NEURO STEP 1

3) Papez circuit**

-how info is transferred from short to long term memory

Spinal Cord and associated tracts $$$TEP

"Legs (Lumbosacral) are Lateral in Lateral corticospinal/spinothalamic tracts" *Dorsal columns are organized as you are, with hands at sides, Arms outside, legs inside

1) How Neurological exam helps with localization**

Temporal Profile + Anatomical Localization = Pathophysiological Process

Hordeolum**

-Acute bacterial infection of the sebaceous glands -painful pustule formation and lid lump -Tx: drain and topical ocular antibiotic to lash line if injection suspected

Apraxia

-a motor planning problem to make sounds

Acetaminophen***

-analgesic

Classic Epidural Hemotoma MRI

-convex or lens

1) Components of the pupillary exam**

1) Exam both pupils in room li

Uvea

= Iris, Ciliary body, and choroid

2) Perform a standard opthalmologic examination**

A) Visual Acuity Technique: 1) one eye followed by the other 2) measure sc and cc then ph 3) measure near visual acuity 20/20 20/40 etc. if VA<20/400 follow this order if continous negative 1) Bring chart closer 2) CF (count fingers) 3) HM (hand motion) 4) LP (light perception) 5) NLP (no light perception) = dead eye 4) Color vision test -use isochromatic plates, color sorting techniques, red desaturation (if one eye sees more grey then other there is red desaturation) 5) Contrast Sensitivity -differentiate different shades of grey using pelli-robson charts best indicator for MS 6) Visual Fields -Confrontation - peripheral vision** 1) cover eye and ask to see something in periphery -Tangent screen-peripheral vision -Goldman - peripheral -Automated perimetry 7) Confrontational campimetry -look at face or two fingers to test facial recognition -test standard 5 degrees 8) Amsler Grid -test standard 10 degrees -test the retina -automated - -peripheral vision B) External Eye: 1) Face-comon innervation with eye-Hutchinson sign 2) Orbit - look for protosis (forward displacement of eye) 3) Ductions = monoculary movement test eye movement* 4) Versions = binocular, simultaneous conjugate movements in same direction* 5) Vergences = binocular, simultaneous, disconjugate movements (convergence reading) * 6) Superior muscles intort and inferior muscle extort 7) Lids a) ptosis (dropping of lid) b) retraction = scleral show inferiorly c) lagophthalmos = inability to close lids d) Entropian = inward turning of eye lid e) ectropion = outward turning of eye lid f) trichiasis = lashes rubbing against cornea 8) Lid Margins = inflammation, mass lesion, madarosis (loss of eyelashes), test CN 7 see if can close eye C) Conjuctiva and Sclera 1) Conjuctiva: a) Palpebra = lid margin to fornix b) Forniceal = in fornix c) bulbar = anterior sclera to the limbus -look for inflammation , color, vasculature 2) Vessels a) conj vessels = superficial b) superficial episcleral plexus vessels = straight c) deep vascular plexus = dark purple vessles D) Cornea E) Anterior chamber: blood in eye = hyphema infiltrate = hypopyon Cells and Flare = signs of inflammation Flare = can see beems of light Anterior chamber depth: very important to avoid angle closure glucoma attack, gonioscopy (gold standard), do not dilate F) Iris 1) color shape of pupil, dilation, adhesion G) Angle -site of aqueous drainage-need gonioscopy to visualize H) Lens -opactiy in lens = cataracts -slit lamb exam needed to determin location I) Pupil -size, shape, reflexes, RAPD- relative afferent pupillary defect -aniscocaria = unequal pupils means either a structure problem with iris or problem with EFFERENT problem J) Intraocular pressure -tonometry = measures pressure needed to deform cornea -normal IOP is 10-21 mmHg K) Posterior segment undilated = disc and macula dilated = all the way to the ora serrata -media, disc, macula, vessels, periphery

Anterior Segment and Posterior Segment

Anterior Segment anterior to the lens, contains aqueous humor -contains tear film, conjuctiva, cornea, iris, angle, lens, ciliary body Posterior: -anything behind the lens -contains vitreous, retina, optic nerve

encephalitis and Meningitis**

Causes: -enteroviruses is most common> arbovirus (west nile, La crosse encephalitis) S/S (just encephalitis) -Fever and Altered level of consciousness** (confusion and crazy behavior)** , focal or generalized seizures, aphasia, ataxia, hemiparesis, involuntary movements PE: -parotitis = mumps encephalitis in unvaccinated -Flaccid paralysis = west nile -maculopapular rash = west nile -tremors of eyelids, tongue, lips, and extremetites = St. Louis or West Nile -Hydrophobia, areophobia, paryngeal spasms and hyperactivity = rabies -grouped vesicles in a dermatomal pattern = varicella zoster Labs: -CT/MRI, EEG, CSF, Serum electorlytes and osmolarity, Urine osmolarlaity LP: -Enteroviruses -> CSF: RT-PCR -HSV1 and 2 -> CSF: RT-PCR -arboviruses-> CSF & Serum: virus specific IgM & IgG Exception/Caveats: -enterovirus in stool or throat isnt diagnostic -focal findings on MRI/CT/EEG is HSV encephalitis until proven otherwie -WNV IgM may persist for a year

Suprachiasmatic Nucleus $$TEP (part of the hypothalamus)

Circadian rhythm. You need SLEEP to be CHARISMATIC

3) Projections of the lateral lemniscus**

Contains axons from the: 1) cochlear nucleus 2) Superior olivary nucleus 3) Nucleus of the lateral lemniscus -travels withing the dorsal lateral pons to the inferior colliculus (MIDBRAIN [mesencephalon])

Anterior Nucleus $$$TEP (part of the hypothalamus)

Cooling, parasympathetic. Anterior nucleus = Cooling = A/C

Disc

Disc Pallor -need a full workup -can be tumors and many other diseases Disc swelling -papilledema

Frontal Lobe lesion $$$TEP

Disinhibition and deficits in concentration, orientation, and judgement. Reemergence of primitive reflexes

6) Higher Order visual processing

Dorsal visual stream goes to parietal lobe and determines " Where is it" Ventral visual stream goes to temporal lobe and determines the "What is it"

9) Differentiat an anxiety disorder from mood disorders**

GAD: -worry -anxiety -muscle tension -GI distress BOTH: -difficulty concentrating -fatigue -irritability -psychomotor agitioanton -sleep distrubrbance MDD: -depressed mood -andhedonia -worthlessness -suicidal ideation

Disease-Specific Findings**

Helps with the WHAT

CNS and PNS origins ***$$$TEP

Neuroepithelia in nerual tube => CNS neurons, ependymal cells(inner linings of ventricles), oligodendrocytes, astrocytes Neural crest => PNS neurons and schwann cells Mesoderm=> Micoroglia (like Macrophages and Muscle)

T4 Dermatome $$$TEP

Nipple T4 let the teat pore

9) Two forms of axonal degeneration**

Retrograde = toward cell body

Progressive muscular atrophy**

Secondary to motor nerve cell degeneration with secondary muscle atrophy -only LMN

Light Reflex Pathway

She didnt talk about it but make sure you know it from lab

Homunculus $$$TEP

Topographic representation of motor and sensory areas in cerebral cortex Distorted image is due to certain body regions being more richly innervated and thus having ↑ cortical representations

Rule VIII: Use highly localizing signs***

UMN: Babinski, Pronator Drift-> CNS LMN: Fasiculations, arreflexia -> PNS A sensory level -> CNS (spinal cord)

Nucleus Solitarius $$$TEP

Visceral Sensory Information (taste, baroreceptors, gut distention), CN VII, IX, X

Rooting Reflex $$$TEP

a baby's tendency, when touched on the cheek, to turn toward the touch, open the mouth, and search for the nipple

Supratentorial

above the tentorium cerebelli

5) Describe the auditory radiations***

axons from the medial geniculate nucleus traveling to the anterior transverse temporal gyrus

Subthalamic nucleus lesion $$$TEP

contralateral hemiballismus

Superior Rectus

elevation, adduction, intorsion, -superior division of CN III

Periorbita

eye socket -lines the bones of the orbit and is continues with the 1) Peristeal layer of dura 2) Pericranium on external sufurce 3) Orbital septa 4) Fascia of extra-ocular muscles 5) Fascial sheath of eyeball

C4 Dermatome $$$TEP

low collar shirt

raphe nuclei location

medulla, pons, midbrain

Venous Drainage of eye

via sup and inf ophthalmic veins into the cavernous sinus. Blood is finally drained into internal jugular vein.

T7 Dermatome $$$TEP

xiphoid process

Plantar Reflex $$$TEP

Dorsiflexion of large toe and fanning of other toes with plantar stimulation Babinski sign- presence of this reflex in an adult which may signify a UMN lesion

1) Describe levels of the meninges $$$TEP

Dura mater (most superficial) -though, thick external fibrous layer -derived from mesoderm Arachnoid mater -thin intermediate layer -compressed against the meningeal dura -archnoid traveculae- spider web tissue -derived from neural crest Pia Mater -delicate internal highly vascular layer -adherent to the brain and spinal cord -derived from neural crest -CSF flows in the subarachnoid space -Epidural space is the potential space between the dura mattur and skull containing fat and blood vessels

5) Schizophrenia DSM***

Dx: -2 or more present (1 must be 1-3) for at least 1 month period (Criterion A the active phase) with signs persisting for at least 6 months , causes a dec in level of function at work, relationship, or self-care, must rule out other causes. Positive Symptoms (mostly)*** 1) Delusions -fixed, false belief such as paranoid, grandiose, jealous, erotomanic, somatic 2) Hallucinations -sensory experience with NO corresponding stimulus can be auditory>visual> tactile, olfactory, gustatory 3) Disorganized speech -incoherence, derailment, looseness of associations, thought blocking, neologisms (made up word), echolalia(repeat question rather than answering ) 4) Grossly disorganized (manifests as deficts in self-care) or catatonic behavior (3 or more of the following: stupor, catalepsy, mutism, waxy fleibility, posturing, mannerism, sterotypiy, agitation, grimacing, negativism) 5) Negative symptoms **** -affective blunting (dec emotional expression) -avolition (lack of motivation to engage in social activities) -apathy (lack of interest in engaging in social activities) -anhedonia (lack of pleasure in activities) -alogia (decreased speech output) Cognitive Symptoms: -problems with executive functioning, deficits in working memory, deficits in attention and focus Facts: -1/100 people 1:1 M:F ratio -primary relative means 12% chance of develop schizo -both parents means 40% chance to develop -Monozygotic twin = 50% chance to develop -AOO in men = late teens and early 20s -AOO in women = late 20s and early 30s -155 billion dollar cost per year

4) Major Depressive Disorder** (Pathophys, tx, and DSM-5 dx)

Dx: -Depressed mood (can be irritability in child) or diminished interest/pleasure -Plus 4 additional sympotms (SIGECAPS) for 2 weeks nearly day SIGECAPS S- sleep changes I - diminished interest or pleause G- excessive Guilt E- low Energy C- loss of concentration A- appetite or weight changes P- psychomotor (movement) slowing or agitation S- Suicidal thoughts or actions Children vs adults: -kids dont verbally express feelings/depression as well, can be more irritable, low frustration tolerance, temper tantrums, somatic complaints, hallucination, and social withdrawal, less suicide attempts, less melancholic sysmptoms, less sleep and appetite issues, more heterogeneous in children, decline in school perfomance Mental Status Exam Recurrence is very common, 40-70% within 3-5 years, highest risk within 4 months of symptomatic improvement, must treat fully Tx: 1) SSRI -for moderate to severe -one year process -continue for 6-12 months during asymptmatic period (continuation phase) -Prescribe therapy always 2) CBT -work on cognition (thoughts) work on cognitive reconstruction , mood (feelings), and behavior (actions) with behavioral activation -can decrease suicidality 3) Interpersonal therapy for adolescents (IPT-A) -adapted for adolescents 4) Fluoxetine -best choice in pediatric populations 5) Atypical/Non-SSRI antidepressents -usually no better than placebo for children 6) TADS study showed combo tx of fluoxetine and CBT for depression in peds is optimal tx****

Dementia with Lewy Bodies (DLB)***

Dx: -Subcortical dementia = impaired executive cognitive function, memory retrival, slower processing, visual hallucinations + 2 of 3 of: extrapyramidal features (bradykinesia, rigidity, resting tremors), fluctuating cognition, visual hallucinations -REM-sleep behavior disorder, RLS, -second most common degenerative dementia -faster progression and shorter survival Tx: -respond well to cholinesterase inhbitiors -balance their dopamine levels

2) Elicit the appropriate historical elements to dx and tx depression in the elderly**

Dx: -collateral can be a helpful tool**** -PHQ-2 only asks 2 questions. Are you less interested or sad -PHQ-9 the diagnostic test, less than 5 = remission you are aiming for a lower score -asks the 2 questions from PHQ-2 plus about sleep, energy, appetite, feeling of failure, trouble concentrating, moving/talking slowly, thoughts of being better off dead -4 steps to asking about suicide 1) Break ice (people with depression have thoughts of suicide) 2) Identify presence of a plan (do you have a plan) 3) Expand in detail (gun, knife, rope, OD) 4) Establish intent (do you feel like you would do it) -MiniCog is a screener (repeat 3 words, draw clock with specific time, ask for the 3 words again) if remember they pass if only get 1 or 2 words need to get clock right to pass. -MoCA = diagnostic test, depressed pts will put little effort (not the case for dementia) and depressed patient will respond after prompt dementia still wont remember -Check thyroid levels, vitamins, anemia, and infections with blood work -Imaging not routinely done

2) Utilize the nernst equation to calculate the diffusion potential for a single monovalent ion**

Eion = RT/ZF ln Ion (out) / Ion (in) for a postive charge -if calculating for a negative charge its Ion(in)/Ion (out) -For K+ the nernst equation Equals to -65.8 mV and that is the typical membrane potential of the cell -Shows the importance of appropriate K+ levels -Nearst equation doesnt do permeability -Goldman-Hodgkin-Katz equation does

Epilepitform**

Epileptiform = spike and wave complexes, sharp waves, polyspikes (not all sharp or spike waves are epileptiform -abnormal brain signal that could lead to a seizure

Episcleritis and Scleritis**

Episcleritis = focal inflammation of episclera tisue, blanches with neosynephrine Scleritis = inflammation of slcera, with blue hue of underlying choroid Tx: urgent referral

Seperation Anxiety Disorder

Excessive anxiety over separation from home or whom attached, must last 4 weeks and begin before age 18.

5) Describe spatial and temporal summation of post-synaptic potentials***

Excitatory response: -opening channels pereable to Na+ increases Na+ influx leading to depolarization (NON-SELECTIVE CATION CHANNELS) -Examples are Glutamate and Acetlycholine ionotropic receptors which open non-selective channels which are equally permeable to Na+ and K+ however drives membrane potential to 0 which ends up depolarizing cell this is called EXCITATORY POST-SYNAPTIC POTENTIAL (EPSP) Inhibitory Response: -no neurotransmitters that directly only open ionotropic K+ channels, but some can open GPCRs selective K+ channels (will be slower) -Ionotropic GABA and glycine receptors trigger opening of Cl- channels, causing hyperpolarization cuz influx of Cl- -Inhibitory post-synaptic potentials Temporal Summation: -Thicker dendrite = faster rate less resistance -Longer length constant = faster rate -Temporal and spatial summation is ultimately having enough EPSP over IPSP in the same location at the same time to reach threshold to fire an AP **

Degenerative Disc Disease**

Extramedullary/Compressive: 1) Herniated disc 2) Vertebral pathology (Spondylolithesis/Stenosis) 3) Tumor (Metastatic, meningioma) 4) Epidural abscess (IS pt, IV drug user, TB (potts), known infections) 5) Epidural hematoma -Can have a trauma that may have damaged the spinal cord, must CT, stablize, reduce swelling, call surgeons Intramedullary: 1) Vascular infarct (upper thoracic, aterry of adamkiewicz) 2) Inflammatory/ Infection (MS, post-infectious, infectious, polio, syphilis, HTLV-1) 3) Cord masses 4) Deficiencies (Vit B12, copper defiency) 5) Genetic (familal spastic paraplegia, adrenomyeloneuropathy) 6) Syringomyelia (dilated central canal)

Extramedullary vs Intramedullary **

Extramedullary: -radicular pain -somatotopic organization -early sacral sensory loss = lateral spiothalamic tract -spastic leg weakness (corticospinal tract) Intramedullary: -poorly localized burning pain -somatotopic organization -spares sensation in perineal and sacral areas -later corticospinal tract

rubrospinal tract

Extrapyramidal motor tract responsible for motor input of gross postural tone, facilitating activity of flexor muscles, and inhibiting the activity of extensor muscles -neurons in midbrain project to the contralateral spinal cord via the rubrospinal tract, the axons travel in the lateral funiculus and influence lateral LMNs -Limb flexors

Paramedian Pontine Reticular Formation Lesion $$$TEP

Eyes look away from side of lesion -inability to look toward side of lesion

5) Flumazenil** (FLUFFY MUZZLED DOG)

FLUFFY MUZZLED DOG = THE AGITATED, FORGETFUL, SHAKING (SEIZURE AND DIZZINESS), WITHDRAWING DOG (PRECIPATES WITHDRAWAL SYMPTOMS OF BZDS) -BZD receptor antagonist MOA: -competitive antagonist at BZD receptor on GABA-A -blocks effects of BZDs and Z drugs doesnt reverse barbiturates, ehtanol, general anesteics or opiods PK: -IV Uses: -NOT USED AS AN ANTIDOTE FOR BZD usually** -reverese sedative effects of midazolam after anesthesia SE: -Amnesia -Agitation, dizziness, N, may precipitate BZD withdrawal -seizures -BBW**

Holoprosencephaly ** $$TEP

Failure or left and right hemispheres to seperate -usually occurs during weeks 5-6 -Range from cleft lip/palate to most sever cyclopia -associated with trisomy 13 and fetal alcohol syndrome MRI shows monoventricle and fusion of basal ganglia Causes= genetic(loss of function mutation in SHH (sonic hedgehog signaling pathway) and teratogens Outcome = intellectual disability

General defintions of motor systems exam**

Fasciculations- muscle spasms, either benign vs pathologic, contraction of a motor unit, random or involuntary and dont result in movement of joint Deep Tendon Reflexes- stretch reflex is main dx indicator of UMN or LMN Babinski-extensor plantar response: -oppenheimar sign = firmly stroke the medial tibial surface (extendeds) -Gordon sign = firm compression of lower calf causing extends -Chaddock sign = stoking the skin beneath the lateral malleolus causing extension (+ babinski) Clonus- most common in ankle, indicates lesion in descending motor neurons Superficial reflexes- response to scraping to the skin, present or absent , utility is that they are decreased or abolished by UMN lesions = no longer flex Muscle tone- hold on to knee and move it around, a flaccid leg will drag on bed = LMN, a spastic leg will jerk upward = UMN Spasticity-characterized by velocity-dependent increase in muscle tone, associated with corticospinal tract, seen with catch and release, UMN Flaccidity or hypotonicity- decrease muscle tone due to alpha motor neuron loss, limb feels like a rag doll, LMN

Layers of Eye

Fibrous layer -sclera (posterior 5/6)= maintain shape, provides attachement for extra-ocular muscles, covered by conjunctiva (palpebral and bulbar forming conjunctival sac) -Cornea (anterior 1/6) = most significant refractive media of ey, avascular, highly sensitive Vascular layer: -choroid (posterior 5/6) = pigmented layer located between sclera and retina, provides oxygen supply for the photoreceptors fed by the cilary branches of ophthalmic a. -ciliary body (processes and muscle)=produce aqueous humor giving nutrients to cells on retina and cornea, -Iris Neural layer: -retina (optical, cilary, and iridial parts) = optic part is the outer layer is pigmented epithelium, inner layer contains light receptive nerons, cilary and iridal part are non-visual portions

Anterior Cranial Fossa**

Frontal lobe of brain 1) cribiform plate 2) Crista galli (attachement for falx cerebri) 3) Frontal crest 4) Orbital plate of frontal bone 5) Lesser wing of sphenoid 6) Optic canal (optic nerve, opthalmic a.) 7) Anterior clinoid processes

2) Assess and triage eye and orbital trauma**

Functional Aspects 1) Visual acuity 2) External adnexa (lids, brow, nodes/bony margins) 3) Alignment and motality 4) Visual fields 5) Pupillary exam 6) Anterior segment (conj, cornea, AC) 7) Posterior segment (retina, choroid, ONH) 8) Intraocular pressure

3) Neurochemicals that are responsible for arousal and sleeep

GABA: -primary inhibitatory ( sleep-promoting neurotransmitter), inhibits the arousal system -located in the preoptic area (VLPO) Orexin (Hypocretin) -wake promoting neuromodulator -synthesized in lateral and post. hypothalamus -stablized sleep-wake status (narcolepsy) -also apart of appetitie, motivation, substance abuse -hypocreetin neurons innervate ascending arousal system and cerebral cotex -promotes wakefulness, -maintains motor control, - inhibits REM sleep by activating histamine, NE, 5-HT Adenosine: -by product of breakdown of ATP -this is where the methylxanthines work (caffeine and theophylline) -interacts closely with Dopaminergic systems -caffeiin is an andensoine antagonists causing you to produce adrenaline and boost DA

4) Describe how information is processed in the retina and brain***

Ganglion Cells: 1) On center = respond most strongly when lights on the center of the receptive field 2) Off Center = respond most strongly light restricted to the area surrounding the center of their receptive field *Weaker response if light is on and off center for both types

3) categories of cerebral hypoxa including types of cerebral infarction**

Global Hypoxia: -due to hypotension (watershed/borderzone first affected at MCA-ACA and MCA-PCA areas) -cardiac arrest (diffuse hypoxia) -hypoexmia (diffuse hypoxia) Focal Hypoxia: -vascular occlusion-> focal hypoxia in specific vascular territory -vascular disruption with focal hemorrhage -red dead neurons (acute neuronal necrosis) -foamy macrophages in subacute infarct

4) Describe the pathologic findings in the retina with HTN, diabetes, and macular degeneration**

HTN: -endothelial damge leads to edema and exudate -arteriolosclerosis with vascular wall changes (red-> copper-> silver) -infarcts - nerve fiber layer and choroid Diabetes Mellitus: -affect lens, iris, cilliary body -vessels -retinal microangiopathy 1) non-proliferative -early sage, dilated, leaky BVs, edema and ischmeia 2) proliferactive- breaches internal limiting membrane, neovascularization, and significant hemorrhaging and scarrign Age-related macular degeneration (ARMD) -leading cause of blindness in elderly -loss of central fovea -drusen-> damaged RPE -atrophic (dry) to exudative (wet in range) -Atrophic - atrophy/RPE and photorecpetor degeneration, excess BM material -Exudative (wet) - neovascularization, hemorrhage and scarring, detached Retinal pigment epithelium (RPE)

HINTS testing**

Head Impulse Nystagmus Test of Skew INFARCT = Impulse normal, fast-phase alternating, refixation on Cover test -these mean central etiology and can be dangerous -if normal head impulse test = eyes dont slip off = central etiology -benign HINTS with acute dizziness rules out stroke 1) Head Impulse test = focus on nose and move their head, then start moving head fast if normal = central problem 2) Nystagmus: Changing in direction = central Doesnt change in direction = peripheral 3) Skew test -cover one eye and eye moves = refixation + test = central - test = peripheral

Posterior Nucleus $$$TEP (part of the hypothalamus)

Heating, sympathetics. Destruction -> poikilotherm Heating = Posterior Nucleus = HotPot

Nondominant parietal cortex lesion $$$TEP

Hemispatial neglect syndrome (agnosia of the contralateral side of the world).

2) Unique way CNS responds to injury such as inc intracranial pressure and major types of herniation**

Hernination: -Inc cerebral edema -> areas of least resistance -3 main patterns 1) Transtentorial (uncal) -ipsialteral CN3 palsy -ipsialteral peduncle/corticospinal tract injury = contralateral hemiparesis -ipsialateral posterior cerebral artery compression (infarction of occipital lobe) -hemorrhage and necrosis of rostral brainstem (Duret hemmorrhage) 2) Subfalcine (cingulate) -displacement of cigulate gyrus from one hemusohere to the other, under falx cerebri 3) Cerebellar tonsillar -cerebellar tonsils are displaced into the foramen magnum and the medulla is compressed

C3 Dermatome $$$TEP

High turtleneck shirt C3,C4,C5 keep you alive

Lateral Nucleus $$$TEP (part of hypothalamus)

Hunger. Destruction -> anorexia, failure to thrive (infants). Stimulated by ghrelin, inhibited by leptin Lateral injury makes you Lean

Trinucleotide repeats**

Huntington's, Fragile X, Friedreich's Ataxia, -repeats are normal but if they increase above a certain number they can cause disease -CAG repeats = polyglutamine = neuronal death -Repeats may increase with each generation leading to earlier onset

4) Different types of hydrocephalus**

Hydrocephalus= increased size of ventricle system due to increased CSF, see increased head size Hydrocephalus ex vacuo= atrophy or lesion of brain due to hydrocephalus Congenital vs. acquired hydrocephalus: -Congenital = genes or events in fetal development -Acquired = after birth due to trauma or disease Communication vs. non-communicatiing: -Communicating= CSF can flow beetwen ventricles, problem at the arachnoid villi leading to inc in CSF in ventricles -Non-communicating = CSF flow is obstructed, commonly at cerebral aqueduct Normal pressure hydrocephalus = increased CSF but CSF stays normal

2) Locate hypothalamic nuclei and fiber bundles within medial-lateral and rostral-caudal regions of the hypothalamus***

Hypothalamus divided into 3 regions: 1) Anterior -SCN, SON, and PVN 2) Tuberal -VMH (ventral medial nuclei of hypothalamus) receives input from the amygldala -Arcuate nucleus -contains nuerons which produce molecules which are released into median eminence, directly dorsal to the median eminence and transported to anterior pitutary gland. include dopamine and GHRH 3) Posterior Mammillary nuclei - important in long term memories 2 Major fiber bundles in hypothalamus 1) Medial forebrain bundle (MFB) 2) Dorsal longitudinal fasiculus (DLF) -

Stages of Anesthesia

I: Induction; the period between administration of anesthesia and loss of conciousness II: Maintenance; the period after loss of consciousness and during surgery III: Emergence; waking up after stopping adminstration Kids get gas (slower), adults get IV for induction (faster) Adults and kids get inhalation during maintenance cuz more control Emergence= N/V given 5-HT3 antagonists to treat, tachycardia and hypertension, shivering give meperidine

Etomidate**

INTRODUCING INTIMIDATOR=ETOMIDATE INTRODUCTION STAGE -POTENTIATE CHLORIDE CURRENT THROUGH GABAa RECEPTOR -STABILIZIES CV (give to heart problem pts.) -ALTERNATIVE TO PROPOFOL IF THEY HAVE CV ISSUES MOA: -GABA-A -non-angelsia need fentyl -minimal CV and respiratiry effects Uses: -induction and maintenace -procedural sedation -Pts with HYPOTENSION SE: -CAN CAUSE NAUSEA -injection site pain, myclonic movements

Spinal cord-lower extent $$$TEP

In adults, the spinal cord extends to the lower border of L1-L2 Subarachnoid space [Which contains CSF] extends to lower border of S2 vertebrae Lumbar puncture is usually performed at L3/L4 or L4/L5 [Level of the cauda equina] KEEP ALIVE GO BETWEEN L3 and L5

L4 Dermatome $$$TEP

Includes patella "Down on L4s (all fours)"

2) Common indications and contraindications for LP **

Indications: -Diagnostic: 1) Infections: Meningitis/encephalitis 2) ICH: Subarachnoid hemorrhage 3) Inflammatory diseases: MS, NMOSD, GBS, Sarcoid 4) Neoplastic: Carcinomatous and lymphomatous meningitis -Therapeutic 1) Pseudotumor cerebri 2) Intrathecal medications Contraindications: -Absolute: infected skin over needle entry, unequal pressure between supratenetorial and infratentorial level, seen on CT scan -Relative: Inc Intracranial pressure, coagulopathy, brain abscess Indications of Brain CT scan Before LP: -above 60 -IS -known CNS lesions -seizure within 1 week of presentation -abnormal level of consciousness -focal findings on neuro exam -papilledema seen on physcial exam, with clinical suspicion of elevated ICP -suspected SAH in awake and alert patients with neurologic exam -diagnose any significant intracranial mass effect that might be present

Common causes of Seizures**

Infancy and childhood: -prenatal or birth injury -inborn error of metabolism -congenital malformation Childhood and adolescence: -Idiopathic/genetic syndrome -CNS infection -Trauma Adolescence and young adult: -Head trauma -drug intoxication and withdrawal (causes acute syndromes seizures, not epilepsy) Older Adult: -stroke -brain tumor -acute metabolic disturbances (causes acute symptoms not epilepsy) -neurodegenerative

Lateral Medullary (Wallenberg) Syndrome**

Infarction of PICA resulting in: - contralateral: sensory deficits of trunk and extremities -ipsilateral: sensory deficits of the face as the primary deficits, ataxia of limb, nystagmus, nausea, vertigo, horner's syndrome, dysphagia, hoarseness, vocal cord paralysis

Innervation/Arteries/of the Dura

Innervation of Dura: 1) Supratententorial innervation: -dura of anterior and middle cranial fossa floor and posterior cranial fossa roof are innervated by the Trigeminal Nerve (CN V) and all 3 branches V1, V2, V3 2) Infratentorial Innervation -dura of the posterior cranial fossa FLOOR are innervated by C2, C3 cared by the Vagus and Hypoglossal (CN XII) nerves Arteries of Dura: -middle meningeal arteries (from Maxillary) -Intracranial cerebral arteries (within the subarachnoid spaces) -Small meningeal arteries (from external carotid branches)

6) Describe how the hypothalamus regulates different parts of the autonomics**

Input: -visceral info from ANS especially from the solitary nucleus (contains special receptors for blood temp and salt concentration) -sensory info received by hypothalamus from the reticular formation -emotional info received from the limbic system especially from the septal nuclei, amygdala and hippocampus Output -hypothalamus influences blood pressure, HR, temp, digestion via the ANS via the hypothalamospinal tract (from MFB) projects to the IML of the spinal cord -neurons in several hypothalamic nuclei, especially in the paraventicular nucleus project directly to the preganglionic sympathtetica and parasympathetic neurons and indirectly influence these neurons via the reticular formation -Horner's syndrome is due to to damage of the hypothalamospial trac in the pons, medulla or spinal cord

LGN lateral geniculate nucleus $$$TEP

Input: CN II, optic chiasm, optic tract Sense: Vision Destination: Calcarine Sulcus LATERAL = LIGHT

MGN (medial geniculate nucleus) $$$TEP

Input: Superior olive and inferior colliculus of tectum Senses: Hearing Destination: Auditory cortex of temporal lobe Medial = MUSIC

VLN (Ventral Lateral Nucleus) $$TEP

Input: basal ganglia, cerebellum Senses: Motor Destination: motor cortex

Ischemic brain disease/stroke $$$TEP

Irreversible damage begins after 5 minutes of hypoxia [Due to glucose dependence] Most vulnerable: 1. Hippocampus (vulnerable hippos) 2. Neocortex 3. Cerebellum 4. Watershed areas Ischemic HYPOxia = HYPOcampus most vulnerable

13) Two main types of strokes**

Ischemic vs Hemorrhagic strokes: -Ischemic = blockage of arteries (artherosclerosis) -Hemmorrhagic = rupture of arteries

1) Explain how ion diffusion generates membrane potentials**

K+ = IN, higher concentration IN and is pumped IN Na+ = OUT, higher concentration OUT and is pumped OUT -Na/K conteracts the natural diffusion of ions to maintain the membrane potenital -accumulation of positive charge extracellularly and the charge of negative charge intracellarly causes a potential voltage difference called the diffusion potential -Cell membrane is much more permeable to K+ than to Na+ resulting in a more negative membrane potential (-65)

Amygdala (bilateral) lesion $$$TEP

Kluver-Bucy syndrome - disinhibited behavior (hyperorality, hypersexuality, hyperphagia) -HSV-1 enchephalitis

SBMA

Labs; Inc HnA1c, CK midly elevated EMG is supportive for dx -definitive diagnosis by genetic confirmation of AR expansion -treatment is supportive (PEG-tube), cramps medication, PT/OT

Lacrimation

Lacrimal gland => Canaliculi => Lacrimal sac => Nasolacrimal duct -tear flow = superior lateral to inferior medial to inferior nasal meatus -From CN VII parasympathetics (greater petrosal nerve) ultimately reach lacrimal nerve (CN V1) to be distributed to the gland

dural venous sinuses $$$TEP

Large venous channels that run through the periosteal and meningeal layers of the dura. Drain blood from cerebral veins and receive CSF from arachnoid granulations. Empty into internal jugular vein.

Brainstem: (Pons and Medulla) Lesions*

Lateral Pons/Medulla -the lesion involves anterolateral pathways and the spinal trigeminal nucleus on same side -it causes loss of pain and temp* sensation in the body opposit the lesion, and loss of pain and temp sensation in face on the same side as the lesion** Medial Medulla: -the lesion involves the medial lemniscus, causing contralateral loss of vibration and joint position sense

Anterior Inferior Cerebellar Artery (AICA) stroke $$$TEP

Lateral pons-->vomiting, vertigo, nystagmus, paralysis of face, decreased lacrimation/salivation/taste from anterior 2/3 of tongue, ipsilateral decreased pain and temp on face, contralateral of pain and temp from body, ipislateral horner syndrome , ipsilateral sensorineural deafness, vertigo middle and inferior cerebellar peduncles-->ataxia, dymetria -affects the facial nucleus, vestibular nuclei, spinothalamic tract, spinal trigemnial nucleus all part of the lateral pons, sympathetic fibers, and labyrinthine artery -Lateral pontine syndrome -Facial droop means AICAs pooped

9) Describe the lateralization of function in the cerbral cortex**

Left Hemisphere = usually dominant for language ( 94% of the time) Right Hemisphere = visual spatial processing, and facial recognition

Mitochondrial mutations**

Leigh syndrome-MT-ATP6 gene -intellectual disability and other neurological signs -Often fatal -exclusively inherited from the mother -usually due to de novo mutations

Blood supply of basal ganglia

Lenticulostriate vessels off of the middle cerebral artery

X-Linked Recessive**

Lesch-Nyhan - HPRT1 -Sons will have symtoms and daughters will not (extra X) -tendency to self-injury and intellectual disability -Males are unlikely to have offspring

Optic Chiasm**

Lesions of chiasm characteristically cause bitemporal scotoma*** -Central or peripheral -superior or inferior -rarely monocular -Will always respect the vertical meridian Symtoms: 1) Bitemporal VF defect 2_ Junctional scotma 3) Paracentral bitemporal 4) Incongruous homonymous hemianopi 5) hemichiasm

Cranial nerve Nuclei $$$TEP

Located in the tegmentum portion of brain stem [Between dorsal and ventral portions] Midbrain = Nuclei CN III, IV Pons = Nuclei CN V, VI, VII, VIII Medulla = Nuclei CN IX, X, XII Spinal Cord = Nucleus of CN XI Lateral Nuclei = Sensory [aLar plate] --- Sulcus limitans Medial Nuclei = Motor [Basal Plate]

Posterior Inferior Cerebellar Artery (PICA) stroke $$$TEP

Location of lesion: -Lateral medulla (symp fibers, vestibular nuc, spinal trigeminal nuc, lat corticospinal tract, and nucleus ambiguus), inf cerebellar peduncle Symptoms: -Vomiting, vertigo, nystagmus -Limbs face have dec pain and temp sensation -dysphagia, hoarseness, dec gag reflex -IL horner's syndrome -ataxia, dysmetria Lateral medullary (Wallenberg syndrome)

1) Explain the differences between upper and lower motor neurons***

Lower Motor Neurons: -innervate muscles -CN motor nuclei: III, IV, V, VI, VII, IX,X,XI,XII, and ventral horn of spinal cord -lesions cause flaccid paralysis (decreased tone, reflexes) regardless of state of other components of motor system -final common pathway Upper motor neurons: - terminate on lower motor neurons -pyramidal neurons in precentral gyrus, red nucleus, superior colliculus, vestibular nuclei, retricular nuclei -Lesions cause spastic paralysis (increased tone, reflexes) which can only be seen if lower motor neurons are intact

Comparison of NMJ disorders**

MG: -lot of ocular and bulbar -DTR is normal -Normal CMAP -Autonomics are negative -Slow RNS are decrement (fading -Fast RNS are decrement (fading) -Paraneoplastic 20% of the time -Autoimmune LEMS: -not so much ocular and bulbar -dec DTR -autonomics + -dec CMAP -Decrement Slow RNS -Facitation of Fast RNS -Paraneoplastic 50% of the time -Autoimmue Botulism -lot of bulbar affects -dec DTR -autonomics + -dec CMAP -decrement of slow RNS -Facitation of fast RNS -Paraneoplastic no -autoimmune no

9) Esketamine*** (NASAL ANTI-SUICIDE DRUG)

MOA: -S-isomer of ketamine; may also inhibit re-uptake of DA PK: -nasal spray -no apparent onset latency period Uses: -treatment-resistant depression/suicidality* -avoid suicide attempt SE: -sedation and dissociation (ketamine); patients are monitored

7) Suvorexant ** ORX ANTagonists

MOA: -blocks oX1R and OX2r (which are orexin receptors that promote wakefulness) -differs from other hypnotics by blocking wakefule circutray Uses: -insomnia -schedule 4 drug SE: -similar to BZDs (next day drowisness is major SE), some mild cataplexy (half asleep half awake and cant move your limbs)

1) Explain proprosed mechanism of efficacy of lithium for the tx of mania and describe major adverse rxns***

MOA: -no AP generation -no apparent psychotropic effects -No known MOA SE: -Acute effects = tremors, mild N/D, polyurea, polydipsia, weight gain -Long-term effectus = neuphorgenic DI, hypothyroidism -Toxic OD = serum levels >2, risk increases with renal impaiment, dehydration, presents with N/V/D, arrhythmias, and neurologic effects confusion, ataxia, seizures

Succinylcholine***

MOA: Depolarizing neuromuscular blocker -phase I block due to high affinity for Nm and resistance to AChE PK: -onset is 1-2 mins, given IV bolus -Duration dpendent on plamsa BuChE activity, to test a patients BuVChE you do a dibucaine number: >80 = wild type and 7-12 min duration 50-60 = heterzygous atypical = 15-25 min duration <25= homozygous atypical = 8 hours duration SE: -hyperkalemia in patients with extra-junctional Nm receptors like children with MD, or burn patients, or paralysed -bradycardia (high doses = tachycardia) -increased intracranial/gastric/ocular pressure -malignant hyperthermia -Myalgias- Use NSAIDs -anaphylaxis

1) List the categories and functions of eye movements**

MR = adduction LR= abduction SR= elevate, intorsion, adduction IR = depress, extorison, adduction SO= Intorsion, depression, abduction IO= extorsion, elevation, abdcution 1st action is primary, 2nd action is secondary, and third action is teriary Resistance to movement: 1) Viscosity - doenst want to initially move, overcome by high frequency neural burst called PULSE-velocity command 2) Elasticity- wants to go back, overcome by sustained neural activity called STEP-position command by the common neural integrator Gaze stabilization = stay focused even when you move your head done by 1) Vestibular mediated reflex (VOR) = vestibular system senses head rotation 2) Visual mediated reflex = optokinetic response and smooth pursuit Gaze shifting= want to look at something new done by 1) Saccades 2) Vergence

7) Demyelinating diseases**

MS -disease of oligodendrocytes -ataxia and double vision -myelin basic protein may be attacked Guillain- Barre disease: -sudden and severe weakness -rare -autoimmune disease involving schwann cells -increased incidence with Zika infections

Inferior Orbital Fissure

Maxillary nerve (infraorbital, lacrimal, and zygomatic branches), communication between inferior opthalmic vein and pterygoid plexus

Menignitis vs encephalitis

Meningitis: -inflammation of the meninges -clincal evidence of meningeal signs -abnormal CSF examination Encephalitis: -inflammaotry porcess of the brain -clinical evidence of parnchymal dysfunction -abnormal or abnormal exam

Prophylaxis for Meningitis**

Meningococcal: -may be helpful if came in contact with dx patient give them rifampin, ciprofloxacin, ceftriaxone H. influenzae; -may be helpful if come in contact with dx patient give them rifampin Pneumococcal conjugate vaccine is HUGE

5) Id types of glia, their origin and function** $$$TEP

Microglia: - mesodermally derived, they invade the CNS during development -Macrophages of the CNS -respond to infection or injury in brian -HIV infected microglia fuse to form multinucleated giant cells in CNS Astrocytes: -most common glial cell in CNS -derived from the neural tube (neuroectoderm) -Marker = GFAP -regulate extracelular milieu taking up extra K+ and extra neurotransmitters -regulate the BBB -respond to injury with reactive astroglisis -express large amounts of glial fibrillary acidic protein -glycogen fuel reserve Ependymal cells -ciliated simple columnar form that line the ventricles and central canal of spinal cord -apical surfaces covered in cilia (circulate CSF) and microvilli (CSF absorbers)

1) Understand the anatomy of the middle and inner ear related to hearing **

Middle -ossicles -tympanic membrane Inner 1) cochlea-sensory -tontopically organized -organ of corti rests on basilar membrane, basal turn (high freq) , and apical turn (low freq) -oval/round windows 2) Cochlear duct -outer/inner hair cells -endolymph -stria vascularis (battery for inner ear) one of the most metabolic active structure in body 2) cochlear nerve Mechanisms: -area ratio of TM/stapes oval window 17:1 ratio so I can hear small sounds -lever action of ossicular chain = more gain -lever action of curved(conical shaped) TM = more gain -overall its a 30db gain

Cerebellum $$$TEP

Modulates movement, aids in coordination and balance Input: 1) Contralateral cortex via middle cerbellar peduncle 2) Ipsilateral proprecieptive info via inferior cerebellar peduncle from spinal cord Output: 1) Cerebellar cotex is via purkINje cells (alwasy INhibitory)-> deep nuclei of cerebellum -> contralateral cortex vai superior cerebellar peduncle 2) Deep nuclei (lateral-> medial) : Dentate, Emboliform, Globose, Fastigal DON'T EAT GREASY FOODS Lateral lesion: affects voluntatry movement of extremities (lateral structutes), propresity to fall toward (ipsilateral) injured side Medial lesion: -vermis, fastigial nuclie, flocculonodular lobe -truncal ataxia (wide based cerebellar gait), nystagmus, head tilting -gernaly result in bilateral motor deficits affecting axial and proximal limb musculature (medial structures_

Brown-Sequard Syndrome**

Motor Findings: -Spinal shock = intially, primarily flaccid paralysis, spastic paralysis emerges over time -Spastic paralysis in the ipsilateral limbs below the level of the lesion -Flaccid paralysis in the ipsilateral limb at the level of the lesion Sensory Findgings: -ipsialteral loss of fine touch and conscious proprioception -Contralateral loss of pain and temp (often 2-3 segements below lesion)

1) General pathologic reactions of the motor unit**

Motor Unit Components: -anterior horn cell -myelinated axon -NMJ Segmental demyelination = loss of myelin, can cause hypertrophic changes such as onion bulb formation (proliferation of schwann cells) Axonal degeneration = loss of axons Reinnervation ? Myopathy = atrophy of myocytes

Nucleus aMbiguus $$$TEP

Motor innervation of pharynx, larynx, upper esophagus (swallowing, palate elevation), CN IX, X, XI

1) Nerve conduction studies, elctromyography, indications, limitations, and usefulness

NCS(nerve conduction study) /EMG (Electomyography needle part looks at muscles) -extension of PE -tells pathology -not helpful in joint disease, fibromyalgia, CNS, -this helps with LMN system -larger diameter the more myelin the faster the conduction -these studies A and B nerve fibers Nerve Conduction Studies -peripheral nerves stimulated with a controlled electrical stimulus 1) Compound muscle action potential (CMAP) tells amplitude (negative is up, post down) durantion of response, and latency , conduction velocity (>50 UE and >40 m/s LE) -responses are recorded at muscle -G1 on belly G2 on tendon of muscle 2) Sensory NCS: studied antidromatic (opp of anatomy) typically study sural, superficial perneal, ulnar, median, and radial, sensors on the nerve record duration, amplitude, latency 3) Late responses: follow motor and sensory responses, used to study proximal nerve conduction, used for radiculopathy, guillain barre, dyemelyinating neuropatheis , peripheral neuropathy F-waves 4) H-reflex: -used for proximal nerve conduction -helpful in eval of polyneruopathy, early GBs, and S1 neuropathy 5) Repetitive Nerve stimulation: -try to fatigue muscle, see muscle fatigue in MG -U shape response in MG Findings: -Axonal loss = reduction of amplitude, CV normal (70-130%), DL normal, F wave latency is normal, H reflex is normal -Demyelinating = normal amplitude, CV reduced, DL is prolonged, F wave latencies is prolonged or absent, H reflex latencies significantly prolonged or absent, acquired conduction block and temporal dispersion -preganglionic lesions can hide as normal in sensory test due to ganglion -motor nerve conduction in skin: with fall in 1 degree C of skin, the conduction velocity is reduced 1 m/s

4) Practice responding to strong emotion*

NURSE Naming (You sound frustrated) Understanding (It helps me understand where u r coming from) Respecting (you have done everything you can) Supporting (I will be here to help) Exploring (Tell me what you mean) -Develop rapport, address illness and prognostic awareness, focus on symptoms and coping, talk about end of life issues -Emotional openers and emotional closers are things we sometime miss, make sure you address emotion

Neuroeptielial tissue Tumors

Neuroepithelial tissue tumors=> glioma (most common)=> astryocytomas=> pilocytic astrocytoma (grade I) OR Diffuse astrocytoma (3 types) => Astrocytoma (grade II), Anaplastic astrocytoma (grade III), and glioblastoma (Grade 4)

2) Explain how medical conditions can cause many psychiatric symtoms**

Neurological Causes of Mood Disorders: -MS -Trauma -Parkinson's: may present as depression (40-70%) -Stroke: 35% have depression -Endocrine : hyper- and hypothyroidism, addisons disease, cushing (excessive glucocortcoid levels) -Pancreatic carcinoma: 19-75% depression -HIV: 2x more depression than general -Typhoid Fever -Hep -Substance/Meds (there are alot)

Central post-stroke pain syndrome $$$TEP

Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia. -Occurs in 10% of stroke patients.

2) Given muscle biopsy list the histological distinction between neurogenic atrophy and a myopathy and dystrophy***

Neuropathy: -angulated atrophic fibers of both fiber types -group atrophy -fiber type grouping -target fibers Myopathy-Dystrophy -round atrophic fibers -myofiber necrosis -myophagocytosis -degeneration -regeneration -internal nuclie -endomysial fibrosis

5) Nonpharm and pharm tx for depression in the elderly**

Non-Pharm: -Care-giver education and help -activities (social, cognitive, PHYSICAL***) -excercise reduces depression symptoms and should be prescribed for all that are able**** -psychotherapy -co-morbid factors -enhance sensory Meds: -treat for 6 months after symptoms remiss -consider safety, SE, and drug interactions -ease in and out of use -50% respond to 1st line and 1/3 respond to 2nd line -Most common is SSRI (-pram and -tine) (start low and go slow) see GI distrurbances, insomnia, and jitteriness -SNRIs not more efficacies, benefit in chronic px, less GI -Bupropion (Wellbutrin) = activating drug, helps with low activity, smoking cessation, no sexual SEs, no weight gain -Mitrtazapine = sedative, good for insomnics and low appetite pts, alpha 2 antagonist, H1 antagonist -Psycostimulants = (ritolin, adrehal) last line for depressed elders, quick response, -Tricyclic antidepressants = not used anymore too many SE -ECT= not used very often, used in nonresposive in depression, highly effective

3) DDx of acute red eye**

Non-Vision Threatening Disorders: -most common type -Lid disorders = blepharitis, hordeolum, chalazion -dry eye syndrome -conjuctivitis - bacterial, viral, allergic -corneal abrasions (most) -small foreign body -subconjunctival hemorrhage -pterygium Vision Threatening Disorders -orbital cellulitis -scleritis/uveitis -chemical injury -keratitis -acute angle-closure glaucoma -penetrating trauma/cornea perforation -corneal ulcerations

Stroke imaging $$$TEP

Noncontrast CT to exclude hemorrhage [Before tPA can be given] CT detects changes in 6-24 hours Diffusion weighed MRI can detect ischemia w/in 3-30 minutes

Global aphasia $$$$TEP

Nonfluent aphasia w/ impaired comprehension, no repitition. Both Broca's and Wernicke's areas affected.

Broca's aphasia $$$TEP

Nonfluent aphasia w/ intact comprehension, impaired repetiton . Broca's area -- inferior frontal gyrus. ("Bro ca's Bro ken Boca " [boca = mouth in Spanish])

Vertebral disc herniation $$$TEP

Nucleus pulposus (soft central disc) herniates through annulus fibrosus (outer ring); usually occurs posterolaterally at L4-L5 or L5-S1. -nerve is usually affected below the level of the herniation (L3-L4 disc spares L3 but involves L4) -Compression of S1 nerve root leads to absent ankle reflex

Medial inferior pontine syndrome**8

Occlusion of the paramedian branch of basilar artery; -characteristics- ipsilateral to lesion: cerebellar ataxia, nystagmus, diploplia, paralysis of conjugate gaze to side of lesion -contralateral to lesion: hemiparesis UE/LE, impaired sensation

4) Anatomy of a chemical synapse**

Oligodendrocytes myelinate axons in CNS Schwann cells myelinate axons in PNS 1) Presynaptic terminal: 2) Synaptic cleft 3) Postsynaptic membrane 4) Neurotransmitters Types of Synapses: 1) Axodendritic= most common, axon terminal -> dendrite 2) Axosomatic = axon -> cell body 3) Axoaxonic = axon -> axon 4) Dendrodendritic = dendrite -> dendrite (rarest)

2) Describe the clinical presenstations and pathologic features of tumors of the eyelid, conjunctiva, uveal tract, and retina**

Orbit: -encapsulated vs. unencapsulated -most are vascular: Cavernous hemangioma (adults and encapsulated) Capillary hemangioma (infants, unenapsulated) -lacrimal glandm (peleomorphic adenoma and salivary glands) -some malignant (lymphoma and rhabdimyoscarcoma) Eyelids: 1) Basal cell carcinoma -locally invasive, lower lid, medial canthus 2) Sebaceous carcinoma- (meibomian glands, glands of zeis, caruncle) elderly, mimmizs chalazion, blepharitis, pemphigoid, upper lid, local invasion via pagetoid spread, lymph nodes, hematogenous, lipid/fat stains**, 20% mortality Conjuctiva: 1) Squamous cell carcinoma- solar damaged conjunctiva, some HPV 16/18 connection, near libus, can invade cornea, preceded by dysplasia, treat locally 2) Pigmeted lesions- nevi so congentital, benign, be concerned if extends to cornea and/or involves fornix or palebra conjunctiva 3) Melanocytic neoplasms-primary acquired melanosis (PAM) without atypia (begnin), PAM with atypia = pre-cancerous (melanoma precursor), PAM with severe atypia is worse 4) Melanoma- middle age to elderly, better prognosis than uveal melanomas, metasize to lymph nodes (parotid, submandiblular, pre-auricular) Uveal tract 1) Melanoma- most common primary intraocular malignancy in adults seen in caucasions at age 50-60 -choroid or ciliary body is worse than iris -80% at 5 years -spreads via emissarial canal, vortex veins, and hematogenous to the LIVER -Spindle cells, mixed, epithloid (lateral extension is seen with worse prognosis), rarely invade optic nerve Retina: 1) Retinoblastoma- neuronal orgin(retina) , #1 primary intraocular malignancy of peds, genetic (RB gene), -encephaloid, uni/mulitfocal, necorsis, and Calcifaction -Flexner-wintersteiner rosettes (photoreceptor differentiation) -prognosis: smaller than 3 mm better, vitreous seeding (bad), >50% of globe (bad) , optic nerve invasion (bad) , extraicular extension (bad) , -5 year 95% survival -metasized to bone marrow, brain, local spread to orbit -hereditary - 25% early onset, bilateral, multiffocal -sporadic -75% late onset, unilateral, unifocal

5) Common infections that affect the anatomic compartments of the eye**

Orbital Cellulitis: -bacterial, fungal, viral, parasitic -can lead to sinus infections -life-threntening if spreads to the brain

2) Temazepam** (PASSED OUT KIDS, FOR A MEDIUM AMOUNT OF TIME teMAzepam ENDS IN PAM)

PASSED OUT KIDS AFTER EATING PANCAKES Uses: -insomnia = medium acting

Lateral Medullary (Wallenberg) Syndrome

PICA infarct → NVNV, ipsilateral Horner's, loss of pain/temp to ipsilateral face & contralateral body,CN X loss (dysphagia, hoarseness, ↓ gag reflex) -ataxia due to lesion of the inferior cerebellar peduncle and cerebellum

1) Benefits of palliative care*

Palliative care = extra layer of support by an interdisciplinary team. -focus on physcial, emotional, and psychological symptoms and spiritual distress Offer: -Symptom managenment -Coping -Advance care planning -Legacy work -increases patient experiences -Increases or keeps survival the same -Decreases or keeps cost at the same time

1) Explain the pahtophys of sexual development in males and females including paraphilia's****

Paraphilia: -recurrent intense sexualy-arousing fantasies/urges/behaviors involving nonhuman objects, suffering or humiliation of onself or one's partner, children or other nonconsenting persons -If it causes personal harm or risk of harm to others it is a paraphilic disorder

Dorsal Midbrain lesion $$TEP

Parinaud syndrome- vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus -stroke, hydrocephalus, pinealoma

2) Reduplication and infolding of dura partitions and which dural sinuses pass through each partition**

Partitions-extension of the dura mater that seperate the cerebellum hemispheres from one another and the cerebrum and the cerebral hemispheres 1) Falx cerebri-divides the two cerebral hemispheres 2) Tentorium cerebelli-roof for the cerebellum 3) Falx cerebelli-divides two cerebellum hemispheres 4) Diaphragma sellae- opening for infundibulum and roof for pitutory gland

4) Explain how normal anxeity can become pathologic** ON TEST

Pathological anxiety: 1) Excessive fear/anxiety response that is impairing or distressing rather than helpful or manageable and/or 2) Occurs in contexts or with response to cues where there is no real threat

1) Describe common pathophys of seizures**

Pathophys: -result due to imbalance between excitation and inhibition produces runaqay excitation and hypersynchrony within neural circuits -generalized epilepses see epielptogenic networks are widely distrubuted involving thalamocortical structures bilaterally -focal epilepsies networks involve neuronal circuats in one hemisphere -epileptogenesis = sequence of events that converts a normal neuronal network into a hyperexcitable network -paroxysmal depolarization shift (PDS) = cellular events in which rapidly repetiitve APs are not followed by the usual refractory period, thereby generating a prolonged membrane depolarization -a interictal spike is caused by PDSs in large numbers of neurons that are synchronixed such that each involved neuron generates one PDS at the same time -An electroclinical seizure occurs when large numbers of neurons in one or more brain regions are repeatedly genertating PDSs in sustained repetetivve firing with synchronization

Thought Content

Perceptions: -Illusions= misperception of a stimulus -Hallucinations= perception in the abscence of a stimulus Delusions: fixed, false beliefs not congruent with societal norms or culture -Paranoid -Grandiose -Erotomanic-famous person loves me -Nihilistic- feel like they've done something bad, or they are dying -Bizarre- stranges thoughts Assessing the risk of harm -sucidial ideation -thoughts of harm to self -homicidal ideation -thoughts of harm to others Obsessions-recurrent, intrusive, uncomfortable thoughts Cumpulsions- behavior in response to obsession Phobias Recurring themes: -self-esteem, hopelessness, worthlessness, guilt, anxiety, somatic preoccupation

Sexual masochism disorder**

Period of recurrent fantasises/urges/behaviors involving in the act of being humiliated, beaten, bound, or otherwise made to suffer causing impairment/distress for more than 6 months

1) General awarness of gait exam**

Phases of Gait: 1)Stance Phase (anytime foot on the ground) 60-65% -Heel strike -Foot flat -Midstance -Push off 2) Swing Phase (anytime foot is in the air) -Acceleration - Midswing -Deceleration -Left and leg will touch the ground at the same time = double support 20-25% , this gets longer as you get older (also have shorter strides, broader base, dec pelvic rotation, dec velocity) Step length = length of one step Stride length = 2 consective steps Cadence = # of steps per minute Stride time = time of full gait cycle (heel strike to heel strike)

Brain stem - dorsal view (cerebellum removed) $$$TEP

Pineal gland - melatonin secretion, circadian rhythms Superior Colliculi - conjugate vertical gaze center Inferior Colliculi - auditory -Your eyes are ABOVE your ears, and the superior colliculus (vision) is ABOVE the inferior colliculus (auditiory)

11) Prenatal and postnatal development of the brain**

Postnatal: -400 g -> 1400 g -Myelination continues until age 20 -environmental stimulation affects morphology, a lack of stimuation will have permanent effects on synapse and cognitive functioning

2) Describe primary and secondary motor cortex areas***

Primary motor cortex: -in the precentral gyrus in the frontal lobe -contributes to the corticospinal and corticobulbar tracts (Upper motor neuron) Secondary Motor cortex: -involved in planning movements -projects to the primary motor cortex -contributes to the corticospinal tract -Made up of the supplementary motor cortex and premotor cortex -Supplementary motor cotex = receives info from the basal ganglia via the Ventral Anerterior nucleus of the thalamus -Premotor cortex = receives info from the cerebellum via the Ventral Lateral (VL) nucleus of the the thalamus

6) Management of Glaucoma and MOA of Topical and systemic glaucoma***

Prostaglandin analogues all end in -prost -MOA: INCREASE UVEOSCLERAL OUTFLOW*** Topical Beta-Blockers; end in -olol MOA: REDUCES SECRETION OF AQUEOUS HUMOR (yellow caps) -Betaxolol-Beta-1 selective less pulmonary effect but less ocular hypotensic effect*** (Blue cap) Alpha-2 Agonist (Purple cap) MOA: decreased aqeuous production and increased uveosleral outflow -SE: DONT USE IN PEDS and elderly cuz of CNS suppression, hypotension, and apnea*** Carbonic Anhydrase Inhibitors MOA: decrease aqeuous production -many SE Glaucoma Lasers: POAG = laser trabeculoplasty laser applied to travecular meshowrk but requires open angle to apply PACG= laser iridotomy used for closed angle

3) Delineate each of the comonents of the dorsal column -medial lemniscus pathway and the modalities by this system**

Pseudounipolar neuron: -peripheral process extends into skin -central process extends into spinal cord -Large cell bodies = fine touch and propioception -small cell = pain and temp 1) Spinal cord: -pseudoumipolar cells -central process of pseduounipolar cell extending into spinal cord with the dorsal roots -axons from the DRG ascend ipsilaterlly within ghe spinal cord as dorsal columns (gracile and cuneate fasciculi) 2) Myelencephalon (Medulla) -axons in the dorsal column will terminate on the gracile and cuneate nuclei in the caudal medulla -axons from the gracile and cuneate nuclei cross the midline as internal arcuate fibers in the medulla -these axons will ascend as the medial lemniscus to the entral posterior lateral VPL nucleus of the thalamus 3) metencephalon -medial lemniscus 4) Mesencephalon-medial lemniscus 5) Diencephalon (Thalamus) - axons traveling via medial lemniscus and terminate at the VPL -Axons from VPL in the thalamus project via the posterior limb of the internal capsule to the post central gyrus of the cerebral cotex 6) Telencephalon (cerebral cortex) -fine touch and conscious proceprimetion for the body

Horner syndrome symptoms

Pupillary constriction (miosis) and dilation lag Ptosis Anhydrosis (Decrease sweating)

5) Amitriptyline** (TRICYCLE)

RECESS THEME -Abandoned Tricyclic= Tricyclic antidepressants (no longer used) -Inhibit NET and SERT (reuptake of serotonin and NE) (Smiley ball and compass ball) -Reserved for unresponsive depression -Used for neuropathic pain (FAT KID) , migraines (BELL) , OCD (DWIGHT) , depression, -SE: Sexual dysfunction (Rejection of advances), anticholerngic effects (dry mouth, constipation, blurred vision, urinartion reterention), contraindicated in elderly, block H1 histamine receptors can cause sleepiness, increased appetite, orthostatic hypotension, MOST COMMON CAUSE OF DEATH is fatal cardiac arrhythmias due to block of fast Na+ channels and wide QRS complex and torsades twisted streamer (NEED Na+ bicarb therapy) 3 C's Cardiac, COMA (antihistamine effects), Convulsions (induce seizures due to affect on GABA-A receptors), and serotonin syndrome (bunch of smiley balls) MOA: -Inhibit NET>SERT, also antagonize H1, a1, M receptors Uses: -MDD, pain syndromes - migraine prophylaxis, Diabetic neuropathy SE: -sh*t ton and OD can be lethal -OD is neurologic (agitation/delirium) prior to loss of consciousness; seizures, AND Cardiovascular like severe tachycardia, hypotension, and arrhythmias

8) Nueronal migration**

Radial Migration: -from ventrical surface to pia mater Tangential Migration -going parallel with pia mater Radial Migration in Cerebellum -post-natal -granule cells migrate from an external layer near the pial surface to a deeper layer after birth -developing cerebellum occurs in the first year of life Radial Migration in Cerebral Cortex -six layers of the cerebral cortex are built inside-out -neurons that will reside in deeper layers of the cerebral cortex are born and migrate first, -new neurons must migrate past exisiting neurons Tangential Migration in the Cerebral Cortex -GABAergic interneurons migrate tangentially into the olfactory bulb via the rostral migratory stream and to the cerebral cortex from the medial ganglionic eminence (MGE)

Reticular activating system (midbrain) lesion $$$TEP

Reduced Levels of arousal and wakefulness (coma)

sucking reflex $$$TEP

Reflex that causes a newborn to make sucking motions when a finger or nipple if placed in the mouth

Retina

Retinal Detachments: 1) Non-rhegmatogenous- due to fluid accumulation in subretinal space, retina intact, -seen with trauma, tumors and severe HTN 2) Rhegmatogenous- primary defect, full thickness tear, often requires surgery

Neostigmine**

Reversal agent for non-depolarizing neuromuscular blocker

2) Idiopathic Intracranial Hpertension**

Risk factors: females of childbearing age, obese 456xc(rapid gain) , meds (tetracyclines, growth homone), systemic disorders (hypoparathyoidism) S/S: -Headache similar to migraine -severe bilateral pain, nothing seems to help -pain is often excebated by position changes worse when laying down and exertion** -Pulsatile tinnitus** -horizontal diplopia** -sustained vision loss that may be perminent** -retro-ocular pain or pain w/ eye movement* -pulsating throbbing or dull pain PE: -papilledema** (means elevated pressure) -bilareral 6th nerve palsy Dx: 1) Neuroimaging : MRI >> CT 2) LP opening pressure >25*** 3) Ophthalmologic elevation, dilated fundoscopic exam Tx: -weight loss main thing* -Carbonic anhydrase inhibitors (acetazolamide)* -loop dieurtics (furosemide) -Surgery for those to perserve vision or severe pain* : CSF shunting, optic nerve sheath fenestration

3) Define the function of each of the retinoreceipient nuclei**

Rods= low light environments, found outside the fovea, responsible for peripheral vision -rhodopsin 498nm Cones= color detection and fine visual descrimination, requires lots of light, fovea is packed with cones -3 types of cones 1) Blue cones 420nm 2) Green cones 534nm 3) Red cones 564 nm

1) Discuss the basic clinical criteria for psychiatric emergencies ***

Role of ED: -Rapid stabilization of acute crisis -to ensure the safety of the patient, staff, and the community -Most patients who kill themselves have a mental illness -Any disturbances in thoughts, feelings, or actions which warrant immediate psychiatric intervention -leading to a threat to self or others -occur due to chronic psychiatric illness, adverse med reaction, intoxication (or withdrawl), victims of trauma, consequence of medical illness -Examples: suicidial ideations, violence, panic attack (severe anxiety), abuse, tardive dykinesia -Considerations: sudden onset, hx of organic illness, confusion, VH, and disorientation to time and place, substance use disorder, symptoms unrelated to specific psychiatric dx, poor response to psychiatric tx, ab vital signs, ab labs, coexisting signs of specific organic illness, sudden fluctuation of psychiatric symptoms

Subdural hematoma $$$TEP

Rupture of bridging veins (crescent shaped) -can be acute or chronic -seen in shaken babies at times -predisposing factors: brain atrophy, trauma -Crescenbt shaped hemorrhage that crosses suture lines -can cause mideline shift -Left is acute right is chronic

Epidural Hematoma $$$TEP

Rupture of middle meningeal artery (branch of maxillary artery) often secondary to skull fracturem(commonly at pterion (thinnest part of lateral skull) ) -lucid interval and rapid intracranial expansion under systemic arterial pressure -> transtentorial herniation, CN III palsy -CT shows lentiform hyperdense blood collection not cossing suture lines

Bacterial Meningitis**

S/S- fever and chills, headache stiff neck and back, abdominal and extremity pains, nausea and vomiting., photophobia, altered level of consciousness, seizures Triad = Fever, headache, and meningismus but dont usually all present at once** -Extra-cranial infection can also show arthrits (gonorrhea), non-blanching petechiae and cutaneous hemorrhages, and severe vascular collapse -Exanthem = erythematous macular-> petechial-> purpuric -Infants= irritability or lethargy, full fontanel, poor feeding, elevated or subnormal temp, vomiting, altered consciousness, seixures, Kernig (pull up head and knees will come up) and Brudzinski (lay down and bring up leg resistance or pain is + ) PE: -Kernigs sign, brudzinski sign, nuchal rigidity, papilledema, CN 3,4,6,7 abnormalities Labs: -CT maybe, -LP: cell count, protein, glucose, bactieral culture and gram stain -Bacterial culture, cyrpto antigen, histo antigen, fungal culture, herpes panel, enterovirus DNA, adenovirus DNA, WNV IgM, and IgG, AFB culture Tx: -start off with empirical antibiotics with dexamethasone, then once get dx specify antibitiocs, and continue for typically 7-21 days -dexamehasone only helpful when given immediatlely with antibiotic and usually only helpful in pneumococcal mengigitis

2) Congenital Glaucoma**

S/S: Epiphora = tearing Photophobia= light sensitive Blepharospasm = sqeezing eyes** Tx: SURGERY -Trabeculotomy is for a cloudy cornea** -Goniotomy is for a CLEAR cornea**

Orbital fracture

S/S: globe dystopia (displaced globe) (enophtlamos), diplopia restricibe (double vision) , (low upper lid) blepharoptosis (mechanical), hypoesthesia (decreased sensation) (infra-orbital n.) Tx: -postural drainage -no asprin, nsaids and blood thinners -no nose blosing -antibiotics -nasal decongestion -oral steriods Sx: -when dystopia of globe (enopthalmos, 2mm or greater) -restrivtive diplopia -defect >50% of orbital wall

Screening Tests

SBIRT: Screening, Brief Intervention, and Referral to Treatment -for substance use disorder AUDIT-C DAST-10

3) Describe the steps involved in synaptic vesicle exocytosis and the roles of synaptogmin and SNARE proteins in vesicle fusion**

SNARE proteins: -mediate fushion -V-SNARE- vesicle associated, synaptobrevin -T-SNARE- targer associated , syntaxin -Munc18-1 - helps SNARE complex stay intact and place -Synaptotagmin= Ca+ sensor and fusion clamp, releases the SNARE and allows vesicle to fuse with presynaptic membrane -Complexins - helps synaptotagmin clamp the SNARE complex -SNARE proteins can cause spontaneous fushion, to prevent this the SNARE complex is clamped by complexin and synaptotagmin*** -Without synaptotagmin and complexins the vesicles would automatically bind to presynaptic membrane -Ca+ causes synaptotagmin to virtually become inactive leading to fushion

Ventromedial nucleus $$TEP (part of the hypothalamus)

Satiety. Destruction (craniopharyngioma) -> hyperphagia. Stimulated by leptin VentroMedial injury makes you VeryMassive (

2) Describe the neurobiological components of psychotic disorders***

Schizophrenia: -primarliy related to dopamine dysregulation -mesolimbic system = inc dopamine causing + symptoms -prefrontal cortex = dec DA causing - symptoms -other possibilities are inc serotonin, inc NE, dec GABA, dec Glutamine receptors -Drugs used to treat Dopamine actually block dopamine which treat the + symptoms but worsen the - symptoms, also will cause an increase in prolactin due to less DA -Dopamine can be produced nigrostriatal and tuberoinfundibular system

Schwann Cells and Oligodendrocyes $$$TEP

Schwann cells = PNS Olgiogendrocytes = CNS COPS = CNS -> Oligodendrocytes, PNS -> Schwann Cells Olgiodendroglia -derived from the neural tube (neuroectoderm) -fried egg appearance histologically -injured in MS, progressive multifocal leukoencephalopathy (PML), leukodystrophies -each ogiodendryocyte may melinate 30 axons Schwann Cells -only myelinates one axon -important in axonal regeneration -derived from neural crest -Injured in guillain-barre syndrome

Dorsal Motor Nucleus $$$TEP

Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI. CN X

S2, S3, S4 dermatomes $$$TEP

Sensation of penile and anal zones S2,3,4 keep the penis off the floor

Migrainine treatment**

Serotonin: -inhibits trigeminal pain pathways -5HT1B = selective vasoconstriction (want to stimulate) -5HT1D = reduces activity of painful pathways, rescues release of CGRP (want to stimulate) Dopamine: -D2 plays a role -Dopamine antagonism of DA receptors relieves migraine pain, N/V -meds work best if you diagnosis -medication overuse HA use meds too much so get headache seen with all migraine meds but highest risk for opiodis/barbs, aspirin-APAP caffeine combos, medium risk = triptans, lowest risk is NSAIDs -Midrin is a combo of analgesic, dichloralphenazone, and isometheptene

3) How the hypothalamus uses the ANS to respond to short term stress**

Short term stress: - the ANS is used -the hypothalamus projects to the IML via the hypothalamospinal tract -adrenal medulla receives direct input from the preganglionic neurons in the intermediolateral cell column and releases catecholamines into the general circulation Long Term stress: -endocine system is used -Hypothalamic neuroendocrine cells release CRH into the median eminence. -CRH is transported to anterior pituratiry gland via the portal vessels where it stimulates the release of ACTH -ACTH stimulates the release of steroid hormones from the adrenal cortex

Autosomal dominant mutation**

(Amyotrophyic lateral sclerosis) ALS-SOD1 gene -degeneration of motor neurons and is utimately fatal -10% are famililal

Medial midbrain (Weber's) syndrome

* Symptoms: *Ipsilateral eye down and out (CN III), contralateral hemiparesis of body and face (CST).* Lab Values: ** Pathophysiology: *PCA infarct.* Treatment: *

Tongue Development $$$TEP

- 1st and 2nd branchial arches form anterior 2/3 (thus sensation via CN V3, taste via CN VII). - 3rd and 4th branchial arches form posterior 1/3 (thus sensation and taste mainly via CN IX, extreme posterior via CN X). -Motor innervation by CN XII Hyoglossus = retracts & depresses tongue GENIglossus = PROTRUDES tongu (GENIE sticks his tongue out) Styloglossus = draws side of tongues inward -CN X innervates palatoglossus = elevates posterior tongue for SWALLOWING Taste = 7,9,10 Pain= 5 V3, 9,10 Motor = 10, 12

Biological Basis of Depression

- The downregulation of receptor density better correlates with therpeutic effects more than the amount of Neurotransmitters Neurotrophic theory: -depression is due to suppression of neurogenesis due to a deficency in BDNF, monoamines are known to regulate BDNF expression, so monamine deficiency could lead to BDNF defiency

Dystrophinopathies***

- X-linked, largest gene in humans - Gene product dystrophin links actin to muscle cell membrane - Duchene (early, no dystrophin, out of frame mutation,) - Becker (late, some dystrophin, cardiac, inframe mutation) - Difference in two diseases depends on whether or not the mutation shifts the reading frame - LOWER weakness mainly, can progress to upper and eventually respiratory - Calf pseudohypertrophy, lumbar lordosis, Gower's sign, gross motor delay, scoliosis, toe walking and waddling gait - Diagnosed by genetic testing

Posterior Cerebral artery stroke $$$TEP

- affects occipital lobe -symptoms are contralateral heminaopia with macular sparing, and alexia without agraphia (dominant hemisphere)

2) Wilson Disease**

- completely treatable -can present with any type of movement phenomenology S/S: -Kayser-Fleisher rigngs Labs: -low ceruloplasmin, elevated copper in urine -MRI = Panda sign -liver biopsy Tx: -includes chelators

vertebral osteomyelitis

- injection drug users, sickle cell anemia pts, and those that are immunosuppressed are at highest risk - *most common pathogen = staphylococcus aureus* -Night pain** - *tenderness to gentle percussion over spinous process is most impt clue* - *WBC MAY BE NORMAL OR NOT ELEVATED BUT PLATELETS WILL BE ELEVATED AS MARKER OF INFLAMMATION/STRESS* - *ESR - ELEVATED > 100mm/h) - *MOST SENSITIVE DX TEST = MRI* - *HIGH SUPSICION FOR PT w/VERTEBRAL OSTEOMUYELTIIS SHOULD BE PRESENT IF THERE IS PT W/HX OF INJECTION DRUG USE OR RECENT DISTANT SITE INFECTION (UTI) - *Tx = Long Term IV antibiotics*

7) Dectoricate Posturing Lesion**

- lesion above the level of the red nucleus loosing the corticospinal tract and disinhibiting the rubrospinal tract leading upper limb flexor posterioring

3)Brain Abcess**

- rare and often mixed pathology -Frontal> temporal> frontoparietal> parietal>cerebellar> occipital Stages: 1) Early cerbritis = perivascular inflammatory response surround a developing necrotic center with profound edema 2) Late cerebritis = well-formed necrotic center peripheral fibroblasts and neurovascularity 3) Early capsule formation = peristent cerebritis with well developed layer of fibroblast, neovacularity and reactive astrocytes 4) Late capsule formation = thickening of capsule and large amounts of reactive collagen S/S: -duration of S/S for more than 2 weeks -triad: fever, headache, focal neurologic deffictis -N/ V, nuchal rigidy, papillaedema Workup: -medical emergency -WBC -leukocytosis -LP contraindicated -CT/MRI Tx: -Antibiotics= Cefotaxime/Ceftriaxone + Metronidazole + vanco if suspected Staph -Surgery for large abscess >2.5 cm, neuro decline, or loss of consciousness

4) Describe common presentations of acute hemorrhagic strokes**

- severe headache that develop suddenly -thunderclap headache -neck pain -confusion and drowisness -loss of consciousness at onset of symptomsis strongly correletd with an aneurysm** -N/V -seizure

3) Analyze risk factors for suicide and attempted suicide in children with mood disorders**

-#2 leading cause of death in 10-34 year olds Risk factors -Hx of suicide attempts, cormorbid psychiatric disorders, impusivity and aggression, availability of lethal agents, exposure to negative events, Fhx of suicidal behavior, percieved burdensomeness, thwarted belongingness -Firearm most common method, > hanging/suffocation>poisoning -Copycat suicide -Safety planning: 1) avoid second attempt of suicidie by preparing for home environment, leave contact information

retinotopic arrangement

-1 million RGC per eye -5 degree = 12% of cells -10 degere = 1/3 of ganglion cells

Dementia Causes**

-1) Alzheimer disease = #1 - 2) Vascular dementia: caused by CVAs - stepwise progression -3) Lewy body dementia: visual hallucinations, parkinsonism - 4) Frontotemporal dementia: personality changes - Parkinson's disease - Creutzfeld-Jakob prion disease -Seems to be reduced with increased years of education and increased with TBIs

2) Risk factors and epidemiology for epilepsy**

-1/26 Americans will develop epilepsy in their life Risk factors: -non compliance or inadequate AED treatment -sleep deprivation -fever or systemic infection -metaboli and electolyte imbalance -stimulant/ other proconculsant intoxication -concussion and or closed head injury -hormonal variations -stress

2) Fluexetine** (FLY OUT)

-1st Line for MDD, Major anxiety disorders, PTSD, -Helpful for OCD, Bulimia, social anxiety disorder, Premenstrual dysphoric disorder (PDD) -2 month calendars = takes 1-2 months to work at max strength -SE: Sweating daren, hyponatremia, sexual dysfunction (Pam denying Roy) , Weight gain (Fat Roy), Sleepiness (insomnia**) (sleeping Pam), serotonin syndrome=hyperthermia and HTN, with hyperreflexia, and clonus (boucing foot) (happy faces everywhere) and tricycle (SSRI + SNRI+ MAOIs*** can cause serotonin syndrome), withdrawl results in flu symptoms (out with flu) -SSRI MOA: -selective inhibition of 5-HT reuptake by SERT -SERT>>>NET -little action on a1, H1, and M receptors (limits SE) -multiple postsynaptic 5-HT receptor subtypes are stimulated (not wanted overdone) -advantage over older antidepressants are SE are less and less OD, less likely to worsen CV, and less sedating -after 18 months stops working -SE: start immediately (usually go away when therapeutic effects kick in [except sex problems]), -5HT3 = GI complaints (N/V/D) -5HT1A/2A SE = over activition = serotonin syndrome, most common when SSRI+MAOI therapy -5-HT2 receptor related SE= tolerance develops for agitation, extrapyramidal symptoms, initial anxiety and panic attacks, insomnia and no tolerance is sexual dysfunction -Other SE = QT prolongation -Drug interactions with MAOIs and tamoxifen

2) Tension-Type Headache**

-2 of the following = bilateral, pressure-like or squeezing quality (not pulsating), mild or moderate, not aggravated by routine physical activity, no nausea or vomiting, photophobia or phonobobia (not both) Treatment: -Tricyclic antidepressants = amitryptiline -SNRI -Muscle relaxers = tizanidine -Botox -EMG biofeedback -CBT -Relexation, acupunctiure, PT

6) Describe the somatotopic relationships within the somatosensory systems**

-2nd neuron in each system has axons that cross to the contralateral side

7) Microcircuitry and histology of the cerebellar cortex**

-3 cellular layers in the cerebellar cortex 1) Molecular layer = purkinje cell dendrites, parallel fibers from granule cells, climbing fibers from the inferior olivary 2) Purkinje cell layer = 1 cell layer, purkinje cells receive info from granule cells and the inferior olive and then project to deep nuclei 3) Granule cell layer = granule cells receive synaptic input from spinocerebellar tract, vestibular nuclie, pons, granule cells axons synapse on purkinje cell dendrites in molecular layer Microcircuitry: 1) Mossy fibers from many sources terminate on granule cells 2) Purkinje cells receive input from granule cells (parallel fibers) and climbing fibers (orginate at inferior olivary nucleus) 3) Purkinje project to deep cerebellar nuclei 4) Both mossy and climbing fibers have collateral projectons to the deep nuclei 5) Deep cerbellar nuclei project out to the cerebellum

Eating disorders overview**

-3rd most common chronic illness of adolescent females -occur before age of 25 and are typically seen 6th-7th grade -AN have highest mortality among all mental disorders -suicide attempt can be cormorbid condition -Used be seen as a SWAG problem -now we see it as a disease that effects everyone and need further public education Eating disorder workup: -vitals include pulse, BP, current age, height, and weight to calculate an expected body weight

7) Role of cell death in neural development**

-50% of neurons die during development -neurons are dependent on trophic factors for surivial -neurons which do not make correct connections and dont then recieve trophic factors from targets undergo apoptosis -Failure to undergo apoptosis may lead to autism -Overactive apoptosis can lead to microcephaly

Exhibitionistic Disorder **

-6 month + period of recurrent fantasises/urges/behaviors incloving exposure of one's genitals to an unsuspecting stranger -causes significant distress or impairment in social or occupational functioning

Diffuse astrocytoma

-70% of all gliomas -infiltrative tumors in which neoplasma astroyctes migrate into the adjacent brain -these tumors cannot be completly remove tumor = poor prognisis -Grading criteria AMEN Atypia Grade II = diffuse astrocytoma Mitoses Grade III = anaplastic astrocytoma Endothelial proliferation or necorsis is Grade IV = Glioblastoma***

1) Describe the epidemology, common etiologies and risk factors for back pain**

-84% lifetime prevalence -85% will be non-specific musculoskeletal low back pain Risk Factors: -obesity -age -tobacco use -female -strenousus acitivity -sedentary activity -low education -psychological factors

MS**

-900,000 americans and 2.5 mil worldwide -Histology: inflammatory cells , demylination, (loss of blue cells on stain) -Age of onset is 30 yoa -Females -Causes: unknown may be geographic (environment), low vitamin D, viral trigger such as EBV, obesity, higher in tobacco use, complex polygenetic influence -Genetics: twins 20-40%, dizogytic twins 3-5%, patent 2% no relative 0.1%, may be incloving around 200 genes -Major histocompatibility complex on chromosome 6 the HLA-DR2 allele Symtoms** -optic neurits -internuclear opthalmoplegia -upper motor neuron weakness -sensory disturbances -ataxia -tremor -bladder/bowel dysfunction Dx: -McDonald MS Diagnositic criteria: includes clinical, supportive testing, and MRI, can do CSF but not as much anymore -Must have dissemination in TIME and SPACE, meaning it is progressive , and will have Attack then rest, then another flare up very diagnostic** -Must see evidence of progression to differentiate from Isolated syndrome Course: 1) Relapsing remitting = 85% of all cases 2) Secondary Progressive = comes and goes and then complelety progresses 3) Primary progessive = 10% of caes, 1:1 M:F, just purely progressive 4) Progressive Relapsing = 5% of all cases -A common first sign of MS is Reflective Afferent Pupillary Defect, when there is only one symptom it is termed CLINCALLY ISOLATED SYNDROME and must then get a MRI Common Signs of MS: -RAPD -Periventricular scars -Juxtacortical Lesion -Dawson's Fingers -Spinal cord lesions -With Contrast may see open ring scar which may be reletevely new -Internuclear opthalmoplegia Tx: -anti-inflammatory corticosteriods for acute attacks -plasma exchange -symptomatic management Disease Modifying Therapy for Chronic tx 1) Platform therapy: -interferon Beta -Glatiramer 2) Advanced Therapy -natalizumab 3) New Oral Agents -fingolimod, teriflunomide, dimethyl fumurate -alemtuxumab, daclizumab

Cardioembolic Stroke**

-A fib high risk for stroke 5% of all strokes -Patent foramen ovale is low risk of stroke

Duchenne muscular dystrophy**

-A human genetic disease caused by a sex-linked recessive allele; -onset 3-5 -S/S falls, difficulty running and jumping, proximal muscle weakness and neck flexors -characterized by progressive weakening and a loss of muscle tissue. -cardiomyopathy, restrictive PFT -Tx: Supportive, steriods, ASO, wheelchair by 12, shortened life expectancy, predinosione helps delay need for wheelchair

Alzheimer's disease (AD)***

-A progressive disease that destroys the brain's neurons, gradually impairing memory, thinking, language, and other cognitive functions, resulting in the complete inability to care for oneself; the most common cause of dementia. -Memory loss is initial most prominent symptom** -Risk Factors: Age, Genes (PSEN1,2, APP, and APOE) , Lifestyle -Amyloid-beta -Amyloid plaquing occurs long before symptom onset -Tx: -B-secretase inhibitors (early intervention) -antibodies to target AB and amyloid plaques -chlonesterase inhibitors (donepizol, rivastigmine, galatamine) (inc Ach) -Glutamate modulators (memantine) (reduces the Ca flow)

Head Trauma Work up**

-ABCD's -Immobilaization -Neuro exam : GCS, pupils, EOM, motor, sensory, reflexes (DTR, pathologic) , rectal exam -Imaging : full body CT without contrast -GOAL IS TO PREVENT SECONDAY INJURY -Prevent : Hypoxia, hypotension, hypercapnia, seizures, and elevated ICP (manage all of these if they occur)

Myotonic Dystrophy***

-AD, CTG trinucleotide repeat -Frontal balding, testicular atrophy, muscle wasting (no fatty deposits), catracts, cannot release grip (muscle can contract but hard time relaxing) -CK is normal or mildly elevated Labs: EMG, muscle biopsy -genetic testing > CTG repeats -Tx: must treat with early pacemaker/defibrillator cuz cardiac arrhythmias kill them,

Entacapone** (Entrance Capone mobster)

-AL CAPONE GANG -ENTERENCE GUY -PERIPHERAL COMT INHIBITOR (DOESNT CROSS BBB) -COMT WILL CONVERT LEVODOPA TO 3-OMD WHICH ISNT HELPFUL -ENTACAPONE IS HOLDING UP THE OFFICERS TRYING TO SHOOT THE ROBBERS -ADD WHEN PATIENTS HAVE MOTOR FLUCTUATIONS = GANGSTERS ONLY SHOWED UP WHEN THERE WERE motorCARS -Dopamine metabolism (MAO/COMT) inhibitor - when DOPA decarboxylase is inhibited COMT compensates MOA: -reversible inhibitor of COMT, doesn't cross BBB Uses: -prolongs and enhances the effect of levodopa SE: - increases SE of levodopa = dyskinesia, naseua, hypotension, confusion

CN VI*$$TEP

-Abducens -Exits via the SOF -Motor -Somatic motor -emerges ventrally and medially from the junction of the pons and medulla -cell bodies located in abducens nucleus IN pons axons exit the ventral brainstem at junction of pon and medulla and terminate on lateral rectus muscle -does eye movement -CNS region = pons -Lesion= abnormal eye movement

Central retinal artery occlusion

-Acute, PAINLESS, monocular vision loss Retina CLOUDY with attenuated vessels and CHERRY RED spot on fovea [Center of macula] -occulusion of central retinal artery proximal to its bifurcation at the optic nerve -Vision never gets better -STROKE IN THE EYE

3) Describe SUDs and the assoicated intoxication, OD, and withdrawal syndromes**

-Addiction = severe substance use disorder -Intoxication = being impaired -Withdrawal -Tolerance/Dependence DSM-5 SUD: -use in larger amounts or for longer periods of time than intended -unsuccessful efforts to cut down or quit -excessive time spent using the drug -intense desire/urge for drug(craving) -failure to fulfill major obligation -tolerance -withdrawal -activities hobbies reduced given use -TOLERANCE AND DEPENDENCE IS NOT ENOUGH TO DX A SUBSTANCE USE DISORDER -Score of 0-1 no diagnosis, 2-3 Mild SUD, 4-5 Moderated SUD, 6 or more Severe SUD Risk Factors: -Pain, history up to 50%

Sedatives**

-Alcohol -Benzodiazepines -Barbiturates -Downer's -OD and withdrawal can be fatal Intoxication: slurred speech, ataxic gain, disinhibited, impaired judgement -OD = respiratory depresion -Withdraswal symptoms = tremulous, inc BP, inc Pulse, N/V, Diaphoresis, Seizure, delirium tremens (alcohol)

Local Anesthetic drugs

-All end in -caine -All inhibit the Na+ channel -All have similar SE -Difference is mainly in potency -Block peripheral pain pathway by blocking primary afferent nerves -Block A, B, C-fibers A-fibers = largest, myelinated, noxious cold, transmit first pain signals B-fibers= smaller, myelinated, C-fibers= smalles, non-myelinated, for second pain signal (Spine column to CNS) -Type B and C fibers are targeted the most for local anesthetic

3) Compare common personality types that interfere with patient care

-All of these are tough to treat because they dont think they have a problem -Cluster A hard due to fantasy and projection -Cluster B is tough to treat because they act out, splitting, dissociation, devaluation**** -Cluster C is hard cuz passive aggressive, help rejection, complaining -countertransferense dont let them affect you

8) Mirtazapine** (Mirth and Misery Cam)

-Alpha 2 blocker (double alpha candles on jumbotron) leading to increase in release of serotonin (smiley ballons) and compases balloons (NE) - blocks 5Ht-2 and 5HT-3 receptors = retired jerseys (52 and 53) -H1 anti-histamine receptor antagonists (bee swatter) can lead to sedation and weight gain (FAT KID EATING) used for patients with DEPRESSION AND INSOMNIA AND ANOREXIA -SE= WEIGHT GAIN (FAT KID) and SOMNOLENCE -KISS CAM = NO SEXUAL DYSFUNCTION

Divisions of the cerebellar cotex

-Anterior lobe -Posterior lobe -Floculonodular lobe

Circulation*

-Anterior stroke = carotids* EMERGENT -Posterior stroke = vertebro-basilar -If seeing strokes in both the liklihood of its source being the heart is high -If only one not very high probablity ACA = medial portion of the brain MCA = lateral portion of the brain

Lambert-Eaton Syndrome**

-Antibodies agaisnt presynaptic calcium channels of the NMJ S/S: -decreased or absent DTR's -50% paraneoplastic (small cell lung cancer) Dx: -

Neuromyelitis Optica Spectrum Disoder**

-Aquaporin-4 antibodies -Aquaporin-4 is a water channel of CNS tissues, which is more concentrated along optic nerve as well as spinal cord

CNS Depression with Pharm **

-Ascending arousal system = wakeful and is inhibited by H1 antagonists, H3 agonists, Alpha-2 agonists, muscarinic antagonists -Orexin system maintains wakefulness -GABA makes you sleepy

Steppage gait**

-Associated with anterior compartment syndrome -foot drop, : paralhysis of the tibialis anterior -L4 radiuculopathy -neuropathy of deep peroneal nerve -common peroneal nerve injury (compression around the fibular head -compensatory excessive hip flexion -foot slaps the floor -Falls are due to tripping

3) Aripiprazole** (APPROPRIATE in sign)

-Atypical -A 5-HT2A antagonist and D2 AGONIST* -stimulate D2 levels at low levels so actually treats the excess Dopamine with having lower risk of the ESPS side effects -Negative symptoms are still treated with the 5-H2TA antagonists

7) Olanzapine** (ONLY WHISPERING)

-Atypical (second gen) -biopolar disorder and other pscychotic disorders

8) Quetiapine** (QUIET PLEASE)

-Atypical (second gen) -biopolar disorder and other pscychotic disorders

9) Ziprasidone** (ZIPPER ON BLACK DRESS)

-Atypical (second gen) -biopolar disorder and other pscychotic disorders

5) Clozapine** (CLOSET)

-Atypical (second gen) Uses: -for recalcitrant (refractory or persistent) schizophrenia and suicidal behavior in schizoaffective disorder, may take >6 months -reserved due to boxed warning of risk of agranulocytosis (increased risk of infection only 1% of patients) -No risk of EPSE/TD -SE: CV events and seizures -PULLS THE D2 ROPE = BLOCK D2 RECEPTORS -SMILLEY WHEEL OF CHEESE = BLOCKED SEROTONIN RECEPTORS (5-HT-2A) -POSITIVE AND NEGATIVE SYMPTOMS = BOTH WHISPERING INTO EARS -TREAT RESISTANT DEPRESSION = OPENING WINE BOTTLE -TOURETTES = MARIONETTE -H1 ANTIHISTAMINE EFFECTS(SEDATION) = BEE SWATTER -A1 RECEPTOR BLOCKER = ORTHOSTATIC HYPOTENSION -ANTI-MUSCARINIC EFFECTS = TEA PARTY EFFECT(WORST IN CLOZAPINE, BUT STILL MILD -WEIGHT GAIN = FAT PAINTING = -METABOLIC PROBLEMS = BUTTER (DYSLIPIDEMIA) AND CANDY (DIABETES) -EXTRA PYRAMIDAL HAT = EXTRAPYRAMIDAL SYMPTOMS (reduced in second gen) -HYPERPROLACTINEMIA = less milk in nose (not as bad as 1st gen) -NUEROLEPTIC MALIGNANT SYNDROME = EXTRA SPICY CHICKEN BUCKET (less in second gen) -TWISTED STREAMER = TORSADES strictly clozapine: -AGRANULOCYTOSIS = MELTING GRAINULES -DROPPY HEART = CV EVENTS -SHAKING CLOCK = SEIZURES

Corticobulbar tract**

-Axons from pyramidal neurons in layer 5 of primary motor cortex give rise to corticopsinal and corticobulbar tracts -Projections are bilateral with the exception of Facial and Hypoglossal nucleus -unilateral lesion of Motor nucleus of trigeminal, nucleus ambiguus, Vagus, and accessory will not see signs due to bilateral nature -Facial motor nucleus of pons receives partial bilarteral input of the forehead, BUT completely crossed input (neurons of lower face) from corticobulbar tract -Hypoglossal nuclesu receives primarily contralateral input from the corticobulbar tract -Lesion: if left side of face is drooping and they can wrinkle their whole forehead its a corticobulbar tract problem (CONTRALATERAL) , if left side of face is drooping and they cant wrinkle the side of the face with the drooping face its CN 7 lesion (IPSILATERAL)

Non-Benzodiazepine BZD receptor agonists**

-BIND TO THE GABA-A CAB -CHLORIDER = OPEN CL CHANNELS AND INCREASED CL FLOW THUS DEC CNS ACTIVITY -SE NOT AS PRONOUNCED BUT CAN STILL GREATLY AFFECT OLD ADULTS CAUSING COGNITIVE IMPAIRMENT, ATAXIA, AND SOMNOLENCE= OLD GUY KNOCKING OUT STUFF -selective for GABA-A receptors containg alpha-1 subunits -have no anit-anxiety, muscle reflexants, long term memory and learning deficits cuz doesnt bind to alpha-2,3, and alpha -5 -ultra short acting -schedule IV -doesnt supress REM or N3 sleep -recommend 7-8 hours of sleep before taking

Rule V: A bilateral HP= Quadriplegia

-BL Hemishpheres -BL Face, arm, and leg involvement

1) Common effects of neurogenetic mutations*

-Because so many genes are expressed in the brain we see many genetic diseases** -74% of all human proteins are expressed in the brain 1) Inteectual disability-cerebral cortex is affected 2) Hyperkinetic and hypokinetic movement disorders- basal ganglia affected 3) Ataxia- cerebellum affected 4) Deafness - cochlea affected 5) Blindness - retina affected

3 Basic shapes of neurons**

-Bipolar- found in vestibular ganglion, olfactory epithelium, and retina -Psuedo-unipolar-found in DRG and trigeminal ganglion -Multipolar- most common

Depolarizing Agents

-Blockers are Nm agonists that reemble ACh and prevent diffusion -results in fasciculations -depolarization is prolonged and membrane becomes unresponsive called phase 1 block and results in flaccid paralysis -Under certain conditions, convert to phase II block- membrane repolarizes but cannon depolarize due to densensitazation resembling non-depolarizing block -use spontaneous recovery

8) S/S attributable to progressive and visually significant cataract**

-Blurred vision, glare, starbust -2nd sight increased lens thickness -post-subcapsular is more rapid vision decline due to corticosteriods and diabetes

3) Environmental factors that can modulate neurogenetic diseases**

-Brain is very plastic, can alter brain by affecting the environment -Many of these genetic diseases can be variable due to environment - Intellectual disability is a good example of environmental or genetic (700 genes)

Benign Paroxysmal Positional Vertigo (BPPV)**

-Brief episodes of vertigo (< 1 min.) assoc. w/position change; result of degen. of the utricular otoconia -otoliths in semicicular canals (canalithiasis) causes inappropriate movement of endolymp during linear movement -Everything else is normal -Dix-Hallpike will confirm diagnosis , nystagmus in opposite direction when sitting up ,only postivie on affected side Tx with epley maneuver and semont maneuver

Binge eating disorder**

-Bulimia without the compensatory behaviors -can result in diabetes and other metabolic disorders, sleep apnea, depression

Orbital hemorrhage

-Bullulos subconjunctival hemorrhage -proptosis, -corneal exposure -elevated IOP -vascular and neural compromise Tx: -systemic corticosteriods -ocular hypotensive agents (eyedrops) -canthotomy/cantholysis -therapeutic orbital floor fracture

5) Ethosuximide** (ETHOS class)

-CLASS ROOM SETTING = ABSCENCE SEIZURES -3 SPIKES = 3HZ SPIKE WAVE COMPLEX -ETHOS=ETHOSuximide -BLOCKS T-TYPE CA CHANNELS = CLOSED BOTTLE OF CALCIUM CHOCOLATE MILK WITH T Therumus -SE= PAIN, N/V KID GETTING BEAT UP, SLEEPING KID IN CLASS -traditional -Only helpful in abscence seizure -Only targets T-type Ca+ channels Uses: -absence seizures (3-Hz spike and wave) in kids SE: -GI complaints and CNS effects

Other Rare Viral Encephalitis**

-CMV, -EBV -HSV 6 -Caricella-zoster -Herpes B -Influenza -JC virus -Measles -Rabies

2) Recognize presence of facial asymmetry*

-CN 7 palsy aka bell's palsy

4) Recognize the presence of palate and tongue weakness**

-CN 9,10, 12 -CN 9 Does posterior 1/3 of taste, incharge of swallowing, and the GAG REFLEX*** , parotid gland -CN 10: innervates palae and pharyngeal muslces, esophageal motlity, gastric acid secretion, gallbladder emptying, HR, autonomic. PALATE MUSLCES SAY AWWW is to test this CN nothing else. -CN 12: deviates to the affected side, impaired speech, (Genioglossues, hyoglossus, and styloglossus*** DOESNT DO THE PALATOGLOSSUS)

3) Recognize the prescence of ocular misalignment and ptosis**

-CN III Palsy, eye in down and out position with ptosis, with dilated pupil that is unresponsive to light ( loss of pupillary light reflex (could be 2)), loss of accomendation -Know the H test (obliques tested in the medial plane and rectus in the lateral plane) -Superior are IN Inferiors are OUT - Obliques abduct, Rectus Adduct

2) Id the cochlear nuclei (LOCATION AND PROJECTIONS) **

-CN VIII enters the brainstem at junction between the medulla and the pons and terminates on the cochlear nuclei -located dorsally and laterally withing the ROSTRAL MEDULLA -Cochlear nuclei projections (3) 1) to the superior olivary nucleus, 2) to the nuclei of the lateral lemniscus, 3) to the inferior colliculus -most axons orginationg in the cochlear nuclei cross via the dorsal acoustic stria, intermediate acoustic stria, and the trapezoid body -some of the projections stay ipsilateral

1) Id the cranial nerve nuclei, CN, and foramen they exit**

-CN nuclei are organized both in rostrocaudal columns and in transverse cross-sections of the brainstem -Columns: bilateral, discontinuous, organized via functional modalities -multiple CN nuclei exist in each column -Multiple CN can share a nuclei (3 nuclei do this) Neuroectoderm of develping hindbrain: 1) Dorsal Region: -Alar plates = contains columns of sensory nuclei 2) Ventral region: -Basal plates = contain columns of motor nuclei 3) 4th ventricle expands and pushes alar plates laterally 4) Sensory columns are lateral in brainstem*** 5) Motor columns are medial in brainstem** -Sulcus limtans divides the two

9) Determine common meds and systemic conditions that can lead to the development of certain types of cataract**

-CORTICOSTEROIDS and diabetes increase risk***

7) Summary of CSF Lecture**

-CSF is formed in the choroid plexus -CSF is essential for physical protection of the CNS -Physcial and chemical analysis of CSF is essential for dx -MS panel is a misnomer and is better referred to as a CSF protein electophoreisis

3) Flow of CSF through ventricular system**

-CSF is made in the choroid plexus of the lateral, third, and fourth ventricle's -The flow goes from: 1) Lateral ventricles -> through interventricular foramine-> 2) Third ventricles-> through the aqueduct of the midbrain-> 3) Fourth ventricle -> through lateral and median apertures-> 4) Subarachnoid space-> 5) Arachnoid villi of dural venoous sinuses-> venous blood-> 6) Heart and lungs-> arterial blood-> lateral, 3rd, or 4th ventricles

4) Path of CSF**

-CSF is produced by ependymal cells of the choroid plexus located within the 4 brain ventricles -CSF helps maintain EC fluid balance and provides nourishment and cushoning for the brain Seen in the: 1) Lateral ventricles (x2) in the interventricular foramen (Monoroe) 2) Third ventricle in the cerebral aqueduct 3) Fourth ventricle in lateral (x2) and median apertures and central canal of spinal cord 4) Subarchnoid space with arachoid granulations how CSF drains into the sinus 5) Superiror sagital sinus (primarily)

Diffuse Axonal Injury (DAI)

-CT is essentially normal -shear injur to neurons -classically occurs in corpus callosum and the pons

1) Describe the general principles of MRI and CT imaging of the brain**

-CT is fast, MRI is better -CT for acute problems, then MRI brain later -Outpatient MRI is generally preferred CT: -good for brain hemorrhages: 1) brain parenchymal 2) subachnoid = layers in sulci and fissures 3) subdural = cresentic venous blood, not into sucli 4) Epidural = lens shaped arterial bleed -Good at mass effect = shows where it is not what it is -Ventricle size/hydrocephalus -Fractures -Aneurysms = with CTA -Vessel occlusion on a coronal CTA MIP reformat - Head CT with contrast not very helpful MRI: -better at everything in brain except fractures -Stoke -Brain Mass characterization -MS=Dawsons finger

CT before LP? for meningitis*8

-CT slows things down and delays therapy -it is indicted in pts with: 60+, IS, hx of CNS disease, hx of seizures a week before present, neruologic abnormalities (abnormal level of consciousness, abnormal vision, gaze palsy, facial palsy, arm and leg drift, abnormal language)

2) Recognize the back pain patients who need work-up (imaging & neurophysilogical studies) vs those who dont**

-Cant miss Mass lesion or tumor, abscess, osteomyelitis, cauda equina syndrome, conus maedullaris syndrome Concern for nerve or cord injury: -loss of function (weakness, numbness, incontinence falls) -abnormal neuro exam -bowel or bladder dysfunction Concern for cancer or injection: -constitutional symptoms (fever, sweats, weight loss) -history of cancer -recent infections or bacteremia -IV drug use -recent spine procedure

3) Id CN II-X and XII on MRI**

-Cassidy said she will go over in lab

6)Huntington Disease**

-Cause of chorea,dystonia, and atazia -AD, CAG trinucleotide repeat in huntingtin protien on chromosme 4 -see loss of caudate nucleus -slowly progressive, fatal within 15-20 years -Tx chorea, depression, irritability

Vestibular Migraine Vertigo**

-Central etiology -known migraine history -vestibular history = car sickness, feel like moving when they arent, dizzy at grocery stores -symptoms get better with rapid head movement -Start migriane preventation and lifesytle modicifications -Benign (not stroke) , chronic, recurrent can last 20 mins to 24 hours

10) Gyri and sulci of external cerebral cortex**

-Central sulcus divides the frontal lobe from the parietal lobe -Precentral gyrus is the only one in the frontal lobe that runs medial to lateral. -Find Precentral gyrus then you can find the central sulcus and then you are orientated -Lateral fissure divides the frontal and temporal lobe -To find the supramarginal gyrus find the lateral fissure follow it back and superiorly will be the supramarginal gyrus

Positive visual phenomena

-Cerebral diplopia or polyopia refers to 2 or more images of a single visual object in space -Palinopsia = persistence of visual afterimages -illusory visual spread = spread of object beyond spatial boundaries -May be associate with paretal lobe structural esions and with neurodegenerative impariments

3) Clinical description of the opthalmoscopic exam**

-Characteristics of the optic disc: disc margins, cup to disc ratio -Id the retinal vessels-central and branch retinal arteries and veins: A:V ratio -Id the macula and fovea -Describe common findings such as swollen wool spots, hard and soft exudates, retinal hemorrhage, A:V nicking

1) Trigeminal Neuralgia**

-Characterixed by paroxysmal sudden severe stabbing or shock-like pain involving one or more trigeminal nerve usually V2 or V3 -Pain triggered by contact in trigger areas* -Duration of attacks is often one to several seconds -continous pain inbetween attacks 1) Classical -demylination of primary sensory trigemental root entry zone due to neurovascular ompression by abnormal vascular loop, caused by herpes virus 2) Painful Trigeminal neuropathy -usually caused by direct trauma to the nerve and post-herpetic neuralgia (shingles) -characterized by continous pain Tx 1st line :oxycarbazepine or carbamazepine 2nd line: baclofen, gabapentin, pregabatin, topiromate, Surgical options -Gamma knife -Percutaneous rhizotomy -micorvascular decrompression

Traumatic optic neuropathy

-Closed head injury ptss and mid facial fractue pts -Adults = accidents, falls,assualt, accidents -Kids= falls, motor vechile accidents -S/S: subnormal VA, visual field loss, dyschromatopsia (color vision problems) , ipsilateral RAPD

1) Describe the components, filters, and apertures of the direct ophthalmoscope**

-Cobalt -Red-Free or green light -Focus whee -Slit beam and filters -Anti-glare filter

1) What must we develop in our brain

-Cognitivie Function -Emotion/Emotional Regulation -Self-Regulation -Attachment -Interpersonal connection -Sense of Self -Integration

3) Describe treatment options for primary and secondary prophylaxis of strokes**

-Control modifiable risk factors -Carotid revascularization: carotid edentocomy (best for severe stenosis), stenting -Oral anticoagulation: a) a fib = warafin b) HF with LVEF<35 = aspirin c) 2nd preventin in non-cardioembolic stroke = aspirin d) patent foamen ovale = recurrence risk is low may use anticoags -Lipid lowereing -Anti-HTN -Antiplatlet therapy used for secondary stroke avoidance and high risk patients

Major Fiber Bundles of the Cerebral cortex**

-Corpus callosum= fiber bundle that connects the 2 cerebral hemispeheres and allows communication, biggest fiber bundles -Cingulum= connects the cingulate gyrus with the entorhinal cortex -Fornix= connects hippocampus with the mammillary bodies o they hypothalamus

ocular dominance columns

-Cortical columns in the V1 consisting of neurons that receive signals from the left eye only or the right eye only

Basic Circuitry

-Cortical eye fields = plan movements -Basal ganglia= modulates movements -Cerebellum = optimize movements, makes smooth -Brainstem nuclei = PULSE and STEP signal generators -Nuclear and infranuclear = motor nuclei, CN, EOM -Supranuclear = above motor nuclei -Nuclear = at motor nuclei -Infranuclear = below motor nuclei

Upper Motor Neurons**

-Corticospinal tract axons terminate either directly on LMNs or on internuerons in the ventral horn of the spinal cord -all sysnapses that the corticopsinal neurons form are excitatory, except many internourons inhibit LMNs -Lesions of LMNs cause paralysis regardless of other lesions to the motor system

3) Recognize ocular side effects of systemic drugs**

-Corticosteroids can cause increased intraocular pressure (secondary glaucoma) and cataractogenic (ingreased risk of posterior subcapsular cataract) and a topical corticosterioid for the eye should only be prescribed by an ophthalmologist -Hydroxychloroquine used to treat RA can cause a Bull's Eye maculopathy causing irreversible damage following 6 years of tx (regular eye check ups are needed if being prescribed this med -Topiramate used to treat seizures and migraine prophylaxis, ocular side effects is bilarteral angle-closure glaucoma due to ciliary body effusions forcing everything in the eye forward, presents as sudden myopia -Ethambutol used to treat mycobacterial infections, cau cuase optic neuropathy ( optic nerve pallor) see rapid vision loss within 1 month of tx, may be reversible -Tetracyclines and retinoids can cause intracranial HTN manifesting as bilateral optic nerve edema (papilledema)

3) Unique symptoms of depression in the elderly**

-Depression is less common in older age, unless you live in a nursing home*** -The cause is rarely one cause more likely to think multifactorial*** -Elders are more liekly to have somatic complaints, feelings of worthlessness, and demonstrate hypochondriasis****

S/S of CNS tumors

-Diffuse (mass effect, CSF obstruction) headache, N/V, altered mental status, personality changes, papilledema -Focal (dependent on loncation of tumor) Motor, sensory, visual -Seizures

Process when Suspect SUD

-Do a sample mental stauts: apperance, behavior, attitude, motor activity, speech, mood and affect, thought process, thought content, cognition, insight, judgement -Do a urine drug screen (only screening test, cannot diagnosis anything based on this) -oxy wont show up on drug screen

Headache treatment in pregenancy**

-Dont use valproate *** Not Safe: -valproate -topiramate -NSAIDs -Beta blockers -SNRIs -CGRP -Botox Safe: -Tylenol -Mg sulfate -excedrine -Metoclopromide -opiods -verapamil -amtriptykine -diphenhydramine

Acamprosate**

-Drug for alcohol dependence -MOA: modulate GABA and glutamate receptor -reduces craving and relapse -used for patients who take px opoids -SE; diarrhea, and fatigue -MUST HAVE STRONG MOTIVATION TO QUIT

4) Primary Angle Closure Glaucoma**

-Due to iris being in contact with lens not allowing eye fluid to drain -S/S: unilateral eye px, headache, rapid onset of blurred vision, halos, nausea/emesis *** -PE: fixed, mid-dilated pupil, ciliary flush, corneal edema, narrow or closed anterior chamber angle*** -Tx: NEED A LASER IRIDOTOMY which creates a laser opening in the iris to allow fluid to flow

4) Summary of EEG lecture**

-EEG records electrical activity from the brain -ordering an eeg is indicated in patients with paroxysmal disorders, new onset seizures, in patients you suspect have epilepsy and in work up of an encephalopathic or comatose patient -Stat EEG is rocommeneded in status epilepticus, specially non convulsive status epilepticus. Always remember do not wait to treat

8) Levetricetam** (Elevator)

-ELEVATOR = LEVETRICETAM -BROADSPECTRUM -SE = SOMULANCE = FALLING ASLEEP WORKER -BLOCKING FUSION OF SV2A OF GLUTAMATE = ELEVATORS BLOCK THE FINISHING OF YOUR sUPER vERY nice ASS (sv2a) (GLUTS) -New MOA: -unknown may block vesicle fusion SV2A of glutamate (i think) Uses: -add on for partial or generalized tonic-clonic and myoclonic seizures SE: -well tolerated -fatigue, dizziness, HTN -Behavioral symptoms

3) Valproic acid (divalproex) ** (emporer VAL or festiVALs)

-EMPOREROR VAL = VALPROATE -BROAD SPECTRUM SEIZURE MED, -FOCAL SHAKING OF ARM = TX FOCAL SEIZURES -WHOLE SHAKING INCA = TX GENERALIZED SEIZURES -JUVENIALE MYOCLONIC EPILEPSY = YOUNG INCA DOING CHICKEN DANCE -HOLDS THE BASKET OF PEANUT BASKET CLOSED = BLOCKS NA CHANNELS -ELEVATED GABA = TAXI CAR PATTERN -SE: EMPOREROR= N/V, FAT, SHAKING (TREMORS), HEPATOTOXICTY BABY COW, PANCREATITIS, TARANTULA ON SHIELDS (SPINA BIFUDA) -FARM festiVAL = VALPROMATE can be used for abscence seizures , farm in the classroom sketch, use if have history of other seizures -traditional -Main MOA is Na+ channel blocker, also blocks t-type Ca++ channels, and stimiulates synthesis and inhibits degradation of GABA Uses: -broad spectrum anti-seizure drug** -afective against absence, myoclonic, focal, and tonic-clonic seizures -bipolar disorder and migraine prophylaxis -Divalproex** is a 1:1 acid/salt ratio that is valproic acid to help with less N/V SE: -anorexia, N/V, -CNS effects and weight gian -hepatic toxicity/pancreatitis is BW in kids less than 2 and it is immediate liver failure -Teratogenic neuroal tube defects and give them a butt to of folic acid

Treatment of Increased Intacranial Pressure**

-Elevate head of the bed -watch BP -maintain good CO2 -prevent fevers -Drain CSF -pain meds and sedations meds, and mannitol -surgical decompression -profound hyperventilation -barbitiuates -forced hypothermia

Meningitis vs. Encephalitis ON SET***

-Encephalitis will have focal neurologic signs and behavior changes** Most common cause is HSV and is the most severe* -Mengitis will not have these signs

2) Pathophysiology of various traumatic intracranial hemorrhages**

-Epidural hematoma = most commonly bleeding from the meningeal artery damage (trauma) loss consciousness (tears medial meningeal) , 15 mins later starts vomiting and keeps getting worse gets (increased intracranial pressure) into coma (due to uncal shift due to blood pooling) , and starts dying -this is why when you get a concusion you need to go to the hospital to make sure you didnt get a middle meningeal artery ruputre -Subdural hematoma = from bridging vein ***,

6) Summary of Seizure lecture**

-Epilepsy = 2 or more unprovoked seizures -seziures are either focal or generalized in onset -seizures have multiple etiologies -distinguish between provoked and unprovoked seizures -First time seizures= get work up, discuss risks, and conusel patient -Focal is one half of the body, or the frontal lobe ones where you freeze, or the kinetic ones -Generalized is the entire body and everything else

Halothane**

-FAST LITTLE KID -PASSED OUT AT THE END OF THE RACE= LATER ONSET, SLOWER RECOVERY, AND LONGER DURATION -HIGHER PARTITION COEFFICEINT -GRADUAL ARTERIAL TENSION CURVE -HEPATIC NECROSIS = CRACKED LIVER -High solubility and very high potency .77 Uses: -induction/maintencance of anesthesia, esp. pediatric Advantage: -non-pungent, rapid induction and recovery, bronchodilator Disadvantage: -Halothane hepatiitis- toxic metabolite

4) Carbamazepine *8 (Cool CAR)

-FOCAL SEIZURES -CLASSIC CAR = CARBAMAZEPINE -CHIP CLIPS = BLOCK NA+ CHANNEL -USED FOR TRIGEMinal neuralgia =THREE GEMS -SE = ATAXIA = FALLING PATTYS, DIPLOPIA = MISS ALIGNED HEAD LAMPS, SIADH, AGRANULOCYTOSIS = SAND TIMER, EOSINOPHILIC DRESS SYNDROME, TARANTULA JACKET (SPINA BIFIDA), SJS (HLA-B*1502 allele) = ASIAN GUY WEARING ASIAN MASK -CANNABOLS' CLASSIC CAR = EATS SELF = INDUCES OWN METABOLISM Traditional -Main MOA is Na++ channel blocker -Very similiar to phenytoin PK: -linear kinetics so more reliable with blood levels -induces its own metabolism by CYP3A4 Uses: -trigeminal neuralgia -tonic-clonic seizures, simple and complex partial seizures -bipolar disorder (mania) SE: -drowsiness, ataxia, vertigo, diplopia, and blurred vision, N/V/D -rash and SJS boxed wraning screen for HLA-B*1502 allele -blood dyscrasias -Boxed Warning- serious aplastic anemia, agranulocytosis -Teratogenic - and decreases BC

CN VII** $$$TEP

-Facial -Exits via internal acoustic meatus and sytlomastoid -Both Sensory and motor -Visceral motor, branchial motor, General sensory, and special sensory -emerges ventrally from the junction of the pons and meddulla lateral to CN VI -Cell bodies of sensory are in geniculate ganglia and terminate on the nucleus solitarius -Motor cell bodies are located IN the pons and axons loop over abducens then go ventral -Doe taste, muscles of facial expression, and autonomic -CNS region = pons -Lesion = ipsilateral weakness of facial expression muscles, dysgesusia (lost of some taste)

5) Id the components of the vestibulospinal system**

-Facilitates extensor muscles -patients with damage to the vestibulospinal system may have difficulty with balance and motor coordination (ataxia)

Viral Meningitis**

-Fever/severe headache/ stiff neck/ vomiting/ large parotid glands, caused by many enteroviruses, meningeal irritation, malaise, myalgia, anorexia, N/V, lethargy/drowisness

9) Axon pathfinding**

-Finding correct target tissue or neurons -growth cones are found at the ends of the developing axons and respond to molecules in their environment -guidance molecules are soluble and act a distance -Some molecules are attractive to growth cones while others are repulsive

2) Ascertain the presence of ocular, speech, truncal, and appendicular ataxias using basic exam techniques**

-Fludonoccular segment = eye movements, test eye movement 1) Speech could find dysarthria -Spinocellebellum (vermis, paravermis) = trunk, gait, posture = check out gait, posture, steps and stride, rising from seating to stand, standing alone, walking, turning while walking, more complex movements, stand on one foot, hop on foot, can they walk in a straight line, stopping, tandem gait (walking straight tight rope) 1) Trunkal tretebration = jerking of upper body -Cerebral cerebellum = hand control/limb control, tap fingers together, tap feet, finger to nose test, foot on shin, handwriting and pen and paper tests, 1) Intential tremor= reaching for something will cause shaking 2) dismetria= overshooting or undershooting target with corrective behavior 3) disdigokinesia = shin test, or salmon test, are testing for a break in the action -Cerebellar lesions are on the same side

5) Id the frontal eye fields and the pathways related to eye movements*8

-Frontal eye fields projects to the contralateral Paramedian Pontine Reticular Formation (PPRF) -The reticular formation projects to the ipsilateral cranial nerve nuclei III, IV, and VI via the medial longitudinal fasciculus (MLF) -Internuclear neurons in the abducens nucleus project to the contralateral occulomotor nucleus via the MLF to coordinate lateral and medial rectus muscles

7) Identify the locations for object and facial recognition**

-Fusiform facial recognition area is in the occiptotemporal gyrus on the inferior surface of the cerebral cortex -Object recognition involves the parahippocampal gyrus

Friedriech (autosomal recessive) ataxia

-GAA trinucleotide repeat -accumulation of iron in mitocondria kills neurons with long axons preferentially -Symptoms: spasticity (loss of corticospinal tract) , loss of fine touch, vibration (dorsal root ganglion loss), ataxia, including stoming gait (dorsal root ganglion and spinal cerebellar tract loss), sensory ataxia -Dysarthria occur later in life

3) Identitfy major pathways and neurotransmitters involving the basal ganglia**

-GABAergic medium spiny neurons of the striatum project to the globus pallidus . Degeneration of these neurons cause Huntington's chorea. -Glutaminergic neurons of the subthalamus project to the internal segment of the globus pallidus. Damage to the subthalamus results in hemiballismus

6) Gabapentin** (Ice cream truck)

-GRAB A PINT = GABAPENTIN -ICE CREAM TRUCK= BINDS TO CA2+ CHANNELS -ZEUS' ICE CREAM = BINDS TO HIGH VOLTAGE CA2+ CHANNELS -TREATS PAIN = FRAYED WIRE -SELLING SWEETS = TREATS DIABETI NEURALIGA -SELLING FIBER BARS = TREATS FIBROMYALGIA -ZUES ICE CREAM = TREATS POSTHERPETIC NEURLAGIA (REACTIVATED VARICELLA-ZOSTER VIRUS) -SE: DIZZINESS, ATAXIA, SEDATION = TIRED WORKER HOLDING FALLING ICECREAM CONE -newer -not a GABA receptor agonist** -Binds to High voltage Ca+2 channels, may decrease release of glutamate Uses: -focal, generalized seizures -postherpetic neuralgia -migraine, neuropathic pain, fibromyalgia, bipolar SE: -sedation, dizziness

CN IX**$$$TEP

-Glossopharyngeal -Exits via the jugular foramen -Both Motor and sensory -Visceral moter, branchial motor, general sensory, visceral sensory, and special sensory -Best friend with CN X -emerges ventrally from the medulla, lateral to the olive -Sensory cell bodies located in associated ganglia they enter the brainstem, and terminate on nucleus solitarius -Motor neurons located in nucleus ambiguus axons exit the medulla dorsal and lateral to the inferior olive -Has a critical role in respiration and cardiac function via autonomic nervous system -does pain in ear, taste, sytlopharygneasu muscle, parasympathetic efferent, general visceral efferents -CNS region = medulla -Lesion= dysgeusia (lost of taste), problems swallowing, dysfunction of parotid

Pilocytic Astrocytoma

-Grade 1 tumor -5-6% of all gliomas -most common glioma in childhood -majority occur in the cerebellum -relatively cricumscribed = better prognosis -often cystic -elongated cells(piloid cells), rosenthal fibers, eosiniphilic granular bodies

Medulloblastoma**

-Grade IV -embryonal small cell tumor of the cerebellum which is a subtype of the neuroepithelial tissue tumors -usualy occur in children -Predominatnly neuronal differentiation -Tendency to spread through the CSF -Located in the midline (childhood) or lateral hemisphers (adults) -Homer wright rosettes on histology

Glioblastoma

-Grade IV tumor -2 year prognosis is 10% -A subtype of diffuse astrocytoma which is a subtype of gliomas -Primary GBM (de novo)** -Secondary GBM(evolution of a lower grade** astrocytoma into a grade IV tumor) -AOO is 60-65 -Ring-enhancement and mid-line invasion common radiographic features -microvascular (endothelial) proliferation, pseudo-palisading necrosis common histo findings - O6-Mehtylguaunine-DNA-methyltransferase (MGMT) -DNA repair enzyme: -methylated MGMT is seen in cancer -low levels of MGMT activity by GMB tumor cells is associated with enchancehd response to TMZ and longer surgival EGFR amplification = primary GBM**=62 AOO TP53 mutation = secondary GBM ** = 45 AOO

Muscle testing **

-H test: positions the eyes such that each muscle function can be isolated -must first minipulate the gaze and then can test individual muscles 1) Medial rectus = adduct eye, inferior division of CN III 2) Lateral rectus = abduct eye, CN VI 3) Superior rectus = lateral postition look up (superior division of CN III) 4) Inferior Rectus = lateral position look down, inferior division of CN III 5) Superior oblique= medial position DOWN, CN IV 6) Inferior oblique = medial position look UP, inferior dividions of CN III

Infectious neuropathies

-HIV is most common, painflul symmetric, sensory predomonant -Hep C, leprosy, lyme disease

Herpes Viruses**

-HSV1 is more common get via oral transmission -HSV2 get via genital transmission -Latency is in sensory root ganglion Menigitis: -HSV2 is more common to cause meningitis (Fever, headache, vomiting, photophobia, nucal rigidity) Dx: HSV DNA PCR in CSF Tx: Acyclovir (IV acutely) Encephalitis -The most common cause of acute sporadic viral encephalitis in US with HSV-1 being the most likely culprit, -can see necrotizing hemorrhagic encephalitis -Temporal lobe involvement -Fever and focal neurologic signs Dx: -HSV DNA in CSF -MRI with contrast -HSV antibodies are postitive in CSF after 10 days Tx: Acyclovir (acutely IV)

Motor Neuron Disease Summary**

-Hallmark is progressive painless weakness, fasciculations, and atrophy (pure motor syndrome) -No significant sensory loss or sphincter disturbance -Mixed UMN/LM in classic ALS -Crams more common with LMN -Focal/regional limb onset: ALS -Regional with asymmetry: polio-like : WNV, AFM -Symmetric, generalized, proximal>distal: SMA +/- asymmetric limb and bulbar LMN weakness = Kennedys disease -almost never ptosis, opthalmoparesis Treatment -multi-disciplinary clinics -PT, OT, bracing -S;eech pathology, swallow evaluation. PEG-tube for moderate-severe dysphagia prevents malnutrition, reduces aspiration risk -Rstrictive pulmonary mechanics: BiPAP -symptom management: sialorrhea, cramps, spasticity -Scoliossi surgery (SMA) -Specific therapy: Riluzole and Edaravone (ALS), Nusinersen (SMA)

Bupivacaine**

-Highly hydrophobic slow onset 15-30, highly potent -long duration, not used with epiphenrien -uses: spinal, epidural, peripheral nerve block, and infiltration anesthesia, labor -SE: cardiotoxic at higher doeses, black box warning for obstetrical anesthsia and cardiac arrest and death -Amino amide class = have 2 "i's" -Most common one used for central nerve blockade Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Clearance: -dependent on liver and heart function SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy

Perforating ocular injuries

-History is essential - must determine nature of injury -speed, projectile, metal -note warning signs of open globe: laceration, pigment, pupil, AC -shield eye (NOT A PATCH) and refer, no pressure, no topicals -signs: irregular pupil, subconj hemerrohage, uveal prolapse, lens opacity/dislocate -If suspect a ruptured globe: 1) stop the exam and asses visual acuity 2) Shiled the eye (dont patch) 3) Do not apply topical meds 4) If narcotics given also give antiemetics 5) Give tetanus prophylaxis 6) Tell not to eat 7) REFER IMMEDIATELY TO OPHTHAMOLOGIST

CN XII **$$$TEP

-Hypoglossal -Hypoglossal canal -Motor -Somatic motor -Emerges ventrally from the medulla, medial to olive and lateral to the pyramids -Cell bodies in hypoglossal nucleus axons exit ventrally between the inferior olive and the pyramids and terminates on the hypoglossal muscle of the tonugh -Does movenemtn of tongue -CNS region = medulla -Lesion = ipsilateral weakness of the tongue

1) Projections from the hypothalamus to the autonomic system**

-Hypothalamospinal Tract control both the sympathetics and Parasympathetics nervous system via its projections to the preganglionic neurons

1) Locate the hypothalamus within the brain

-Hypothalamus is inferior and anterior -Located in Diencephalon' -mammillary bodies are the caudal most part of the hypothalamus -hypothalamic sulcus seperates thalamus and hypothalamus -column of fornix comes from hippocampal formation and terminates at the mamillary bodies -optic chiasm and pitutary gland is immediately ventral to the hypothalamus

Parahippocampal gyrus

-IN TEMPORAL LOBE -close to the hippocampal formation -entorhinal cortex is located in the rostral parahippocampal gyrus

Ketamine***

-INHIBITION OF THE NMDA RECEPTOR -SNAKE CHARMER -DISSOCIATIVE TRANCE = OPEN EYED STATE -UNPLEASANT HALLUCINATIONS= VIVID COLORFUL DREAMS, OUT OF BODY EXPERIENCES -INCREASES IN BP HR, CO = HEART SHAPED COBRA HOOD MOA: -NMDA receptor antagonist -produces dissociative sediation, produces significant ANALGESIA and bronchodilator, minimal CV affects Uses: -unpleasant emergence in adults -induction and maintence in kids cuz wont see bad emergence SE: -CNS psychotomimetic effects = unpleasant emergence, -some N/V, tachycardia and hypersalivation

Propofol**

-INTRODUCING PROSPERO = INTRODUCTION -MAINTAIN YOUR SLEEP=MAINTENCE -POTENTIATE CHLORIDE CURRENT THROUGH GABAa RECEPTOR -DILATED SLEEVES = VASODILATION -MOST COMMON ONE USED IN U.S. -KILLED MJ MOA: -GABA-A agonist Uses: -induction, maintaencance, procedural sedation, post-op anti-emetic (anti-nausea) -non-anselgic have to give them fentonyl Onset; -40 sec duration 6 mins SE: -hypotension, respiratory depresion -pain at injection site, hypertriglyceridemia

2) Correct technique for direct opthamoscopy **=

-Id the red reflex -Id the optic disc, optic cup, retinal vessels, and macula

Parahippocampal formation myelin stain

-Id: 1) Fimbria of Fornix (alveus of the fornix) on gross brain can be seen its a sheat of axons on top of fimbria) 2) Hippocampus proper 3) Dentate gyrus 4) Subiculum 5) Ventral Tegmental Area 6) Cingulate gyrus 7) Cingulum 8) Body of Forinx

Review of Movement disorders emergiencies** KNOW THIS FOR THE TEST

-If induced DA definency = NMS -If induced 5-HT excess = SS -myoclonus = SS -High CK = NMS -HTN = SS, NMS -Hypotension = NMS -Peak within 6 hours = SS -Peak after 12 hours = NMS -leukocyotsis = NMS or sepsos -Hyperreflexia = SS -NMS and SS first line tx = ABCs and stop offending -NMS specific Rx = levodopa, DOPA agonists, BDZ -SS specific tx = BDZ, cyprohepatdine (anti-serotonin) -Acute dystonic rxns, oculo-gyric crisis tx = Benydraly IV -

3) Id presence of neuroimmunlogical disorders in CSF***

-IgG can be obtained from the BBB if it increased permeabilty or locally synethsized from plasma cells within CSF (MS) *MUST DIFFERENTIATE BETWEEN THE USE CALCULATION Q Albumin = CSF Albumin x 10^3/ Serum albumin -normal is <9.0 if <9 no increase in BBB permeability IgG index = normal <0.7 it can be elevated in MS, CNS immune reactions, it is decreased in cases of increased BBB permieability in stoke, tumor and meningitis

4) ID the prescence of meningitis/encephalitis in CSF**

-Increased neutrophils = bacterial meingitis -Increased lymphocytes = aseptic or viral meningitis -can see decreased CSF/Plasma glucose ratio (bacterial infection) (due breakdown of glucose) -With viral infection CSF glucose is usally normal -Bacterial and fungal CSF may increase CSF proteins due to breakdown of CSF -Bacterial menigitis can have increased lactate

1) S/S of acute red eye**

-Increased vessels (hyperemia) of the conjunctiva, episclera, or sclera

11) Id structures in the cerebral cortex related to reading**

-Inferior Frontal Gyrus = vocalization and articulation -Parieto-Temporal = word analysis -Occipito-temporal = word recognition, automaticity -dyslexia readers are depending more on frontol lobe and dont have axis to the parieto-temproarl and occipito-temporal regions -Some forms of dyslexia are associated with periventicular nodular heteropia, a neural migration disorder, see abnormal gray matter adjacent to the lateral ventricles on the right

2) Role of genetic evals in patinets with neuropathy

-Inherited neuropathyies are relatively rare 1) most common is Charcot-Marie-Tooth type 1a -CMT1 = demyelininating , AD -CMT2 = axonal , AD -CMTX = X-linked -gradual onset/progession with classic stigmata see a high arch and hammer toe feet 2) Fabry disease -X-linked -angiokeratomas (freckles) -GLA boold activity -Tx: ERT 3) TTR amyloidosis -congo stain -AD (chromsome 18) -Dx: genetic testing -Tx: liver transplant, ASO/RNAi

Brachial Motor Nuclei**

-Innervates muscles that develop from paryngeal/branchial arches -CN 5, 7, 9, 10, 11 = 5,791,011 -Motor nucleus of trigeminal = CN V (mastication) -Facial nucleus = CN VII (facial expression) -Nucleus ambigus = CN IX and X (pharynx and larynx) -Spinal accessory nucleus = CN XI

Cerebellar hemisphere lesion $$TEP

-Intention tremor -Limb ataxia -Ipsilateral deficits -Fall towards side of lesion Cerebellar hemispheres are LATERALly located -affects LATERAL limbs

2) Describe the vascular anatomy of the brain as it relates to major stroke distrubtions**

-Internal Carotid Artery -Vertebral Artery (subclavian artery) -circle of willis -Anterior Cerebral Artery = 3 segments A1, A2, A3 and has recurrent artery of heubner -Middle Cerebral Artery = 4 segments M1, M2, M3, M4, has lenticulostriate artieries and leptomeningeal branches Posterior Circulation: -Posterior Inferior cerbellar artery = PICA -Basilar artery = pontine arteries, paramedian arteries, circumferetial artieris -Anterior Inferior Cerbellar artery = AICA -Posterior Cerberall Areteries (PCA)

Uveal Tract

-Iris, cillary body, choroid -all have pigmented-melanocytic layers Uveitis: -acute vs. chronic -ant., intermediate, post, panuveitis -due to infectious agents (pneumocystis, toxoplasma, CMV, mycobacteria) -due to autoimune (anklosying, RA, sarcoid) -due to idiopathic -Granulomatous vs. nongranulmatous -Can see nevi usually small and dont transform -

Chemical/Contact injury to eye

-Irrigate!! -topical anesthetic -check for occult FB, consider nature of injury -Check pH, acid vs. base -cycloplegia (immoblize eye reducing px) -topical antibiotic, referral, avoid patch -True vision emergency need to copiously irrigate

4) Explain how K+ channels modify the action potential waveform**

-K+ channels modify how quick we return to resting potential, contributing to relative refractory period -Open slower than Na+ channels but also opened once reach threshold -Due to the slow opening/closing of K+ channels overshoot repolarization causing after-hyperpolaraztion

Nitrous oxide**

-LAUGHING GAS -FAT KID = LOW SOLUBILITY -STEEPER ARTERIAL TENSION CURVE -solubiltity and extremely low potentcy Uses: -alone as a sedative/analgesic for outpatient dental procedures -used in combo Advantages: -good analgesia, amnesia, rapid induction and recovery, minimial CV effects, reduced SE Disadvantages: -not complet anesthetic, can cause diffusion hypoxia (treat by pumping oxygen to 100%), expansion of closed airspaces (problem in lungs)

Visual Fields and Visual Pathways**** ON TEST

-LEFT PART OF THE RETINAS GO THE LEFT BRAIN BUT REPRESENTS RIGHT VISUAL FIELD -RIGHT PART OF RETINA GOES TO THE RIGHT BRAIN BUT REPRESENTS LEFT VISUAL FIELD -Nasal retinal ganglion cell axons cross at the optic chiasm -Temporal retina ganglion cell axons do not cross at the optic chiasm and remain ipsilateral

7) Lamotrigine** (Llama)

-LLAMA = LAMOTRIGINE -BROAD-SPECTRUM -LIDS ON PEANUT BASKET = NA+ CHANNEL BLOCKER -SE: RED MASK = SJS, DIPLOPIA (CROSSED EYE LLAMA) , WEARING A TERTANTULA SMACH -LLAMA IN THE CLASSROOM SKETCH AT THE FARM FESTIVEL -LLAMAS NAME IS LENDARD-GESTAT (tX LENNOX GESTAT SYNDROME) -newer MOA: -blocks Na+ channels, reduces release of glutamate -block Ca+ channels -5HT3 antagonist Uses: -lennox-gastaut syndrome -monotheapry for partial and generalized tonic-clonic seizures; absence seizures -bipolar disorder-depression SE: -dizziness, ataxia, blurred vision, N/V -Rash/SJS-BW -teratogen

3) Describe the organization of lower motor neurons**

-LMN's axons form neuromuscular junctions with muscle cells -LMN's are located in the ventral hornsin the spinal cord -The ventral horn is larger in lumbrosacral and cervical enlargements -LMN's organzed somatotopically: Medial = axial muscles Lateral region = limb muscles Flexors = more dorsal Extensors = more ventral -LMN's in ventral horns exit in the ventral horns -Spinal reflexes occur when sensory information directly reaches the ventral horn cells from somatosensory neurons in the dorsal root ganglia -LMN's associated with CN III, IV,V, VI. VII. IX,X. XI.XII, azons from these brainstem CN nuclei terminate in muscles of head and neck

Inhalation general anesthetics**

-LOW SOLUBLITY PASS OUT EARLY CUZ FASTER SATURATION = EARLY ONSET AND FASTER RECOVERY -LOW MAC = HIGHER POTENCY -MYOCARDIAL DEPRESSION, LEADING TO DEC CO AND HYPOTENSION = DEFLATING HEART BALLOON -DEFLATING LUNG BALLOONS = RESPIRATORY DEPRESSION -INC CEREBRAL BLOOD FLOW = RED CEREBRAL HAIR MOA: -targets in CNS are the enhancement of GABA-A* and inhibition of glutamate/NMDA (THESE ARE GUESSES) -Potency is defined by MAC, 1 MAC = vol% that prevents movement in 50% of patients -MAC HAS NO EFFECT ON ONSET -1.3 MAC is our goal -Can be additive -Potency increases with age (give old people less GAs) -Acute alcohol intake, pregnancy, opiods, sediative, hypothermia will increase potency (dec MAC so give less) -Infancy, chronic alcohol intake, hypernateremia, sympathomimetics increase MAC(dec potency and give more)

Hallucinogens**

-LSD/PCP, mesacaline/peyote, psilocybin/shurms -acute intoxication = anxeiety and hallucinations -chronic intoxication = prolonged psychoses, flashbacks, exacerbate psychiatiric illnesses -Serotonin agonists -no withdrawal -mescaline/psilocybin less potent than LSD -PCP and ketamine are anesthetic agents, no loss of concisousness, flat facies, dissociatives

Meissner's Corpuscle $$TEP

-Large, myelinated fiers -adapt quickly -light touch, dynamic, fine touch, position sense -located in glabrous (hairless) skin

Risk Factors of CNS bacterial infections**

-Less than 5 more than 60 -IS -Crowding (military recruits and college dorms) -Splenectomy and Sickle cell -Alcoholism and cirrhosis -DM -Sinusitis and otitis

Posterior Cord Syndrome**

-Loss of dorsal columns bilaterally, bilateral loss of proprioception, vibration, pressure, stereognosis, 2 point discrimination; preservation of motor function, pain and light touch; very rare! -Neurosyphillis and B-12 defiency, MS, HIV associated vacuolar myelopathy

3) Id the presence of hyperreflexia and provide a ddx**

-Loss of inhibition coming from the corticospinal neuron in the brain (must be in the brain) -can be due to CNS structural lesion, or toxins -Stroke can be a cause -MS can be a cause

spinal muscle atrophy**

-Lower motor neuron disorder -rare -most common fatal genetic disease of infancy -AR -neurodegeneration of anterior horn -due to homozygous deletion or point mutation of SMN1 gene on chromsome 5 S/S: -tongue atrophy with fasciculations -facial and EOM are spared -hypotonia -fine tremor -refelxes are usally absent -waddling gait -impaired swallwing and ventialrty insuffiency Dx: -genetic confirmation Tx: -supportive care -intrathecal ASO nusinersen Prognosis -normal life expectancy in type 4

Progessive Bulbar Palsy**

-Lower motor neuron disorder -symptoms restricted ot bulbar muscles (CN 9-12) -prgessive dysarthria, dyspahgia, weight loss -handkercheif sign to wipe drool

Amantadine** (Manatee statue)

-MANATEE STATUE -CAN TREAT SOME MOTOR SYMPTOMS -BREAKS OPEN ROPE BOX = INCREASING SYNTHESIS AND DEC REUPTAKE -MANATEE WAS THE FIRST THING THEY STOLE = EARLY THERAPY -SE: MANATEES ARE BIG DUMB CREATURES = EDEMA AND CNS IMPAIRMENT, LIVEDO RETICULARIS , MOA: -increase DA release from presynaptic terminals, some Anticholinergic, NMDA antagonist Uses: -short term -monotherapy in early PD, improving bradykinease/rigidy -drug induced dyskinesia, caused by levodopa* SE: -cognitive impairment, livedo reticularis, edema

Superior Colliculus

-MIDBRAIN -recieves direct retinal input fro the retinal ganglion cells via the brachium of the superior colliculus *** -involves visual reflexes -projects to the spinal cord via the tectospinal tract to have movement when you see something flying at your head -Also reieves input from the visual cerebral cortex and the pretectal nuclei -Also projects to the pulvinar of the thalamus

6) Phenelizine** (FUNNEL OF WINE)

-MOA inhibitors -Nichloas Cage = slowly falling out of favor, only used when other actors are unresponsive -MAO-A = deminates serotonin, dopamine, and NE (ALBANIO MOUCE EATING SMILEY FACE, NORTH COMPASS, AND DOPAMINE ROPE) -MOA-B = Deaminates dopamine (BLACK MOUCE EATS DOAPMINE ROPE) -MOA INHIBTORS = MOUSE TRAPS, IRREVERSIBLE, USED IN ATYPICAL DEPRESSION, TREATMENT RESISTANT DEPRESSION -SE: Orthostatic HTN, Weight gain, sexual dysfunction, avoid food with tyramine cuz can cause HTN crisis , blurred vision, diaphoresis, serotonin syndrome, avoid use with drugs that increase serotonin Uses: -MDD 3rd line PK: -onset is faster than other antidepressants

Other Tests do differentiate central and periperal

-MRI brain -Electronystagography -Videonystamography -Videooculography Eye tests: -H test Ataxia and Gait Tests: -finger to nose -heel to shin -coordination -have patient walk Hearing test: -Rinne test, air>bone, hold a fork outside ear, and on mastoid process conductive hearing loss, bone better than air -Weber test, place on vertex, Sensorineural hearing loss, tone louder on the normal side

9) Bipolar disorder DSM-5 dx**

-Mania is usually increased focused goal directed behavior -more likely to show up depressed (as that is the majority of the symtoms) -Untreated results in work problems, lifetime loss of earning, social impairments, high rates of divorce, legal problems, increased incarceration, high rate of emergency -Giving bipolar pts antidepressents can worsen condition Dx: -80% OF TIME ILL IS DEPRESSED , 20% MANIC -presence of one life-time manic episode with or woithout a hx of depressiive episodes -Manic episode = period of abnormally elevated, expansive, or irritable mood plus 3 of 7 manic symptoms (4 if mood is irritable) that occurs daily for at least one week. Symptoms = drandiosity, dec need of sleep, overly talkative, subjective experience of racing thougts, distractibility, increased goal-direxted behaviors or psychomotor agitation, impuslive behaviors -Must be impairment in function hospitalization or psychotic symptoms -must not be due to direct effects of drugs -50% of manic pts experience psychotic symptoms -Age of onset usually 25 -Late middle age or elderly onset is usally secondary (alzheimers, post-stroke, subdural hematoma, steriods, amphetamine) Types: Bipolar Type 1: recurrent manic episodes with or without episodes of major depression. The majority of patients have both depressive and manic episodes Bipolar Type 2: periods of hypomania with major depressive episodes, it is NOT more mild because it is has more impairment and more suicide attempts Cyclothymia : mood swings that don not meet full DSM criterial for major depression or mania Hypomania = same symptoms just not as severe to cause marked functional impairment, no psychotic symptoms are present, symptoms mus be present every day for at least 4 days in a row Mania= euphoric can be used, but more commonly mood is not epuphoric but expansive or irritable and angry Expansive mood = exaggerated behavior, poor boundaries, poor reading of social cues Comorbidities: -Anxiety/Panic disorder, Adult ADHD, Substance abuse disorders (50%) Screening:**** -MDQ = + score = 7 or greater symptoms, tool to eliminate a bipolar dx, can id 70% of persons w/ bipolar disorder Tx: -mood stabilizers -majority of pts will take mor than 2 mood stabilizers and 3 or more psychiatric meds in maintence phase -Drugs for Acute mania = lithium, valproic acid, carbamazepine, 4 new- generation antipsychotics, Haldol and lorazepam (ACUTE SETTING) -Drugs for Bipolar depression = seroquel, latuda, zyprexxa/prozac combo (symbiax) (UNMET NEED FOR MORE) -Drugs for maintence= lithium, lamictal, zyprexa, abilify, seroquel (UNMET NEED FOR MORE) -advise patients to avoid mood de-stabilizers such as (lack of sleep, stress, meds (steriods, and amphetamines), alcohol and drugs Antidepressants for bipolar: -Most common effect is no improvement -can have mania or hypomania respnse -may cause more rapid-cycling and worsening or disease -Seems to be more beneficial for those with severe Type 2 - Avoid if bipolar type 1 with no depression

5) OCD due to another medical condition**

-Many causes of it -He talked about: 1) Pediatric Autoimmune Neurophyschiatric Disorders associate with Streptococcal infection (PANDAS) -antigens on cell wall of the streptococcus mimic proteins of basal ganglia 2) Sydenham chorea can also follow stretpococcal infections and may include obessions, compulsions, cognitve impairment, emotional labilty

Metabolic Myopathies**

-McArdles: Glycogen storage dz, PAS+ -CPTD: Fat droplets in muscle, Rhabdomyolysis w/ exercise/stress Mitochondrial dz: Fancy stains, Ragged red w/ Gomori & loss of stain w/ COX -dynamic rather than static symptoms: usually complain of exercise intolerance with muscle pain and cramps -can worsen in tyimes of increased physiologic stress -includes disorders of glycogen, lipids, and mitochondiral metabolism

5) Pharm tx for kids and adults with ADHD***

-Meds or Meds + behavioral tx are the best tx with Med+ behavioral treatment being Gold standard especially if under 8 -1st line treatment is methylphenidate or amphetamines (stimulant) increases DA and NE (stimulate the breaks) -1st or second line is atomoxetine (non-stimulant) * less effective than stimulants but is used 1st line if there is a cormorbid substance use disorder, a NE reuptake inhibitor -2nd line is guanfacine and clonidine (non-stiumulant) -All meds cause appetitie suppression -Screen for cardiac problems due to sudden cardiac death risk

Visual Distortion

-Micropsia = object appear smaller than shou;d -macropsia -metamorphopsia = distortion of objects as if in a carnival mirror -most commonly seen in retinal disorders like macular degeneration

2) Neuroanatomy related to horner's**

-Miosis, mild ptosis, anhydrosis are S/S -3 types of lesions 1) Central = interruption of the hypothalmospinal tract in the CNS, may result in lack of sweating on one side of the body 2) Preganglionic = damage to the IML axons , may result in lack of sweating on one side of the FACE 3) Postganglionic = damage to postganglionic axons, may result in limited facial sweating or no sweating effects at all

3) Explain how open, closed, and inactivated states of a voltage-gated sodium channels can give rise to an action potential**

-More permeable the K+ channels (open) will drive membrane more negative -More permeable the Na+ channels (open) will drive membrane more + -depolarization= membrane potential is less negative than resting membrane potential (more +) -hyperpolarization (repolarization) - membrane potential becoming more negative -AP = rapid depolarizing change in membrane potential = primary signal of the nervous system -AP requirements= 1) Resting membrane potential 2) Transmembrane Ion channels -Ion channels different than leak channels**** -Two properties of ion channels: 1) Selectivity = sixe and arrangement of channel 2) Gating = may be open or closed -3 types of Ion channels: 1) Ligand-gated ion channels -intracellular ligand dependent (cyclic nucleotide, Ca++) 2) Ligand-gated ion channels- external neurotransmitter dependent 3) Voltage-gated ion channles -Voltage-gated Na+ channels: 1) enter an inactivation state following activation where it is inactive and cannot be opened due to gate blocking channel (3-4 linker) , different from a closed channel where it is closed but has the potential to be opened 2) Composed of 4 domains with 6 trans-membrane segements 3) P-loop forms Pore by S5 and S6 4) Voltage sensor involved + charged arginine residues on S4 -K+ channels inactivated by ball and chain plugs

Delirium again** (3 Questions from this card)

-Mortality is 22 percent at 6 months, 2x more likely then patients without delirium ** -Morbiditiy = inc risk of complications, inc cost, inc length of hospital stay, poor functional recovery, future cognitive decline, inc rate of institutionalization, inc risk of subsequent delirium, inc rates of PTSD, depression, and anxiety** -Acute mental disturbance characterized by confused thinking and disrupted attention, usually accompanied by disordered speech and visual hallucinations that fluctuations throughout the day, can affect psychomotor activity, sleep-wake cycles, and affect*** -risk factors: old, men, dementia, hospitalization DSM-5: -disturbance of attention and awareness -disturbance develops over a short period of time, is distinictly diffrent from baseline**, fluctuate throughout the course of day** -caused by another general medical condition** -has an additional disturbance in cognition -Pathophys: dec of cholinergic (Ach activity) and excess of dopamine Causes: a bunch, stroke, imbalances, NSAIds, TBI, psychiatric disorders, hypoxia BUT ANOTHER MEDICAL CONDITION** Work up: Hx*, PE, mental status exam, bedside cognitive test, basic lab tests Tx: - dopamine antagonists have been used -more sleep at night -no approved meds -continue to reorientate -keep blinds open during day -have more direct care

1) Migrane**

-Most common primary headace (no secondary cause) -Females mor common -most common in 30-39 -Hypothalamaus seems to be the key player -Hyopthalamic neurotransmitters: 1) Orexin A &B = sleep disruption, feeding, and arousal disruption 2) Chlecytsokinin = appetite supression 3) Doapine = yawning and nausea 4) Somatostatin = modulation of trigminovascular pain signaling 5) Antidiruetic hormone = excessive thirst and urination 6) Melatonin = sleep distruption 1) Premonitory Phase (Prodrome) -starts hours to days before onset -fatigue and yawning, mood alteration (irritability, dysphoria) ** -food cravings, sleep disturbance, sensory symptoms 2) Migraine Aura -sensory symptom before or during migrane usually a visual aura -can be sensory, speech, hemiplegic migraine, stroke mimacry, basilar migraine (stroke like presentation) , 3) Attack -last 4-72 hours usually -pain is usually unilateral, throbbing, pulsating, pressure-like (especially behind eye) , phophobia, phonophobia, (usually more pronouned on one side), nausea, vomiting 4) Postdrome -tiredness>dif concentrating> neck stiffness> photoobia -usually lasts 18-25 hours 1) Chronic Migraine= 15 or more headaches day in a month and at least 8 of those with migraine symptoms lasting for more than 3 months -Tx: onabotulinumtoxinA (botox) 2) Vestibular Migraine = vestibular symptoms of moderate or severe intensity lasting 5 mins to 72 hours. -vertigo with or without headache symptoms, -tx with regular migraine therapy Treatment: 1) Abortive/Acute -Class A= Outpatient -triptans (within 30 mins of onset) (not used in pregnancy and HF) -NSAIDs, Acetaminophen, excedrin migraine -can cause rebound headaches (especially excedrin) -level B= more seen at ED level -Ergots (level B) more serious triptans (vasoconstrictors) (Dihydroergotamine) -ketrolac, metoclopramide, prochloperazine (antiemetics), magnesium sulfate -Level C= valpromate, opiodis, dexamethasone, butalbital 2) Preventative -Antihypertensives = propanolol, verapamil, -sartan -Antidepressants = Amitriptyline, Dualextine -Anticonvulsants= toprimate, gabapentin -calcitonin gene related peptid (CGRP) inhibitors= erenumab, glaanezumab, fremanezumab (NEW KID ON THE BLOCK 3) Chronic Migriane -Botox

8) Explain how myelination increases action potential velocity**

-Myelin leads to membrane dropping capacitance allowing the charge to to spread further down the axon increasing length constant leading to faster AP its like a chunnel -Saltatory condunction = AP skipping from one node to the next -C-fibers are unmyelinated and small diameter and are slow as sh*t -One test for MS is to measure nerve conduction velocity

Red Flags of back pain **

-Neuro deficit (bilateral or progressive) -Recent trauma -Mild trauma in patiens over 50 -Prolonged corticosteriod use -oseteoporosis -older pt with new onset back pain -hx of cancer -hx of recent infection -temp over 38 -drug and alcohol abuse -unexplained weight loss -low back pain that is worse at rest or during the night -disablilty from pain for more than 4 weeks -perianal numbness with bowel and bladder sphincter dysfunction

1) Id the neurobiological hypotheses for mood disorders**

-Neurobiologic changes: EEG changes (reduced activity over the left frontal lobe) -cortisol abnormalities -Catecholamine = decreases in major serotonin metabolite in CSF and in CNS brain receptors -PET scan show inc blood flow and dec volume in subgenual prefrontal cortex (regulates social behavior)

5) Morphology of neurons related to the ANS***

-Neurons of the autonomic ganglia have a multipolar shape and receive synpatic input from the preganglionic neurons in the CNS -Postganglionic nuerons of sympathetics and parasympathetics are multipolar

7) Summury of neurodevelopment**

-Neuropsychiatric development is a lifetime process there is no final accomplishment -Gene-environmental interaction is the mode of neuropsychiatric development -Understanding the neuropsychiatric development puts emphasis on prevention/early intervention of mental illnesses

Articaine**

-New drug used for dental work, medium onset, medium duration -Has a secondary amine group and thiophene ring and ester group -metabolized by plasma cholinesterases and liver (rapid metabolism may decrease potential toxicity) - SE: methemoblobinemia and local tissue toxicyt -Amino amide class = have 2 "i's" Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Distribution: -administered with epinephrine to vasoconstrict vessels to keep in local Clearance: -dependent on liver and heart function SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy

Hydrocephalus**

-Non-communicating = obstructive -communication = nonobsrtuctive -hydrocephalus ex vacuo

Mivacurium**

-Non-depolarizing NMB that is a benzylisoquinoline -Cannot be used in patients with BuCHE deficient patients -alternative to SuCH

Cisatracurium**

-Non-depolarizing NMB that is benzylisoquinoline -more potent but doenst cause seizures compared to laudonsine

Pancuronium**

-Non-depolarizing NMB that is steridial -Long acting used in long surgeries -rarely used due to residual muscular weakness and tachycardia

Rocuronium***

-Non-depolarizing NMB that is steriodial -Fastest onset -Alternative for SuCh -not associated with histamine release and doesnt affect CV response -used off label to prevent SuCh-induced fasiculations

4) Id common and emergeny retinal pathology**

-Normal fundus findings -Papilledema (swollen optic nerve) due to increased intracranial pressure -Diabetic retinopathy-exudates, neovascularization, must see an opthalmalgoist once a year -HTN retinopathy-narrowing of arterioles, AV nicking, cotton wool spots -retinal vein occlusion- -Glaucoma- -Macular degeneration-see drusen (clumps of protein that becomes calcified) Dry or Wet. Wet means increased blood vessels leading to fluid leakage -Central retinal artery occlusion- opthalmic emergency, stroke in the eye, at high risk of strokes -Vitreous hemorrhage -Retinal detachment

Spinocerebellar ataxias (SCA)

-Numerous types Cause: autosomal dominant, trinucleotide repeats Clinical: non-episodic, gradual onset gait/balance difficulties, dysarthria, clumsiness, incoordination of limbs, abnormal eye movement, degeneration of cerebellum - SCA 2, SCA 3, SCA 6 are most common

2) Members of palliative care team**

-Nursing -Medical providers= physicians and advance practice and providers -Social work -Chaplaincy -Pharmacy -Home health aids -Bereavement counselors

5) Describe the organization of the olfactory bulb**

-OB is part of telencephalon -granule cells seen

4) Summary of OCD, tourretts, and RLS**

-OCD is a disorder of though and or movement that is based in feelings of anxeity or distress -There is a high co-morbidity between OCD and tic disorders, as well as other neurologic disorders (KNOW HOW TO DIFFERIETATE AND PANDAS) -the neurocicrucity of OCD is very different from other anxiety disorders -Cortico-striato-thalamo-cortical loop for OCD -OCD is highly treatable with exposure and response prevention and SSRI, or other meds working on serotonin, while tics require other meds

Visual Acuity Technique

-OD= Right eye -OS = Left eye -OU= both eyes -SC= without correction -CC= with correction -ph= pinhole 20/40 most people see at 20 people you see it at 40

6) Zolpidem** (The 3 Zs)

-ONE OF THE 3 Zs -LESS ADDICTIVE -USED FOR SHORT TERM TX OF INSOMNIA -FALL ASLEEP FAST SIGN = QUICK ONSET AND SHORT DURATION AND WORK FOR THOSE WHO HAVE TROUBLE GETTING TO SLEEP BUT STAY ASLEEP -LESS LIKELY TO SEE TOLERANCE AND DEPENDANCE = RETURNS NOT TOLERATED -CAN USE FLUMAZEIL AS ANTIDOTE AS WELL= FLUFFY THE DOG -selective for GABA-A receptors containing alpha-1 subunits , non-benzodizepine BZD receptor agonist MOA: -selective for GABA-A receptors containing alpha-1 subunits PK: -ultra short acting -schedule IV -doesnt supress REM or N3 sleep (maintain quality of sleep) -recommend 7-8 hours of sleep before taking -tolerance will be seen SE: -residual daytime sedation*, ataxia*, and cognitive impairment -sleep while driving, cooking, having sex, make phone calls, increased with alcohol intake

CN III** $$$TEP

-Oculomotor -exits via the superior orbitial fissure -Motor (Afferent) -Somatic and visceral motor -emerges from the ventral mesencephalon medial to the cerebral peduncles -cell bodies located in oculomoter nuclear complex in the midbrain and terminate in medial rectus, inferior rectus, superior rectus, inferior oblique muscles, levator palpebrae surperioris, and ciliary ganglion -Does eye movement, upper eyelid movement, and pupillary response to light -CNS region = midbrain -Lesion = abnormal eye movement, ipsilateral ptosis, no pupillary reaction to light ipsilaterally

1.5) EEG findings**

-Odd numbers = left side of brain -Even numbers = right side of brain -Z= Central sagittal -FP = frontal pole -F= frontal -P= parietal -T= temporal -O = occipital -G= -C= Central coronal -Channels are the numbers -Fp2-F8 is channel and the difference between the two

CN I** $$$TEP

-Olfactory -exits via Cribiform plate -Sensory (Efferent) -Special sensory -small fila attached to olfactory bulb in telencephalon -cell bodies are located in olfactory epitheium -CN 1 terminates in the olfactory bulb in telencephalon -Does smell -CNS region = olfactory bulb -Lesion = ipsilateral ansomia (olfaction)

3) Location, conent, and drainage of the cavernous sinus**

-On the right and left side of the sella tursica -CN III, CN IV, Opthalmic V1 and Maxillary V2 of CN V, and CN VI all pass through -Cartoid artery passes through -If this structure is resticted can lead to weakness of all the innervations of those CNS

4) Delusional disorder DSM***

-One or more delusions with a duration of 1 month or longer -Criterion A for schizophrenia hasnt been met -able to function fairly well apart from the delusions -if any other symptoms of schizophenria has occured it is related to the delusions

3) Determine the most likely eating disorder diagnosis when given a case scenario***

-Only one single specific feeding or eating disorder diagnosis can be made for a patient (exception is PICA which can be cormorbid with all the other eating disorders) -Priority list 1) AN 2) BN 3) ARFID 4) BED 5) Rumination disorder -Lack of expressed fear of weight-gain or stating weight loss was unintentiinal does not screen people out for an eating disorder **** -High risk sports: wrestling, gymnastics, dance, figure skating, cheerleading, long and middle distance running

Mesencephalic Nucleus of CN V

-Only place with a pseudounipolar in the CNS -conscious proceiption for face especially the jaw -projects to the primary sensory nucleus -projects to the trigeminal motor nucleus Neuron 1: mesencephalic trigeminal nucleus -pseudounipolar neuron in midbrain Neuron 2: neurons in the main trigeminal nucleus receive input from mesencephalic V nucleus. Neuron 2 axons project to the VPM Neuron 3 VPM Neuron 4 Primary somatosensory cortex-face

Childhood absence epilepsy

-Onset 3-9 years of age -many seizures per day lasting 5-20 seconds -3/sec spike and wave on EEG -hyperventilation can provoke a seizure

CN II** $$$TEP

-Optic -Exits via the optic canal -Sensory -Special Sensory -connects to the eye to the diencephalon and mesenchephalon -CN II orginates from ganglion cells in the neural retina, the cells give rise to axons that form the optic nerve-> optic chiasm-> and optic tract -Axons terminate in the hypothalamus and thalamus in diencephalon -Does sight -CNS region = thalamus -Lesion = blindness

Levodopa** (Coiled Rope)

-PARK & SON'S BANK -COILED ROPE -TIED ROPE = DOPA DECARBOXYLASE OUTSIDE OF BRAIN = HOSTAGE THROWING UP, CARDIAC ARRHYTHMIAS, SLEEPING, ORTHOSTATIC HYPOTENSION = PERIPHERAL SIDE EFFECTS -BANK TELLER HOSTAGE = CENTRAL SE= ANXIETY, AGITATION, INSOMNIA, CONFUSION, HALLUCINATIONS -END DOSE EFFECT = THIN ROPE = RECURRANCE OF PARKINSONS SYMPTOMS -OFF AND LIGHT = ON OFF PHENONOMEN DUE TO CHRONIC TX -LONGER YOU ARE IN THE VAULT NARROWER THE WINDOW FOR ESCAPE = NARROWING WINDOW OF DOPA THERAPY -DYSKINESIAS = SHAKING MAN -VAN GOUGH PAINTING DAMAGED = CONTRAINDICATED IN PSYCHOTIC PTS -Dopamine synethesis adjuvants -immediate precursor of dopamine -can cross BBB converted to Dopamine via DOPA decarboxylase (which is everywhere in body, so to minimize peripheral metabolism its given with carbidopa*) -most effective drug -increases lifespan and improves quality of life -In Early PD there are plenty of neurons to reuptake DA and see normal action of DA release, but in later PD lose more neurons so the DA is then just directly binding to postsynaptic receptors so have too much DA effects then leading to dyskineia and motor fluctuations Uses: -preserved for later use cuz it eventually leads to motor fluctuation -RLS SE: -Peripheral SE (not as common now due to carbidopa) = N/V, anerexia, CV othrostatic hypotension, arrhythmias -Central SE = psychiatric (hallucinations, psychosis, depression, somnolence, insomina, impulsive and worsens schizo remember) , these will be worsened by carbidopa -Motor fluctuations and dyskinesia

Pramipexole**(Pecks)

-PECKS ROBBER = PRAMIPEXOLE -D3 DOPAMINE RECEPTOR AGONIST -INTITIAL TREATMENT OF PARKINSONS AND USED AT THE END (BEGINNING OR END) -RESTLESS LEGS ON THE ROPE LATER = TX RLS (1ST LINE) -SE SIMILIAR TO LEVODOPA BUT CAN MAKE CNS (BANK TELLER) SE WORSE, ESPECIALLY CAN MAKE YOU MORE IMPULSIVE (THINK OF TAKING OFF SHIRT) SHOW OFF YOUR PECKS AT THE BEGINNING OF THE POOL PARTY AND AT THE END -dopamine receptor agonist -D2 receptor agonist -simple require no metabolism and not inhibited by BBB Uses: -early PD and combo with levodopa for advanced PD -RLS

Plexopathy **

-PNS involvement at the point where spinal nerves intermingle (in plexuses) before forming nerves that go to the extremities

2) Carbidopa** (Cop Car)

-POLICE CAR -BLOCKING THE DOPA DECARBOXYLASE ROBBER -ROBBER PULLS ON SE ROBBER REDUCING SE, EXCEPT THE BANK TELLER SE (CENTRAL SE) HES COMING WITH THEM AS INSURANCE -Dopamine synthesis adjuvants -given with levodopa -inhibits peripheral metabolism of DOPA decarboxylase then decreasing the SE (on heart and GI system) seen with giving massive amounts of Levodopa -Will not cross the BBB

2) hemorrhagic strokes** (Indicatcations ad contrindications for tx of acute ischemic strokes)

-Parenchymal or Intracerebral Hemorrhage -Causes: HTN> amylid angiopathy> anticoags> neoplasm> presc or illegal drugs> AVMs and aneyryysms> miscellaneous -Charcot-Bouchard microaneurysms TX** -monitoring and management in ICU -consider reversal of anticoag, platelets replacement causes -Acute arterial HTN managemetn need <140 -DVT propophylais : compression, LD anticoagulation -dysphagia screening, nutrition, hydratio -hyperglycemia and electrolyts -intracranial HTN monitoring -hydrocephalus -seizure treatment and NO prophylaxis -surgery and decompression, indicated for cerebelar ICH, and possibly ICA

2) Gait disorder dx of

-Parkinsonian: -Hemiplegic -Paraplegic -Myopathic -Steppage -Functional

Menieres disease vertigo*

-Peripheral etiologies -In 40s -deficient absorption of the endolymp -feel ear fullness, pressure, hear rining and seashell, -can be triggered by salt make sure to restrict salt and dieurtics -MRI and auditometry -Chronic recurrent dizziness that lasts 20 mins to 24 hours WITH HEARING LOSS (sensionerual, fluctuating, and progressive)***

1) Summarize the basics of human development including principles of personality, temperament, and regression under stress**

-Personality = who we are -Character = habits/experiences -Temperment = innate preferences -character + temperment = personality

Personality Disorders*

-Personality disorders are EgoSyntonic = limited insight, its everyone else's problem NOT MINE -Personality disorders = enduring pattern, deviates markedly, pervasice and inflexible, onset in adolesce, stable over time, leads to distress and impairment -Manifested in 2 or more ways : Cognition (how the see the world and themselves) , emotional response (full range of emotions) , interpersonal functioning (how they get along with others) , impulse control -Tx with psychotherapy= CBT (problem solving) and dialectiaal behavior therapy (DBT) more for borderline PD, helps patients have more control over their feelings pharmocological treat the symptoms such as depression or anxiety

Optic Radiations (Temporal Lobe) **

-Pie in the sky defect**

1) Examine temperature and pinprick sensation**

-Posterior columns and anterolateral sensory system are most important for somatosensory deficits -Somatosensory refers to bodily sensations of touch pain, temp, vibration, and proprieception** -Comparisons should be made from one side of the body to the other and from proximal to distal on each extremity -If needed the exam may be repeated to make sure the findings are reporducible Light Touch: exactly as it sounds Sharp touch: exactly as it sounds Temperature: cool touch with tuning fork Two Point Discrimination:

6) Major landmarks and levels of the spinal cord**

-Posterior median sulcus = smaller -Anterior median fissure = wider

Amyotrophic lateral sclerosis** (ALS)

-Protein defect = TDP-43 -degenerative disorder of motor neurons -presents in middle age with weakness of the extermities -may develop bulbar signs and symptoms such as dysphagia and dysarthria -males more commonly affected -3 Types: 1) Sporadic = 90-95% of cases 2) Familial see SOD1 gene mutations in 20% of familial cases, SOD1 encodes superoxide dismutase on chromosme 21 , are AD 3) Western Pacific ALS (ALS-PDC)

Frontal temporal dementia**

-Protein defect = Tau -causes personality change, language dysfunction, and globial cognitive decline -Frontotemporal lobar degeneration (FTLD) is the neuropathy of FTD -Most common type is Pick's Disease Pick's Disease - Tau -See it frontal and temporal

Alzheimer's Disease**

-Protein defect = beta amyloid, Tau -extracellular deposition of beta amyloid are insoluble and will lead to senile plaques (Primary) -intracellular accumulation of hyperphosphorylated tau protein are insoluble and will lead to neurofibillary tangles (NBT) (secondary) Etiology: -familial (5-10%), -early onset AD commonly linked to chromosome 14 -sporadic and familial AD patients exhibit increassed aneuploidy particulary trisomy 21 Histo; -neurtic plaques not diffuese lead to pathology -amyloid angiopathy (thanos ship) (not dx of alzeheimers) -NBTs -increased risk for hemorrhage when have amyloid angiopathy (thickened BVs walls prone to rupture)

Hintington's Disease**

-Protein defect = polyglutamine-expanded (PolyQ) -AD -presents in 30s-40s -chromosome 4 problem -See CAG repeats (more the worse the disease) -striatal medium-sized neurons undergo selective degeneration -Caudate atrophy leads to enlarged ventricles

Prion disease**

-Protein defect= prion -Spongiform encephalopathy -Transmissible dementia -Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker disease, fatal familial insomnia, Kuru -Accumulation of prion protein that contains no DNA or RNA -age of onset in familial is 55-75 -rapidly progressive demetia followed by death with 1-2 years

9) Tiagabine** (Tie in the car door)

-RAISING THE GABA CAB -INCREASES GABA BY DEC REUPTAKE = TIE GETTING TAKEN UP BY BLOCKING GAT-1 -SHIT WILL HANG YOU IF YOU USE IT WRONG = DONT USE IF DONT HAVE EPLIPSEY CUZ CAN GIVE YOU EPLISPSY -BLOCKS GAT-1 = GABA UP TAKE-1 (GUT-1 = GAT-1) -newer MOAL -inhibtis GAT-1 mediated reuptake of GABA Uses: -Add on for refractory partial seizures -off-label use discouraged cuz can cause seizures in pts without epilepsy SE: -dizziness, somnolence, tremeor, can enchance absence seizures

Optic Radiations***

-RETINOTOPCIALLY ORGANIZED = fibers from superior radiation reprsent INFERIOR visual field -fibers representing inferior retinal quadrants represent the SUPERIOR visual field -Meyer's loop = superior visual field, terminates in inferior quadrant in calcarine fissure or lingual gyrus -Superior retinal quadrant terminate superior to the Calcirne fissure or the Cuneus gyrus

Dix-Hallpike maneuver*

-Rapidly moving the pt from a sitting position to the supine position with the head turned 45 degrees to the Right. After waiting apx. 20-30 sec, the pt is returned to the sitting position. If no Nystagmus is observed, the procedure is then repeated on the Left side. Peripheral: -nystagmus 2-20 second latency and resolves in <1min -fatigues with repetition -severe vertigo -nystagmus occurs in one direction Central: -nystagmus occurs right awas -lasts >1 minute -doesnt fatigue -nystagmus may change direction in a single head position -less severe to no vertigo

7) Clinical indicators for referral with glaucoma**

-Recognize risk factors, characteristic optic nerve appearance, and refer appropriately -A cup: disc > 0.5 -Cup: disc asymmetry of >0.2 (non urgent referral) -Symproms of angle closure glaucoma like headache, eye px, decreased vision, halos, N/emesis (URGENT referral) **

Spinal Cord Lesion Summary **

-Red = motor loss -Green = pain and temp sense loss -Blue= Vibration and position sense loss

7) Describe the stages of sleep**

-Reticular formation is important in the regulation of sleep -orexin is involved in wakefulness and appetite, loss of this = narcolepsy -Melatonin regulates circadian rhythms -Suprachiasmatic nucleus (SCN) controls relaease of melotonin from the pineal gland via projections to paraventricular nucleus the to the intermediolateral cell colomn, then to the superior cervical ganglion t -SCN also projects the lateral hypthalmamus which releases orexin -Sleep wake cycles are controlled by SCN in hypothalamus Stage 1 &2 = light sleeo Stage 3&4 = deep sleep REM sleep

Sugammadex**

-Reverse Steroidal non-depolarizing NMBs MOA: -slectively binds sterodial NMBs in plasma, reversing the concentration gradient and driving transfer from NMJ into plasma, produces faster reversaly than ACHEIs SE: -anaphylaxis, bradycardia, inactivates BC

Allergic Conjuctivitis

-S/S: Itching -Tx: H1 R antagonist and mast cell stabilizer

Corneal Abrasion***

-S/S: pain and tearing -epithelial defect with flourescein stain

4) Describe the function of the suprachiasmatic nucleus in generating circadian rhythms**

-SCN regulates daily rhythms henced called circadian pacemaker -it receives info from the photosenstivte ganglion cells in the retina -SCN projects to region near PVN then projects to IML of spial cord, preganglinionic neurons in IML project to superior cervical gaglion which project to the pineal gland, the pineal gland secretes melotonin at night

2) Identify the commonly used topical agents, including their ocular effects and potential side effects (ocular and systemic)*

-SE: local type 1 IgE mediated hypersenstiivty rxn , be careful with old people -Chronic repeated use of -caine anesthetics can lead to perforation to the corneal epithelium and lus should never be prescribed to a patient -Eye decongestant meds those ending in -zoline and phenylephirne can cause acute angle-closure glaucoma in patients with narrow angles -Topical antibiotics should be avoided if an open globe is suspected

3) Trazodone** (TRAMBONE PLAYER) (TrazoBONE)

-SEROTONIN MODULATIOR -antagonizes 5-HT receptors and inhibits 5-HT reuptake = drummer hitting the smiley drum while wearing 52-Ht -Antagonized Alpha 1 recptors = leads to vasodilation can lead to 4 hour erection (priapisom) can cause perminent damage AND orthostatic Hypotension , and bleeding -H1 antihistamine receptor antagonist -Not first line only used for patients with insomnia and major depression (sleeping basketball team ) -Not used with old people and other sedators -Does cause sexual dysfunction (splashes water on band) -Sertoinin syndrome = smilely basketballs getting knocked over -Anatagonizes 5-HT2A* and inhibits SERT, blocks a1, and H1, No effect on M receptor -5-HT2A antagonism may decrease SE associated with SSRI

Selegiline** (Sledge Hammer)

-SLEDGE HAMMER KILLING THE BLACK MOUSE THE MOA-B WHICH IS EATING UP THE DOPAMINE ROPE -USED AS AN ADJUNCTIVE MED -CAN WORSEN LOVADOPA SE -SE THINK OF OLD VIDEO SS, INSOMNIA, DIZZINESS, DYSKINESIA, -MONOTHERAPY EARLY AND AGAIN LATE TO HELP IN PHASE 2 = KILL MICE IN THE BEGINNING OF THE SPRING AND IN THE END OF FALL -Dopamine metabolism (MAO/COMT) inhibitor -inhibits degradation of endogenous dopamine in CNS -enhances and prolongs the effects of levodopa Uses: -monotherapy in early PD -used with levodopa-carbidopa to reduce motor fluctuations , helps treat off stage SE: -Headache, insomnia, dizziness, will increrase dyskinesia, Sertotonin syndrome

4) Duloxetine** (DUAL COPIER/SCANNER)

-SNRI (NORTH SOUTH COMPASS) -1st Line for MDD, major anxiety disorders, PTSD, -Useful for diabetic neuropathy, low back pain, osteoarthritis, fibromalagia (FIBER BARS) -SE: HTN (Stanely w/HTN) , serotonin syndrome, flue like symptoms with withdrawl (out with the flu) -2 month calendars = takes 1-2 months to work at max strength -inhibit the presynaptic reuptake of norepinephrine and serotonin MOA: -inhibition of SERT and NET (SERT>NET), no action on a1, H1, M receptors

Rule VIII: Use highly localizing signs: Horner's Syndrome**8

-SPAM -> Sunken (enophthalamus), Ptosis, anhidrosis, miosis -horner's contralateral to muslce weakness-> CNS. -Horner's ipsilateral to muscle weakness-> Consider PNS -Central Horner's can associate to weakness due to UMN injury (say a stroke on the pons) -Peripheral horners can associate to weakness due to LMN injury (say a tumor outside the spine)

Assessment of Visual association

-Screening tools -detailed neuro-psychological profile (boston cookie theft picture)

LGN Lesions*

-Sectoranopia = two more hemi VFs -caused by lateral choroid artery and anterior chorodial artery occulsions

Magnocellular Neurons histo

-Seen in the PVN the axons are what the arrows are pointing to

3)Trigeminal Autonomic Cephalgias**

-Severe unilateral pain within the trigeminal nerve distribution -ipsilateral cranial autonomic features (lacrimation, conjuctival injecton, nasal congestion, rhinorrhea) -differentiation depends on severity and longevity 1) Hemicrania Continua -continus unliateral sharp or throbbing pain in the frontal or temproal region -lasts 24 hours -photophobia, phonophobia, Nasue common -Responds to indomethacin 2) Cluster Headache -Most common ** -lasts 15mins - 3 hours -sudden severe pain stop them in tracks -unbarable pain -get a lot of autonomics sysmptoms -more common in men -can happen 8x a day but can be inbetween months -Triptans, oxygen 100%, greater occipital neurve block, steroids -Prevent with verapamil** , topiramte, lituum and melatonon 3) Paroxysmal Hemicrania -duration 2-30 mins -responds to indomethacin 4) Short lasting unilateral neuralgiformm headache attack -1 minute headache -autonomics involved -happens 59 a day -tactili stimuli can trigger

Parkinsonian gait*

-Shuffling gait, turns accomplished in very stiff manner, decreased stride length -Flexed posture: Stooped-over posture with flexed hips and knees. -Narrow base -Cadence initally inc -Gait speed slow -festination, freezing, difficulaty with gait initation -postural instablity, retropulsion (cant stop going backwards) -dec or lack or arm swing -turn en bloc (several steps to turn)

Varenicline* (Chantix)

-Smoking cessation -MOA= partial agonist of Nn receptors containing a4B2 subunits, acts as a nicotine subsitute (decreases withdrawal symptoms) but also antagonizes full agonist effects of nicotine in cigarette smoke (reduces reward if you do smoke) -SE: N/V, headache, insomnia, and abnormal dreams, CNS depression, hypersensitivity reactions, SJS, CV events boxed warning for neuropsychiatric response

CN XI ** $$$TEP

-Spinal accessory -Exits via the jugular foramen -Motor -Branchial motor -emerges ventrally from the medull, inferior to CN X -cell bodies in accessory nucleus in the caudal medulla and C1-C5 in the spinal cord and terminate on the sternocleidomastoid and trapezius -Does the movement of the traps and SCM -CNS region = caudal medulla/spinal cord -Lesion = ipsilateral weakness of the SCM and traps

3) Spinal cord injury understand the pattern and location of injury**

-Spinal facture ISNT a Spinal cord injury but can occur together -Spinal cord ends at L1-L2 area -Spinal shock: 1) Loss of DTR after spinal cord injury, despite intact reflex arc, DTR come back and are hyperreflexive when they due 2) Decreased organ perfusion due to low BP secondary to lack of sympathetic output (neurogenic shock = low BP, low HR** (should be fast if losing blood) -20% of spine fractures have a secondary level of injury -Spinal cord and brain injury go toghether -Can use a ASIA score system to assess Management: -ABCD's -Immobilaization -Neuro exam : GCS, pupils, EOM, motor, sensory, reflexes (DTR, pathologic) , rectal exam -Imaging : full body CT without contrast -BP goal is >90 mmHg -airway must be open -Methylpredinsolone protocol = no longer used but typically used for spinal cord trauma

10) development of the spinal cord and spinal nerves**

-Spinal nerve development exemplifies axon pathfinding -Primary somatosensory neurons differentiate in the dorsal root ganglion (neural crest deritive). The neurons begin as bipolar cells but change into psuedounipolar neurons, one enters spinal cord dorsally and other extend towards periphery -Motor neurons differentiate in the ventral horns of the spinal cord (neural tube derivative) their axons exit the ventral roots and terminate on muscles -30 segments = 30 spinal nerves -Vertebral column grows faster than spinal cord leading to a lumbar cistern allowing a space for CSF to be tap

Necrotizing autoimmune myopathy**

-Subacute, severe progressive proximal weakness -Very high CK (5200) -seriology = anit-SRP, anti-HMGCoA, CT disease, paraneoplastic -1/3 dysphagia and 1/3 dyspnea -Early aggressive dual immunotherapy improves prognosis

2) History and exam of acute red eye**

-Sudden or progressive? -Timeline of symptoms, intermittent? -Co-workers or family w/ red eye -Trauma or unusual activyt -Contact lenses? How worn? -Recent URI? -Vision disturbances? -Discharge? Classify -Itching? -Do symptoms change with environment? -Photophobia? -PMH, meds, allergies, FH, SH? -OTC or Rx eye meds Key Exam points: -Visual acuity** -Pattern of hyperemia (one eye goes up) -detect and classify any conjunctival discharge -detect opacities of the cornea -search for disruption of corneal epithelium using fluorescein strips -estimate AC depth as normal or shallow, detect any hyphema or hypopyon -Detect pupil irregularitis, anisocoria, rxn to light -IOP meausurement if suspected elevation of pressure or angle-closure -detect proptosis, lid malfunction, or EOM deficity

4) Asses cutaneous reflexes and provide a ddx based on the findings**

-Superificial or Cutneuas reflexes is stimulation of receptors in the skin (and mucous) eliciting superficial (skin-muscle) reflexes -Deep Reflexes = stimulation of receptors deep to skin in muscles causing muscle stretch reflex Cutneaus Refelexes: -corneal reflex -gag reflex -abdominal reflex -anal reflex -bulbocacernous reflex -Plantar reflex = supposed to be the most reliable cuz its the furthermost from brain (scratching S1 area ) = lateral and plantar side, normal reflex is a negative babinski sign (curling toes). Babinski = stretch out toes, helps differentiate UMNs from LMNs, MUST obtain a response if not getting stimulus you can first change length, then pressure, then and or velocity + Babinski's = UMN lesion No reflex = LMN lesion

11) Effects of lesions in different parts of the cerebellum and related pathways**

-Symtoms are ipsilateral -patterns of loss = ataxia -Includes vestibulocerebellum, spinocerebellar, and cerebrocerebellum lesions -Can also include slurred speech, and abnormal swallowing

Dopamine $$TEP

-Synthesized in Ventral tegmentum, SNc -decreased in depression -increased in schizophenria -increased in huntington -decreased in parkinsons

Serotonin $$$TEP

-Synthesized in the Raphe nucleus -decreased in anxiety -decreased in depression -decreased in parkinsons

lateral geniculate nucleus (LGN)**

-THALAMUS -the part of the thalamus that receives information from the optic tract and sends it to visual areas in the occipital cortex -primarily receives input from the fovea -LGN projects to the area 17 (primary visual cortex) via the optic radiations -CELL BODIES OF THE OPTIC RADIATIONS IN LGN

6) Haloperidol** (HALO IN STARRY NIGHT PAINTING)

-TYPICAL Drug -High potentcy = higher risk of EPSE but less sedating Uses: -Schizophrenia, behavioral problems in peds, tics/vocalization in tourettes, delirium, OCD, N/V, sedation of severly agitated pts HALO HIGH IN THE SKY = HIGH POTENTCY -USED IN ACUTE PSYCHOSIS AND VIOLENT PATIENTS -PULLS ON D2 ROPE (REDUCES DA) -BLOCK POSITIVE SYMPTOMS = BLOCKING POSTITIVE VOICES CUZ VAUNHGO CUT IS EAR OFF -HIGHLY LIPOPHILIC = LONG FLAG = LONG HALFLIFE SE: -EXTRA PYRAMIDAL HAT = EXTRAPYRAMIDAL SYMPTOMS (EPS) (most common with haloperidol) - actue dystonia = viewer with cocked head -akathisia = restlessness = flipping chair - parkinsonism = cog wheels on carriage -tardiva dyskinesia = guy sticking out his tongue -HYPERPROLACTINEMA= guy with milk coming out of nose -Neuroleptic malignant syndrome = EXTRA SPICY CHICKEN BUCKET, LEAD-PIPE RIGIDITY, CRAXY, SWEATY, TACHYCARDIA, RHABDO, -QT PROLONGATION THEN TORSADES = TWISTED STREAMER -SHAKING ESCAPEE ON ROPE = SEIZURES

Gene-environmental Interaction

-Temperament is based both on genes and environment -Goodness of fit

1) Somatic symptom Disorder****

-The DSM 5 changed the rule from that the somatic symptoms being medically unexplained TO somatic symptom disorder can be diagnosed in patients with general medical disorders DSM-5: -Presence of atleast one somatic symptom that coauses distress or impairment -pattern of abnormal behaviors, thoughts, or feelings related to physical symptoms -may or may not have a diagnosed medical condition -symptoms not intnetionally produced -Last for at least 6 months Risk Factors: -Female, fewer years of education, lower SCS, Hx of childhood chronic illness, Hx of sexual abuse or trauma, concurrent general medical disorders, concurrent psychiatric disorders**, FHx of chronic illness Gen: -greater number of somatic symptoms = worse prognosis -doctor shopping is common -high risk of attempted suicide Cormobid Conditions: -30-60% have anxiety and or depressive disorders -increased risk of a personality disorder -risk to have cormorbid cond is recent stress, poor self-reported helath status, greater # of somatic symtoms Tx: -regular visits with PCP -establish collaborative therapeutic alliance -acknowlege health fears -limit dx testing and referrals -make sure assure dont have serious medical disorders -may need referral to psychiatrist for pharm or psychotherapy -explicititly make functional improvement the goal of tx

The Arcuate nucleus and Infundibulum histo

-The ZI or inter zone is where axons for the posterior pituatory pass through -The ZE is the external zone is where the median eminence is and where axons will terminate and sysnapse and end up in the anterior pitutartory gland -Squiggly lines are the capilllaries

5) Describe the anatomy, connections and function of the amygdala**

-The amygdala is rostral to the hippocampal formation and the inferior horn of the lateral ventricle -involed fear learning and the link between emotion and memory, involved in feeding and reporductive behavior -the mark for it is the uncus -typically discussed with the limbic system but is technically part of the basla ganglia -Receives info from olfactory bulb via the lateral olfactory stria and entorhinal cortix -Has reciprocal connections with the frontal and temporal neocortex -Lesioned amygdala pt cannot differentiate emotional expressions from fearful facial expression -Uncinate fits = lesion of uncus and amygdala can lead to strange unpleasant odor and feeling of unreality (amygdala)

11) Blood supply of the spinal cord and brain**

-The anterior 2/3 of the spinal cord including the ventral horn and lateral funiciulus are supplied by the anterior spinal artery -Posterior 1/3 of the spinal cord including the dorsal horn and dorsal columns are supplied by the posterior spinal artery -Circle of willis is in close proximity to the optic chiasm and the pituitary gland -Most of the lateral surface of the cerebral cortex is supplied by the middle cerebral artery (MCA) -Most of the medial surface of the cerebral cortex is supplied by the anterior cerebral artery (ACA) -Posterior part of the brain is supplied by the posterior cerebral artery (PCA) -Basal ganglia is supplied by lenticulostriate arteries -borders between the cerebral arteries are espically vulnerable to strokes

6) Describe the mesolimbic system including the anatomy, connections and function of the ventral tegmental area**

-The axons of the ventral tegmental area make up the mesolimbic system and project to the nucleus acumbens (part of striatum of basal ganglia and is invovled in motivation and reward and is connected to addiction) as well as many other areas of the limbic system -VTA found in MIDBRAIN and contains dopamine -It is a reward pathway -main transmitter is dopamine

Cerebellar pathways***

-The motor cerebral cortex projects to the pons -The ventral lateral nucleus of the thalamus (VL) receives info from the dentate nucleus of the cerebellum and projects to the premotor cerebral crotex -Deep nuclein of the cerebellum project to the red nucleus and the VL via the superior cerebellar peduncle (SCP) -Purkinje cells (PC) project to deep cerebellar nuclei (DN). the pons project to the contralateral cerebellar cortex via the middle cerebellar peduncle (MCP) -neuronal cell bodies in the vestibular ganglia (VG) project to the vestibular nuclei (VN) which project to the granule cells in the cerebellar cortex via the inferior cerebellar peduncle (ICP) -Unconscious propreciption, mediated by neurons with their cell bides in DRG is conveyed to granule cells in the ipsilaterl spinocerebellar tracts

Alzheimer's

-The risk of getting alzheimers is strongly related to the APOE genotyple but none of the APOE genotype makes it certain you will get alzheimers -2 APOE4 genes = high risk of developing alzheimers (67%) -APOE 2 is a rare protective gene against alzheimers -APOE3 is most common, contray to note -Increased education seen to reduce the risk of developing of alzheimers due to development of alternative pathways

Inner and outer hair cells histo

-The tunnel of corti is the triangle in the middle -On the left towards the middle of the cochlea with only 1 cell is the inner hair cells -On the right of the tunnel of corti towards the lateral part of the cochlea with 3 cells are the outer hair cells - Organ of corti conatains everything above -tectorial membrane is above the organ of the corti, the sterocilia of the hair cells is embedded in this gelantinous membrane -

5) Describe how the hypothalamus regulates feeding**

-The ventromedial nucleus of the hypothalamus (VMH) is invovled in regulating satiety. it may contain receptors for glucose lesion in this structure leads to obesity -Lateral hypothalamus is involved in regulating hunger. Lesions in this area result in anorexia Leptin = releases signals of satiety if lesioned = obesiety. Leptin is a protein secreted by fat cells Ghrelin = signals hunger, released by stomach

1) cerebellar peduncles**

-There are 3 cerebellar peduncles which connect the cerebellum wit the brainstem 1) Superior cerbellar peduncle is attached to midbrain 2) Middle cerebellar peduncle is attached to pons 3) Inferior cerebellar peduncle is attached to medulla

3) Psychotic Disorder Due to Another Medical condition**

-There are a lot One's He Talked about: 1) Temporal Lobe Epilepsy-40% experience psychosis,esp olfactory and religious delusions 2) Lesions of occipital lobe= may cause visual hallucinations 3) Metastatic renal cell carcinoma 4) Subarachnoid hemorrhage = may cause capgras syndrome (everyone is an imposter) 5) Subdural hematoma = may present with blunted affect mimicking negative symptoms of schizophenria, catatonia 6) Argyll robertson pupils (syphilis) = pupils accommodate but don't react to light -Catonia is a lot of things but talked about holding fixed positions and can be caused by many medical causes

4) Anxiety Disorder Due to Another Medical Condition**

-There are a lot of medical causes -Talked about a basal ganglia stroke -Tx: to avoid future stroke and can treat with normal anxiety meds

4) Describe the corticospinal and corticobulbar projections**

-These are UMN's -The cell bodies origin in the precentral gyrus of the cerebral cortex Corticobulbar: -axons terminate in LMN's of brainstem (aren't found in pyramids of the medulla or in the spinal cord) -bilateral projections with exceptions OF Facial and hypoglossal -control muscles of the head -lateral area of the precentral gyrus controls the face and head movements and give rise to the corticobulbar tract. Corticospinal tract: - axons terminate on LMNs in the ventral horn of the spinal cord -control muscles of the body -projections is primarily contralateral -Besides the lateral area of the precentral gyrus the rest gives rise to cortiocospinal

5) Define threshold, absolute refractory period, relative refractory period and "all-or-none" as they apply to action potentials***

-Threshold = membrane potential above which the depolarization is sufficient to generate an AP -Absolute refractory period = a new AP cannot be generated no matter the how strong the stimulus -Relative refractory period = the threshold is elevated, due to inactivated Na+ channels further down the line, need a larger stimulus than normal to reach threshold -All-or-none= doesnt matter the amount of stimulus receives as long as it reaches threshold it will result in same magnitude of AP

1) Recognize different presentations of tics (Tourettes) **

-Tics = abrupt, often repetitive, sudden movements or vocalizations that are preceded by an uncomfortable feeling that is relieved by the act -fast movements they are trying to conceal (speech counts) -Transient tic disorder = child disease -Chronic tic disorder = motor or vocal but not both -Tourette syndrome = motor and vocal tics fluctuation for at least 1 year -childhood onset -males more -familial -utterance of foul language is uncommon -increases with stress, waxs and wans with transient remission -Tx: many do not need treatment, if effets self-esteem should treat First line = behavioral reversal therapy (CBT)**, Second line is pharmacological therapies (clonidine) -Can use Botox and DBS

3) Clinicial characteristics of acute and chronic vertigo**

-Time course is huge Chronic = bening Acute= severe -Triggers is important to know 1) Standing = orthostatic

3) Primary Open Angle Glaucoma**

-Trabecular meshwork is the primary site of resistance*** -Hx: very important 1st degree relative -Risk Factors = Cup-to Disc Ratio -POAG has open angle on gonioscopy

Optic Tract Syndrome**

-Traid 1) Homonymous heminopia= lose one half of total visual field 2) Optic atrophy 3) Contralateral RAPD

1) Traumatic brain injury describe the spectrum of injury types**

-Trauma leading cause of death in young people -multiple injuries will often occur together look for more Scalp Injuries: -abrasiaon, contusion (bruises), laceration Skull Fractoures: -linerar vs comminuted (pieces) -depressed vs non-depressed (not shoved in) -open vs closed (skin not pierced) -basilar skull fractures - battle's sign (bruising) = from a mastoid fracture raccoon eyes (bruising) = from a frontal skull base fracture, -depressed cominuted, open fracture = hit by hammer or golf club -Injuries can be focal = contusion or diffuse = concussion, diffuse axonal injury

1) Movement Disorders General**

-Tremor = oscillation -Chorea = jerk -Dystonia = excessive muscle contraction -Myoclonus = very fast jerk -Tics= fast movements they are trying to conceal -Akathisia = jittery, need to move -Sterotypiae= usually kids, -All dystonia and parkinsonism patient deserves a trial with levodopa

Normal Pressure Hydrocephalus (NPH)***

-Triad of symptoms: gait apraxia (magnetic gait), incontinence, mild cognitive impirment -Tap-test (does it get better following a spinal tap) used to dx and treated with VP shunt -If have all 3 symptoms =better prognosis or if its secondary (menignitis, subarachnoid bleed) -70% of selected patients improve

CN V*$$TEP

-Trigeminal -V1 exits via the SOF -V2 exits via Foramen rotundum -V3 exits via Foramen ovale -Both Sensory and Motor -Branchial motor and General Sensory -emerges from the lateral pons -cell bodies located in the sensory trigeminal ganglia and cell bodies of motor located IN brain IN motor nucleus of V in the pons, sensory axons enter and motor axons exit -Does somatosensation in face and muscles of mastication -CNS region = pons and medulla -Lesion= ipsilaterla loss of somatosenesation of face and ipsilateral paresis of muscles of mastication

CN IV**$TEP

-Trochlear -Exits via the superior orbital fissure -Motor -Somatic motor -emerges from the dorsal mesenchephalon and then proceeds ventraly outside the brain -Cell bodies located in trochllear nucleus in the midbrain, the axons cross* to the contralateral side and exit dorsally* and terminated on the superior oblique muscles -does eye movement -CNS region = midbrain -Lesion = abnormal eye movement

2_ Understand the initial work up of hearing loss**

-Tuning Fork: 512/1024/2048 Hz 1) Weber (localization) -CHL = lateralizes to poorer ear -SNHL = lateralizes to better ear 2) Rinne (conduction) -Air Conduction > Bone conduction postive test is within normal limits or SNHL -Air conduction < bone conduction negative test is CHL -Audiogram Hearing level 0-20 is norma 20-40 mild hearing loss 40-70 = moderate hearing loss 70-90 = severe hering loss 90=120 = profound hearing loss -Specialized Audiometric testing used in the hospital for a newborn either an Audiometric brainstem response > or an Otoacoustic Emission

Neurotransmitter Loading**

-Two ways to do it: 1) Exchange: -cationic (5HT{serotonin}) transmitters are exchanged for protons with proton transporter and vesicular transporter 2) Electrochemical gradient: -proton pump generates electrochemical gradient for anionic neurotransmitter uptake (this example was glutamate) -creates + environment in vesicle attracting the (-) anion (glutamate)

Pompe disease**

-Type II glycogen storage disease (AR) -Lysosomal acid a-1,4-glucosidase with a-1,6-glucosidase activity (acid maltase) deficiency -Cardiomegaly -Hypertrophic cardiomyopathy -Hypotonia -Exercise intolerance -Systemic findings lead to early death (heart, liver, muscle) -all types of onset -Adult onsest = prxomal, axial myopathy with fewuent respiratory failure, 1/3 scapular winging -Dx: EMG with myopathy and myotonic discharges, GAA activity in blood, genetic testing, vacules full of glycogen -Tx is ERT (enzyme replacement therapy )

4) Chlorpromazine** (STARRY GAZING)

-Typical -Low potency = lower risk of EPSE but more sedating Uses: -psychosis, N/V, behavioral problems in peds, intractable hiccups, control behavior in elderly w/ dementia, huntington' chorea -COLORS ON THE FLOOR = LOW POTENCY -PULLS ON D2 ROPE (REDUCES DA) -BLOCK POSITIVE SYMPTOMS = BLOCKING POSTITIVE VOICES CUZ VAUNHGO CUT IS EAR OFF -HIGHLY LIPOPHILIC = LONG FLAG = LONG HALFLIFE SE: -ANTI-CHOLRINERGIC EFFECTS (dry as hair (urinary retention and dry mouth) constipation, blind as a bat (blurred vision) -ORTHOSTATIC HYPOTENSION DUE TO ALPHA A EFFECTS -H1 HISTAMINE EFFECTS DUE TO H1 ANTAGONISTS = SEDATION AND WEIGHT GAIN -QT PROLONGATION THEN TORSADES = TWISTED STREAMER -SHAKING ESCAPEE ON ROPE = SEIZURES -CORN YELLOW PAINT = CORNEAL DEPOSITS

hemiplegic gait**

-Unilateral lesion of the corticospinal tract -due to weakness and spasctiity there is decreased knee flexion and ankle dorsiflexion -stiff extended leg that cricumducts during swing -associated with weakness in pyramidal distribution and hyperreflexia -UMN problem

ALS**

-Upper and lower motor neuron disorder -cause of death is respiratory weakness -Risk factor: Age, male, white, -Increase oxidative stress, astrocyte disfunction, glutamate reuptake impaired, -familial ALS is 5% rare is AD, most common mutation is C9orf72 expansion > SOD1 mutation Histo: bunina bodies in cytoplasm of neurons S/S: -starts as focal asymmetric limb onset -fsyarthria, dysphagia, drooling, reduced ability to cough -fasciculations muscle twitching of tonge/limb muscles -cramps -hyperreflexia -spasticity stiffness of legs or arms -weight loss, muscle loss, worsening fatgue -pseudobulbar affect (emotional rollercoaster) -cognitive impariemtnt in 50% -UMN and LMN signs -DONT usually see pain, tinghling, incontinence, EOM abnormalities Dx -UMN and LMN involvemetn -progessive weakening -EMG in ALS helps confirm diagnosis -PFT test shows restrictive DDx: -cramp-fasciculation syndrome, motor only neuropathies, SMA, SBMA, Management: -no cure -Riluzole (glutamate antagonizes) -non-invasive ventilation * -symptom management Prognosis: Poor -3-5 year survival -5% choose mechanical ventilation

Alcohol**

-Use AUDIT-C as a screening tool -BAC = each drink adds about to 0.02-0.03, zero-order kinetcs drop of 0.015 BALs (Blood alchol levels): -degree of tolerance predicts symptoms of intoxication -Non tolerance (alchohl) 0-100 mg tranquil, 100-150 clunsy belligerent 150-25 lethargic, labile >250 confusion stupod, >350 disorientation ocma >450 respiratory depression, death Liver Functi0on tests: -Aspartate aminotransferase (AST) :muscles -Alanine aminotransferase (ALT) : exclusively found in liver** -Ratio of AST: ALT over 2 suggests alcoholic liver disease -ALP is alkaline phosphatase: cells lining the biliary ducts of the liver Complications: Liver disease, pancreatitis, esophegeal tears and bleeding, amllory-weiss tears, gastritis, intestinal malabsorption, malnuttrion, THiamine (Vit B1 defiency) Wernicke-Korsakoff Syndrome: -Wernicke's encephalopathay (reversible) TRIAD = ocular changes, altered mental status with confusion, ataxia Korsakoff's Psychosis: -irreverisible memory loss, confabulation, personality changes, caused by thiamine B1 defiency -Tx: naltrexone (Mu opioid receptor antagonist), disulfiram (antabuse, alcohol dehydrogenase inhibitor), Acamprostate (glutamate receptor modulator), Topiramate (Glutamate and GABA receptor modulator)

3) Effects of cocaine, hydroxyamphetamine, and pilocarpine on pupils and how they are used to id pupillary pathology**

-Used to test Adie's tonic pupil

Utricle Histology

-Utricle is big space -Macula -Sensory epithelium = contains hair cells and support cells -Otolith membrane with calcium crystals

5) Glaucoma PE**

-VA, recognize cupping -measure IOP with many devices -confrontation vision field test (test to determine visual field ability the 2 circles with 8 total pieces of pie)

CN X**$$$TEP

-Vagus -Exits via the jugular foramen -Both motor and sensory -Visceral motor, brachial motor, general sensory, and visceral sensory -emerges ventrally from the medulla, lateral to olive and inferior to IX Sensory cell bodies located in associated ganglia they enter the brainstem, and terminate on nucleus solitarius -Motor neurons located in nucleus ambiguus axons exit the medulla dorsal and lateral to the inferior olive -Has a critical role in respiration and cardiac function via autonomic nervous system -does pain in ear, taste, motor in pharynx, larynx, and palatal musles, general visceral afferent, parasympathetic efferent -CNS region = medulla -Lesion = Ipsilateral weakness of soft palate, pharynx, larynx, and autonomic dysfunction

7) Location of medulla, pons, cerebellum, midbrain and Id major nuclei and nerve bundles of these structures*8

-Ventral side -Cerebral peduncles tell us its ventral side

2) penetrance and expressivity relating to common neurogenetic diseases**

-Very uncommon for common diseases to have high penetrence

CN VIII*$$$TEP

-Vestibulocochlear -Exits via internal acoustic meatus -Sensory -Special sensory -Emerges ventraly from the junction of the pons and medulla and is lateral to CN VII -Cell bodies in coclear ganglion and vestibular ganglia terminate on the rostral medulla/caudal pons junction -Does hearing and balance and orientation -CNS region= pons/medulla junction -Lesion= ipsilateral deafness, impaired balance, vertigo

Agnosia **

-Visual agnosia = cannot recognize what you see -Auditory agnosia = pure word deafness (cant recognize spoken language) -Tactile Agnosia/asterognosisa: cant recognize objects throug touch -Anoscognosia: unable to recognize presence of disease or abnormality -Prsopagnosia= unable to recognize faces

11) Vigabatrin** (Viagra, lift and take out Transmission)

-WORKING ON THE GABA CAB -IRREVERSIBLE INHIBITS GABA TRANSANIMINSE WHICH BREAKS DOWN GABA= VIGABATRIN IS TAKING OUT THE TRANSmission -Vigabatrin = sounds like vigra and see the cab going up on the hydrolyic lift -GIVE VIAGRA TO SHAKING BABY AND REFRACTORY FOCAL SEIZURES BUT WATCH OUT VIAGRA CAUSES PERMINENT BLINDNESS*** -newer MOA: -analog GABA not an agonist -irreversibly inhibits GABA transaminase, reducing degradation of GABA Uses; -restrictured for refractory focal seizures -monotherapy for infantile spasms (children less than 2 years) SE: -progressive and permanent bilateral vision loss*** TEST

TCM and TCS aphasias**

-Watershed infarcts -seen in the setting of strple TCM: Not fluent, can comprhend, can repeat, like broca, ACA-MCA TCS: Fluent, cant comprhend, can repeat, like wernicke's . MCA-PCA

10) Id structures in the cerebral cortex relevant to spoken language and the connections between them**

-Wernicke's Area is Area 39,40 = superior temporal gyrus, on the dominant hemisphere -responsible for receptive speech -FOR UNDERSTANDING SPEECH -Lesion= can talk fine but understand what you said -Broca;s Area is Area 44,45 = inferior frontal gyrus, it is located in dominant hemisphere, -it is responsible for expressive speech -FOR MAKING SPEECH -Has phonological processing (sounds) and semantic processing (meanings) -Pars tringularis,pars orbitalis, and pars opercularis make up brocas area -Lesions = Can understand but can't respond appropriately, the guy that was making no sense Arcuate fasiculus= connects Wernicke's and Broca's area Lesion = conduction aphasia, which is inability to repeat what is heard Prosody is represented in the right hemisphere -it will do inflection You are going to the store can be a statement, command, or question

Global aphasia**

-When both production and understanding of language is damaged -Not fluent, can't comprhend, cant repeat

3) temporal profiles build the differential diagnosis **

-When? = onset and trajectory Onset: (hyperacute, acute (mins to hours), subacute (hours to days) , subacute to chronic (weeks to months) , chronic (months to years) Trajectory: Static, progressive, transient (happens then goes away) , recurrent or paroxysmal, fluctuating Acute: 1) static = vascular (stroke), structural 2) Transient = vascular (TIA) , metabolic 3) Recurrent = migraines, epilepsy, vascular 4) Fluctuating = metabolic 5) Progressive = vascular (bleeding) Chronic: 1) Static = congenital 2) Transient = structural 3) Fluctuating = structural 4) Progressive = degenerative, neoplastic

Pterygium**

-Winged growth, fibrovascular proliferation of conj that grows towards and over the cornea -Tx: surgery if problematic

Rett Syndrome**

-X-linked dominant -MECP2 gene affected -Sons will die in uterus -Daughters can have microcephaly, intellectual disability, autstic like behavior. They will have a mosaic brain -Rarely inherited it is most commonly de novo mutation

3) Consider appropriate radiologic studies for post-traumatic patients**

-X-ray and CT the main ones -CT is the best for fractures and FB and dont do an MRI -CT of head get a cut every 5 mm and only due axial cut with orbit its every 3mm -orbital need to get in all 3 planes axial, coronal, sagittal head its only axial

5) Id acute subarachnoid hemorrhage using CSF analysis**

-Xanthochromia = bilirubin in CSF indictive of hemorrhage -No change in CSF over 3 taps -Presents of marcophages -See RBCs in CSF (may be traumatic tap, whcih should be bright red color and disapate as fluid is collected)

myasthenia gravis (MG)***

-a chronic autoimmune disease that affects the neuromuscular junction and produces serious weakness of voluntary muscles -Hallmark is variable weakness and fatigability -Most common subtype is AChR -S/S: Ocular drooping(ptosis is usually asymmetric) , bulbar (facial weakness with dysarthria and dysphagia), respiratory dysfunction, axial and proximal limb muscles more affected, no sensory symptoms PE: -ocular = ptosis/diplopia with prolonged upgaze, weakness of eye closure -bulbar signs = jaw weakness, facial diplegia, palatal weakness, tongue weakness -respiratory signs = respiratory rate, use of accessory muscles, ease of speach and neck strenght -Limb strength examine for fatigue -Deep tendon reflexes Labs: -Single-Fiber EMG is most sensitive detecting NMJ disorders -AChR antibodies in 85% -MuSK antibodies in 10% GMG Dx: -RNS slow rate -single fiber EMG Tx: -pyridostigmine inhibits AChE (works very well for ocular MG) -if systemic MG need the big guns, IS drugs, surgery Myasthenic crisis -severe bulbar/respiratory weakness, -tx with IVIG or Plasma exchange MG and thymoma -associated with AChR only -striational antibodies predict -screen with contrast every new MG case -mandatory thymectomy MuSK + MG -alot of bulbar sysmtoms -young females -poor respnse to pyridostigmine -Tx: sterioids and rituximab MG+ Pregnancy: -dont give mycophenolate -can have neonatal MG (only last 3-4 weeks cuz IgG will wear off)

8) Dysthymic disorder DSM-5 dx**

-a chronic form of deprssion with fewer symptoms than MDD -dx requires low mood plus 2 other depressive symtpoms that have been present for at least 2 years -signicficant morbidity from the chonicity of the illness - new term is dysthymia is Persistent depressive disorder -Double depression = a major depressive episode superimposed on persistent depressive disorder. Common presentation in mediacal and psychiatric settings

Specific Phobia***

-a disorder that involves an irrational fear of a particular object or situation (flying, heights, animals, injections, blood) that markedly interferes with an individual's ability to function -6 months -Tx: CBT = exposure to phobic object non-FDA approved benzodiazepines and B-blockers

Fornix

-a fiber tract that extends from the sibculum of the hippocampal formation to the mammillary body (columns of fornix)

Sexual Dysfunction

-a group of heterogeneous disorders that are typically characterized by a clinically significant distiburbance in a person's ability to respond sexually or ability to experience sexual pleasure -Can occur in the : 1) Desire Phase -lack of interest in/desire for sex 2) Arousal/Excitement Phase -inability to acheive sufficient physiological or emotional arousal during sexual acticity 3) Organism Phase -premature ejac

EMG (electromyography)**

-a measurement technique that records the electrical activity of a muscle or group of muscles. It indicates the muscle activity -aka needle exam -used for diagnosis, localization, prognoisis How to distinguish between nerve and muscle: -Duration increases with number of muscle fibers, correlates with pitch (dull or crisp -Polyphasia multiple blimps not clean and crisp Findings: 1) Normal insertional activity -confirms needle in muscle -breif lasts less than 300 ms 2) Abnormal spontaneous activity -anything that persists for more than 3 sec 3) Postivie sharp waves (fibrillation potentials): -called rain on roof tell you that there is denervation (muscle and nerve are not connected, but doesnt tell us if its muscle or nerve) 4) Myotonic discharges: -sounds like a plane engine from WW2 -seen in myotonic dystrophy*** , myotonia, paramyontina, myopathies 5) Fasiculations potentials -sounds like popcorn at end of microwave -spontaneous involvuntary discharge -LMN problem 6) Voluntary activity -MUAP = extracellular recording of a motor unit 7) Myopathic disorders -less muscle fibers = smaller, shorter, polyphasic -clicking sound, crisper -SMALL AND SHORT 8) Neuropathic disorders Acute = recruitment decreased Chromic = decreased recrutiment, polyphasic, large ampiltude - LONG AND LARGE

Conduction aphasia***

-a speech disorder characterized by the inability to repeat words with intact spontaneous speech production and comprehension; usually due to injury to the arcuate fasciculus -Fluent, can comprehend, cant repeat

3) Provoked seizures**

-a toxin or metabolic cause withing the previous 24 hours can be identified. -causes are: 1) Hypoglycemia 2) Severe hyponatremia, and other metabolic derangements 3) Alcohol withdrawal/benzo withdrawal 4) Exposure to certain illcit drugs 5) Prescribed drugs such as Tramadol or bupropion *Treatment should target the provoking factor rather than starting an anti-seizure meds

4) SAD DSM-5 dx**

-a true seasonal form of depression vs. chronic depression with seasonal worsening

Alexia without agraphia**

-able to write but unable to read what they have written -presents with right honomyous hemiopnia

Generalized Slowing EEG**

-abnormal Mild = Theta, distruption of PDR Moderate = Prodominant: theta, superimposed: delta Severe= persistant delta, Delta>theta Profound = bursts supression

Triphasic Waves EEG**

-abnormal -liver failure, renal failure (metabolic problems) -generalized usually

Tardive disorders**

-abnormal movements -delayed -On Dopamine blockers long-term -Neuroleptics> SSRI and lithium Tardive Dyskinesia: -oro-bucco-lingual sterotypes = look like chewing gum and swallowing -elderly at higher risk -irreversible Tardive akathisia: -moving hands and legs around -restlessness Tardive dystonia: -rigid neck dystonia Parkinsonism: -cant be differentiated from normal parkinsons, a DaT SCAN can help differentiate -tx withdrawal symptoms and maybe levodopa Tardive tics: -tics due to long-term exposure to dopamine blockers -hard to treat, try to avoid dopamine blockers for touretts -tx by eliminating offending drug, anticholnergics, gabeergics, dopamine agents, Botox, DBS, VMAT-2 inhibitors (deutrabenazine)

Myopathic Gait (Waddling Gait)**

-abnormalitites caused by proximal muslce weakness -weakness of hip abductors, dropping of pelvis toward swing leg, compensatory lean toward stance leg -Penguin

Trauma brain pathology

-acute diffuse-loss of consciousness transient (concussion) or persistent (death) -acute, focal, progressive or non progressive -cerebral hematoma -subdural hematoma can be acute or chronic. Chronic can mimic a neoplasm

delirium***

-acute disorder of attention and cognition -acute brain failure -attention fluctuates -Reversible Risk factors: old, restraints, catheter, new meds, depression, dementia, hx of alcohol abuse, or stroke Tx: -nonpharm most sucessful (reorientation, avoud restaraint, reduced dose of psychoactive drugs, sleep, providing hearing and vision aids) -Pharm: anti-psychotic meds (low dose)

Vascular Pathology**

-acute onset usually -ischemic or hemmorhagic -focal or diffuse Cerebral infaraction (stroke) = acute, focal, nonprogressive Intraparenchymal hematoma = acute, focal, progressive Global anoxia-ischemia or subarachnoid hemorrhage = acute, diffuse

Acute dystonic or oculogyric crisis** ON TEST

-acute state of DA defiency** due to blocking DA or withdrawal DA agonists -causes focal, segemental and generalized dystonic (muscles contract uncontrolabally) -oculo-gyric crisis are usually accompanied with opisthosomas, rigidity, rage or fear, catalepsy or block -Fix with diphenyladramine (benadryl) treat for a week

1) Define addiction as it relates to substance use disorders**

-addiction is chronic, relapsing disease of brain reward, motivation and memory and related circuits -Dopamine Pathways: 1) VTA 2) Goes to frontal cortex 3) Goes to amygdala (memory) -reward, pleasure, euphoria, motor function, compulsion, perservation -Serotonin Pathways: 1) should give you satiety (brakes) -mood, memory processing, sleep, cognition -Dopamine flooding: reward pathway hijacking -MOA: faster the reward the higher the addiction is IV>inhale>IM>ingestion

BASilar artery stroke $$$TEP

-affects pons, medulla, lower midbrain, corticospinal tract, corticobulbar tract, ocular cranial nerve nuclei, paramedian pondtine reticular formation -RAS spared so remain conscious, Quadreplegia, loss of horizontal eye movement but can move them up and down -Locked-in syndrome (Locked in the BASment)

carbon monoxide poisoning

-affects the Globus pallidus

Facioscapulohumeral muscular dystrophy**

-affects the face, upper arms, and scapular region. -AD a. Onset usually occurs in adolescence. b. This type of dystrophy is characterized by sloped shoulders and limited ability to raise arms above head. c. Decreased mobility in the facial muscles results in a "masklike" appearance. -S/S: hyperlordorsis, asymmetrical*, scapular wing, triple hump sign, abdominal laxity, CK slighlty increased -FSHD1 is a D4Z4 is a decreased repeats* -normal life expectancy -Tx: AFO, PT/OT, scapular fixation

Pre-chiasmatic Lesion

-affects vision in only one eye -diseases of the eye ball are visible on clinical exam -optic nerve lesion will cause slow pupil reaction in that eye resulting in RAPD on swinging flashing test -RAPD + test = pre-chiasmatic optic nerve lesion -optic nerve swelling or pallor -characteristic visual field defects

Recurrance Risk**

-after an unprovoked first seizure the likelihood to have another withing the first 2 years is 50% (only 25% if normal EEG or MRI. 60% for patients with epileptiform EEG, prior brain injury, or signifcant MRI) -increased risk of hx of stroke, trauma, EEG with epileptiform abnormalitis, significant brain abnormality, or nocturnal seizure -if no additional risk an antiepleptic meds does not have to be started after a first lifetime seizure -Driving is the biggest concern for patients -In NE only have to go 3 months seizure free in iowa it is 6 months -Once they have a second seizure = epilepsy

Toxic Neuropathy

-alcohol, meds (flurowuinolones), chemo exposure (taxanes, paltin, thalidomide), heavy metals (talium, arsenic ,lead) -Produce a predominantly painful axonal peripheral neuropathy -must see deficits around time of exposure

5) Summarize the cognitive processes and basic neurobiology of fear and anxiety**

-all species have inborn ways to deal with a threat -defenses are elicited automatically by circumstances -role of learning and memory is fear conditioning Fear conditioning is a variation of Pavlivian classical conditioning : -Habitiuation -Unconditioned stimulus= momscremms -Conditioned stimulus = dogs -unconditioned reponse = fear and anxiety due to mom scream cuz of dog -conditioned response = fear and anxiety for all dogs -Amygdala = (fear and emotion) gas pedal -> activiates hypothalamus -> pituatory -> adrenal glands -> stress (slow response) -Sympathetics = triggered to engage defensive behaviors immediately -Adrenal glands = release epinephrine/noepinephrine (acute) and glucocorticoids (prolonged stress response) -HPA axis= cortisol response to stress, can be prolonged= -Prefrontal cortex = breaks

Primary Visual Cortex

-along the banks of the calcarine fissure -Meyer's loop = superior visual field, terminates in lingual gyrus -Superior retinal quadrant= inferior VF, terminate superior of the Calcirne fissure -Images are represented upside down on the retina -Fovea has a disprportionately large representation in primary visual cortex

Social Anxiety Disorder (Social Phobia)***

-an intense fear of being humiliated or embarrassed in social situations, worrying about scrutiny from others -6 months -Consequences of untreated can increase unemployment, more likely signal, more likely divorced, less likely to go to college, more likely to get substance use disorders and major depressive disorder -DDx ; introvert -Tx: SSRI, SNRI, MAOIs, CBT, can use benzos and beta-blockers (but not for long term use)

Caffeine ***

-analgesic

NSAID**

-analgesic -for people with mild to moderate headaaches -aspirin, ibuprofen, naproxen +/- caffeine -naproxein has been added to triptian with combo cname treximet and has been helpful SE: dyspeepsia and GI irritation

4) Thalamus Lesions***

-anatomically may include thalamic Bentral posterior lateral VPL and Ventral Posterior Medial VPM Nuclei or Thalamic Somatosensory Radiations -deficit is contralateral to the lesion -not neatly in midline -deficit may be more noticeable in the face, hand, and foot compared with trunck or proximal extremities

6) Id the projections of the olfactory tract**

-anterior comissure allows crossing -mitral cells will project to the piriform cortex, entorhinal cortex, amygdala, and olfactory tubercle via the olfactory tract -entrorhinal cortex involved in associatin between odors and memories -The piroform cortex to the orbitofrontal cortex is involved in fine discrimination between smells -amygdala projects to the hypothalamus and is involved in feeding behavior and other limbic system functions -olfactory tubercle for smell and walking away or towards

Acute Flaccid Myelitis **

-anterior horn cell disease -onset 7 years of age -fever and or respiratory illness -acute onset of focal limb weakness - Gray matter is affected -Causes by coxsakievirus A16, EV-A71, and EV-D68 -Tx: supportive

Prochlorperazine* (ANTI-PSYHCOTIC MED look at chlor part)

-antiemetic/prokinetic agent -1st gen D2 antagonist -used for antiemetic -alternative for metoclopramide -SE: akathisia/dystonia, prolonged QT

Metoclopramide* (METRO GIVES ME NO JOY)

-antiemetic/prokinetic agent -DA antagonist -helps relieve N/V -Prokinetic = stimulates M3 receptor which Increases GI motility helps with gastricc emptying and helps pts take drugs again SE: Fatigue akathsia, dystonia

4) List of meds at risk to cause depression in elderly**

-antihistamines - benzo -opiates -NSAIDs -hormones

Panic attack disorder

-anxiety disorder in which the person experiences frequent and unexpected panic attacks -must meet 4 + criteria to be a panic attack: palpations, sweating, shaking, SOB, choking, chest px, N/Ab distress, dizziness, chills, parathesias, feelings of unreality, fear of losing control or going crazy, fear of dyging -Must have 1 panic attack with 1 month of worrying about having a panic attack -you get afraid of having a panic attack so you avoid -Ddx: anxiety due to a medical condition, substance-induced -Types: social, obessional, PTSD, specific, GAD, unexpected

1) Anxiety Disorder Epidemology**

-anxiety disorders are the most common mental illness in the US -most common women -social phobia>specific phobia> PTSD > GAD > Panic d/o > OCD -higher anxiety increases risk for developing chronic anxiety disorder

1) Explain the basic theories of anxiety and the associated neurobiological components**

-anxiety disorders are the most common mental illness in the US -most common women -social phobia>specific phobia> PTSD > GAD > Panic d/o > OCD -higher anxiety increases risk for developing chronic anxiety disorder

Summary of ANxiety disorders**

-anxiety is normal response to stress/threat, until starts to get in the way of things -highly prevalent -resul in cost due to treatment, mortality and reduced workplace output -associated with somatic symptoms -cormorbidity is common -seperate disoderose -understand mechanisms and neurobiology can help you

Benzodiazepines**

-anything ending in -AM -frequently misused by alcoholics -cross-tolerance with other sedative-hypnotics (alcohol) -Withdrawal: replace with longer acting BDZ at equivalent dose and taper

Large Vessel Disease**

-artherslcepsos -cerviacal, intracranial arterial dissection -sinus venous thrombosis -moyamoya -reverible cerebral vasoconstriction syndrome -fibromuscular dyspasia -radiation scaculopahty -vasiculitis

Functional Gait*

-astasis-abasis -inconsistent, draumatic -uneceonmical posteures with sense of energy being wasted -lurching but rarely falls -sudden knee buckling -extreme slow motion -wide fluctations over shor period of time -distractible, exaggerated with observation (normalize if distract) -have excellence balance -no structural damage or disease, its like a conversion disorder

7) bupropion** (Basketball hoop)

-atypical antidepressant -NO serotonin affect -NET DAT ball pro = inhibits reuptake NE and Dopa -useful with depression with those who are sleepy cuz they are CNS activating agent (WAKING UP FRIEND) -PROS dont' SMOKE = Reduces urge to smoke -SE: RATTLES THE RIM WHEN HE DUNKS = SEIZURES -SKINNY PLAYER = CONTRAINDICATED WITH BULEMIA AND ANOREXIA PTS -kissing under the hoop no sexual side effects -Poster says "stay awake, stay fit, lose weight" = WEIGHT LOSE and LESS SOMNOLENCE Uses: -MDD (mono or add-on), SAD, smoking cessation SE: -dry mouth, N, insomnia -boxed warning = neuropsychiatric effects, depression, anxiety, psychosis, suicidal/homicidal ideation (ONLY WHEN USED FOR SMOKING CESSATION)

Post-Septal or Orbital Cellulitis

-bacterial infection of periocular tissue deep to oribital septum -Findings: febrile, proptosis, reduced or painful EOM, decreased VA, APD, papilledema -Tx: IV antibiotics stat

Medial lemniscus*

-begins medial and ventral (on top of pyrimids) -Gradually moves laterally and dorsally

Early warning signs of eating disorders

-behavior focuses on food, dieting behavior or sudden change in food preference, increased picky eating, always going to the bathroom after eating, multiple showers a day, skilling meals or large amounts of food missing, excessive exercise, visiting pro-anorexia web sites SCOFF questionnaire 1) Do you make yourself vomit (Sick) 2) Do you worry you have lost Control over how much you eat 3) Have you recently lost more than One stone (14lbs) in 3 months 4) Do you believe yourself to be Fat when others say you art too thin 5) Would you say that Food dominates your life * score of 2 indicates likely case of AN or BN

4) Discuss the effect of hippocampal dysfunction on memory***

-bilateral destruction of hippocampal formation for tx of temporal lobe epilepsy (HM) -He was able to remember past things however could not form new info into long term mememory (anterograde amnesia) -deficit declarative (event) NOT procedural information

Paraplegic Gait**

-bilateral hemiplegic gait -stiffness of both legs with scissoring -UMNs

Bulimia nervosa***

-binge eating and inappropriate compensatory behaviors both occur at least once a week for 3 months -can be forced emesis, long fasting, laxitives, intense workout for compensatory behavior -calluses on back of dominant hand (Russell's sign) -salivary gland hypertrophy (parotid gland) Medical complications: -esophageal rupture (boerhaave's syndrome) -More than 50% of people recover or improve

5) Generate a basic management plan for a patient with moderate to severe alcohol withdrawl**

-biological= meds, detox, abstinence -psychological and social = therapy/conseling. AA, residental programs Alcohol Pharm tx: -disulfiram = prevents acetaldehyde metabolism = aversive agent makes you sick -nalterxone= mu opiate blocage (less privelige) -Acamprosate = decreases glutamate neurotransmission

West Nile Virus WNV **

-birds are resevoir hosts Transmession: -mosquitos, human-to-human, blood transfusion, organ transplant, maternal-infant Manifestations: -most are asymptomatic (80%) -20% self limited febrile illness (WN fever) like a bad flu but rash is a prognostic indicator for severe disease and death -<1% develop severe neuroinvasive diseases (encephalitis> menigitis> acute flaccid paralysis) -at risk for encephalitis is elderly, alcoholics, diabetics Dx; -CSF IgM and IgG -surum IgM and IgG -PCR not useful -MRI show diagnositic signs but can't dx solely -Hosipatlized persons >75 years of age are 9x more likely to die -motality is less than 1% -high risk of death is change in level of consciousness, dysarthia, and dysphagia -Tx: supportive care

Non-depolarizing agents

-blockers are Nm antagonists that resemble ACH but conceal it inside a large righ structures -antagonism of postysynaptic receptors result in weakness progressing to flaccid paryalysis -motor endplates do not depolarize and fasculiculations do not occur -presynaptic receptors are also blocked resulting in decreased release of ACh with each subsequent depolarization (fade) -Recovery you use neostigmine and atropine (most the time)

2) Tuberous Sclerosis ** and associated neuropathy

-bourneville-pringle disease -2nd most common neurocutaneous disorder -AD -Mutations can be multiple: TSC1 = most common TSC2 *both are tumor supressors in mTOR pathway Dx: -2 major or 1 major with a few minors: Majors: -hypomelanotic macules (ashleaf spots) -angiofibroma or fibrous cephalic plawue -ungual fibromas (around nail) -Shagreen patch (orange lesion) -Multiple retinal hamartomas -Cortical dysplasia -Subependymal nodules -Subepednymal giant cell atrocytoma -Cardiac rhyabdomyoma -Lymphangioleiomyomatosis -Angiomyliplipmomas Minor: -confetti skin lesions -dental enamel pit -intraoral fibromas -retinal achromic matic -renal cysts -nonrenal hematomas Characteristic signs: -Ash leaf spots -Shagreen patches -Periungal fibromas -Facial angiofibrobamas CNS manifestations: -Seizures -Intracranial lesions: SEGA (Subependymal giant cell astrocytoma), Cortical tubers (hamartomas), Subendymal nodules Systemic Manifestations: -single or multiple cardiac rahdomyomas occur in 50% of pts -renal angiomyolipomas -lymphangiomyomatosis -ophthalamilogic manifesations

Classic Subdural Hemotoma MRI

-bridging vein -concave

Contusion**

-bruise of the brain -focal injury Coup lesion = contusion under the point of impact Contrecoup lesion = contusion under area of impact on the opposite side of impact -associated with rapid deceleration and torsional forces or impact to thte skull -basal fronal lobes and anterior, medial temporal lobes (neear rough areas of skull) -Torsional forces produce deep hemorrhages

Foreign body**

-can be conjunctival, corneal, or intraocular

Anterior Chamber Depth**

-can do on a slit lamp -very important for avoiding angle closure glaucoma attakc -Do not dilate if you suspect a narrow angle -Van Herick, flashlight, gonioscopy (gold standard)

Psychosis**

-can present with the majority of other psychologic diseases

Antiseizure random facti**

-can withdrawal after 2 years of seizure free but should taper and be careful cuz can take a year to get under control -all have an increased risk of suicidal thoughts or actions

Lipid storage myopathy

-carnitine defiency -cant use lipid for engery -carnitine carries FA into mitochondia -causes weakness -caritine palmutoyl tranferase (CPT) transfers FA from carnitine to acetyl-Coa -CPT defiency causes myonecrosis, precipteated by exercise

mitochondrial myopathy**

-causes weakness and intolerance to exercise and muscle deterioration -hearing loss, short stature, peripheral neuropathy Types: -Isolated myopathy -chronic progessive external opthalmoplegia (CPEO) or -Kearns-Syare syndrome (ptosis, before 20, heart arrhytmisas) -Encephalomyopathy of infancy and childhood -Multisystem disease with myopathy (MELAS, MERRF) -stroke like episodess tx with arginine, red ragged fibers -Lactate will be high in thsese patients -Red ragged fibers

4) Locatae neuronal cell bodies in the preganglionic and postganglionic ganglia related to both the sympathetic and parasympathetic nervous system*

-cell bodies of the postganglionic neurons are located in autonomic ganglia -preganglionic neuronal cell bodies of the ANS are located in the CNS -postganglionic neuronal cell bodies of the ANS are located in the PNS specifically in the paravetebral or prevetebral ganglia Sympathetics: -preganglionic sympathetic neurons are located in the intermediolateral cell column at T1-L2 of spinal cord and project to the postganglionic neurons Parasympathetics -preganglionic neurons are located in the brainstem and sacral spinal cord

Complex Regional Pain Syndrome (CRPS)***

-characterized by an overactive sympathetic nervous system; typically follows an insult (no matter how minor) to a nerve -color changes, temperature changes, increased hair growth over affected area -insists not to touch the area -Exam and imaging usually looks normally -autoimmune injury of a nerve thats been injured -Type 1 is most common and usually follows an event -Type 2 less common Tx: -early treatment helps within 6 months -sympathetic nerve blocks -Desensitazation PT*** MOST IMPORTANT

Abscence seizure EEG

-child not paying attention in class, they zone out for a few seconds -grow out of it -3 hertz spike and wave -hyperventilation onset

Chalazion**

-chronic lipo-granulomatuous inflammation of meibomian gland -painless, hard lid lump -tx: drain and topical ocular antibitotic

Degenerative disorders brain pathology

-chronic, progressive deficites that reflect bilateral loss of specific populations of neurons -alzheimers

6) Normal CSF fluid**

-clear and colorless -equal viscosity to water -color or turbidity only seen w/ path -1-5 lympocytes/HPF -blood free -50-80 mg/dl glucose with CSF glucose/plasma glucose ratio of 0.6-0.7 -15-45 mg/dL Protein (mostly albumin) -Lactate 11-22 mg/dl -Glutamine normal 8-18 mg/dL Turbid CSF -Bacteria -WBC cells or pus cells = meningitis or encephalitis -Blood = suggestive of hemorrhacge (subarachnoid or artifactual traumatic tap) Yellow Color: -Jaundice (bilirubin in CSF) -Xanthochromai suggests that a subarachnoid hemorrhage has recently occured Traumatic Lumbar Puncture: -different CSF in 3 tubes -clear tubes -no macrophages -Increased CSF protein

4) Ataxia**

-clumsiness and inaccuracy of movement seen in cerebellar disorders -most common cause of ataxia is toxic*** -Acute: stroke, drugs, hydrocephalus, migraine (mostly in children) -Ataxic tremors are intention tremors

1) Describe the structure and function of the cochlea and the organ of corti***

-cochlear duct contains endolymph, excessive endolymph may cause meniere's disease which results in low freq ringing of ear -Sound waves -> move endolymph in cochlear duct-> basilar membrane moves->stereocillial hair cells (embedded in tectorial membrance) move -> activates the hair cells -> stimulate the auditory component of CN VIII -Hair cells do not regenerate -Superior olivary complex in pons have axons which project to the unipolary type II ganglion cells in the spiral ganglion. Outer hair cells receive efferent input from these ganglion cells and move in response to stimulation to enhance hearing -Apex of cochlea is in the middle -Base of cochlea is on the outside Base = high frequencies , as we age we lose some of the abilitiy to hear high freq (base is more sensitive) Apex = low frequencies

HIV associated Neurocognitive Disoder (HAND) *8

-combination antirtrovialr treatment has decressed pervalence, BUT milder forms of HAND have increased in prevalence -associated with decreased survival, quality of life, medication adherance

Refractive error**

-common cause of functional amblyopia (lazy eye) -defect in ability of eye to bend light rays to focus image properly on fovea centralis (refraction); occurs in myopia (near-sighted) and hyperopia (far-sighted) -astigmatism

Dacryocystitis***

-common in infants -inflammation of the lacrimal sac casued by flow obstruction and subsequent bacterial infection -Congentital obstruction should by patent by 12 months of age -S/S: erythema and edema over the lacrimal sac -Tx: broad spectrum antibiotics

Brocas aphasia**

-condition resulting from damage to Broca's area, causing the affected person to be unable to speak fluently, to mispronounce words, and to speak haltingly -can fully undersatnd words -Non-fluent, expressive ** -Non-fluent, can comprehend, cant repeat

Wernicke's Aphasia**

-condition resulting from damage to Wernicke's area, causing the affected person to be unable to understand or produce meaningful language -Fluent, "receptive"** -Fluent, cant comprehend, cant repeat

carbon monoxide poisoning***

-confusion, loss of conscousness, deep coma to death, headache all possible -injury to the GPi and hippocampus

Neurocutaneous syndromes general

-congenital disorders often inherited, and present in early childhood or adolescence -affect skin, eye, and CNS -can be progressive -inc risk of neoplastic formation in many of them Types: -NF type 1 and 2 -Tuberous sclerosis -struge weber sydrome -ataxia-telangiesctasia -incontinentia pgmenti -von hippel lindua syndrome

Summary of Trauma Lecture**

-consider an adjustment disorder if patient has a significant reaxtion to a non-tramuatic stressor -the main difference between an adjustment disorder and ASD/PTSED is the latter is the acute stressor is traumatic vs getting fired or divored (if it is in the grey area (cancer dx) then asses for PTSD -previous truam, mental helath problems, and other conditions may presidose someone to a maladaptive stress response -there may be variable cutlrual presentations to stress/trauma -victims of trauma often present to PCPs who need to be vigilant by screening for ASD/PTSD -PTSD is treatable and should not be considered a normal response to a traumatic experience

peripheral nerve** $$$TEP

-contains axons, schwann cells, and CT (endoneurium, perineurium, and epineurium) 1) Endoneurium invests single nerve fiber layers (inflammatory infiltrate in Guillian Barre Syndrome) 2) perineurium surround each group of axons termed fascicles. -blood-nerve permeability barrier -must be rejoined in microsurgery for limb reattachment 3) epineurium surround fasciles and blood vessels. -dense connective tissue endo = inner peri= around epi= outer

Middle Cerebral artery stroke $$$TEP

-contralateral paryalysis and sensory loss - face and upper limb -aphasia if dominatnt and hemineglect if nondominant -loss of sensation in the arm and face due to lesioning motor and sensory cortices in those areass -Teproal lobe (wernike area) lesion -Frontal lobe (brocas area) lesion

Violence***

-contribution to vioolence made by persons with mental illness is no larger than the contribution made by persons who do not have a mental illness -*people with mental illness are much more likely to be victims than perpertatros -History of violence may lead to future violence -Risk Factors: late teens to early 20s, males, Low SES, less education, inverse relationship to IQ, substance abuse (alcohol), childhood exposure, borderline PD, antisocial Assessment: -Look for raised voices, threats, abrupt movements, pacing, clenching, posturing, intoxication -Tarasoff Rule must inform -Management: restraint, meds, seculusion, careful documentation

Animal Bites

-copious irrigation -reduce bacterial colony count -debride nonviable tissue -early primary wound closure -antibiotic coverage

11) Risk factors for suicide and attempted suicide in adults with mood disorders**

-cormorbid alcohol use -presence of psychosis -impulsivity (bipolar patients) -asking about suicide does not increase risk

peripheral neuropathy

-damage to nerves in lower legs and hands as result of diabetes mellitus; symptoms include either extreme sensitivity or numbness and tingling -Causes: Diabetes*, toxin, paraproteinemic, HIV idiopathic genetic -Work up = what, when, where, what setting What: -Small sensory fibers = dec pain/temp, dysesthesias, allodynia -Large sensory fibers = dec vibration/propreciption, hyporeflexia, sensory ataxia, and paresthesias -Large motor nerves = wasting, hypotonia, weakness, hyporeflexia, orthopedic deformity, fasiculations, cramps -Autonomic nerves = dec sweating, hypotension, urinary retention, impotence, vascular color changes, inc sweating, HTN When: -convincing date and rapid onset = immune or infectious -less exact onset and gradual = toxic, metabolic, inheritied, or idiopathic -Acute = <4 weeks -Subacuse = <8 weeks -Chronic progressive = progression continuing after 8 weeks Where: -feet before hands = diabetes What setting: - Mee's line = chronic arsenic or thallium poisoning -distal sensory polyneuropathy w/ brisk reflexes, mild memory loss and red raw tonghue = vitamin B12 deficienncy and pernicious anemia -progressive sensory-motor painful neuropathy and M-protein = POEMS (cancer related neuropathy) Tx: -frequent foot inspection -adequate shoes -mes gabapentin, pregabalin -specific treatment for B12 replacement, DM, etoh reduction, immunotheapy, infection treatment, cancer or blood dyscrasia treatment

Spinal Cord: Central Cord Lesions**

-damage to spinothalamic fibers crossing in the ventral commissure causes bilateral regions of suspended sensory loss to pain and temp -lesions of the cervical cord produce the classic cape distribution -causes: spinal cord contusion, nontrauma and trauma syringomyelia, intrinsic spinal cord tumors (hemangioblastoma, ependymoma or astrocytoma

Spinal Cord: Anterior Cord Lesions**

-damage to the aneterolateral pathways causes loss of pain and temp sensation below the level of the lesion -damage to the anterior horn cells produce LMNs weakness at the level of the lesion (helps localize) -Common causes include trauma, MS, and anterior spinal artery infarct

Dorsal Midbrain syndrome

-damage to upper brainstem -loss of up gaze -convergence retraction nystagmus-eyes converge and retract with attempted up gaze -light-near discoation of pupils- pupilas are mid-dilated and respond poorly to light-typically equal in size -eyelide retraction

Antipsychotics sexual SE

-decrease in libido, Erectile dysfunction -hyperprolactinemia in both sexes

Amblyopia**

-decreased corrected vision -not an eye problem its a brain problem -4% of the population -photoscreeners ONLY detect risk factors -Must do an eye exam Organic: -problem with the anatomy -less common -must rule out Functional: -most common -anatomically normal eye -Causes: 1) refractive error 2) Strabismus -May lead to brain atrophy due to LGN froming 6 layers 2,3,5 ipsilateral and 1,4,6 contralateral eye with amblyopia leading to the atrophy of 3 of the corresponding layers cuz one eye isn't functioning it is fixable before the critical period ( in humans its 6-8 so 7 is party line) Eye Exam: 1) Eyelid and orbits, external exam 2) Cover test: muscle imbalance/motility exam 3) Visual acuity testing*** (Best test) 4) Pupil and red reflex-Bruckner's test -looking for symetrical red feflex and central light reflex 5) Fundus exam Tx: -best therapy is early detection check vision at 3,4,and 5 and vision screening devices if available -glasses (severe far-sighted without anything else going on) -eye patches (not far-sighted or near-sighted have muscle imbalance so patch good eye) -atropine theraphy into the good eye to prevent accommodation, blurring the sound eye -eye excercises -surgery: 1) cut and reattach muscle further back to reduce torque and influence of muscle if medial rectus fixing intorsion 2) Detach muscle and resect some muscle and reattach in same spot to increase strength of muscle if medial rectus could pull muscle in to fix extorsion -chemodenervation of extraocular muscle (botox)

3) Primary Somatosensory Cortex Lesions

-deficit is contralateral to lesion*** -sensory does not begin neatly at the midline -cortical sensory loss = extiction (dont feel certain spots) , decreased stereogenosis (cant id object in hand with eyes closed), and graphesthesia (cannot recognize writing on the skin)

Ruffini's Corpuscles $$$TEP

-dendritic endings with capsule; adapt slowly -located in finger tips, joints -pressure, slippage of objects along surface of skin, joint angle change

Dependence and Withdrawal Symptoms for each agent**

-dependence can be psychological or physcial Nicotine: -stimulates Nn receptors (a4B2 in the brain) and release of other transmitters (dopamine) -withdrawl symptoms are listed and you should know Ethanol: -stinulates at multiple CNS sites and activates the reward system at several sites in the mesolimbic system -activates GABA-A receptor and inhibits glutamate (NDMA) receptor -withdrawal= craving, poor sleep, hallucinations, anxiety, tremors, insomnia, agitiation, irritability, and delirium tremens with circulatory collapse arrhythmias Opiods: -withdrawal = craving, anxiety, fear of withdrawl, insonmia, rhinorrhea, sweating, lacrimation, restlessnes, GI, tremors, N/V/D, muscle spasms, tachycardia, chills

3) Unique features of neurons and how it relates to disease**

-dependence on oxygen (aka why strokes are bad) -high metabolic activity -2/3 of lysosomal storage disorders affect the nervous system, need to clear debris

6) Id specific strategies to foster mutual support*** (task assistance, feedback)

-dependent upon info gathering thtrough situation monitoring -moderated by the communication of info -enhanced by leaders who encourage and role model mutual support behaviors 1) Task Assistance = team members foster a climate in whic it is expected that assistance will be actvely sought and offered as a method for reducing the occurence of error 2) Feedback= information provided for the purpose of improving teaqm performance can be formal (case conference) and informal (huddles debreifs) 3) Advocacy and Assertion = invoked when team members viewpoints don't coincide with that of the decision maker and concern that there is unsafe patient condition Assertive Statement: - respectful and supportive of authority, -clearly asserts concerns and suffestions -is nonthreatening and ensures that critical information is addressed -5-step processes 1) Open the discussion 2) State the concern 3) state the problem- real or perceived 4) Offer a solution 5) Obtain an agreement 2-challenge rule -invoked when an initial assertion is ignored -responsibility is to assertibvely voice the concern at least two times to ensure that it has been heard** -member being challenged must ackowledge -if outcome is not acceptable you make a stronger course of action and utilize chain of command -empowers any team member to stop the line if they sense or discover breach of safethy -action is to be take seriously and requores immediate cessation of process and resolution of safety process Use CUS words C = I am concerned U = I am uncomfortable S= Stop this is a Safety issue

Disruptive mood dysregulation disorder

-depressive disorder with some conduct problems

Development of Cerebral Cortex**

-derived from telencephalon -becomes convoluted during development allowing you to increase the surface of the cerebral cortex forming gyrus and sulci

Meningioma**

-derived from the covering (meninges) of the brain; arachnoidal (meningothelia) cells -typically attached to the dura mater -Single most common of all CNS tumors -can cause hyperostosis due to invasion into skull -See cellular whorls on histo* Benign meningioma = Grade 1 (5% recurrence at 5 years) Atypical meningioma = Grade II(40% recurrence) Anaplastic Menigioma = Grade III (median survivial <2 years)

3) Describe Bordmann's Area***

-determined histological analysis of the cerebral cortex -defined differences in the 6 layers of neocortex which relates to functional differences -Primary sensory cortices have large layer 4 (lot of information from the thalamus ) -Primary motor cortices have large layer 5 (due to large cell bodies cuz of long axons)

critical illness myopathy**

-diffuse inflammatory myopathy that involves both limb & truncal muscles, causing diffuse flaccid weakness in the limbs & even the diaphragm, symetric, usually extraocular muscles are spared -Hx of ICU stay -Risk factors: illnesses that cause you to be ICU

Rule 1: Direct HP (Face, Arm, Leg on same sade) **

-direct HP localize contralateral to the weakness, and usually above affected level of the BS-> Contralateral

Mononeuropathy**

-disease affecting a single nerve (such as carpal tunnel syndrome) -Risk factors: diabetes, amyloidosis, peripheral neuropathy, hypothyroidism, HNPP -S/S: sensory symptoms are predominant in CTS, meralgia paresthetica and ulnar at the elbow -motor symptoms predominant in common peroneal and radial neuropathies (foot and wrist drop) -pain alone is not seen -prognosis depends on pathophysiology (axonal or demyelinating are bad news)

Burn Out

-disengagement, emotions blunted, hopelessness and helplessness, loss of motivation, ideals, and hope -Leads to detachment and depression -Primary damage is emotional -May not make life seem like living

Dysarthria***

-disorder of speech production that is characterized by poor speech** -many causes stroke, TBI, PD, MS, ALS -may includ respiration, phonation, articulation, resonation, prosody due to breakdown in movement control of muscle gorups 1) Flaccid dysarthria = LMN problem, causes weak tongue, tongue fasciculations, poor articulation, hypernasal, monoptich, ALS, MG, (Sound like stephen hawking, monotone and hypernasal) 2) Spasctic Dysarthria = UMN lesion, stained, strangled, slurred, slow speech, common in stroke, MS, cerebral palsy (slurred and sounds struggled) 3) Ataxic Dysarthria = dysfuction of cerebellum, drunk speech seen in MS, stroke, degenerative diseaes (sounds like elmer fud) 4) Hypokinetic Dysarthria = basal ganglia dysfunction, hypophonia, dec articulation, monopitch, increased rate, seen in PD Tx: -speech and language therapy -no meds currently -Lee Silverman Voice treatment is very helpful for PD patients

2) Describe Autism spectrum disorders with the associated levels of support required**

-disorders with persistent (pervasive) deficits in social communication and interaction and restricted, repetitive patterns of behavior, interests or activities -social impairment -communication: verbal and nonverbal impairment, poor comprehension, difficult understanding gestures, facial expression -echolalia,= meaningless repetition of what someone else says -perseveration of an idea or word -wrong pronouns -Preoccupation and restricted patterns, infexible adherence to routine or ritual, repetitive motor mannerisms, preoccupation with parts of objects, rocking clapping, fascinated with movement of object -restricted/fixated interests, insistence on sameness -hypo or hypersensitive to sensory input -similiar features to OCD differentiate with other symptoms -repetitive patterns seen in aspergers = high functioning autism with poor social interactions especially conversation endless learning on topic of interest -clumsiness, awkwardness -variablity in cognitive functioning Course: -symptoms must be present in early development period -75% may have intellectual disability -25% may develop seizures in adolescence -language skills and higher intelligence have better prognosis -more frequent in men Autism Spectrum Disorder = autistic disorder, asperger's, or pervasive development dissorder Dx: -must id if intellectual impairment, if language impairment, if genetic or environmental factor, id if neurodevelopmental, mental or behavioral disorder Level 1: Requiring Support -Dont need a bunch of help, but without support can see impairment -atypical or unsuccessful responses to social attempts of others -full sentences but to-and fro conversation fails -problems of organization and planning hampering independence Level 2: Require Substantial Support -limited initiation -reduced or abnormal response to social attempt -simple sentences -inflexibility and behaviors obcvious to causal oberserve Level 3: Require very substantial support -cant function without assistant -severe deficits in verbal and nonverbal social communciation -few words of intelligible speech

4) ODD*** (Opposition Defiant Disorder)

-disruptive, impulse-control, and conduct disorders -Angry, defiant, vindictiveness for at least 6 months acted on one idividual that is not a sibling -No meds have been approved, Behavioral Management Training, most successful under 8 -Scared straight programs do not help

3) CD *** (Conduct Disorder)

-disruptive, impulse-control, and conduct disorders -more malicious -Aggressive, Destructive, Deceitful, and serious violations of rules occurring with in the last 6 months with at least 3 criteria in past 12 months -Lack of remorse or guilt, callous (lack of empathy), unconcerned about performance, and shallow or deficient affect -No meds have been approved, Behavioral Management Training, most successful under 8 -Scared straight programs do not help

Rhabdomyolysis**

-dissolution of striated muscle (caused by trauma, extreme exertion, or drug toxicity; in severe cases renal failure can result) -acut muscle necorsis and release of intracellular muscle constituents into circulation -CK usually over 5,000 (1,500-100,000) -Toxin*** is #1 cause (alcohol, cocaine) , car accident -Tx: stop offending, hydration, CK should decrease within a week of treatment

Peripheral Nerves Lesions**

-distal symmetrical polyneuropathies cause bilateral sensory loss in a glove and stocking distribution, in all modalitis -specific nerve or nerve root lesions cause sensory loss in specific territories -associated deficits of lesions of the peripheral nerves or nerve roots often include LMN type weakness -vascular risk factor like diabetes alcholism, toxins, infection or idiopathic are your DDX**

Delirium**

-disturbance in attention/awareness -an additional disturbance in cognition -lasts short time (hours to days) & fluctuates in severity throughout the day -Causes: illness, meds, substances -often reversible

3) Explain managment strategies in psychiatric emergencies**

-do a complete eval -develop rapport, be nonjudgemental, supportive, -get a psychiatric consult, chaplain if wanted, -maintain safety Approach to Self-Harming Pt or Suicidal Pt: -assessment: engagement, understand the desire, identify risk factors for harm/SI -Management: assertive follow up, treat psychiatric disorder, locked psychiatric unit with suicidal precautions, court order may be necessay for involuntary hospitalization, family members can be supportive

Neurons $$$$TEP

-dont divide in adulthood -cell bodies and dendrites can e seen on Nissl stain, not the case with axons -injury to axon leads to wallerian degeneration (Anterograde (wallerian) = away from the cell body) allows for potential regen of axons if in PNS. Macrophage will remove debris and meylin

Apomorphine

-dopamine receptor agonist -injected SC to treat hypomobility off episodes in advanced PD -rapid onset -strong emetic action requires 3 day pretreatment with an anti-emetic -can suffer from hypotension SE: -N/V, hypotension, simialar to levodopa but less dyskinesia and more impulsive behavior

Spinal cord**

-dorsal roots enter the spinal cord** -ventral roots exit the spinal cord** -Cell bodies that give rise to the dorsal roots are in the DRG -Cell bodies that give rise to the ventral roots are in the spinal cord -Spinal cord has a distinct appearance at different levels associated with different needs of motor control -

Dura Venous Sinuses**

-drain internal (cerebral) and external (diploic, emissary, frontomaxillary) veins and CSF into Internal Jugular veins Midline Sinuses -superior sagittal -inferior sagittal -straight -occipital -confluence Paired Sinuses -transverse-drains into sigmoid -sigmoid -becomes the internal jugular vein -superior petrosal-drains into transverse (starts where transverse becomes sigmoid and ends [anteriorly] where sigmoid becoes IJV) -inferior petrosal- -cavernous

2) Advanced Dry AMD (age related macular degeneration) **

-drusen, pigmentary changes, plus the presence of center-involving geographic atrophy ***** -vision is usually 20/100-20/200

1) Recognize serotonin syndrome**

-due administration of serotonigin drugsw -seen in combo of MAOi with other Serotonin drugs S/S: -hypertension, myoclonic, hypertheremia, tapping, hyperrefexia Tx: life support and ciproheptamine

6) Describe the role of the vestibular system in N/V**

-dysfunction of the vestibular system can cause N/V -vomiting center is in the MEDULLA

3) Recognize effective infromation exchange strategies**

-effective communication skills are vital for patient safety -enables team members to effectively relay info -critical strategies and tools of TeamSTEPPS -communication is the lifeline of the core team -effective when it permeates every aspect of an organization -challenges of communication are language barrier, physcial proximity, distractrions, workload, personalities, varying communication sytles, conflict, lack of information verification, shift change -strategies for info exchange: 1) SBAR (situation-Background-Assessment- Recommendation), = a framework for team members to effectively communicate information to one another 2) Call-Out= a strategy to communicate important or critical info, informs team memers simultanelusly during emergent situations helps team members anticipate next step 3) Check-Back= sender initiates message, recieveer accepts message, proveids feedback confirmation, sender verifies message was recieved 4) Handoffs = transfer of info during transistions, have verbal communication, clarity of info with anticipatory guidance, formal transfer of responsibility and accountabolitity, acknowlegment by reciever, includes an opportunity to ask questions, clarify and confirm

3) Giant cell arteritis key features**

-elderly pts, headaches, scalp tenderness, jaw claudication, fever, maliase, visual loss, associated with polymyalgia rheymatica -EMERGENCY -Stat ESR, CRP, CBC -Immediate high dose steriods -confirm with 7-10 days with temporal artery biopsy

Pseudopapilledema

-elevated, but no edema -vessels sharp and distinct -spontaneou venous pulsations -crowded disc -optic nerve drusen = calcifed deposits

Generalized cortical myoclonus**

-emergency -due to brain being damaged by hypoxia -Triad is the lance adams syndrome = mycoclonus, ataxia, and gait disturbance

3) Sturge Weber** and associated neuropathology

-encephalotrigeminal angiomatosis -GNAQ gene on chromosome 9q21 -earler mutation is more symptomatic -Port wine nevus: V1 with involement of the inner canthus of the eye CNS effects: -Progressive cortical desturction can cause seizures, contralateral hemiparesis, visual field deficits, and development delay -25% get glaucoma ipislateral to skin lesion Types: 1) type 1= classic form including facial and leptomeningeal angimatosis w/ or withou gluacoma 2) Type 2= facial angima and possible glaucoma (no intracranial involvement) 3) type 3 = leptomeningeal angioma, no facial angioma or coular manifestation Neuroimaging: -gyral calcifications -cereabral hemiatrophy can be scenne -dyke-davidoff-maison syndrome (compensatory hypertrophy of petrous part of brain) -MRIa used

8) Describe how common phyiscal illnesses and substances can lead to anxiety**

-endocrine problems (thyroid and parathyroid disease, pheochromocytoma, hypoglycemia) -Pulmonary disease (hypoxia, PE) -CV-arrhythmias, angia, CHF -Neurologic (head injury) -Autoimmune -Meds (steriods, bronchodilators, benzo, opiods, thyroid replacement) Substance use: -caffeine -psychostimulants -cocaine, meth -alcohol/benzo withdrawal -cannabis -discontinuation/withdrawal

5) Explain situational awarenss and id undermining conditions**

-ensures new or changing information is ided for communication and decision-making -continuous process -leads to effective support of fellow team members -it is the state of knowning the current conditions affecting one's work -it includes knowing status of the patient, status of other team members, environmental conditions, current progress toward the goal -should have shared mental model- the preception of, understanding of or knowledge about a situation or process that is shared among team members through communication -undermined by failure to share informatiomn

VOR cancellation

-equal and opposite saccade/smooth pursuit signal -decrease manitude of vestibular response -neural basis: vestibuocerebellum-flocculus and paraflocculus -If the VOR is not canceled you know the problem is in the vestibuocerebellum-flocculus and paraflocculus -you should be able to follow an object while moving your head if you cannot there is a problem

Dystonia**

-excessive muscle contraction that causes abnormal movements or postures, or tremor -when they come in with crazy shit -nystagmus like movement -Should be considered for levodopa tx -Chemodenervation (Botox) can be very helpful -Deep brain stimulation or lesional surgery are last resort but be can be helpful

1) Compare the clinical and pathologic features of thyroid opthalmopathy (GRAVE's) with the other orbital inflammatory conditions**

-exophthalmos (bulging eye) , lid retraction, enlarged muscles -tendons and fat are spared -may be independent of thyroid function -muscle enlargement due to lympocytic cell infiltration, severe, edema, variable fibrosis

Disruptive Behaviors

-externalized behavior exhibited when a cognitive or emotional challenge exceeds capactiy for an accepted adaptive respnse -sociocultural and contextually defined

1) Basic physiology of ophthalmic drops and learn how to apply them*8

-eye drops enter systemic circulation via nasolacrimal system, conjunctiva, ciliary body, or iris, - the most direct patway is via the nasal mucosa and will avoid first pass metabolism -To improve absorption patient should occlude nasolacrimal by closing eys and pressing fingers over the medial part of the eye

3) Describe the role of the reticular formation in movement control**

-eye movements are influenced by two gaze centers in the reticural formation 1) Vertical gaze center = Nucleus of Cajal in the Midbrain and rostral interstitial nucleus of the MLF (riMLF) 2) Horizontal gaze center = PPRF in pons -one function of the reticular formation is to act as UMN that influence movement -the reticular formation coordinates rhythmic movements such as walking via the reticulospinal tract

Strabismus**

-eyes do not properly align with eah other Esotropia: -one or both eyes turn inward Exotropia: -one or both eyes turn outward

Traumatic Brain Injury

-falls, -unintentional blunt trauma -MVA -Assualts Symptoms: -emotional labile, impusle, exucative dysfunction, depression, anxiety, psychosis, sleep disorders

6) collatreral source historians effective to obtain info

-family members and friends -must first get approval from patient -ask how they are doing cuz care-giver stress is challenging

Benzocaine**

-fast onset, well absorbed on mucus membrane -Uses: mouth/gum irritation, sore thoart/mouth -SE: methemglobinemia -Secondary amine (exception) -Amino ester class = cuz they have 1 "i" in their name -pKa 2.5 more af Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Distribution: -administered with epinephrine to vasoconstrict vessels to keep in local Clearance: -metabolized by cholinesterase to a PABA (can cause allergic rxns) and alcohol SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy- -methemoglobinemia = seen in amides minus cocaine, treat with 02 and methylene blue

agoraphobia***

-fear or avoidance of situations, such as crowds or wide open places, where one has felt loss of control and panic, fear of not being able to escape -lasts for 6 months or more -Ddx: Panic disorder -Tx: SSRI, SNRI, MAOis , CBT, avoid caffeine benzo and beta blockers (not for long-term use) -CBT is very improtant

1) Locate and know organization of the taste buds**

-filiform papilla and fungiform papilla -fluids on the tongue enter the taste bud through the taste pore -microvilli on receptor cells contain taste receptors -taste receptors have one of the 5 receptors = salty, sweet, bitter, sour, and umami (GPCRs are important for sweet, bitter, and umami) -receptor cells release transmitter onto the afferent nerve fibers -alot of taste comes from olfaction

Suicide**

-firearm suicides are highly impulsive -parasuicidal = range of acts from attempts, gestures, threats, and suicidal thoughts (death not intended) -male, older, careful, increased lethality, dec chance for help are all characteristics of completers -15% of people with depression will commit suicide -asking doesn't increase the risk -"Have you thought about ending your life?" -"Have you ever you gone so far as to think about how you would do so?" -"Do you have access to a way to carry out your plan?" -Previous attempt is big risk factor along with availablity of lethal means

Hommunculus of cerebellum

-flocculonodular lobe is vestibulocerbellum -vermis receives info from procreicptors -Cerebellum cortex is in charge of fine movements

Aqueous Humor

-fluid produced by the ciliary body and found in the anterior chamber -maintians shape of the eye glove -maintains proper distances between refractive surfaces: cornea-lens-retina -glacuoma = too much aqueous humor -Cataracts= not enough aqueous humor

6) Summarize the idea of harm reduction with traditional models of addiction treatment**

-focus on problems, does not insit abstinence, active participation of person -pretty much like if i cant get you to stop then lets make it safer, safe needle program, methadone mainetence,

Vascular Dementia**

-form of dementia caused by a stroke or other restriction of the flow of blood to the brain -step-wise decline kind of like MS -See focal problems -Risk Factors: HTN, smoking, DM, hyperlipidema, a fib, mechanical valve, HF Tx: -stroke prevention -anti-platelet therapy

Orbital emphysema

-fracture of the bones of the orbit -increases the air in the orbit -increased risk of poptosis, increased intraocular pressure, Central retinal optic occulsion Stages: 1. no dystophia, no visual problems, no elevated IOP, no CRAO, bone broken 2. Dystophia (affected globe) , no visual problems, no elevated IOP, no CRAO, bone broke 3.Dystophia, visual problems, +/-elevated IOP, no CRAO, bone broken 4. Dystophia, visual problems, elevated IOP, CRAO, bone broken No nose blowing for 1,2,3,4 oral antibiotics for 1,2,3,4 Mucosal decongestion for 1,2,3,4 CT imaging for 1,2,3,4 Corticosteriods 3,4 Needle decongestion 3,4 Cantholysis (cut the lateral palbrea tendon) IV

Botulism**

-from wound, food borne, infantile, inhalational -neurotoxins degrade proteins needed for docking and fusion of ACh vesicles to synaptic membrane, preventing release from synamptic cleft -Descending affects including dysphagia, diplopia, dsyarthria, eventually leading to limbs and respiratory muscles -GI and autonomic Dx: -toxin in serum in foodborn, toxin in stool of infant and wound scraping in wound related Tx: -equine serum trivalaent botulism anittoxin, antibiotics for wounds, supportive care

7) Explain the relationship between axonal diameter and action potential velocity**

-further the depolarization spreads down a neuron = the faster the AP or nerve conduction velocity will be - The distance of depolarization = length constant -Lower the resistance Rin the faster the AP will be -Larger the diameter lower the resistance (due to more possible paths) leading to larger length constant faster the AP

1) Id the pathophys of eating disorders***

-genetic predispositions -puberty may be a trigger -dieting is the biggest risk factor -childhood anxiety disorders often precede eating disorders -weight-sensitive activities and sports -sexual abuse -peer pressure -Starvation : after 12 week refeeding phrase, most of the food-related andnormal attitudes and behaviors persisted (subjects said they were not back to normal) -Recovery requires more than nutritional resortation; psychological treatment is also needed

2) Id the current DSM-5 criteria for various anxiety conditions**

-gerneralized anxiety disorder -social anxiety disorder -panic disorder -specific phobia -PTSD -Agoraphobia -Substance induced anxiety disorder -anxiety due to another medical condition

Vestibular Projections**

-goal is to provide information about the location of the head in space, ensuring correct eye movement and balance (conjuction with cerebellum) -Vestibular nuclei has ascending projections to nuclei associated with CN III, IV, and VI via MLF to coordinate eye moveent and head coordination

2) Understand dopamine therapy for PD **

-goal is to restore/maintain motor function can due this by restoring DA levels (best response) , block muscarinic receptors to bring balance, exogenous D2 receptor agonist -2 stages: 1) Initial = pt developed disability that requires meds 2) Second = patient develops dyskinesia related to usage of levodopa, therapy is now aimed to reduce motor fluctuations while perserving motor function

1) Follow proper technique in ascertainment of cutaneous and deep tendon reflexes**

-goal is to strike the tendon and stretch the whole muscle -need a full swing and hold inbetween two fingers -a good hammer will bounce back at least half on table top -Use thumb to find tendon and strike own thumb What if you don't get a reflex: 1) Strike a crisper blow 2) Id proper tendon 3) Position patient properly 4) Apply slight tension on the muscle 5) Jendrassik's maneuver for reinforcement (clench jaw to get better reflexes or pull hands right before you strike) 6) Conterpressure for reinforcement Knee Jerk: -normall foot swing back and forth in straight line -spasctically diminishes the amplitutude -abnormal may see irregular rotary or sidewise arcs -hypothyroidism the reflex has a hung up appearance -latency of reflex should be measured

General Antidepressant Facts

-goal is usually response and remisision usally takes 2 weeks but max benefit is 6-12 qeeks -standard to continue treatment for 4-9 months and maintence therapy for pts with high risk of relapse -efficacy is generally equal across the board -all have delayed onset of efficacy -all have boxed warning for suicidial ideation and behavior -have also been used for anxiety, neuropathic pain, premenstrual dysphoric disorder, vasomotor menopausal symptoms, stress incontinence, eating disorders, smoking cessation Types of Fuctions: 1) SERT = serotonin transporter 2) NET = norepinephrine transporter 3) DAT= dopamine transporter 4) MAO= monoamine oxidase (block degradation) 5) 5-HTR= serotonin transporter 6) a1AR, a2AR, BAR = adrenergic receptors

Middle Ear Reconstruction

-goals of mastoid/middle ear surgery is for disease removal, secondary objective is to restore hearing -disease removal may include mastoidectomy/typmanoplasty -hearing restoration is ossicular reconstruction

1) Id key competency outcomes of the TeamSTEPPS training framework**

-gold standard for team work training -made up of leadership, communication, mutual support, and situtation monitoring to then lead to more positive performance, knowledge, and attitudes -works to faciltate teamwork -is dependent upon or moderated by other skills -contributes to team performmance, quality of care and patient safety

muscular dystrophy**

-group of inherited diseases characterized by progressive weakness and degeneration of muscle fibers without involvement of the nervous system -Early childhood = duchenne MD -Childhood/adolescene = Becker, FSH, Emery-Dreifuss, Erb -Adule = ocuopharygneal, mytonic dystrophy (steinert)

Nicotine**

-half-life is 2 hours -most addictive of all substances -most leathal drug in US Withdrawal: craving, irritability, anxiety, difficulty conc, dec hr, inc appetiite

10) Chromatolysis** $$$TEP

-hallmark of retrograde degeneration -reaction of neuronal cell body to axonal injury -changes reflect increase protein synthesis in effort to repair the damaged axons -round cellular swelling, displacement of nucleus, dispersion of Nissl substances throughout cytoplasm -concurrent with Wallerian degeneration

3) Post traumatic Headache**

-headaches almost daily following head trauma for months to years -takes on migrainious features -can excaberate migraine symptoms Tx: -usually self-limited -tricyclyic antidepressants (amitrityline) -beta blockers (propranolol)

4) Primary Cough Headache**

-headaches with cough -must do an MRI to make sure its not secondary -treat with indomethicin but usually resolves on own

Brown-Sequard Syndrome**

-hemisection of the spinal cord -ipsilateral weakness & loss of vibration, position and light touch -Contralateral loss of pain and temp

Opiods**

-heroin, oxycodone, hydrocodone, morphine, fentanyl -OD can be and are often are fatal -withdrawal never fatal -more deaths in US from drug OD than MVAs -intoxication = dec appetitie, respiratory depression constricted pupil, constipation -OD triad= stupor, miosis, apnea or slowed breathening Antidote- Naloxone, lasts 30-90 mins -Tx for OD : methadone (full opiate agonsit) , nalterexone, naloxone, buprenophine (partial opiate agonist)

Insula**

-hidden lobe of the brain -cerebral cortex

2) Summarize risk factors and demographic information of suicide **

-higher amongst psychiatric patients with mood disorders, psychotic disorder, substance-use disorders (alcohol), periosnality disorder -serious physical illness -male, older, careful, increased lethality, dec chance for help are all characteristics of completers

4) Olfactory receptors**

-hundreds of different types of olfactory receptros to detect different odorants -olfactory nerve axons from the same type of olfactor receptors converge on the same mitral cells

Other Causes of NMJ disease

-hypermagnesium -envonmations -tick paralysis -pesticides

Management of herniation and increased ICP

-hyperventilation -mannitol or hypertonic saline -steriods (decadron) helpful with brain tumors, inflammation, not helpful with ischemia or hemorrhage -Neurosurg -Cerebral perfusion pressure (CPP) CPP = MAP- mean ICP try to maintain >50, ideally 60>

2) Trace the path of visual info from the retina to the brain**

-hypothalamus and 3rd ventricle are dorsal to the optic chiasm -infundibulum is ventral to the optic chiasm Retinal ganglion cell projections: 1) Suprachiasmatic nucleus of the hypothalamus- circadian pacemaker 2) Pretectal nuclei= pupillary response to light 3) Superior colliculus = reflexive eye and head movement in response to visual stimulii (mostly rods) 4) Lateral geniculate nucleus (LGN) of the thalamus= fine visual discrimination (mostly cones) -LEFT VISUAL FIELD = RIGHT BRAIN -RIGHT VISUAL FIELD = LEFT BRAIN

Hypothalamus endocrine control**

-hypthalamus is the master regulator

Abrasions and foreign bodies in eye

-illuminate/magnify** -topical anesthetic -topical fluroescein enhances visualization -lid eversion -cotton tip/spatula -Topical cycloplegia (paralysis of cilalary body causing loss of accomendation) -topical antibiotic -eye patch sometimes (downside cant detect vision and can lead to infection) uses contact lens more often DONT PRESCRIBE OR DISPENSE TOPICAL ANESTHETICS (proparacaine, tetracaine) cuz too effective and can lead to corneal melts

Naloxone*

-immediate opiod antagonist for OD binds to MU opioid receptor

Immune Brain pathology

-immune attack on myelin -CNS= MS= focal or multifocal, subacute or chronic, remitting or progressive MS LESIONS TEND TO BE CLOSE TO THE WATER MS plauques can be all over -PNS = Guillain-Barre syndrome -Paraneoplastic- autoimmune response to tumor antigens, can affect any neural tissue

basal ganglia** $$$TEP

-important in voluntary movements and making postural adjustments -recieves cortical input, provides negative feedback to cortex to modulate movement Striatum: 1) Caudate Nucleus -runs with the lateral ventricle 2) Putamen-lateral and ventral to caudate, separted by internal capsule 3) Nucleus accumbens-rostral-ventral to the putamen Claustrum-sheet of cells Globus Pallidus: -medial to the putamen 1) Externa*** 2) Interna*** Lenticular nucleus (Lentiform) = putamen + globus pallidus Amygdala: -rostral to the tail of the audate nucleus and the inferior horn of the lateral ventricle Direct (excitatory) pathway-SNc input stimulates the striatum, stimulating the release of GABA, which inhibits GABA release from the GPi, dishinhibity the thalamus via the GPi (INC motion) D1-Receptor = D1Rect pathway Indirect (inhibitory) pathway- SNc input stimulates the striatum, releaseing GABA that disinhibits STN via GPe inhibition, and STN stimulates GPi to inhibit the thalamus (DEC motion) INdirect (D2) = INhibitory Dopamine binds to D1, stimulating the excitatory pathway, and to D2 inhibiting the inhibitory pathway leading to INC of motion

Conjunctivitis bacterial**

-in the neonate, IS, ocular truama/surgergy, or contact lens wearer can be vision threatening

9) Id the basal ganglia**

-in the telencephalon -includes the caudate nucleus, putamen, globus pallidus, amygdala, claustrum, n. accumbens

4) Relative afferent pupillary defect*8

-indicates damage in the pathway usually in the optic nerve -both pupils respond together

Rule 2- Indirect HP (head contralateral to arm and leg) ***

-indirect HP localize ipsilateral to and at the level of the CN involvement-> Brain Stem

Semi-voluntary movements**

-induced by an inner sensory stimulus, or an unwanted feeling or thought (obsession). Therefore they are supperssible -Examples are RLS, Akathisia, Tics

Lateralized periodic discharges EEG**

-infectious (herpes encephalitis) -brain tumors -Seizures from lesion on one side of brain

4) Id the brachium of the inferior colliculus**

-inferior colliculus projects to the medial geniculate nucleus via the brachium of the inferior colliculus

Preseptal (periorbital) Cellulitis**

-inflammation and infection superficial to orbitbal septum -Staph aureaus, strep pyogens, strep pneumo -Findings: Intact VA and EOM, no proptosis, APD (?), or diplopia -Tx: PO antibiotics

Blepharitis**

-inflammation of the eyelid margins -gritty, FB sensation -collarettes in lashes -Tx: Lid scrubs if staph suspected bacitracin or erythromycin

Myositis**

-inflammation of the muscle -Dermatomyosistis (V-neck rash, periorbital helliotripe rash, mechanic hands, gottron's sign, atrophy) -Polymyosistis -Afects predomenetley shoulder and hip girdle muscle -dysphagia is common -females -Normal CK is typically 200-300

Somatic Motor Nuclei**

-innervate skeletal muscle (which develops from somites) -CN 3, 4, 6, 12 = 34, 612 -Oculomotor nuclueus = CN III -Trochlear nucleus = CN IV -Abducens nucleus = CN VI -Hypoglossal nucleus = CN XII

Visceral Motor Nuclei*

-innervate the parasympathetic systems (viscera, glands, SM) -CN 3, 7, 9, 10 = 37, 910 -Edlinger-Westphal nucleus= CN III -Superior Salivatory Nucleus = CN VII (submandibular & sublingual) -Inferior salivatory nucleus = CN IX (parotid) -Dorsal motor nucleus of vagus = CN X

Intermediolateral cell column histo

-inside these cells are preganglionic cells, if it is T1-L2 like this one then is sympathetic, if it is cervical or sacral then its parasympathetic preganglion cell bodies -the cell bodies will be multipolar

Sympatetic Nerves of Eye

-internal carotid plexus -arise in IMLCC of T1 -synapse in the superior cervical ganglion -postsynaptics travel along internal carotid a. into head -Targets: Superior tarsal muscle Dilatory pupillae

Spinal Cord: Hemi Cord Lesion**

-interruption of the posterior columns causes ipsilateral loss of vibration and joint position sense** -interruption of anterlateral systems causes contralateral loss of pain and temp sensation** -this is ofetren begins slightly below the lesion because the anterlateroal fibers ascend to three sgments as they cross -there may also be a strip of one or two segments of sensory loss to pain and temp ipisalateral to the lesion, caused by damage to posterior horn cells before axons have crosed -Causes: Brown-Sequard syndrome, MS, and lateral compresion from tumors

3) Disuss treatment for neovascular AMD**

-intrvitreal injection of anti-Vascular endothelial growth factor (anti-VEGF) made up of bevacizumab, ranibizumab, aflibercept, 4-6 week intervals (if dry slowly extend interval) for the rest of their lives

1) Basal ganglia overview**

-involved in movement, cognition, and limbic system -basal ganglia modify movements -lenticulostriate arteries supply the basal ganglia

Anterior Cord Syndrome**

-involvement of corticospinal and spinothalamic tracts -weakness & loss of pain and temp sensation -anterior spinal cord occlusion -damage to the aneterolateral pathways causes loss of pain and temp sensation below the level of the lesion -damage to the anterior horn cells produce LMNs weakness at the level of the lesion (helps localize) -Common causes include trauma, MS, and anterior spinal artery infarct

Brain Death**

-irreversible cessation of all brain function, including brain stem 1) Is the exam consistent with brain death? 2) Is the insult irreversible** -must run a neuro exam and apnea test** , cerebral angiography or a nuclear medicine perfusion scan may be used

2) Id the location of the vestibular cortex and the projection to it from the thalamus**

-it is at the pariteoinsular vestibular cortex and it recieves vestibular input from the ventral posterior thalamus -the vestibular cortex is at the parietal operculum and posterior insula

Trauma induced lid injuries

-lacerations/avulsions (sharp vs blunt) -animal bits common -must rule out other ocular injury like globe rupture and hyphema (blood in front of eye) Danger zones of Lacerations: 1) full thickness lid laceration 2) Lacrimal outflow system -lacrimal canaliculus must be repaired canalicular avulsion repair 3) Retractor muscles superior laceration

Merkel cells $$$TEP

-large, myelinated fibers, adapt slowly -found on finger tips, superficial skin -respond to pressure, position, and deep static touch

Pacinian Corpuscle $$$TEP

-large, myelinated fibers;adapt quickly -located in deep skin layers, ligaments, and joints -senses vibration and pressure

4) Describe the tools for leading teams, including breifs, huddles and debreifs**

-leaders hold the team together -ensure a plan is conveyed, reveied and updated -leadership is fascilitated through communication, situation monitoring and fostering of an environment of mutual support, -designated vs. situational -DEFINE, ASSIGN, SHARE, MONITOR, AND MODIFY A PLAN**** -Define the plan by considering time, people, equipment, and information -Assign tasks and responsibilitys by deteriming what must be done, who will do what, communicate clear expectations, request feedback Breif = share the plan, should form the team, designate roles, estamblish climate and goals, short and long term planning Huddle = monoitor and modify the plan, by hold ad hoc (touch base) to regain situation awareness, discuss cirtical issues and events, antipicate outcoumed and likely contingencies, assign resources, and express concerns Debrief = review team performance, should be breif informative and should exchange infor and give feedbakc, should occur after the event, desnged to improve teamwork, designed to improve outcomes

AMD (age-related macular degeneration)

-leading cause of blindness in developed world 1) Dry = non-exudative or non-neovascular = most common 2) Wet = exudative or neovascular= more severe -Risk factors: Older 50<, smoking, Fhx, White, >fat, HTN, light colored eyes, sun exposure -S/S: blurry vision, metamorphopsia, central scotoma -blind spot, in advanced stages see charles bonnett syndrome = visual hallucinations, peripheral vision will be unaffected -Pathology: unknown thought to be inflammation and oxidative stress leading to accumulation of drusen -DRUSEN is a hallmark of AMD*** = yellow/white accumulations of lipid and protein 1) Dry AMD = presence of Drusen and pigmentary changes of RPE w/out hemorrhage, exudate or subretinal fluid Tx: -stop smoking -AREDs vitamins for those with inetermediate to late dry AMD or wet AMD, Vit C, E, zinc, copper, lutein, zeaanthin, slows progression 2) Wet AMD= when damage to the outer retinal layrs leads to neovascular growth into the retina -characterized by hemorrhage, subretinal fluid, macular edema, and presence of retinal pigment epithelial detachments -daily amsler grid testing to catch progression from dry to wet -chorodial neovascularization forms due to break in bruchs membrane caused by drusen , these vessels are very fragile and tend to break and bleed leading to scarring and is irreversible Tx: anti-VEGF

General Glaucoma**

-leading cause of irrevsible blindness in AA, 3 million affected in U.S., only half are aware -lead to progressive damage to the Optic nerve which has CUPPING appearance ** if Cup: disc ratio (CDR) of >0.5, CDR asymmetry between nerves of >0.2*** -ISNT rule** Inferior> Superior> Nasal > Temporal in terms of thickness (Nasal side with thicker vessels) -Intraocular pressure is only modifiable risk factor and focus of all current treatment, should be 10-21 mmHg, from build up of aqueous humor due to increases resistance to outflow -Size of small light spot=size of average optic disc -Obeys the horizontal meridian

Decerebrate rigidity lesion**

-lesion at the level of the red nucleus or little lower leading to loss of the rubrospinal tract and vestibulospinal tract are now dominant (this is lower than rubrospinal)

Spinal Cord: Posterior Cord Lesions**

-lesions of the posterior columns cause loss of vibration and postion sense below the level of the lesion -with larger lesions, there may also be encroachment on the lateral corticospinal tracts, causing UMN- type weakness -Common causes include trauma, extrinsic compression from posteriorly located tumors, and MS. Vitamin B12 deficiency**** and tabes dorsalis (Tertiary syphillis)*** preferentially affects the posterior cord

Graves' Ophthalmopathy**

-lid lag and retraction of upper lid -impaired eye movement with muscle edmea -proptosis/exophthalmos causing exposure to keratopathy -hyperthyroidism is common in these patients

2) Describe the anatomyu, connections, and function of the limbic association cortex***

-limbiv system receives input from several different association cortices. Association cortex by definition is not primary sensory or motor rather it is one that receives input from other cortex. -Association cortex conveys highly processed sensory information which is further processed by the hippocampus (in encoding sensory impressions into long-term memory) and the amygdala (link sensory information with emotional responses)

3) Summarize intellectual disability and common disorders related to this level of functioning**

-limitation in communication, self-care, social and interpersonal skills, ADAPTIVE FUNCTIONING** major thing you are assessing for -must occur before age 18 Borderline Intellectual Functioning: -IQ range approximately 71-84 Mild Intellectual Disability -IQ 50-55 - 70 -most common category -academic skills up to 6th grade level -usually need some assistance/support Moderate Intellectual Disability -IQ 35/40-50/55 -academic level about 2nd grade Severe Intellectual Disability -IQ 20/25-35/40 Profound ID -IQ below 20/25 -most do not live at home

Rule 3: HP without CN involvement** ARM and LEG on same side (No CN involvement)

-localizes below the medulla -> ipsilateral Spinal cord -This is brown-sequared syndromes

1) Describe the anatomy and function of the vestibular apparatus*8

-located within the labyrinth of the temporal bone -Lesions that affect vestibular nerve can also mess up the cochlear nerve -Contains the utricle (sensory) , saccule (sensory) , and 3 ampullas (sensory) associated with each of the semicircular canals 3 seperate semicircular canals: 1) Anterior semicircular canal- 2) Lateral semicircular canal- 3) Posterior semicicular canal - -Cristae within the 3 ampullae detect rotational acceleration, and are emersed in jellylike mass called the cupula -Rotation occurs->fluid (endolymph) moves-> moves the cupula-> moves the cilila of the hair cells-> stimulate the axons of CN VIII Utricle and Saccule: -Maculae within in the utricle and saccule detect linear acceleration and head posistion -Urticle = detects acceleration in horizontal plane -Saccule = detects acceleration in vertivcal plane -Hair cells are in the cristae and maculae and are the sensory receptors and are emersed in jellylike mass that contains cyrstals of calcium slats called otoliths -Movement-> moves endolymph-> moves macula-> moves cilia of hair cells-> stimulates axons of CN VIII -Vestibular ganglion has BIPOLAR neurons** so axons in the vestibular apparatus cell bodies are in the vestibular ganglion and then have axons projecting to the vestibular nuclei which is located at the junction of the medulla and pons (dorsal lateral)

Tetracaine**

-long acting, high hydrophobicity, high potency -Use: spinal, topical -Amino ester class = cuz they have 1 "i" in their name -tertiary amine Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Distribution: -administered with epinephrine to vasoconstrict vessels to keep in local Clearance: -metabolized by cholinesterase to a PABA (can cause allergic rxns) and alcohol SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy -methemoglobinemia = seen in amides minus cocaine, treat with 02 and methylene blue

1) Neuropathic problems underlying Parkinsons and clinical features**

-lose the dopamine (thus losing the inhibitory affect leading to more activation of the GABAergic neuron in striatum (which is inhibitory) Dx: -need bradykinesia plus one of the other two cardinal manifestitations (Tremor, rigidity) -improved UPDRS score 1 hr after challenge with levodopa -Bradykinesia (most responsive to levodopa) , rigidy, tremor (resting), and postural instability (least responsive to levodopa)

Parkinson's Disease**

-loss of dopamine in the substantia nigra -Less movement due to decrease in overall dopamine -Hypokinetic -Decreases inhibition of globus pallidus interna -Increases inhibition of the globuls pallidus externa -Leading to an overall increased inhibition of the thalamus resulting in less output from the cerebral cortex

7) Clinical picture and pathology of MS**

-loss of myelin with variable loss of axons (transmission of impulses) -findings are most prominent in white matter -CSF has increased gamma globulin (IgG) with oligoclonal bands of IgG

1) Optic Neuropathy

-loss of vision -RAPD -optic disc edema or atrophy -optic disc may be normal initially Two most common acute optic neuropathies: 1) Optic neuritis -young pts, acute unilateral oss of visual acuity, px w/ eye movement, ipsilateral RAPD, disc edema (papillitis) or more common is normal appearing nerve -strong association with MS (must do MRI to test) -IV steriod tx -oral steriods at convential dose causes inc attack -they are going to improve over time 2) Ischemic optic neuropathy -older pts, acute, unilateral loss of vision, ipsilateral RAPD, almost always with swollen optic nerve, little revocery, non-arteritic vs aretric -no tx for non-artertic -must rule out giant cell arteritis -must reduce risk factors HTN, heart disease

Sevoflurane**

-low solubility and 2 MAC Uses: -widley used for induction and maintance Advantages: -very low pungency- peds -rapid induction and recovery -Good CV profile and bronchodilator -Great AG

Desflurane**

-low solubility and 6 MAC (low) Uses: -widely used for maintenance during outpatient surgery due to fast onset and revoery Advantages: -rapid induction and emergence -Good CV profile Disadvantage -pungent- bronchial irrtation/cough

Isoflurane**

-low solubiluty and 1.15 MAC Uses: -commonly used for maintenance Advantages: -good CV profile, bronchodilator Disadvantages: -pungent-induction performed with other agents

Kennedy Disease (Spinal Bulbar Muscular Atrophy)**

-lower motor neuron disorder -X-linked trinucleotide CAG repeat expansion of the androgen receptor gene on chromosome 11-13 Dx: -slowly pregressive weakness and atrophy affecting facial, bulbar and limb muscles, cramps are fequent -associated with endocrine distrubances include late-onset gynecomastia defective spermatogenesis -weakness all over -most likely cause of death is aspiration

Leukodystrophies

-lysosomal stroage and peroxisomal defects that wrec the olgiogendrocytes and myelin which affect white matter -Adrenoleukodystrophy= X-linked, inability to oxidize Long FA chains, defiency in perioxisymal acyl coenzyme A synthetase, onset 4-8, school failure, spastic paraparesis, vision and hearling loss, vegatibit state within 2 years, tx with BM transplant

2) Recognize the epidemiology of SUDs an the associated public health crisis**

-major cause of death in U.S. -it is very costly

5) Primary exercise headache**

-make sure its not secondary -important to rule out structural causes -reassurance, indomethacind

5) types of vascular malformations such as arteriovenous malformatinns and sccular aneurisms**

-may cause parenchymal or subarachnoid hemmorrhage -Ateriovenous malformations (AVM) = due to high pressure and can get very large its like a ball of vessels in the brain

Orientation of Orbit

-medial wall extends farther anteriorly than lateral wall -Lateral sidee of eye is more exposed

2) Summarize treatment interventions for eating disorders***

-medical stabilization and safety -psychotherapy is the primary intervention for all eating disorders : family based treatment for adolescent AN and CBT for BED and adult BN focused on restoring weigtht and addressing disordered thinking and stopping behaviors -ongoing medical and psychiatric monitoring -psychotropics are not helpful for primary symptoms in AN, -Fluoxetine and other antidepressants (at higher doeses than depression) are useful for binge suppression in BN and BED

7) Schizophreniform disorder

-meet the criteria for schizophreniz except dont meet the time requirement been more than a month but hasnt been 6 months

2) Describe the role of Ca++ and Ca channels in synaptic transmission**

-membrane depolarization opens a voltage gated Ca++ channel to allow Ca+ to influx into the presynaptic terminal -Ca+ influx stimulated vesicles to fuse to the membrane and release neurotransmitter into synaptic cleft (exocytosis) -Similar structure to Na+ channels -Myasthenic gravis targets the P/Q channels (Ca+ channels) and damages them

Antidepressants sexual side effects

-men experience SE more often -women experience more severe SE -most common lack of desire and orgasm delay -SSRIs can decerase libido, ejact, delay organisms -Trazodone can cause priapism -Bupropion usally no problems/may improve some aspects of sexual function -

Stimulants**

-meth smoked is fasts ingestion route lasts for 12-24 hours ** -amphetamines -cocaine (crack is the base form) : half life is 20-40 mins, used in binges or runs, speedball when injected with heroin, snorted, IV or smoked** tx with disulfiram inhibits dopamine catabolizing enymes -bath salts -nicotine -cafeeine -MDMA: can casue hyperthermia and serotonin ** syndrome** -prescribed stimulatnts

Lidocaine**

-moderate hydrophobicity, rapid onset, medium duration, moderate potency -low pKa so largerly neutral at physiologic pH -Onset 1-3 mins last 120-240 mins -Uses: local infiltration -PK: metabolized by CYP1A2 -SE: Black box for seizures, cardiopulmonary arrest, high incidience of TNS with spinal procedures -Amino amide class = have 2 "i's" Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Distribution: -administered with epinephrine to vasoconstrict vessels to keep in local Uses: -Lidocaine is antiarrthymic drug Clearance: -dependent on liver and heart function SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy -Neural: severe pain often worse than the surgical procedure (only in lidocaine and procaine)

Prilocaine*

-moderate hydrophobiticy, rapid onset, medium duration, moderate potency -low pKa, largely neutral at phsyiologic pH = rapid diffusion and onset -will cross BBB -SE: TNS, methemogloinemia (G6D patients) -Uses: anesthetic of choice when vasoconstrictive additives (epinephrine) must be avoided** -EMLA = prilocaine and lidocaine used as cream for pediatrics, lumbar puncture, dental -Amino amide class = have 2 "i's" Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Clearance: -dependent on liver and heart function SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy

1) Elderly Depression**

-more somatic complaints (GI = less appetite, N/V) -fatigue and lack of energy -not much depression or low self esteem reporting -psychotic -present masked -bereavement will not typically result in depression -bereavement may lead to depression in hx of depression and out of proportion loss -seeing the lost loved one all the time -loss of function = depression -grief = still function maybe not as well -Secondary depression due to hypothyroidism, cancer, ERSD, arthritis, heart disease, stroke (MOST COMMON), cognitive dysfunction -depressive pseudodementia (dementia symptoms of depression) = dementia due to depression reversible with antidepressants -Delirium = hypoactive or hyperactive, people will confuse hypoactive delirium for depression (goes up and down unlike low state of depression) need to do serial cognitive testing to id -Substance induced depression= alcohol and weed -Iatrogenic depression = med induced (antihistamines, benzo, opiates, NSAIDs, hormones)

2.5) Aneurysmal SAH**

-most common cause is trauma -most common non-trauma is berry anerysm -deadliest stroke 12-15% die before they get to hospitial -Presentation: worst headacke of life, can present like menignties -Dx: do a LP if you get pink means recent SAH, yellow fluid meaning xanthocromia and bleeding few days ago, traumatic tap red to pink to clear -Tx*** -admit to ICU, nurtition, and hydration, treat hyperglycemia, and electrolytes -acute arterial HTN management <160 -treat intracranial HTN -hydrocephalus -DVT prophylaxis -Seizure treatnment and possible prophylaxis -Aneuyrsm treatment: COILING most common but will clip in more severe cases Complications: -Cerebral vasospasma dn delayed cerebral ischemia (DCI) = leading cause of death and disability in SAH, occurs 7-10 days post SAH, dx with TCD, CTA, MRA, angiography Tx with nimodipine***, maintain euvolume, treat HTN, hypervoleuma, hyeprosmorlar

10) Cataracts**

-most common cause of reversible decreased vision in US and world -Lens is suspended by zonules -elective surgery

Gliomas

-most common group of primary brain tumor 1) Astrocytoma 2) Oligoastrocytoma 3) Oligodenroglioma 4) Ependymoma 5) Choroid plexus tumor

Conjunctivitis Viral**

-most common is adenovirus -S/S: watery/mucoid discharge -preceded by URI -tender preauricular node -extremely infectious

1) Epidemiology and risk factors for cerbrovascular disease**

-most common life threatening neurologic disease -Leading cause of disability in adults -97% ischemic, 10% ICH, 3%SAH -Risk factors: age, gender, and ethinicity -Non-modifiable stroke factors: -HTN, hyperlipidemia, DM, a fib, tobacco use, obesity, alcohol intake, lack of physical activity, sleep apnea

1) Neurofibromatosis Type 1** and associated neuropathy

-most common neurocutaneous syndrome -AD -100% of pentrance -mutatated tumor supressor gene NF1 on Chromosome 17 -RAS becomes trapped in active stage with this mutation Dx: -Fhx, 6 or more cafe-au-lait macules, 2 or more neurofibromas, freckling under arms or in groin, two or more lisch nodules (bumps on eyes), distincitve bony lesion: dysplasia of the sphenoid bone or lower leg, optic glioma CNS manifestations: -intracranial gliomas (CN 2, cerbellum, brainstem) -Astrocytomas (asymptomatic) Other Manifestations: -Renal artery stnosis, pheochromocytoma secondary HTN, vascular dysplasia (moyamoya), gastrointesnal stromal tumors -Scoliosis, sphenoid wing, short stature, long bone dysplasia, promeninet forehead and brow

Cannabis***

-most frequently used illicit drug worldwide -Withdrawal: irritabliltym anger, aggression, nercousness, anxiety, sleep difficulty, dec appetite, weight loss, restlessness, depressed mood, with at least on of the following (abd pain, shakiness/tremors, sweating, fever, chills, or headache) need 3 of them -withdrawal is worse at 2 weeks cuz it is lipophilic -Spice and K2 synthetic marijuana -Chronic effects: increased rate of anxiety, depression, schizophenria, affect memory, verbal fluency, attention, learning, perception of time, sensory perception, short term memory deficits, high dose can cause acute psychosis*, early use associated with more problems -cannabinoid hyperemesis -cyclical nausea and vomiting, colicky ab pain, can use hot shower for relief

8) Explain the role of the corpus callosum and its function in the cerebral cortex**

-most information is transmitted between the left and right hemispheres via corpus callosum

2) How does the neural crest contribute to PNS and other cells***

-most neuronal cell bodies of the PNS orginate from the neural crest -schwann cells orginate from the neural crest -Much of the face is formed from neural crest cells -Retinoic acid (Vit A) is a morphogen which interacts with developing neural crest cells. Carniofacial malformations occur -In hirschsprung disease neural crest cells that should form parasympathetic enteric ganglia fail to migrate to correct position leading to megacolon, lack of peristalsis and constriction of the colon

multi-infarct dementia (MID)**

-multiple ischemic lesions in cerebral cortex, cumulatively resulting in enough neuronal loss to produce dementia -focal neurologic deficits can be present, depending upon the size and location of the infarcts -vascular dementia -marked cerbral arterial atheroscleorsis and/or thrombembolic disease -often small and scattered infarcts

Rule VII:m Pure Proximal motor (no sensory), decreased Deep tendon reflex**

-muscle -pure proximal, eye or bulbar motor (no sensory) , normal DTR-> NMJ (fatigability is typical)

Reflex Arc***

-muscle fibers in the spindle are attached to the muscle tendon and thus stretch when the muscle tendon is stretched -they adjust their length to constantly remain sensitive to stretch as the muscle changes its length -slow stretch of spindle (voluntary control( the spindle signals intermittently and asynchronously resulting in readjustment of the length of spindle reducing its activity -rapid stretch of spindle (tendon jerk) the spindles fire strongly and syncronosuly resulting in activation of LMNs causing muscle contraction (TEST YOUR REFLEXES) -rapid contraction of muscle quickly reduces stretch and thus ending the reflex quickly -Muscle fasiculations = muscle twitching. It is the result of minor local muscle contractions or the uncontrollable twitching of a single muscle group served by a single motor nerve fiber or filament.

Rule VI: Distal all-limb or LE sensory

-nerve -can be with or without prescence of distal weakness

Ampulla Histology

-nerve cells -Ampulla crest -sensory epithelium contains hair cells and support cells -cupula= gelantinous mass of proteins and carbohydrates covering the hair cells

Diabetic neuropathy

-nerve damage from impoverished blood flow can lead to erectile dysfunction, incontinence, poor wound healing, and loss of sensation from area

1) Epidemiology, risk factors, pathophys and presentation of Parkinsons*** (3 Qs coming from this one flashcard)

-neurodegenerative disease -Males> Females -55 is AOO but can happen at any age Risk Factors: -age&sex, lifestyle, coffee and smoking protective, nutrition, rural living, environmental exposure, occupation, concomitant illness, genetics, milk linked to parkinsons, high stress jobs -May start in the gut, dopamine containing neurons in gut have shown lewy bodies 10-20 years before onset Stages: 1 and 2 = in brainstem see autonomic and olfactory disturbances, 3 and 4 = in midbrain see sleep and motor disturbances 5 and 6 = affects cerebral cortex, see stereotypical symptoms Clinical Presentation -Resting tremor -Bradykinesia-Akinesia = dont cross legs when sitting, not much shifting *** Have to have this to diagnosis -Gait changes = slouching, rigid limbs, -Small handwriting and slowing of handwriting -soft speech Tx: -Levodopa -Decrease destruction (COMT) -Increase reuptake (MAOB) -agonists -Anticholinergics -Give just enough to not cause side effects -Major SE includes dyskinesia (moving a lot) Pathophys: -loss of pigmented neurons in substantia nigra -Origin of the neuromelonin cells is catecholamines -Lewy body form in hypopigmented cells -Lewy body made up of alpha-synuclein -There are a few causal genes for parkinsons -There are associated genes that maybe present in up to 30% of parkinsons

Chronic Traumatic Encephalopathy**

-neurodegenerative tauopathy (abnormal tau) associated with repeated concussive and subconsussive head injuries -seen in athletes and soliders exposed to blasts -grouped by severity: mild, moderate,severe -Mild TBI associated with concussion -Trauma causes stretching and tearing of axons, which leads to diffuse axonal injury

2) ADHD***

-neurodevelopmental disorders with core characteristics being deficits in behavioral and response inhibition** -Put simply is a disease where your brain considers everything to be important cannot filter well -Poor developed inhibition control in prefrontal lobe (inferior frontal cortex) -Not ADD -3 subtypes: 1) Inattentive presentation 2) Hyperactive/impulsive presentation 3) Combined presentation -DSM5: 1) Inattentive= 6+ items for 6+ months (careless, inattention, not listening, not follow through, difficulty organizing, avoids tasks that require sustained mental effort, often loses things, easily distracted, often forgetful) 2) Hyperactive = 6+ items for 6+ months (fidgets, leaves seat, restless, unable to play/do quiet activities, always on the go, excessive talking, blurting out, cant wait turn, interrrupts) 3) Must have hyperactive-impuslive symptoms were present prior to age of 12 4) Must have hyperactive-impulsive present in two or more settings 5) Interfere with functioning -ADHD adapts as you get older -Gold standard for dx through clinical interview and history getting info from more than 1 source -IQ helps establish id of intellect may say hey should be getting As, or may have a learning disorder (presents similarly) -Medical/Neruologic workup is NOT necessary -11% US school-aged Children (most common childhood disorder)*** -1:5 boys and 1:12 girls -4-6% adults -Highest cormobidity disorder is oppositional defiant disorder Causes: -inhertiable -biological risk factors are inutero smoking, severe head injury, lead exosure -Not bad parenting Neuropsychology: -Working memmory delineates -Tx has positive impact on brain structure -Life long disorder: 1/3 will grow out, 1/3 will have symptoms but not needs meds, 1/3 continue to need meds -At higher risk for death due to accidents being #1 killer of kids and more prone to those behavior

Delirium**

-neurologic emergency -flutuating levels of consciusness and disorientation, can present with all psychiatric S/S -reletaively common and deadly Risk factors = old age, dementia, and other stuff he didnt talk about Tx: - life support -do a MMSE scale -rule out stoke, opiod over use -give thiamine, folate, consider naloxone -metabolic infection workup -for agitation do not give more drugs (DA blockers) -get sitter -in acute emergency use low dose BDZ -seroquel and clozapine for agiation if BDZ fails

1) Anatomy of the neuron**

-neuronal cell bodies vary grealty in size -metabolically active -critically dependent on oxygen -use a disproportionate amount of glucose -perikaryon of neurons consist abdundant rough ER -mitochondiral cells are very important -Lysosomal functions are vital due to neurons being post-mitotic and are usually not replaced -Dendrites are specialized for receiving information from other neurons Neuronal cytoskeleton: -Microtubules, neurofilaments, and microfilaments -Microtubues support transport of organelles (mitocondria) and synaptic vesicles -Neurofilaments are imporant for growing axons and axon diameter -Actin remodeling is important for sympatic plasticity Axon Transport -dynein transports cargo along microtubules in retrograde way -kinesin transports cargo in the anterograde direction -Tau protein interactis with microtubules which stabilizes the microtubules

14) Limits to regeneration in the CNS and solutions**

-new neurons are produced in the olfactory epithelium. the axons from these cells enter CNS to get to olfactory bulb due to permissive factors released by olfactory ensheathing cells (OECs) -Neurons migrate from the subventricular zone to the olfactory bulb and from the subgranular zone to the dentate gyrus of the hippocampus in adult humans. Factors increasing neurogenesis: -exercise -anti-depressants (pending) -Environmental stimulation helps dendrites grow in rats Neuroregeneration in PNS but not in the CNS after damage to axon: -schwann cells facilitate axon regeneration leading to functional recovy in PNS -Glial scar (astroglosis), inflammation, chondroitin sulfate proteglycans inhbit CNS regeneration -Olfactory ensheathing cells are among the cell types being tested to create a permissive environemetn for axon regeneration

10) Topiramte** (Toupee)

-newer -BROAD SPECTRUM ANTIELEPTIC -TOPEEA OF THE CONQUISTOR = TOPIRAMATE -LIDS ON THE PEANUT BASKET = INHIBITS NA CHANNELS -BINDS TO GABA-A = SHAKING HAND OF CAB DRIVER -SE = SOLIDERS= SOMONELENCE, FATIGUE, CONFUSED, COGNITIVE SLOWING, SKINNY (WEIGHT LOSS), KIDNEY STONES, ACUTE MYOPIA = EYE TEA KETTLE = HIGH PRESSURE = GLAUCOMA -USES= BROAD SPECTRUM, ATONIC-CLONIC, MIGRAINES = BALD HEAD, TAKES LENNARD-GASAT (LLAMA) MOA; -Blocks Na+ channels -neuronal membrane hyperpolarization, -enhances GABA -limits glutamate Uses: -monotherapy for partial and generalized tonic-clonic seizures; ajunct for Lennox-Gastaut syndrome -prophylaxis of migraine -pain and eating disorders (off label) SE: -generally well-tolerated -metabolic acidosis and kidney stones from CA inhibition -associated with cognitive impairment

IQ scores***** ON TEST

-no longer as important as level of functioning across the domains of conceptual, social ,and practical

Summary of Sleep Lecture**

-normal sleep-wake swtich is due: 1) primary wake promoting neurotransmitters (HA, NE, 5-HT, DA, Ach) 2) primary sleep promotoing neurotransmiter (GABA), 3) the sleep wake modulator ( Hypocretin), 4) REM sleep and REM atonia (which is inhibited by wake-promoting neurotransmitters and hypocretin)

Preoptic area (POA)

-not part of the hypothalamus -it is just anterior to the hyppthatlmus

Post Ganglionic ANS ganglia histo

-nucelolus -nucleus -cytoplasm -multipolar -the cell bodies are in the autonomic ganglion, the axons are in the postganglion

Acetylcholine $$$TEP

-nucleus basalis of meynert -decreased in alzheimer disease -decreased in huntingtons -increased in parkinsons

Lateral inferior pontine syndrome**

-occlusion of the anterior inferior cerebellar artery; -Characteristics- Ipsilateral to lesion: cerebellar ataxia, nystagmus, vertigo, facial paralysis, paralysis of conjugate gaze to side of lesion, deafness, tinnitus, impaired facial sensation -Contralateral to lesion: impaired pain and temperature sesnation half of body

5) Postpartum depression DSM-5 dx**

-occurs i about 10% of women within 1st 2 months of birth -not recognized as a seperate diagnostic category as PPD usually represents a recurrent major depressive episode in a women's life

6) Primary sexual activity headache**

-occurs right before organism -severe -usually no cause -rule out secondary causes -goes away after a few months

5) Explain the significance of the columnar organization in the cerebral cortex***

-ocular dominance columns are an example -columns make up different areas of the brain

6) Premenstrual dysphoric disorder DSM-5 dx**

-officially recognized in DSM-5 for the first time -occurs up to 10 days before onset of menses -symptoms must be severe enough to significantly interfere with function, is not an exacebration of an ongoing underlying depressive disorder

3) organization of the olfactory epithelium and the structure and function of the olfactory receptor neuron**

-olfactory epithelium lines the superior nasal concha -Olfactory cilia at the end of dendritic knobs contain olfactory receptors -axons from the olfactor receptor neurons form the olfactory nerve which projects to the mitral cells in the olfactory bulb -small groups of fila of CN 1 penetrae the cribiform plate to terminate on the dendrites of mitral cells in specialized synaptic zones called glomeruli in the OB -CN1 ensheathed by schwann cells -sustentactular cells are supporting cells -basal cells are stem cells -There are 40 million olfactory receptor neurons (bipolar)

3) Explain development of motor fluctuations and dyskinesia in long-term levodopa therapy**

-on-off phenomenon = alterations between postive and negative responses, striatal neurons become dependent on peripheral avaibality of levodopa -dyskinesia = involuntary movements, occur at peak blood levels (Micheal J Fox) Motor fluctuations — Motor fluctuations are alterations between periods of being "on," during which the patient experiences a positive response to medication, and being "off," during which the patient experiences a reemergence of the Parkinson

Ciliary ganglion

-one of the terminal ganglia of the parasympathetic system, located in the posterior orbit, axons from which project to the iris -the parasympathetics target the ciliary muscle (accomodation) and spincter pupillae

3) Brief psychotic disorder DSM***

-one or more of symotoms 1-4 in schizophrenia descritpion (not negative symotoms) with one being 1-3 -lasts more than a day but less than a month and eventually return to premorbid level of function

Cocaine**

-only naturally occuring local anesthetic, medium duration, medium potentcy -Uses: topical,ENTterm-168 -intrinsic vasoconstirve -inhibits catecholamine uptake -cardiotoxic -Amino ester class = cuz they have 1 "i" in their name -tertiary amine Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) Distribution: -have vasoconstriction property to keep drug in local area Clearance: -metabolized by cholinesterase to a PABA (can cause allergic rxns) and alcohol SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy -Neural: severe pain often worse than the surgical procedure (only in lidocaine and procaine)

Primary Lateral Sclerosis

-only upper motor neurons are involved

7) Causes of papilledema**

-optic swelling, but is excluseively used for optic nerve swelling secondary to increased intracranial pressure** Causes: -tumors, thrombosis, intracranial hemorhage, meningitis/encephalitiss, HTN, and Idiopathic intracranial HTN = dx of exclusion, common in young obese femails, normal neuro imaging, elevated pressure is CSF, tx is acetazolamide -S/S: headache, profound vision loss ver time, blurred swollen margin, disc hyeremia, peripapillary hemmorrhages, enlarged blind spot,

3) Tremors**

-oscillatory movement -shaking is not normal in old age -If ampliptude of tremor decreases during activation of muscle = Resting tremor -If amplipitude of tremor stays the same or increases = Active temor -Does the amplitude increase during target-directed movement if yes = intention tremor if no = simple kinetic (action tremor) Essential Tremor: -aka Familial essential tremor -increase with age -postural and action tremor, mostly in UE and head, must be in HANDS** -bilateral and relativeyl symmetric -more tremor proximally then distally -Tremor occurs with posture holding and with movement, but goes away at rest -drug of choice is propranolol, unless you have asthma then its primidone or Topiramate***

2) When is an EEG indicated**

-outpatient = routine (20-60 mins) or Ambulatory EEG (up to 3 days) (at home) -patients with episodic or paroxysmal events -patients with new onset seizures -patients with a known seizure disorder but unclear dx -patients with unexplained chronic encephalopathy -EEGs are not the most accurate thing in the world. A normal EEG will not rule out an eplipetic disease Inpatient: -for dx, tx, meds titration, and prognosis -can do continous video EEG aka long term monitoring or routine EEG -frequent episodes for seizures or non eplieptic spells -to adjust seizure meds -Epilepsy monitoring Unit (EMU) used when a patient has medically refractory seizures (a patient failing 2 or more antiepileptic meds) -Encephalopathic ptx with unknown diagnosis -Prognosis in comatose patient (often after anoxic brain injury*) -Brain death protocol (not ideal test) STAT EEG: -Non convulsive status epilepticus -encephalopathic or comatose pts where you suspect NCSE -STAT EEG takes 20-30 mins to occur, if after hours may need to wait for tech to drive -Do not wait for EEG, If you suspect status eplipeticus must treat

Autism

-over a 1000 genes involved -3% is de novo (single gene) -4% single gene -3% rare inheritied -49% common inhereted -41% unaccounted

Stress

-over working, tired, leads to anxiety,stretching ourselves out too thin -primary damage is physcial

free nerve endings $$TEP

-pain and temp DRG neurons have peripheral processes with free nerve endings -C-slow, unmyelinated fibers -AS-fAst, myelinated fibers -located all skin, epidermis, some viscera

Medial medullary syndrome**

-penetrating branch of vertebral or lower basilar artery -Ipsilateral: paraylys and atrophy of tongue, ataxia of limb, nystagmus, naseua, vertigo -Contralateral: paralysis of arm and leg spare the face

Vestibular neuritis vertigo**

-peripheral etiology -most common peripheral vestibular cause of acute dizziness** -acute severe symptoms -Hearing preserved = vertibular neuronitiis -Unilateral hearing loss = labrynthitis MUST DIFFERENTIATE BETWEEN THIS AND STROKE -Vestibular neuritis on the right side will have a spontaneous left-beating nystagmus and a postive head thrust test to the right side*** VS -Presence of vascular risk factors, associated neurologic symptoms, direction changing nystagmus, or absent head thrust sign increases the likelihood of a central lesion (stroke) **

Affect

-physical expression of a person's immediate feeling state, typically focusing on facial expression Range: -Full = normal -constricted/blunted = decreased range -increased range -Labile = exaggerated intensitiy, rapid changes Appropriateness -Mood congruent vs. mood incongruent -Matching to subject matter

Optic Radiations (Parietal Lobe) **

-pie on the floor defect**

Definitons**

-plegia: paralysis, palsy -paresia: weakness (sub-total) -hemiplegia & hemiparesis : paralysis or weakness of half of body (most muscle groups affected) -HP: hemiplegia/hemiparesis -Quadriplegia: paralysis of all limbs -Paraplegi: paralysis of LE

The enteroviruses**

-polioviruses -coxsackieviruses Group B -Can cause meningitis and encephalitis Transmission= fecal-oral, person to person, water borne, insect vector (flies and cockroaches) Pathway: -incubation 2-10 days, shedding 1-4 (oropharynx and 1-18 (stool)

4) Summary of Sensory exam lecture**

-position and vibration sense ascend in the posterior column pathway and cross over in the medulla -Pain and temp sense cross over shorly after entering the spinal cord and then ascend in the anterolateral pathway -Intact primary sensation with deficits in cortical sensation such as agraphesthsia or astreognosis suggests a lesion in the contralateral sensory cortex -severe cortical lesions can cause deficits in primary sensation as well -extinction with intact primary sensation is a form of hemineglect that is most commonly associated with lesions of the right parietal lobe, like other forms of neglect, extinction can also occasionally be seen in righ frontal or subcortical lesions, or in the left hemisphere lesions causing mild right hemineglect -patter of sensory loss can provide imprtant information that helps localize lesions to particular nerves, nerve roots, and regions of the spinal cord, brainstem, thalamus, or cortex

3) Common presnetation of OCD and treatment**

-possible mechanism is dysequilibrium of the cortico-striato-thalamocortical conduction pathways with decreased inhibition -major problem is learned behaviors -Thalamus is being hyperstimulated cuz GPi and SNr is not inhibiting thalamus enough Dx: -presence of obsessions or compulsions or both -marked distress that take more than 1 hour/day or significantly affect functioning -marked distress = ego dystonic -diagnosed based on process -AOO is 20 -men and women equal -Familial slightly PANDAS = pediatric autoimmune neuropsychiatric disorders associated with strept infection can cause OCD and tics tx is to treat strept infection Tx: -exposure and response prevention (ERP) **Gold standard treatment -SSRI/SNRI -Clomipramine (TCA) -Psychosurgical procedures Related dieases: -Body Dysmorphic disorder -Hoarding disorder -Trichotillomania = pull out hair causes distress

Huminculus

-post central gyrus map

Acute disseminated encephalomyelitis (ADEM)**

-post viral, vaccination -thought of as a childhood illness -thought of as a autoimmune disorder after environmental trigger -typically monophasic illness, weeks to moths with usual complete recovery -Must differentiate this disease from adrenoleukodystophy -X-linked, metachromatic leukodystrophy, leukodystrophies

Thermal injury

-predominately an adnexal (external) injury (exam status of eyelashes) -lube, lube , lube (to perserve tissue) -often requires late-phase treatment

3) Major Depressive Disorder DSM-5 dx

-presence of at least 5 of 9 symptoms for at least 2 weeks., one of the symptoms must be depressed mood or anhedonia (loss of interest or ability to experience pleasure) -SIGECAPS Sleep = decreased usually can be hypersomnia, insomina in form of intial middle or terminal usually associated with anxious thoughts when awake Interest = less interest (anhedonia) Guilt = inc foucus on guilt Energy = dec energy Concentration = dec focusing Appetite changes = loss of appetite or excessive appetite Psychomotor changes = retardation or agitation Suicidal ideation = preoccupation, passive, active suicidal ideation, and attempt -symptoms must cause distress or disfunction -Mental Status Exam Suicide: -risk factors include comorbid alcohol use, presence of psychosis, impuslivity, asking doesnt increase risk -10% of patients with a major mood disorder will die by suicide = -10-20% of individuals with severe depression experience psychotic symptoms, the hallucinations are delusions are usually mood-congruent S/S of Depression -Single or recurrent (more common) -Severity (mild, moderate, or severe) -with anxious distress -with psychotic features -Chronic Pattern: -most depressive episodes will remit in less than 6 months but some with become chronic -rist of recurrence: 1) one episode = 50% 2) two epidodes = 75% 3) 3 episodes = 90-100% Ddx: -can be a diagnosis or just a symptom -presence of depression should prompt the clinical to perform a comprhensive psychiatric assesment and medical screen -other psychiatric disorders (bipolar, schizo, adhd) -substance use disorder -prescription drugs ( steriods, beta blockers, BC, interferon) -medical conditions (post-stroke, MS, lupus, hypothyroidism) Screening: PHQ-2 = screen for prescence of symptoms in last 2 weeks (screen to see if you need to really screen) PHQ-9***** = real screen, does a screen of all 9 DSM depressive symptoms and rates severtiy of all symptoms, not a subsitiute for full assessment but gives you some help Tx: Mild to moderate depression -Psychotherapy -Exercise -Transcranial magnetic stimulation (TMS) -Electroconsulsive Treatement (ECT) -Serotinin regulate anxietym obsessionality, anger and agitiation SSRIs, SNRI (serotonin-norephinephrine reputake inhibitor) , DNRI (dopamine-noepinephrine reuptake inhibitor) -Dopamine associated with motivation, attention and ability to feel pleasure -Noepinephrine associated with regulation of mental altertness and energy -Tricyclic antidepressants (TCAs) = act on a lot of neurotransmitters and undersirable sites like cholinergic and histamine receptors (too many SE to use including lethality in OD) -Monoamine-oxidase inhibitors (MAOIs) = unique MOA by blocking activity of monoamine oxidase enzymes which degrade Serotonin, dopamine, and NE

1) Describe clinical findings seen in eyes with intermediate Dry age related macular degeneration***

-presence of many large drusen, retinal pigmentary changes or non-center incolving gepographic atrophy -vision is usuaally 20/30 - 20/80 -need to start taking vitamins

2) Discuss epidemiology, path, managment, and prevention of diabetes retinopathy***

-prevelance increases with duration of disease and pts age -exact cause is poorly understood -hyperglycemia -> endothelial cell damage -basement membrane thickening and selective loss of pericytes lead to capillary occlusion and retinal death -can also cause tractional retinal detachment -endothelial barrier decompensation leads to serum leakage and retinal edema -increased vascular permeablilty -> macular edema-> blindess -Prevent with screening Type 1 every 5 years, type 2 once a year, glycemic control, and early tx of macular edema and PDR Tx: NPDR= glyemic and BP control, risk factor modification PDR=panretinal photocoagulation intravitereal injection Macular edema= anti-VEGF -Traction retinal detachment or vitreous hemmorhage = surgical virtrectomy Types: 1) proliferative -creation of abnormal BVs -neovascularulation at disc(NVD) and neovascularization elsewhere (NVE), and neurovascularization in iris (NVI)*** -driven by retinal ischemia, and VEGF -leads to vitreous hemorrhage, retinal traction detachment -use fluorscein-angiography to test -tx with anti-VEGF, and laser destruction of ischemic retina, and surgery 2) Non-proliferative - mild, moderate, severe -microanerysums, lipid(hard exudate), macular edema, cotton wool spots(ischemia) , intraretinal hemorrhages and neovascular changes

2) Id major CNS neurotransmitter that are targeted by CNS drugs and generel functions of these transmitters**

-primary target of most CNS drugs is the neuron -glial maintain ionic gradient and remove transmitters -site of action of drugs is at some portion of neurotransmission -target selectivity is based on 2 concepts: 1) Regions of the brain have different neurotransmitters either completely or with subtypes 2) Specific functions of brain can be targeted by targetting different neurotranmitters completely or with subtypes

Blood supply of visual system

-primary visual cortex is supplied by the calcarine artery (branch of the posterior cerebral artery) and branches of the middle cerebral artery

Mammillary Bodies

-project to the anterior nucleus of the thalamus via the mammilothalamic tract

propriospinal tracts

-projections of white matter that remain in the spinal cord -allows communication between different levels of the spinal cord -allows coordination of movements within the spinal cord -may be improtant for recovry after spinal cord injury

Anterior Nucleus of the Thalamus

-projects to the cingulate gyrus via anterior limb of th internal capsule

6) Describe the function of the reticular activating system**

-projects to the hypothalamus and thalamus -this pathway is involved in sensory control -The reticular formation project to the intralaminar thalamic nuclei which projects to the Ventral anterior (VA) nucleus of the thalamus, which projects to the orbitofrontal gyri of the cerebral cortex -the reticulof formation is determing what senses will get through to the cerebral cortex like feeling my socks or lights flickering

Prefrontal Cortex

-projects to the striatum and receives input from the somatosensory cerebral cortex, the dorsomedial, and anterior nuclei of the thalamus, and the ventral tegmental area (VTA) Dorsolateral Prefrontal Cortex: -Important in attention, abstract thought, and planning (executive function) Ventromedial frontal cortex (orbitofrontal cortex): -function is to inhibition of inappropriate behavior -lesion = impulsiveness and disregard -In

Adjustment disorders***

-prolonged negative emotional reaction following a major life stressor -symptoms occur within 3 months of onset of stressor and once the stressor as terminated symptoms don't last longer than 6 months -Acute = if disturbance lasts less than 6 months -Chronic = if disturbance lasts longer than 6 months -Subtypes: 1) AD With depressed mood 2) with anxious mood 3) with mixed anxiety and deprssive mood 4) with disturbance of conduct 5) with mixed disturbance of emotions and conduct -more common in women 2x

Erenumab* (BIOLOGICS AGAINST CGRP R)

-prophylactic agent -used for worse HA MOA: -CGRP antagonist -monoclonal targted for the CGRP receptor -CGRP is elevated in migraine patients and will cause vasodilation and extravasation of cranial blood vessels Uses: -chronic migraine not acute SE: -hypersensitivity reaction are the main side effect

Propranolol* (HEART MED DONT KNOW HOW IT WORKS)

-prophylactic agent for migraine -used for worse HA -may take several weeks to work MOA: -unclear, may alter cerebral pain sensitization pathway, may due to dec BP lowering effect,

Botulinum toxin* (BOTOX)

-prophylactic agents -used for worse HA -second line therapy for chronic migraine -NOT efective prophylaxis of episodic migraine -must be injected in 36 spots in face

12) BBB** $$$TEP

-protects the brain from toxic substances, bacteria, drugs, from reaching the CSF/CNS -Fromed by tight junctions between nonfenestrated capillary endothelial cells, BM, astrocyte foot processes -transporters can transfer glucose and other necessary molecules like AA -nonpolar/lipid-soluble substances cross rapidly via diffusion -Few specialized brain regions with fenestrated capillaries and no BBB allowl molecules in blood to affect brain function 1) area postrema - vomiting after chemo; 2) OVLT- organum vasculosum lamina terminalis= osmotic sensing 3) Neurosecretory products to enter circulation = neurohypophysis -ADH release -neiplasm and infarction destroys endothelial cell tight junctions-> vasogenic edema -Other barriers are Blood-testis barrier and maternal-fetal blood barrier of placenta

Parkinson's Disease**

-protein defect = alpha-synuclein Causes: -most cases are sporadic -rare familial forms Effects: -affects pigmented neuronal groups which are found in substantia nigra, locus ceruleus, dorsal motor nucleus of CN X -early motor symptoms (bradykinesia, shuffling gait, resting tremor) -Delayed cognitive decline

Electrogiagnosis in polyneuropathy

-provides unequivocal diagnosis of a neuropathy

DDx of psychotic disords***

-psychotic disorder due to another medical condition (dementia) -substance/medication- induced psychotic disorder -delirium -delusional disorder -schizoaffective disorder -schizophreniform disorder -brief psychotic disorder -Cluster A personality disorders (paranoid, schizoid, and schizotypal)

Nystagmus

-quick phase -acheive fixation-resets eyes to incoming visual scene during prolonged rotation

lumbar radiculopathy (sciatica)***

-radiculopathy of the lower back -commonly includes pain radiating down the leg -more they move the better they are -can be due to herniated disk -root problem -Straight leg test to reproduce pain -Most pain will resolve without treatment within 4-6 weeks -weakness and numbness are more concerning -red flags (saddle anesthesia, bowel dysfunction, signs of infection, iv drug use, night sweats, risk for malignancy, thoracic pain, anticoagulation or trauma) will cause further testing with imaging -Image if conservitve care is not affective following 4-6 weeks Tx: -rest, PT, NSAIDs, muscle relaxants, stretches -post 4-6 weeks: MRI, surgery, epidural steriod injection, Gabapentin, lyrica, cymballa

6) Histo features of mitochondrial myopathies

-ragged red fibers (aggregates of abnormal mitochondria) -affect muscle and brain (dependent heavily on oxidative phosphorlyation)

Myoclonus etiologies**

-rapid jerks -most common cause is toxin

Creutzfeldt-Jakob disease (CJD)***

-rapidly progressive dementia (die within 2 years) -tyically associated with myoclonus, tremors, ataxia -can be genetic, sporidic, or iatrogenic -Genetic forms are caused by mutations in prion protein gene -misfolded protein aggregation is pathophy -CSF and MRI are now used to better dx

Neurofibromatosis Type 2

-rare AD, complete penetrance, late onset -mutatuion of Merline gene on chromosome 22 -Merlin encodes for protein schwannomin or merlin (tumor supresor) Dx -onset before 70 -unilateral vestibular schwannoma AND relative with NF2 -ependymomas, meningiomas, and astrocytomas -subcapsular cataract -acustic neuroma

2) Neuroleptic malignant sydnrome**

-rare but grave -due to dopamine loss -antipsychotics especially traditionals or withdrawal of levodopa S/S: - Triad : altered mental status, ridigidty and fever (hyperthermia)**, and dysautonomia -Tx: DA agonists (levodopa) and life support

Cingulate gyrus **

-recieves input from sensory cortex, prefrontal cortex and the thamalus and then projects to the entorhinal cortex -mediates emotion, pain, sadness -Anterior cingulate cortex is thought to play an important role in learning, error detection, and reward-based decision making -Lesions in the cingulate gyrus can caus memory disorders -Cingulum carries input from the cingulate gyrus to the entorhinal cortex -Cingulum also carries info in the orbitalfrontal gyri to the parahippocampal gyrus

Trigeminal neuralgia (tic douloureux)***

-recurring episodes of intense stabbing pain in trigeminal nerve area (near mouth or nose) pain triggered by touch, drinking, washing face treatment may require cutting nerve -typically unilateral and severe pain -high intensity, shock, stab, electrical pain -main be spontaneous or precipated -tic doulorex is grimace following shock -may be related to compression of the nerve by BV, tumors, cysts, berry aneurysm -If you see it bilateral think MS Tx: -MRI -surgery is most likely long term success -Radiofrequency ablation of gasserian ganglian -gamaknife -Carbamazepine -Oxcarbanazipine is more effective** -Baclofen, Clonazepam (droswy SE), gabapentin, TCA as an add in

Fundamental Frequencies**

-refer to chart

Classification of Seizures*

-refer to chart 1) Atonic= goes limp usually kids 2) Tonic= whole body extends 3) Myoclonic-tonic-clonic= jerk then extension then shaking while stiff 4) Behavior arrest = just freezes 5) Hyperkinetic seizure (frontal lobe epilepsy) = legs shaking, same movement everytime, frowning face

Anorexia nervosa**

-restriction of energy intake relative to requirements leading to a significantly low body weight -intense fear of gaining weight or persistent behavior that interferes with weight gain -persistent lack of recognition of the seriousness of the current low body weight Are all the changes in new DSM -Very low weight disorder with dysfunctional self perception along with psychological and behavioral features causing fear and weight-avoidant behaviors Signs: -Emaciation, altered growth curve, hypothermia, menstraul disturbances, lanugo (downy body hair) , hyepractivity or psychomotor retardation, bradycardia, Hypotension, dirty skin, brittle hair and nails, hair loss, cyanotic and cold hands and feet, ankle edema Mental Status Exam - malnourished, appears depressed usually Medical complications: -things smell and taste bad Refeeding Syndrome: -life-threatening condition -compartmental shifts of electrolytes (K, Phos, Mg), fluids, -over aggressive refeeding worsens extracellular (serum) hypophosphatemia -leads to cardiac and diphragmatic failure -More than 50% of people recover or imporve but have a 5% related death (most deadly mental disease)

Huntington's disease**

-results from degeneration of the straitum -results in involuntary choreiform (dance-like) mivements, the indirect pathway is disrupted, hyperkinetic disorder (more movement)

Concussion*

-results in functional rather than structural abnormalities of the brain -may NOT have loss or impairment of consciousness -normal brain imaging -if a person/athlete suffers a concussion they ARE DONE NO EXCEPTIONS

2) Arousal and sleep signaling systems**

-reticular activating system is a big player -The excitatory neurotransmitters are: Ach, DA, Histamine, NE, 5-HT

1) Coma**

-reticular activating system is key to alertness and comas -Causes: Diffuse/Metabolic = hypoxia, hypoglycemia, drug OD, encephalitis, status epilepticus, hepatic failure, renal failure Focal/Mass lesions = tumor, stroke, bleed, brainstem infarct, brainstem bleed, subarachnoid hem, subdural hemoatoma, cerebrallar CVA, bilateral thalamic inf, -Herniations = cingulate (not life threatening) , uncal (life theartening), cental bilateral uncal (life threatening) , cerebellar (life threatening) , transcalvarial (going out of brain)

Aprosodia**

-right hemisphere controls non-verbal aspects of speech and language including producing and understanding intonation, hand gestures, and facial expressions -anatomy mirrors left hemisphere

Acute akathisia**

-rocking in chair, walking on spot, crossing and uncrossing legs when sitting, scratching face or scalp -most common MDS and disstessing side effect from neuroleptic agents -Propranolol is tx of choice

10) Bipolar Depression DSM-5 Dx**

-same criteria as major depression disorder -more likely to see LEADEN depression with profound fatigue and heaviness in body and limbs with hypersomnia often (12+ hours per day )

5) Febrile Seizures**

-seizures that occur in young children 6 mo-5 years old which are triggered by fever usually >101 F -usually begnin -higher risk to develop epilepsy if they are complex= last longer than 10 mins, focal seizure, recurr in 24 hours -patients with prolonged febrile seizures may develop temporal lobe epilepsy -prognosis of simple febrile seizures is good and do not need long term antiepileptic medication treatment.. Treat the fever

1) Id major compents of the ventricular system $$TEP

-series of spaces that contain CSF -two lateral ventricles (C-shaped) -intraventricular foramina of Monro connect the two lateral ventricles with the 3rd ventricle -third ventricle is found in the diencephalon -Cerebral aqueduct is found in the mesencephalon and connects the third ventricle to the 4th -the 4th ventricle drains into the subarachnoid space via: 1) Foramina of Luschka = Lateral 2) Foramen of Magendia = Medial -there is a patent (not normally seen in adults) space in the spinal cord called the central canal -CSF made by ependymal cells of choroid plexus. Travels to suvarcnoid space and is reabsorbed by arachoid granulations and then drains into dural venous sinuses

Dihydroergotamine* (ERGOT HOW ABOUT NOT)

-serotonin receptor agonist MOA: -complex agonist/antagonist effects at alpha-1, 5-HT 1D, and D2 -5HT1D agonists**** is the major affect for migriane -alpha 1 agonist = produces vasoconstriction -antagonist at D2 -5HT1D = reduces activity of painful pathways, rescues release of CGRP (want to stimulate) Uses: -alternative to triptans it is a dirty drug (does a lot o stuff) -patients with prolonged migraine or frequent recurrence SE: -Ergotism = BBW, intense vasoconstriction leading to gangrene -N/V -retroperitoneal/pleural and cardiac valvular fibrosis with long-term use -Contraindicated in pregnancy (can cause uterine contractions) and CV disease

sumatriptan: (a SUMo wrestler TRIPs ANd falls on your HEAD)

-serotonin receptor agonist MOA: -5HT1 agonsit selective for 1B/1D receptor subtypes -produces vasoconstriction and blocks release of CGRP -relieves pain, N/V, and increases GI motality Uses: -1st line for acute migraine headaches -also used for cluster headachs Restrictions: -dont work for everyone -not helpful when auras are occuring -often shorter duration than HA symptoms SE: -CNS depression -CV* due to excessive vasoconstriction can cause coronary artery vasospasm, HTN, peripheral vascular ischemia, dont give IV -Stroke -Serotonin Syndrome

Frovatriptan* (FRO YO when have menstrual migraines and triptan so you know migraine med)

-serotonin receptor agonists -same as sumatriptan -3 hr onset but long half-life; used for short term prophylaxis** of menstrual migraine***

When to suspect a ruptured globe

-severe blunt trauma (car accidents or things smaller than tennis ball) -sharp object -metal on metal contact -bullous subconjunctival hemorrhage -uveal prolapse (iris or ciliary body) -irregular pupil shape (peeked or keyhole) -hyphema or vitreous hemorrhage -post-traumatic lens opacity -flattened anterior chamber angle -intraocular pressure is lowered -anterior chamber is collapsed -seidels sign -gros inspections/symmetry -IF SUSPECT MUST STOP AND SHIELD

Methohexital**

-short acting barbiturate MOA: -activates barbiturate binding site on GABA-A receptors Onset: -30 sec, duration - 10 mins Uses: -induction, procedural sedation

Procaine**

-short acting, low hydrophobicity, low potency, slow onset -Dental applications, infiltration anesthesia -Have intrinsic vasoconstrictive -Little systemic toxicity -Amino ester class = cuz they have 1 "i" in their name -tertiary amine -Carry a + charge at neutral -Weak base (pKa 7.8-9.1) Moa: -block Na+ channels in excitable tissues and prevent signal tranmission along nerves -On B fibers must block 3 nodes of Ranvier -On C fibers binds directly to fibers -Modulated receptor hypothesis = higher affinity for open and inactivated receptor states -More efficiacious on active firing nerves -Pain is first to be blocked and last to be recovered PK: -Topical, Injection (block the nerve ending), Peripheral nerve blockade (block along the axon) , Central nerve blockade (neuraxial blockade) -Neutral form good protonated + bad Distribution: -have vasoconstriction property Clearance: -metabolized by cholinesterase to a PABA (can cause allergic rxns) and alcohol SE: -site irrtation, hypersensitivity, allergic dermatitis, asthma, anaphylaxis, -CNS: metallic taste, tingling lips, tinnitus, agitation, seizures, respiratory depression -CV: bradycardia, hypotension, arrhythmias and cardiogenic shock, treat with lipid emulsion therapy -Neural: severe pain often worse than the surgical procedure (only in lidocaine and procaine) -methemoglobinemia = seen in amides minus cocaine, treat with 02 and methylene blue

Neuron 2 Gross Pictures

-shows both cell bodies and axon bodies

Idiopathic orbital inflammation

-similar to Graves -px, proptosis -diagnosis of exclusion -unilateral, tendons are involved** -can be bilateral

Sleep Physiology $$$TEP

-sleep cycle regulated by circadian rhythm which is driven by suprachiasmic nucleus (SCN) of hypothalamus. -Circadian rhythm controls nocturnal release of ACTH, prolactin, melatonin, norepinephrine -Light ->SCN-> norepinephrine release_> pineal gland-> melatonin -Alcohol, Benzos, Barbitutates, and Noepinephrine decrease REM sleep and delta wave sleep -Benzos helpful with night terrors and sleepwalking by reducing N3 and REM sleepf

Lissencephaly**

-smooth brain -gyri fail to form or are underdeveloped due to neuronal migration fialure -associated with heterotopias= neurons in abnormal locations -Causes= genes (LOF mutation of Lis1 and DCX) and viral infection -Outcome = intellectual disability

5) Summary of Somatic Symptom Disoders**

-somatic symptoms disorders are common and typically present to PCP or ED -healthcare utilization is higher than gen population due to distressing somatic symptoms and/or high anxiety -education and communication are key components of the treatment plan -prognosis varies depending on diagnosis -Management involves a combination of medical and psychiatric treatment

3) Understand the common causes of conductive hearing loss2

-something going on with tympanic membrane or oscular chain 1) EAC blockage (foreign bodies) 2) Tympanic membrane perforation (know location and size) 3) Acute otitis media -complications include extracranial and intracranial problems -Extracranial = acute mastioidits/petrositis, labyrinthitis, facal nerve paralysis -Intracranal = meningitis, abscess, otiitic hydrocephalis 3.5) Chronic serous otitis media -a serous effusion not responsive to medical rx for 3 months -creates CHL like speech delay and risk for infection -PE tubes will equalize pressure and allow improved hearing 3.75) Chronic mastoidits/Otitis media ->3 months fluid/debris within ME/mastoid -prevents proper middle ear function -ETD -can cause ossicular erosion 4) Otosclerosis -fixation of stapes bone to the cochlea at the oval window -most common cause of CHL in women in 20-40 -AD condition -stapedectomy is surgical correction -audiographm = Carhart notch 5) Cholesteatoma -name sucks -begnin skin growth where it shouldnt be -due to closed eustation tube (internal auditory canal) -pressure in middle ear bilds and eventually pulls TM then keeps shedding skin into a ball -tx is surgery 5.5) ossicular chain disruption 6) SSCD, perilymph fistula

4) Understand common causes of sensorineural hearing loss

-something has happended to the cochlea 1) Noise exposure 2) Acoustic Neuroma -8% of brain tumors -most common CPA tumor -unilateral (red flag) -descreased discrimination -instabiloty is more common then vertigo -dx with audio/ABR/MRI -tx: observation, sterotactic radiosurgery, surgical excision 2.5) Presbycusis 3) Meniere's syndrome -vertigo lasting hours, fluctuating SNHL, tinnitus, aural fullness -clinical Dx -Medical tx with diuretics/salt free diet (less than 1,000) -Surgical tx conservative or destructive 3.5) MS -can have vertigo and SNHL -MRI shows areas of demyelinization or plaques in CNS -refer to neurology 4) Sudden sensorineural hearing loss 5) Cerebellopontine angle tumor 6) Aminoglycosides/Toxins 7) Congenital 8) Labrynitihis 9) Syphillis 10) Autoimmune

5) Relationship between the spinal cord and brain**

-spinal cord is a continuation of the brain -caudal medulla merges seamlessly with the cervical spinal cord -Pyramidal decussation is the official seperation between spinal cord and the brain (medulla) this is on the ventral side -Pyramids on the VENTRAL SURFACE** of the MEDULLA -Olive is lateral to pyramids on the MEDULLA and is a marker for the rostral medulla

Metastatic tumors in CNS

-spread by hematogenous routhe -From lung (50%)> breast (15%)>melanoma> renal> colon -Metastatic carcinoma will often be seen with multiple lesions

West Nile Virus**

-spread to humans by the bite of an infected mosquito Presents: -flu liek illness -develop neuro-invasive disease -more common in elderly and IS -attackes anterior horn cells -fever -regional and asymmetric flaccid paralysis -no major pain or sensory deficits Dx: -spnal tap with increased protein, normal glucose -IgM of CSF is dx* Tx: -supportive Prognosis: -good for encephalitis and poor for cord disease

6) How and where neurons divide**

-stem cells of the CNS divide adjacent to the ventricles and central canal in the spinal cord (ventricular zone) -neuroblasts migrate away from ventricular zone towards the pial surface in close contact with glia or axons (radial migration) -Intermediate (mantle) zone will contain most of the neurons in the adult CNS. The marginal zone consits of processes derived from neurons in the indermediate zone

Dementia**

-stroke and ischemic encephaopathy -hippocampal sclerosis -head trauma -hydrocephalus -CNS infectios -Metabolic CNS disorders -Demyelinative diseases -Neurodegenerative diseases -severe medical illness or organ failure -Meds

Thought Process

-structure of thoughts -Goal-directed = organized, coherent to the point -Circumstatial= scenic route getting there but including too many ideas -Tangential = get off topic and stay there -Flight of ideas= shifting rapidly from one idea to another resulting in fragmentary speech, common in mania -Loose associations = incoherence* answers not matching what was asked -Perservation -Blocking

Infections/Inflammatory brain pathology**

-subacute -diffuse, focal, or multifocal -progressive if untreated Meningitis (infection of menigenies)= diffuse and progressive Encephalitis (infection of brain) = focal or diffuse and progressive Myelitis (infection of spinal cord) = focal or mulitfocal and progressive Abscess= focal and progressive

4) Compare the withdrawal phenomena of alcohol, opiates, and nicotine**

-substance is discontinued or reduced -Detoxification is treatment for withdrawal , bind to the same receptors and allow gradual tapering Alcohol: -4 stages 1) Minor Withdrawal-hangover 10x treat with benzos, thiamine before glucoes***, fluids and obtain urine screen 2) Seizure- hospitalize, give benzos, thiamine and fluids, check fluids 3) Hallucinations-tx by hostpiatlize, thiamine and fluids, IV benzos, CT if first seizure, urine drug screen, check levels 4) Delirium tremens -disorientation, agitation, hallucinations, incredased ANS activity, 5% mortalitiy tx: ICU, thiamine and IV fluids, IV benzos, check levels Risk factors for Severe alcohol withdrawal: -years drinking**, older age** , past history of DT or withdrawal seizures, co-morbid medication, Opiate: -Mild: craving, yawning, lacrimation, rhinorrhea -Moderate: restlessness, myalgia, dilated pupils, piloerection -Severe: N/V, increased respiration, inc BP, diarhea, inc pulse, inc temp

Sunconjunctival Hemorrhage**

-sudden onset of increased intrathoracic pressure -uncontrolled HTN -Tx: check BP ,

Central retinal vein occlusion

-sudden, painless vision loss, assoc with HTN, swollen disk, venous stasis retinal hemorrhages, cotton-wool spots, edema of macula -risk factors old, HTN, DM2, vascular disease, hypercoagulable states, glucoma -NOT A STROKE

5) Relative afferent pupillary defect**

-swinging light test -normal = no change or constriction -Nonaffected will constrict both, the affected eye the Pupil dilates in both -ipsilateral optic nerve problem most the time -exception are a large retinal lesion, contralateral tract -NOT cataract, refractive error, cornea

2) Cortical Maturation**

-synapse formation = pruning 1) mainly excitatory, glutaminergic neurons get pruined 2) Local circuit interneurons- GABAergic neurons stick around -Motor functioning thins out before the prefrontal cortex -ADHD is a neurodevelopment disorder, see a delayed maturation of prefrontal cortex

premenstrual syndrome (PMS)

-syndrome involving physical and emotional symptoms occurring in the 10 days before menstruation -not severe enough to significantly interefer with function

GABA $$TEP

-synthesized in Nucleus accumbens -decreased in anxiety -decreased in huntingtons

Noepinephrine $$$TEP

-synthesized in locus ceruleus -increased in anxiety -decreased in depression

Speech Sound Disorder**

-term used to refer to an individual with a phonological or articulation disorder -seen in kids -can result from developmental disorders (Autism), brain injury, genetic disorders (Downs), hearing loss -stuttering is common -more common in boys

Lab tests for polyneuropathy

-test for diabetes by looking at glucose and HbA1c -B12 defiency = 2-8% of PN -Monoclonal protein (SPEP/IFE) = cyroglobulinemia, CLL, Waldenstrom's, multiple myeloma, POEMS, amyloidosis -Highest yield = blood glucose, B12 with MMA and serume IFE

2) Describe how CSF is produced**

-the choroid plexus is found in the ventricles and is a highly vascularized structure that makes CSF from blood -modified ependymal cells form tight junctions which keep cells out of the CSF but allow fluid in

2) Describe the distinctive morphology of some reticular formation neurons

-the dendrites are positioned to sample information that passes through the brainstem -the axons may either descend or ascend long distances -reticular formation receives input from many senses and is especially attuned to extreme stimuli

limbic system $$$TEP

-the function of the limbic system is to reconcile higher level information (cerebral cortex) with more basic drives (subcortical structures) to learn from past experiences, make choices, and formulate long term plans. Emotions evoked by present stimuli as well as associations with long term memories contribute to limbic system output -Limbic system consits of variety of different structures including hippocampus, amygdal, mamillary bodies, anterior thalamic nuclei, cingulate gyrus, entorhinal cortex Responsible for Feeding, Fleeing, Fighting, Feeling, and F*cking (Fab 5)

1) Locate the reticular formation in the pons and medulla**

-the reticular formation includes several nuclei such as the locus ceruleus (noepinphrine) and raphe nuclei (serotonin) as well as less defined reticular areas

Vision Overview***** Multiple questions on test

-the retina is part of the eye and the brain so we process the information immediately -fovea is within the macula and that has the most cones meaning we have the sharpest vision there -Light enters eye via pupil and is focused on retina by the lens -optic disk is where the axons of the ganglion cell exit the retina (blind spot) -central retinal artery runs with the optic nerve and supplies most of the retina --Myelinated by oligodendrocytes

2) Id the presence of hyporeflexia and provide a ddx***

-there is a disconnection in the reflex arc -can be at receptor, at spinal cord, afferent and efferent neurons, could be at NMJ

Spinal Cord: Transverse Cord Lesion***

-there is often a sensory levvel, meaning diminshed sensation in all dermatomes below the level of lesion on both sides -the pattern of weakness and reflex loss can also help determine the lesions spinal cord leve -common causes trauma, tumors, MS, transverse myelitis

3) Describe how neurogenic placodes and derivitives contribute to the PNS**

-thickening of the ectoderm that gives rise to neurons O = olfactory placode - related to CN I ganglion -develops into olfactory epithelium -olfacotry receptor neuron gives rise to olfactory nerve -olfactory nerve makes contact with telencephalon = olfactory bulb -GnRH neurons migrate into brain via olfactory nerve -Kallmann's sydnrome = olfactory bulb not made and then GnRH dont reach the brain T = Trigeminal placode -gives riuse to some of the neurons in the trigemina ganglion Ot = Otic placode - related to CN VIII ganglion -all neurons in the cochlear ganglia and most the neurons in the vestibular ganglia are derived from otic placode Epibranchial placodes -gives rise to some of the neurons of CN ganglia VII, IX, and X G= Geniculate P = Petrosal N= nodose epibranchial places

Temporal lobe seizure EEG**

-this eeg is focal

Reversal of neuromuscular blockade**

-to reverse neuromuscluar blockade the goal is to get TOFR >0.9 -Depolarzing blockers you use spontaneous recovery -Non-depolarizing agens you use neostigmine and atropine (most the time) -New agent is sugammadex- only for steroidal NMBs

Special Sensory Nuclei**

-transmit taste -CN 1,2,7,8 and 9 = 12,789 Solitary nucleus = CN VII and IX (CN VII does taste for ant. 2/3 of tongue and palate, 9 does post. 1/3 of tongue) **Unique nucleus cuz it carries more than 1 modality in a single nucleus Vestibular nuclei = VIII (balance and orientation) Coclear nuclei = VIII (hearing) CN 1 and CN 2 nuclei are not located in the brainstem**

Visceral Sensory Nuclei**

-transmit visceral info to brain (excluding pain) -CN 9, 10 = 910 Solitary nucleus = IX, X ( )

General Sensory Nuclei**

-transmits somatic sensations of the head, neck, meninges, and sinuses back to the brain -CN 5,7,9,10 = 57, 910 -Mesencephalic nucleus of trigeminal = CN V (for propriception (especially of mandible) -Principle sensory nucleus of trigeminal = CN V (for main sensory nucleus of trigeminal, for fine touch and pressure of face) -Spinal nucleus of trigeminal = CN V, VII, IX, X (for pain, temp, and crude touch to face)

Dry Eye Syndrome**

-treat deficent state, abnormal tear film -Tx: with artificial tears

muscle spindles and golgi tendon organs

-two types of proprioceptors -big diameter with myelin = fast Muscle Spindles: -contain 4-12 specialized muscle fibers (intrafusal fibers) -primary function is sensation -in skeletal muscle Golgi Tendon organs -similar structures to muscle spindles in tendons

Uncal Herniation **

-type of transtentorial herniation -usually form unilateral middle fossa epidural hematoma -pupil dilation (due to pressure on CN 3) followed by contralateral paresis** then declined level of consciousness -Kernohan's notch phenomenon = ipsilateral pareiesis with pupil dilation

Nerve roots lesion**

-unilateral, in spinal cord and is near where the lesion is at

6) Schizoaffective disorder DSM**

-uninterrupted period if illness during which there is a major mood episode (major depression or mania) concurrent with criterion A of schizophrenia -delusions or hallucinations for 2 or more weeks in the absenece of a major mood episode during the lifetime duration of the illness

2) Recognize and treat RLS**

-urge to move accompanied by a creepy/craly sensation usually in LE, relieved by movement -most common at rest at night -Familial, gets more common with age -Calves>Legs> arms -Primary -Secondary: Parkinsonism, neuropathy, reneal dysfunction, pregnancy, hypothyroid, periodic limb movements of sleep, anemia Tx: -highly responsive to treatment -first try non therpeutic -then meds use gabapentin, pre-gabalin, then second line dopamine agonists

10) Lithium** (Lithium Lift)

-used in acute mania, maintence, treatment-resistant depression, and reduce risk of suicide = LIFT GOES OVER THE HIGHS AND LOWSS OF THE MOUNTAIN -Narrow therapeutic index = narrow opportunity to get off lift -mood stabilizer -SE= -acute lithium toxicity = N/D/V -Chronic lithium toxicity = neurologic effects = tremors, ataxia,and confusion (KID FALLING OFF LIFT SHAKING THE HIS POLE) -hypothyroid = untied bowtie penguin with FAT GUY leading to weigh gain, dry skin, hair loss, and constipation -Diabetes insipidious caused by lithium by antagonizing ADH in CTs (PEEING SCULPTURE) -Fetal malformation = tarantula hat on pregnant women and misshaped hearts (big right atrium and malformed tricuspid vavle) -Excretion = kidney, drugs that mess with GFR can cause lithium tocicity (thiazides and NSAIDs) or lithium inactivity (HIGH DIVE KID WITH FIRE-EXTINGUISHER) -monovalent cation, doens't generate APs PK: -oral, cleared by kidney, narrow therapeutic window

Naltrexone**

-used to treat ethanol and opiod dependence -MOA: mu opoid receptor ANTAGONIST -reduces craving, binge drinking, makes EtOH less rewarding and more sedating -SE: N, headache, liver toxicity -used for long-term maintence therapy must first be completely withdrawan

Clonidine*

-used to treat ethanol and opiod dependence -used to help the withdrawal symptoms of opoids by decreasing sympathetic activation -SE: can cause several hypotension

Benzodiazepines*

-used to treat ethanol dependence -used for alcohol detox -MOA: bind to BZD site on GABA-A receptor -act by subsitiuting for ethanol to prevent withdrawal symptoms and seizures

Bupropion**

-used to treat nicotine dependence -MOA: inhibts DAT/NET reuptake transporter in CNS -Can help with weight gain probelm and 2x success rate -SE: boxed warning for depression, hostility, agitation, sucididal/homicidal thoughts, and seizures

Nicotine*

-used to treat nicotine dependence -allows you to get nicotine without that dangerous tobacco smoke -MOA is the same as nictotine = stimulation of Nn receptors in the brain (a4B2) -SE: well tolerated can raise BP, HR, Hypersensitivty to dermal patches, headaches, and dizziness

Buprenorphine*

-used to treat opiod dependence -MOA: mixed mu receptor partial AGONIST/kappa receptor antagonists -used in fixed dose combo with mu antagonist naloxone -used for detox like methadone, but also used for long-term maintence

Methadone*

-used to treat opioid dependence -MOA: full opoid receptor AGONIST -dose is titrated to prevent withdrawal but not too high to produce euphoria -used to control withdrawal symptoms during detox but can also be used for long-term maintence -SE: can be lethal due to OD

Metabolic or Toxic Brain pathology

-usually bilateral and diffuse -usually subacute but can be acute or chronic -some conditions can be chronic and progressive and resemble degenerative diseases (ex: Vit B12 deficiency, hypothyroidism, copper metabolism)

Hemidystonia**

-usually injury to subthalamic nucleus or putamen due to injection or stroke -IN YOUNG PEOPLE

NMJ disorders

-usually proximal muscles affected predominantly. -Fluctuation in strength is hallmark -no atrophy -some can involve ptosis, extraoccular, bulbar and neck muscles. -EMG/NCS will have pathogonomnic findings for some disorders. some have serum markers.

5) Non-specific low back pain**

-usually self-limited and resolves <4 weeks -less common etiologies include radiculopathy, spinal stenosis & compression fractures Acute: Chronic:

La Crosse Encephalitis**

-vector and resevour is mosquitos -Amplification in eastern chipmunk and grey squirrel Spectrum: -80% a symptomatic -20% self limitied fevrile illness -1% neruoinvasive (encephaitis>meningits) -98% of cases are <14 years **opposite of WNV -males predominate -Risk factors = live close to forest, 100 M of tree holes, artifical containers or tires, outdoor exposure Manifestations: -Incubation 5-15 days -Fever, headache, malaise, and GI symotoms -Neuro S/S= lethargy, coma, seizures (common and all of them), maliase, GI, meningeal irritation, ofcal neurologic findings Tx: supportive Mortality less than 1 %

Dandy Walker Malformation** $$TEP

-vermis of cerebellum doesnt form -noncommunicating hydrocephalus (4th ventricle enlargement) and spina bifida can be associated -Causes= genetics (chromosomal) -Outcomes= delayed development, movement disorders, intellectual disability

Central etiologies of vertigo presentation:***

-vertigo is more common unilateral -limb dysmetria (lack of coordination of movements) -gait ataxia Causes: -stroke -intoxication -autoimmune or demylinating conditions (MS) -infectious or post infections -if stroke the HINTS will be abnormal (only do HINTS if acute) Tx: -treat the etiology

3) Describe the relationship between the vestibular system and the cerebellum**

-vestibular ganglion neurons project directly to the flocculonodular lobe of the cerebellum and receives a reciprocal projection from the cerebellum -Eye movements are dependent on coordinated input from the cerebellum and the vestibular system

Shingles**

-viral disease that affects the peripheral nerves and causes blisters on the skin that follow the course of the affected nerves -Follows a dermatome outbreak (root problem) -herpes zoster -vesicles, ulcers, papules on skin -Mostly sensory nerves -atropjy of the dorsal horn of the spinal cord with loss of myeline and axons -peripoheral nerve loss of meylin in both PHN and pain free patients -Happens to older individuals Post Herpetic neuralgia -This pain that lasts more then 3 months post infection Tx: -topical agents= capsacin, lidocaine, gabapentin -oral gabapentin -steriod injection -opiods

Visual hallucinations

-visual perceptions in the absence of external visual input -can be uniformed (simple) or formed (complex) 1) Uniformed: (phosphenes) -stimulation of afferent pathway -ossiptial lobe seziures -fortification scotoma (trouble seeing) from migraine 2) Formed -lesion or seizures involving the visual association areas in occcipito-temporal regions Charles-Bonnet syndrome: -visual hallucination in severe vison loss and is believed to be secondary to visual deafferentation -similar to phantom limb syndrome

4) Differentiate between the clinical features of lesions involving the WHERE visual pathways **

-visuo-spatial disorders -simultanagnosia= inability to interpret multiple visual locations simultaneously -optic ataxia = defect of visually guided hand movement -ocular apraxia = inability to voluntarily move/fixate eyes to objects of interst Ankinetopsia: -cant see moving objects, people appear suddently -see things like when in strobe lights -BL lesion to are MT Bilateral Parietal Damage (Balint's Syndrome): -simultanganosia (only see a small portion of picture) -optic ataxia -ocular apraxia cant redirect gaze Alexia with agraphia: -inability to read and write in previously literate individuals -gertsmann's syndrome = alexdia with agraphia(inability to write) accompanied by acalculia (cant calculate) , finger agnosis (loss of sensations) and right-left disorentation -caused by lesions of the left angular gyrus (dominant parietal lobe) corresponding to brodmann area Visuspatial Neglect: -lack of attention to events and actions in one half of space -involve all sensory modalitis and motor acts and motivation

Cistern in brain

-water outside the brain

developmental language disorder*

-when a child has problems acquiring language even though there is no obvious cause -persists into school and potentially beyond -more common in males Tx: -early identification and intervention (3-5 is goal)

7) Treatment options for hyperkinetic disorders

-when oral meds dont work: 1) Clostridium botulinum (Botox) - great for dystonia but works well for other hyperkinetic disorders 2) Deep brain stimulation

4) Delineate the vestibular ocular system**

-when the head move left, both eyes move right to keep the object in the fovea , left medial rectus and right lateral rectus fire. -vestibular hair cells detect this turn and triger the neurons of oculomotor and abducens to fire the muscles -Abducens nucleus projects to the contralateral oculomotor nucleus via the MLF to keep the two eyes in sync

Pediatric leukocoria**

-white eye -white reflex -retinoblastoma -rare -can be commonly misconceived for cataracts -IOP of 39 is a problem apparently** not related to this slide

Ballismus/Chorea**

-wild movements -usually due to injury in subthalamic nucleus or putamen due to infection or stroke -doesnt affect UMN -In old people -Tetrabe

4) Management of coma*8

1) ABCs 2) History 3) Put in C collar 4) Give glucose and thiamine, and naloxone (maybe) 5) Labs, toxicology screen, head CT 6) Coma exam ** 7) Consider LP, and EEG

6) List the primary exictatory and inhibitory neurotransmitters used by the nervous system**

1) Acetylcholine: -excitatory at neuromuscular junction, ANS, parasympathetics, and nucleus basalis -organophosphate poisoning- inhibit AChE = too much ACh, SLUDGEM symptoms 2) Glutamate: -principle excitatory at CNS synapses -taken up by astrocytes where it is degraded into glutamine, which is reabsorbed by neighboring neuron, where its converted back to GLUTAMATE 3) GABA (gamma-aminobutyric acid): -principle inhibitory in the brain -synthesized from glutamate 4) Glycine: -principal inhibitory in the spinal cord -activation of glycine receptors allow Cl- to enter cell leading to inhibitory postsynaptic potential -co-agonist with glutamate for NMDA receptors = excitation 5) Catecholamines: -Dopamine: a) Mesolimbic-mesocortical tract, too much= schizophrenia b) Nigrostriatal tract, too few = parkinson's c) tubero-infundibular tract=DA inhibits prolactin secretion d) medullary-periventricular tract= disregulation of dopamine will lead to obesity and diabetes -norephinephrine: a) dopamine is its precursor b) unlike others DBH is bound to inner surface of vesicles then NE is formed in vesicle c) used in locus coeruleus, and peripheral nervous system -epinephrine a) made by SAM methlyting NE 6) Serotonin: -neurons that use serotonin used in the midline of brain stem -synthesized from tryptophan -Selective serotonin reuptake inhibitors = anti-depressants

Temporal Profile of Diseases Affecting the Brain*

1) Acute -hypoxic, vascular, trauma 2) Subacute -inflammatory/infectious, immune, toxic/metabolic 3) Chronic -congenitial, degenerative, neoplastic 4) Paroxysmal -seizure, vascular/syncope, pain/headaches

3) Discuss a general managment algorithum for acute and chronic back pain syndromes**

1) Acute non-specific musculoskeletal pain -1st NSAIDs (2-4 weeks) + encourage activity -2nd Non-benzo muscle relaxers + physcial therapy -If continues for more than 1 month go see a doctor 2) Chronic non-specific muscluoskeletal pain -1st Duloxetine + Bio-psychological therapies -2nd pain specialist -3rd surgery if nerve damage

10 Bully Brain items (10 Cognitive distortions)

1) All or nothing 2) Overgeneralizations 3) Focusing on negatives 4) Disqualifying the positives 5) Jumping to conclusions 6) Magnification-magnify bad things and zoom out on good things 7) Emotional reasoning- associating emotions to reality (if im nervous- I must not be prepared) 8) Should statements 9) Labeling-if you make a mistake you label yourself to that feeling (I messed up I'm an idiot) 10) Blaming and personalization-leads to guilt

3) Describe common presentations of acute ischemic strokes**

1) Anterior Circulation Syndromes: Most common presentation = pure motor or sensory motor syndrome A) Anterior Cerebral artery -weakness (Leg>arm) -motor hemineglect -transcortical motor aphasia -behavioral disturbances: spincter dysfunction, abulia, mutism, anterograde amnesia grasping B) Anterior Choroidal Artery Infarct -posterior internal capsule -tail of caudate nucleus -posterior corona radiata -lateral geniculate nucleus -optic radiations B) Middle cerebral artery** stroke typically leads to contralateral weakness and sensory loss in the upper extremity and face, hemianopia (visual field defict) , ipsilateral conjugated eye and head devation, if right then mulitmodal neglect, if left hemisphere then aphasia and apraxia -anterior cerebral artery aa) Superior Division of MCA: -contralateral hemipareses (arm>leg) -transient ipisalteral eye deviation -Dominant = brocas aphasia or mutism -Non-dominant = confused neglex inattention bb) Inferior Division of MCA: -contralateral homonyous hemianopia -mild brachiofacial paresis -Dominant = Wernickes aphasia or conduction aphasia -Non-dominant = neglect, confusion, dyspraxia 2) Posterior Circulation Syndromes History = diplopia, tilt of vision, rotatory or linear verigo, drunken type gait, hiccups, BL or crossed motor or sensory symptoms, dec level of consciousness and anmesioa Exam = anisocoria, disconjugate gaze, gaze paresis, nystagmus, skew deviation, Horner's sydnrome, ataxia, unilateral deafness, somoluence and amniesion A) Dorsolateral medullary syndrome (wallenberg's) -ilisplateral thremoalgesic facial defict (CN V nucleus) -contralateral themo defict (spinothalamic) -dysphagia, dysphonia due to vocal cords (CN 9/10) -ipisalateral ataxia (inferior cerebellar peduncle) ** -severe nausea, vomiting, nystagmus, ocular and tronuclu ipsipulsion -psilateral horners syndrome B) Basilar Artery -anteromedial, ventral paramedian, dorsolateral terroties -locked in syndrome = quadriplegia, bL facial palsy, horizontal gaze palsy, C) Posterior Cerebral artery (PCA) -henianopsia -motor symtoms uncommon -thalamic incovlument = amnesia, cognitie impairment, dec consiousness, personalty changes -Embolic etiology 3) Lacunar Syndromes -small sub cortical infarcts less than 1.5 cm -perfortator territories -5 classic symtomes = pure motor hemiparesis*(most common) , pure sensory stroke*, sensory-motor sroke, dysarthria-clumsy hand syndrome, ataxic hemiparesis 4) Watershed infarcts -involve the junction of distal regions of two arterial symtoms -hemodynamic failure -typical patterns (cortical border zone and internal border zone) -clinical presentation is heterogenous -Man in a barrel deficts

Chambers vs Segments of Eye

1) Anterior segment: -anterior chamber -posterior chamber *seperated by iris 2) Posterior Segment

Cluster B personality disorders (Wild) (BAD) **

1) Antisocial PD: disregard for and violation of the rights of others, PSYCOPATH, appearance of normalcy, no regrets, no compassion, -MUST have a prior diagnosis of a conduct disorder by age 15, but this doesnt normally happen usually look back and see CD behaviors 2) Borderline PD: pervasive instability in interpersonal behaviour, mood, and self-image (fear of abandonment, interpersonal relationships are often intense and unstable), can have cormorbid depression and suicide attempts (splitting - view people as solely good or solely bad) 3) Histrionic PD: constant attention seeking, can be sexually provactive , dramatic, shallow, excitable, self-conscious (Scarrlet O'hara) 4) Narcissistic PD: grandiose sense of self-importance or uniqueness (TRUMP) -dramatic, emotional, erratic behaviors -splitting = pits people against each other -Will sometimes be attracted to their polar opposite so this would be cluster C people

2) List 3 types of cerebral cortex**

1) Archicortex : 3 layers Hippocampal formation -Hippocampus proper, subiculum, dentate gyrus 2) Paleocrotex: 3-4 layers -olfactory cortex 3) Neocortex: 6 layers -the vast majority of cerebral cortex 4) Transitional cortex: 3-6 Layers -Subiculum

Association Fiber Bundle Examples

1) Arcuate fasiculus 2) Occipitofrontal fasciculii = connect occipital lobe w/ frontal lobe 3) Superior longitudinal fasiculus = connects the occipital, temporal and parietal lobe with the frontal lobe 4) Uncinate fasiculus = connetcts limbic structures in temporal lobe with the frontal lobe 5) Cingulum = connects the cingulate gyrus with limbic and other structures

5) Trigeminal Sensory Route for Pain and Temperature**

1) Axons from the trigeminal ganglion enter the brain and descend to the spinal trigeminal nucleus as the spinal trigemenal tract 2) Axons from the spinal trigeminal nucleus ascend to the VPM via the trigeminothalamic tract 3) Axons from the VPM ascend to the lateral postcentral gyrus in the posterior limb of the internal capsule

5) Trigeminal Sensory Route for Fine touch of face**

1) Axons from the trigeminal ganglion enters the brain and terminates on the principal sensory nucleus of V 2) Axons from the principle nucleus of V cross the midline and ascend as the trigeminal lemniscus to the VPM 3) Axons from the VPM ascend to lateral postcentral gyrus in the posterior limb of the internal capsule

6) Types of CNS infections such as baceterial, fungal meningitis, viral enchepalitis, and prion disease**

1) Bacterial: -Menigitis: high fever, headache, stiff neck, confusion, skin rash, CSF findings (neutrophils inc, high protien, low glucose, bacteria on stain) Types: 1) Pneumoccocus (strept pneumoniae) is the most common cause and old and babies 2) Meningococcus (neisseria meningitids) seen in adolescents and extremly contingous 3) Hemophilus influenzae = kids 4) Listeria = neonates and IS adults 2) Viral -Meningitis :due to any virus, self-limited, similar to bacterial but less severe, CSF findings (lympocythes high, normal glucose, slight inc in protein) -Encephalitis (most common cause) due to west nile, zika, measles, mupms, HIV, etc enters via insect bites, respiratory tract, GI tract (polio and JV) , animal bites (rabies) , sexual transmit (HIV) 3) Fungal -IS pts, candida, cryptococcus, aspergillus, mucormycosis 4) Parasites 1) Toxoplasmois: seen in neonates, IS pts, necrotizing encephalitis in HIV pts 2) Cystricercosis: ingestion of tenia solium larval cyst in undercooked pork, inflammatory response after organism death 3) Amebic menigencephalits: Naegleria fowleri swimming in warm lakes, primary amebic meningoencephalitis it is fatal 5) Prion disease -causes secondayr spongioform encephalopathy -proteins without DNA and RNA -Creutzfeldt-Jacob disease, Mad cow disease, Kuru -worried in hosptials cuz dont die by disinfectants -see vaculoes in gray matter -rapidly progessive dementia death within in a year or two of onset -epidural/subdural infection are secondary to trauma and form abscesses, incr in patients wht neural tube defect Chronic menigities (infectious): -TBn crypto, syphillis, vascular obstruction due to proliferative changes

Types of Coma*8

1) Brainstem coma -decerbrate posturing -pupil response often abnormal -no or unilateral abnormal cold calorics -apneustic or atxic breathening 2) Bihemispheric coma -decroticate posteruing -normal pupil response ** -col calorics produce slow phase -normal or cheyne-stokes breathening Mimicers -Locked in syndrome = brainstem injured, anarthia and quadriparesis (only communicate w/ eye) -Psycogenic coma = hand drop test to tell if faking (will drop on side in psycogenic, real coma fall on face)

Psychiatric Interview**

1) CC 2) Reason for visit/admission 3) HPI 4) Past Psychiatric History 5) Past Medical history 6) Medications 7) Allergies 8) Family history 9) Social History - more detailed, developmental hx, family bonding, abuse, education, martial status, living situation, home environment, employment hx, legal hx, and support system 10) Mental Status Exam -General appearance, behavior, and attitude -Mood (enduring emotional tone, both pt and dr. reported) and Affect (physical expression of a person's immediate feeling state, focusing on facial expression) -Speech (rate, rhythm, volume, tone, articulation, amount) -Thought Processes (Structure) -Thought Content -Cognition

1) Recognize features of a complete medical history**

1) CC *Handedness 2) HPI -the purpose is to organize the history details in chronological fashion 3) ROS 4) PMH 5) Meds 6) Allergies 7) FHx 8) Shx

3) Describe the role of the hypothalamus in the neuroendocrine system**

1) Cell bodies containing relesing factors. Their axons extend to teh median eminence where they make contact with protal vessels. The releasing factors travel to the adenohypophysis ( anterior pitutary) where they influence the release of hormones into general circulation 2) Cell bodies in the tuberal region of the hypothalamus produce domamine. Dopamin travels to the anterior pitutary where it inhibits prolactin release 3) Cell bodies in SON and PVN have axons that travel to the posterior pitutrary where oxytoci and vasopression are released directly onto general circulation GnRH -Medial POA contains GnRH neuronal cell bodies -GnRH neurons in medial POA have axons that project to the median eminence where GnRH is released into portal blood vessels, then the GnRH is transported to the anterior pitutatary gland where it stiumulates the release of follicile stimulating hormone (FSH) and Luteinizing Hormone (LH) Vasopressin (increased aggression and better memory) (ADH) and Oxytocin(bonding and worse memoryh ) : -SON and PVN are amgnocellular neurons and project to the posterior pitutary gland and release vasopressin (SO THEY MAKE IT) and oxytocin inot the general ciruculation Thryotropin-releasing hormone (TRH) and Corticotropin hormone (CRH) -PVN (parvocellular neurons) prject to the median eminence and produces TRH and CRH -PVN aslo contains a group of neurons whose axons project to the brainstem and intermediolateral cell column of the sponal cord via the medial forebrain bundle and dorsal longitudional fasciulus SCN -receives input from the retina, projects to the area ventral to the PVN and is involved in circadian ryhytms

Intrinsic Arteries

1) Central retinal artery -located deep to the dura mater; pierces the optic nerve -subject to increase in CSF pressure -no significant collateral anastomoses -supplies all retinal neurons except rods and cones 2) Ciliary branches -supplied choroid vascular layer -blood supply to rods and cones

3 Flexures of Brain**

1) Cephalic flexure (Aka mesencephalic flexure) -occurs in the midbrain region on the ventral surface of the brainstem, ONLY ONE THAT STAYS 2) Cervical flexure -occurs during 5th week and seperates the myelencephalon from the spinal cord, occurs on the ventral surface 3) Pontine flexure -occurs dorsally between the 5th and 8th weeks and seperates the metencephalon from the myelencephalon

Localization

1) Cervical cord = arm involvement, C3-C4-C5: phrenic nerve, Horner's syndrome 2) Thoracic Cord = sensory level, landmarks (T4) (T10) 3) Lumbar cord = upper proximal muscles, lower distal muscles 4) Sacral/Conus Medullaris = bilateral saddle anesthesia, prominent bladder/bowel sxs 5) Cauda equina = radicular pain, asymm. leg weak and sensoy hyporeflexia

1) Ocular conditions that result from trauma and injury**

1) Chemical injuries 2) Thermal injuries 3) Ocular abrasions/ FB 4) Perforating/pentrating injuries 5) Orbital injuries

1) Describe proper technique for lumbar puncture**

1) Clean 2) Insert in L3-l4 or L4-L5 3) Let the fill 4) Drip and collect 5) Retract needle -Tube 1 kept in freezer till chemical exam -Tube 2 kept in room temp for microbial investigation -Tube 3 microscopic investigations (cell count; diffrential: cytologoy ) Complete CSF = 3 cc, Cytology (malignacy) = 8cc

1) Classify the different types of glaucoma***

1) Congenital/Newborn Glaucoma: -anterior chamber dygenesis -Surgical disease*** 2) Primary open-angle glaucoma -most common 3) Primary angle closure glaucoma -ocular emergency

6) Conclude which anxiety disorder is most likely represented when given a clinical scenario**

1) Content evoking fear or anxiety (THIS WILL DIFFER) 2) Causes some sort of anxiety 3) Avoidance to prevent feelings of fear or anxiety 4) The fear or anxiety is out of proportion to actual threat posed by the situation 5) Time criterion (probably 6 months) (THIS WILL DIFFER) 6) Functional impairment or significant distress 7) Not due to a medial condition or substance

6) Personality Change Due to Another Medical Condition**

1) Damage to Frontal Lobe = impaired social judgment, difficulty initiating behvior, disinhibition, apathy 2) Damage to Temporal Lobe = impaired memory, emotional response, interpretation of events, may explain hyper-religiosity & seriousness often seen in Temporal lobe epilepsy** 3) Damage to Orbitofrontal region = disinhibted behaviors

4) List major subytupes of inflammatory myopathies**

1) Dermatomyositis -subacute presentation can present in children -rash and other stereotypical signs (gottrons sighn, mechanics hands, erythema, heliotrophe) -inflammory cells predominately perivascular B-cells -look for vasculitis***, perifasicular atrophy 2) Polymyositis -no rashe -endomysial mononuclear cells and myonecrosis -cytotoxic (CD-8 +) lympocytes and macrophages destroy myofibers expression MHC-1 3) Inclusion Body Myosistis -male, usually >50, gradual onset and progession -proximal and distal weakness -NO ASSOCIATION WITH MALIGNANCY (contrast to dermatomyositis) -angular and round atrophy, rimmed vaccules*** 4) Immune mediated necrotizing myopathy - proximal weaknes -myofiber necrosis and regen with minimal inflammatory cell inflitrate on muscle biopsy

Calvaria**

1) Diploe-2 tables of bone 2) Parietal bones -Arachnoid granulations -Emissary formina 3) Frontal bone 4) Grooves for ant. and mid. meningeal art.

Rule IV: Advanced localization on HP*** (BEING MORE SPECIFIC)

1) Direct: Presence of As (except ataxia) goes for cortical 2) Indirect: in the case of multiple CN involvement + hemiplegia, a single contralateral CN (to the UE/LE weaknes side) makes the case an indirect HP -> Localizeds ipislateral to and at the level of the crossed CN 1) Cortical signs (including A's except ataxia) and seizure localizes to the cortex -aphasia, acalculi, agnosisa, agraphia (LEFT) -apraxia, agraphesthsia, astereognosis, aprosody, neglect (RIGHT) 2) Subcortical: A) LE = UE B) Hemianesthesia,(dont feel anything on oneside) : usually thalamus C) Ataxia Hemiparesis (almost always subcortical) Gertman's Syndrome : Angular gyrus/Dominant parietal lobe, agraphia, finger agnosia, acalculi, left-right confusion

1) compare distribution of lipid-soluble small molecule drugs w/ general anesthetic gases and hydrophlic drugs and explain how they interact with BBB**

1) Distribution of Hydrophilic Drugs -Molecules with ionizable functional goups, peptides, antibodies -Unless they engage a specific transporter, dont get into brain; intrathecal injection bypasses BBB -peripheral neurotransmitters are excluded by BBB (Epi, NE, ACh, etc) -AA (happen to be neurotransmitter precursors) readily cross BBB using L-amino acid transporter -passive uptake is increased if BBB is damaged 2) Lipid-Soluble Drugs -lipid solubility directly related to onset time -single dose duration is dependent on redistribution -lipid solubility is inversely related to duration -chronic dosing-duration dependent on renal or hepatic clearance and is prolonged -example is barbiturates 3) Inhaled Anesthetic Gases -highly lipid soluble drugs -goal is to achieve equilibrium from inspired gas into alveolar gas, blood, and brain tissue, it is acheived when exhaled gas = inhaled gas -amount gas needed is measured in partial pressure (P) -7L of N20 + 3L 02 = 70% N20, .7x760 = 532 mm -100mL of halothane vapor in 10L of air = 1% halothane. 0.01 x 760 = 7.6 mm Hg -Dalton's Partial Pressure: P = PN2+ P02+ PC02+ PDrug -3 Factors affect rate of gas equilibrium: a) Blood solubility b) Alveolar Blood flow c) Inspired gas [ ] a) Blood solubility= gas moves according to henry's law partition coefficient = blood [ ]/gas [ ] -time for drug to dissolve into blood will vary -Higher the partition coefficient the more blood soluble the drug is and thus has a slower onset -Lower the partition coefficent the less blood soluble the drug is (cuz you already have some of that compound in your blood) and has a faster onset because the partial pressure doesnt have to rise much to reach equilibrium b) Alveolar blood flow: -reduced CO can lead to OD cuz doesnt take much to rise partial pressure -as alveolar blood flow rises the duration lenghtens c) Inspired gas concentration: self explanitory -Tissue solubility-depends on lipid content and rate of perfusion, the brain is highly lipophilic and receives a bunch of blood. -Elimination of anesthetic is by the reverese process and occurs due to exhalation

Neurulation*

1) Dorsal ectoderm gives rise to the neural plate day 18 2) Neural groove forms in the midline of the neural plate 3) Neural folds appear on either side of neural groove and meet dorsally to form a neural tube. (Neurulation) 4) Neuroepithelial cells of the nueral tube gives rise to neurons and glia that form the CNS (spinal cord + brain)

3) Role of dystrophin-associated protein complex in muscular dystrophies**

1) Duchenne muscular dystrophy -mutation in dystrophin gene (Xp21) -can use Western blot to id amount of dystrophin -can look at immunofloursece for dystrophin 2) Central Core Disease -AD congenital myopathy -cores are devoid of mitochondria

Meningeal Spaces

1) Epidural (Extradural) -potential space -between cranium and periosteal dura 2) Subdural (dura-arachnoid interface) -potential space -between dura mater and arachnoid 3) Subarachnoid -real space* -contains CSF, arterties (Circle of Willis) and veins -withing subarachnoid space 4) Subpial/Intracerebral -potential space -deep to pia/within neural parenchyma

5) Location and source of intracranial hemorrhage**

1) Epidural (extradural) hemorrhage -Source= arterial, usually middle meningeal artery -Hematoma= between cranium and dura mater 2) Subdural hemorrhage -source= venous, usually cerebral vein/dural sinus -Hematoma= between dura and arachnoid mater 3) Subarachnoid & Intracerebral hemorrhage -source= areterial usually cerebral artery -Hematoma= withine the subarachnoid space or within neural parenchyma

Output of Cerebellum*8

1) Fastigual nuclei receive input from vermis (deep nuclei) and project to the vestibular nuclie giving rise to the vestibulospinal tract 2) The inerposed nuclei recieve input from the parvermis and project to the red nuclie which give rise to the rubrospinal tract 3) The dentate nucleus receiveis input from the lateral hemispheres of the cerebrellar cortex and project to the ventral lateral nucleus of the thalamus which in turn projects to the cerebral cortex which gives rise to corticospinal tract

Arboviruses**

1) Faviviruses: -envolped, single straded, + sense RNA virus -Japenese, St. Louis, West Nile Virus, and Powassan encephalitis 2) Bunyaviruses: -envoloped, single stranded, - sense RNA viruses -California, La Crosse encephalitis virus**, Jamestown Canyon, snowshoe, keystone virus 3) Togaviruses -enveloped, single standed, + sense RNA viurs -Western and eastern and venezuelan equine encephaitis -seen in summer and early fall -aseptic menigitsis accounts for 15% of symptomatic infections (more common in children) -Adult infection commonly results in encephalitis

12) Nutrition and brain development/Enhancement *

1) Fetal Alcohol syndrome= intellectual disability, cranial facial malformation, alcohol interfers with adhesion molecule L1 2) Protein deficiency= developmental Intellectual disability, fewer neurons, axon misrouting 3) Iodine deficiency= developmental intellectual disability (ID) , inadequate idodine impairs thyroid function, preventable 4) lead poisoning = linear relationship with lead exposure and IQ decrease 5) PKU = mutuation of pheylalanin hydroxlase gene results in excess phenyalanine when proteins consumed, development problems if not treated, diet prevents disease

1) Describe the different types of somatosensory receptors**

1) Fine touch - dorsal column & medial lemniscus system and trigeminal lemniscus 2) Vibration - dorsal column & medial lemniscus system and trigeminal lemniscus 3) Conscious proprioception -dorsal column & medial lemniscus system and trigeminal lemniscus 4) Crude touch-anterolateral system, trigemino thalamic tract 5) Pain-anterolateral system, trigeminothalamic tract 6) Temperature -anterolateral system, trigeminothalamic tract Pain and Temperature (Anterolateral system) -Free nerve endings -Pain receptors = protease activated receptors -Heat receptors - heat sensitive channels, VR1, VRL-1 -Cold receprot= CMR1 for cold and menthaol-sensitive receptor -Asigma (group III) = smaller diameter but myelinated = 3rd fasttes (pain and temp) -C (group iV)= smalles no myelin = slowest (pain, temp, itch) Mechanoreceptors (Dorsal column/Medial lemniscus system) -Meissner's corpuscles -Merkel's cells -Pacinian corpusces -Ruffini corpuscles -2nd fastest, larger diameter and myelinated (AB or group II) Proprioceptors (Dorsal column/ medial lemniscus system [conscious] or spinocerebellar tracts [unconscious]) -muscle spindles -Golgi tendon organ -Has largest diameter + myelin = fast (Aa or group 1)

1) List the layers of the retina**

1) Ganglion cells axons-FORM THE OPTIC NERVE, CHIASM, TRAXT, and BRACHIUM of the superior colliculus even though they are the first layer to come in contact with photons 2) Ganglion cell layers 3) inner plexiform layer-synaptic zone 4) Inner nuclear layer-horizontal cells, bipolar cells, and amacrine cells all in this layer 5) Outer plexiform layer-synaptic zone 6) Outer nuclear layer 7) Photoreceptor layer** -rods and cones

2) Two types of neuromuscular blockade and when to use them**

1) General anesthetics -require high doseases 2) Muscle relaxants - allow lower doses of GAs but do not ensure unconsciousness, no sedative or analgesic properties. -All given IV bolus Neuromuscluar Blockade 1) Depolarizing Agents -Blockers are Nm agonists that reemble ACh and prevent diffusion 2) Non-depolarizing -blockers are Nm antagonists that resemble ACH but conceal it inside a large righ structures

1) Most common tumor in each of the main categories of CNS tumors**

1) Giloma = most common tumor of neuroepithelial tissue* 2) Meningioma = most common tumor of meninges and mesenchymal tissues* 3) Schwannoma = most common tumor of cranial and spinal nerves 4) Lymphoma(primary CNS) = most common tumor of lymphomas and hematopoietic 5) Germinioma most common tumor of germ cells -Metastatic tumors are the most common brain tumors but are not primary

Exterior of Skull Midline**

1) Glabella - smooth hairless skin 2) Metopic suture-10% have one, not a fracture on x-ray 3) Nasion 4) Nasal bone and nasal cartilages 5) Nasal spine-human characteristic 6) Symphysis menti 7) Genial Tubercle-attachment for tongue muscles 8) Bregma-site of anterior fontanelle 9) Junction coronal and sagittal sutures (closes about 18 months, bulges when baby cries) 10) Sagittal suture 11) Lambda-site of posterior fontanelle, junction parietal + occipital bones 12) External occipital protuberance

Sphenoid Bone**

1) Greater wing 2) Pterygoid process and plates 3) Pterygoid hamulus 4) Body 5) Spine 6) Foramen spinosum 7) Foramen ovale

Dementia Workup, definition, and treatment**

1) Hx and PE -establish time, cormorbid dsease, med review, cognitive test, look for signs of stroke or PD 2) Lab tests 3) Brain Imaging 4) Neuropathology is dx looking for neufibrillary tangles and senile plaques =AD or Lewy bodies = PD 5) Biomarkers = amyloid, tau, metabolic PET scans Spinal fluid analys of amyloid beta and tau levels see LOW amyloid beta and HIGH tau in CSF

6) Erikson development theory**

1) Infancy: Trust vs Mistrust (Hope) 0-1.5 2) Early childhood: Autonomy vs Shame/Doubt (Will) 2-4 3) Preschool: Initiative vs. Guilt(Purpose) 4-5 4) School age: Industry vs. Inferiority (Competence) 5-12 5) Adolescence: Identity vs. role confusion(fidelity) 13-19 6) Early adulthood: Intimacy vs. Isolation (Love) 20-39 7) Adulthood: Generativity vs. Stagnation (Care) 40-65 8) Maturity: Ego integrity vs. depair (wisdom) 65-beyond -development of human mind is abot mastering new challenges of each stage of life -outcome of one stage is not permanent, and can be constantly modified throughout life -symptoms(psychiatric but alsoneurological) can generate from failure or constant struggle of certain stage of life Limitations/Problems: -careful integration between categorical/stage-wise and continuous/dimensional development -neurobiological evidence

4) List PE maneuvers that help in eval of back pain pts*

1) Inspection and palpation 2) Neurologic examination including strength, reflexes, sensation & gait 3) Straight leg raise (identifies radiculopathy) for L4-S1 root compression happens cuz increases root and dural tension. Can use reverse straight leg raise which tests L2-L4 root compression (radiculopathy) 4) Waddell's & Hoover's signs (identifies psychological component) -Waddell's sign push on head and if saterm-12y it worsens pain means there is a psychological component cuz will not actually make pain worse -Hoover's sign = detects patient playing possum with you. Ask them to raise non paralysed leg while holding paralyized leg it will actually move cuz it has to

4) Localize neuro-anatomy of lesions producing common types of nystagmus (rapid uncontrolled eye movements) **

1) Integrator get messed up Acquired pendular nystagmus secondary to MS -due to nerual integrator circuits leaking leading to oscillation 2) Down-beat nystagmus -most comon form of central vestibular nystagmus -lesion of the vestibulocerebellum (nodulus, uvula, flocculus, and paraflocculuus) -problem at spinalcerebellum junction due to poor feedback from vestibulocerebellum -causes: structural lesions (chiari 1, tumor, MS), toxicity (lithium phenytoin, ETOH), wernicke (B1 deficiency) -Tx with clonazepam, aminopyridine gabapentin 3) Internuclear opthalmoplegia: -lesion of the right MLF from acut ischemic stroke -loss of adduction of the right eye; horizontal jerk nystagmus of the abducting left eye

Uses of Neuromusclar Blockades

1) Intubation 2) Mechanical ventilation 3) Surgery 4) Prevention/treatment of convulsions

7) Explain the difference between ionotropic and metatropic neurotransmitter receptors and how they produce breif and long-lasting synaptic changes** (Similarities and differences between group I-III metabotropic glutamine receptors) ***

1) Ionotropic = fast, use ligand-gated ion channels -Binds Acetylcholine, Glutamate, GABA, glycine, serotonin 2) Metabotropic = slow, use receptors coupled to G-proteins -Binds ACh, DA, glutamate, NE, Epi, GABA, serotonin -excitatory or inhibitory -increase or decrease cAMP accumulation -changes in intracellular Ca+ occur** -Metabotropic Glutamate Receptors Group 1) - potentiate the ionotropic NMDA receptor which causes increase of Ca+ influx Group 2) -reduce the ionotropic NMDA receptor which decreases Ca+ influx Group 3 )-reduce the ionotropic NMDA receptor which decreases Ca+ influx

4) Describe how changes in K+, Na+, and Cl- permeability influence synaptic potentials***

1) K+ channels more permeable = hyperpolarizing 2) Na+ channels more permeable = depolarizing 3) Cl- channels more permeable = hyperpolarizing

7) Effects of lesions in the olfactory system**

1) Kallmann's syndrome= Olfactory nerves never enter the brain leading to no olfactory bulbs froming leading to no smell and hypogonadal: LNRH nuerons trapped outside the brain in tangled olfactory nerve axons 2) Uncinate fits: -uncus triggers the system to fire Olfacctory hallucinations = irritation of olfactory cortex Feelings of unreality= irritation of limbic system 3) Olfactory nerve transection(severed) = loss of smell 4) Age related loss of olfactory receptor neurons = diminished smell

5) Describe the role of the reticular formation in sensory control

1) Locus ceruleus = NOADRENALIN and is found in the PONS (metencephalon) -affects so many areas of th CNS and very importantly wakefulness 2) Raphi nuclei = SEROTONIN and is the midbrain (MESENCEPHALON), Pons, and Medulla -affects many areas of the CNS -involved in the sleep-wake cycle, lesion = insomnia -serotonin is involved in mood 3) Acetylcholine -important for mood, sleep, and learning -pedunculopontine and laterodorsal tegmental nuceli are located in the MIDBRAIN and project to the diechephalon and brainstem -medial septal nucleus projects to the hippocampal formation -Nucleus basalis prjects widely within the cerebral cortex and is important in learning

Damage to the ventral-medial medulla (Medial Medullary (Dejerine) Syndrome)

1) Loss of medial lemniscus (body fine touch and conscious proprecitopon) 2) Hypoglossal nucleus- (ipsilateral tongue {tongue would point to side of the lesion} 3) Pyramid -UMN loss, spastic paralysis, contralateral -May be due to occlusion of the anterior spinal artery

Temporal Bone**

1) Mastoid process 2) Styloid process 3) Stylomastoid foramen (CN VII) 4) Carotid canal 5) Juglar foramen 6) Tympanic canaliculus (tympanic brance of CN IX) 7) Foramen lacerum -pterygoid canal (n. of pterygoid canal) 8) Mandibular fossa (head of mandible)

3) Different parts of the neurological exam** ON TEST

1) Mental status = tests cortex 2) Cranial nerves = tests brain stem 3) Coordination = tests the cerebellum and its pathways -will always be ipsilateral 4) Sensory = tests all sensory pathways from sensors to brain 5) Motor = tests all motor pathways from cortex to muscle 6) Gait = tests disease-specific findings 7) Reflexes = checks PNS, muscles, supra-level structure control, and disease-specific findings

Dopaminergic Pathway $$$TEP

1) Mesolimbic mesocortical DA pathway = emotion and congition -primary target of antipsychotic drugs cuz can decrease postivie symtomes 2) Nigrostriatal DA pathway = coordination of movement -decrease activity => extrapyrimadal symptoms (dystonia, akathisia, parkinsonism, tardive dyskinesia) -major dopaminergic pathway in brain -significantly affected by movement disorders and antipsyhcotic meds 3) Tuberoinfundibular DA pathway = prolactin secretion -Decrease activity => increase prolactin => decrease libido and sexual dysfunction, galactorrhea, gynecomasta 4) Mesocortical - decrease activity -> negatice symptoms (anergia, apathy, and lack of sponaneitiy) -Medullary-periventricular = eating behavior

Cellular consequences of neurogenetic disorders**

1) Metabolic = PKU 2) Protein aggregates = Alzheimer's 3) Leukodystrophies = damage to CNS white matter- Krabbe disease 4) Peripheral neuropathy (axons or schwann cells)- Charcot-Marie Tooth disorder 5) Cell signaling = autism

4) Describe the constituents, connectivity and organization of the 6 layers of the neocortex**

1) Molecular Layer = thin, most superficial layer includes dendrites from pyramidal cells and receives input from thalamic intralaminar nuclei and monoaminergic neurons 2) External granular layer = small pyramidal cells and stellate cells, receives inout from cortex 3) External pyramidal layer = pyramidal neurons which project to other areas of the cerebral cortex (ex. corpus callosum) 4) Internal granular layer = receives input from the thalamus, example primary visual cortex 5) Internal pyramidal layer = large pyramidal neurons which project out of the cerbral cote to other regions of the CNS (ex. corticospinal tract) 6) Multiform layer = includes multiple neuro types, projects to the thalamus

1) Distinguish between the 3 types of nicotinic receptors found at the NMJ**

1) Motor endplate Nm receptors = mature form 2) Extra-Junctional Nm receptors = fetal form (dont cause skeletal muscle contraction, cause release of massive amounts of K+ and can cause death via cardiac arrthymias) can see this in burn pts, muscle dystorphy, and paralysed pts 3) Presynaptic nicotinic receptors Muscarninic = stops release of neurotransmitters Nictonic = move neurotransmitter vesicles closer to synapse leading to more release by keeping ACh level steady

6) Explain how action potentials propagate down an axon**

1) Na+ channels closed at resting potential 2) Depolarization causes opening of some Na+ channels, allowing Na+ ion influx leading to further membrane depolarization 3) Positive feedback is regenerative process leading to opening of virtually all Na+ channels 4) Na+ channels begin to inactivate (if this stage is slowed leads to lengthened AP, and epilepsy, and long QT) 5) Hyperpolarization ++ charge in cells (via Na+) repel each other and the - charge further down the axon attract + charge and visa versa --charge outside the cell repel each other and + charger further down the axon attract - charge *** -AP only move in one direction due to inactivation, but if you to stimulate an axon in the middle the AP would move both ways

1) Seizures and potential pharm mechanisms to inhibit them**

1) Na+ channels: -Goal of meds is to block the inactivated Na+ channels to inhibit continual abnormal AP firing 2) Ca+ channels: -Thalamic T-type Ca++ chanels -inhibits absence seizures -Presynaptic HVA Ca++ - suppresses glutamate release; inhibits focal seizure 3) GABA transmission -goal is to get more GABA (inhibitor) A) Activate GABA-A receptors B) inhibit re-uptake of GABA (GAT-1) C) Inhibit GABA degradation (GABA-T) 4) Anatagonize Glutamate A) antagonize glutmate receptors B) Block release of glutamate (SV2A)

1) Describe the clinical features resulting from a lesion of the optic nerve**

1) Nasal Step = 2) Arcuata scotoma = 3) Altitudinal defect = 4) Temproal wedge = 5) Scotoma in arcuate bundle = 6) Ceocentral scotoma+

13) Causes and nature of brain and spinal cord malformations** $$$TEP

1) Neural Tube defects: Neuropores fail to fuse in the 4th week causing persistent connection between amniotic cavity and spinal canal. Associated wwith maternal diabetes as well as low folic acid intake before conception and during pregnancy. -Alpha fetoprotein in amniotic fluid and maternal serum will be elevated (except with spinal bifida occulta) -AChE in amniotic fluid will be elevated -spina bifida = 3 types 1) occulta = gap in vertebral column due to failure of caudal neuropore closure, no herniation. Dura remains intact. Seen at lower vertebral level and is associated with tuft of hair or skin dimple at level of defect 2) Meningocele= gap in vertebral column + meninges protrude. Associated with spina bifida cystica 3) Myelomeningocele= gap in vertebral column + meninges protrude + spinal cord protrudes in that area -Myeloschisis= rachischisis=exposed unfused neural tissue without skin/meningeal covering -Anencephaly = failure of rostral neural tube (neuropore) closure, leads to death due to no forebrain and open calvarium, see polyhydramnios on findings Dandy-Walker syndrome-malformation of the cerebellulum vermis leading to cystic enlargement of the 4th ventricle. associated with noncommunicating hydrocephalus, spina bifida

Neurometabolic Diseases

1) Neuronal Storage Diseases = lysosomal storage of spinolipidids, mucopolysaccharides, and mucolipids which affect grey matter

4) Describe each component of the anterolateral system and the modalities mediated by this system*8

1) Neurons in the DRG have axons that enter the Zone of Lissauer and terminate on the neurons in the dorsal horn 2) Neurons in the dorsal horn have axons that cross in the anterior commissure and ascend in the spinothalmic tract to the VPL 3)Neurons in the VPL ascend in the poserior limb of the internal capsule to the postcentral gyrus -Lissauer's tract can be discerned because it is lightly myelinated or unmyelinated axons -Pain ino also reaches the reticular formation (high pain processing) in the medulla and pons as well as the periaqueductal gray (dampens down pain) in the midbrain -PAG recieves pain information and projects to the reticular formation which provides feedback to the spinal cord -Pain can lead to firing of the cingulate gyrus and insula relating pain to suffering (emotional)

Occipital bone**

1) Nuchal lines-trapezius 2) External occipital protruberance 3) Foramen magnum 4) Occipital condyles 5) Anterior condylar canals/Hypoglossal canal

Pupillary Exam**

1) Observe both pupils in room light, bright light, and in darkness (dim light

2) comatose pt neurological exam with evaulating pt and Brain death**

1) Obtain Coma Hx = time course, symptoms, PMH, hospital hx 2) General insection = vitals, eyes(open or closed) , resp, movements, reflexes 3) Arousal level = response to stimuli (voice, shaking, pain) 4) Brain stem reflexes = pupillary, corneal, oculocephalic, cold calorics (put cold water in ear and eyes move towards ear) , apnea test 5) Motor/Reflexes response 6) Understand 3rd nerve palsy due to ipsilateral uncal herniation see fixed pupil, 7) Brain stem Reflexes a) pupillary reflex - midbrain , CN II n III b) Oculocephalic reflax-normal is lag of eyes when dr. turns head in pons to midbrain, CN VIII and CN III/VI c) corneal reflex - pons, CN V and CN VII d) Gag reflex - medulla, CN IX and X e) respiration - medulla 8) Decebrate rigidity = extension posturing more worriesome 9) Decorticate rigidiy = abnormal flexion 10) Glasgow Coma Scale 3-15 score Best Motor response 1-6 Best Verebral reponse 1-5 Eye opening 1-4 11) Obtunded = arousals to voice Stupor = arousal to pain Coma = no arousa 12) No cold calorics, but pupil is fine think drug OD, pontine lesion, post. herniation

Visual System

1) Optical apparatus = eye structure itself 2) Afferent pathway -transmition of info = optic nerve, chiasm, tract, LGN, optic radiations 3) Primary visual cortex 4) Association cortices= decipher image Dorsal (where) Stream-location, movment, spatial transformations, Ventral (what ) stream-color,texture, shape size, memory portion of brain 5) Pupil pathway 6) Eye movement pathway = efferent system = maintain single vision

4) Freud development theory**

1) Oral 0-1 2) Anal 1-3 3) Phallic 3-6 4) Latency 6-puberty 5) Genital puberty- -development of human mind is derived by sexual desire (libido) and fulfillment of the desire -Intelligence, morality, consciousness are all byproducts of this pathway -Symptoms (psychiatric but also neurological) can generate from fixation on or failure of certain stage of development -Oedipal complex

Exterior of Skull Parasaggittal**

1) Orbital margin-sharp laterally, blunt inferiorly 2) Supraorbital margin-rounded 3) Suprorbital Notch/Foramen 4) Lacrimal fossa -location of lacrimal gland 5) Lacrimal gland 6) Lacrimal groove- location of lacrimal sac 7) Frontozygomatic suture 8) Zygomatic arch 9) zygomaticotemporal suture 10) Infraorbita foramen - exit of infraorbital n. 11) Mental foramen-lined up with 2nd molar 12) Inferior Border of madible- facial artery notch

Cognition

1) Orientation: -person, place and time and ask how they obtained info 2) Memory: 1) Immediate: can you repeat things back 2) Short term: remember these items at end of conversation 3) Long term: historical data 3) Calculations: -Serial sevens- count backwards from 7 at 100 -Money problems 4) Attention/Concentration -digit span -months backwards 5) Insight -what do you understand about the scenario 6) Judgement -decision making

Mitochondrial Syndromes**

1) PEO: progressive external opthalmoplegia -onset 18-40 , mtDNA deletion 2) Kearns-Sayre syndrome -PEO+ pigmentary reintintis, onset before 20, mtDNA deletion 3) MERRF - onset anytime, tRNA for lysine point mutation 4) MELAS -onset 2-15, tRNA for leucine point mutation 5) Leigh syndrome -cytochrom c oxidase (COX) defiency -subacute necrotizing encephalopathy -onset 3months - 2 year

Maxilla**

1) Palatine process 2) Incisive foramen (nasopalatine n and sphenopalatine n)

Exterior of Skull Lateral**

1) Parietal Eminence -prominent on fetal skull 2) Temporal lines 3) Pterion-site of sphenoidal fontanelle 4) External auditory meatus 5) Temporomandibular joint 6) Mastoid process 7) Asterion - site of mastoid fontanelle 8) Angle of mandible 9) Ramus of mandible 10) Superior nuchal line- attachment of trapezius

2) Describe the components and composition of a multi-system team**

1) Patient must partner with the patient to keep them involved in the care, include in bedside rounds, give them tools to communicate 2) Core team = group of care providers who work interdependently to manage a set of assigned patients nurse, Dr, pharmacist, PT, OT (closest contact with patients) 2A) Contingency team = time limited team formed for emergent or specific events and composed of members from various teams (CODE BLUE) 3) Coordinating team = a team comprising those work area members who are responsible for managing the operational environment that supports the core team (techs, secretaries) 4) Ancillary and support services. Ancillary = provide direct, task-specific, time-limted care to patients. Support services = provide indirect service-focused tasks which help to facilitate the optimal health care experience for patients and families (mainteince, janitors0 5) Administration = establish and communicate vision, develop policies and set expectation for staff related to teamwork, support encourgage staff during implementation and culture change, holds teams accountable for team performance, example CEOs, CFOs

Random bones/Crap

1) Pharyngotympanic tube/auditory tube 2) Vomer 3) Choana-opening 4) Ptergyomaxillary fissure (maxillary a, post. sup. alveolar n.) 5) Pterygopalatine fossa (pterygoplalatine ganglion and branches, sphenopalatine a., CN V2) 6) Inferior orbitial fissure (zygomatic brance of CN V2, infraorbital vessels)

3) Characteristics of acute and subacute neuropathies

1) Polyradiculoneurpathy 2) Polyneuropathy 3) Gullain-Barre syndrome -weakness, paresthesias and areflexia -weakness is symmetric and reaches the worse symptoms at 2 weeks then get better -reflexes are often loss early, and are predominantlya sensory phenomenon -can follow infection but not always -Variants: 1) AIDP most common= primarily motor inflammatory demyelination Tx: close monitoring, especially respiratory function may need to intubate, plasma exchange OR IV Immunoglobulin (Not combined and not steriods) 4) Ganglionopathies -asymmetric non length-dependent sensory impairment -rapid onset, subacute progression -Sensory ataxia is common -autoimmune, toxic, infectious, parenoplatic or genetic 3) Multiple mononeuropathies -usally abrupt onset, painful, step-wise subacute progression -asymmetric -weakness and sensory loss mapped to multiople individual nerve territiories -causes: VASCULITIS

6) Describe the types of axonal projections which involve the cerebral cortex**

1) Projection fiber bundles = connect the cerebral cortex with subcortical stuctures (ex. corticospinal tract, optic radiations) 2) Commissural bundles = connect two cerebral hemisphers (ex. ant. commissure and corpus callosum) -anterior commisure connects olfactory and limbic structures 3) Association bundles = connect one area of the cerbral cortex with antother area withing the same hemisphere (arcute fasiculus)

7) Characteristics of High Performing teams**

1) Quality of collaboration = mutual respect and trust 2) Shared mental models 3) Coordination 4) Communication 5) Leadership

8) Describe how the action of neurotransmitters can be terminated ** *

1) Reuptake: a) by the presynaptic neuron, commonly NE, DA, 5-HT b) by the glial cells (astrocytes) can see glutmate get reabsorbed by EAATs 2) Extracellular destruction: a) Diffusion= neurotransmitters drift away b) enzymatic degradation - example AChE

4) Work-up for common seizure presentations**

1) Seizure or not? 2) Provoked? 3) Seizure type? (focal vs. generalized) 4) Syndrome type? 5) Determine studies to do 6) Should treatment be started? 7) What drugs to use? 8) Get hisotry and PE 9) Blood tests including CBC, electorylytes, glucose, calcium, magnesioum, phospate, hepatic and renal function 10 ) LP to rule out menigitis and encephalitis 11) Blood and urine screen for drugs 12) EEG 13) CT or MRI

5) Piaget stages of development***

1) Sensorimotor stage 0-2 2) Pre-operational stage 2-7 3) Concrete operational stage 7-11 4) Formal operational stage 11-20

1) Understand the associations between common systemic diseaseas and the retina**

1) Sickle Cell Retinopathy: -most common type is SC (heterogenous) -due to vascular occlusions = microanerysmusm, salmon patch hemorrhages, black sunburst, retinal neovascuarization (sea fan) -Tx by burnig neovasculariazation with laser photocoagulation of ischemic retina, anti-VEGF (acutely) 2) Sarcoidosis -can affect all layers of the eye -non-caseating granulomatous inflammation -enlargement of lacrimal gland, -granulomatous nodules of conj -Anterior uveitis (MOST COMMON) * (mutton fat keratic preciptitates, iris and conj nodules) -Posterior uveitis (vitreous opaciticies/haze, peri-phlebitis (candle wax dripping) -Tx: steriods 3) Malignancy -most common is uveal metastese; men = lung cancer and women = breast -most common primary is melanoma 4) Vit A deficiency -leading cause of preventable blindness in kids -night blindness and severe dry eyes -more common now due to pts getting bariatric surgery and malabsorption condition -Tx: give Vit A

3) Be able to recognize and understand the principles of basic ophthalmology instrumentation and diagnostics**

1) Slit Lamp examination - looks at reflection in eye 2) Direct ophthalmosope- upright, real image, see disc and macula in undilated pupil, right eye to right eye, set it to 0, adjust to see vessel, follow vessel till optic nerve, then tell them to look straight into light to look at macula and fovea 3) Indirect opthalmoscope- real, inerted image -field-rays from pt pupil caught by lens -lens diameter/focal length = lens diameter x dioptric power 4) SL biomicroscopy lenses- real inverted image between lens and slit lamp -can be binocular or monocular 5) Fluorescein staining is easy and use direct ophthalmoscope have a blue filter to look for corneal abrasisons 6) Dilation is safe if you check AC depth and is often only way to check posterior segment

4) types of intracranial hemmorhage**

1) Spontaneous intracrandial hemmorhage -HTN, vascular malformation, saccular aneurysm, coagulopathies, vasculitis/vasculopathy (amyloid) , neoplasia, other 2) Intraparenchymal -HTN (most common) ,basal gagnlia, thalamus, pons, cerebral edema and herniation 3) Subarachnoid -ruptured saccular berry aneurysm, sudden onset of seere headache, stiff neck, bloody CSF, high morbiditiy, and mortality 4) Epidural/Subdural hemorrhage

1) Common Bacterial Infections of CNS***

1) Stept pneumonia *most common high mortality 2) Neiserria meningitidis -common in kids and young adults, in dorms mortality middle 3) H. influenza much less common following vaccines motality low 4) Listeria monocytogenes very rare most common in old, young, IS, pregos and high mortality 5) Group B strept seen in neonates and elderly mortality can be high or low 6) Gram - bacilli following hosipital stays due to head trauma, neurosurg procedures in neonates, elderly and IS 7) Staph aureus - rare but becoming more common with amount of equipmient put in pts follows trauma, procedures and mortality is extremely high DDx Neonates= Group B strept> E.coli > Listeria>S. pneumoniae Infants and toddlers = S. pneumoniae> N. meningitidis -Early Childhood through adolescence = N. meningititids > S. pneumoniae -Middle age = S. pneumonia>>N. menigiitis > H. influenza -Elderly = S. pneumoniae>> Listeria> N. meningitids> Group B strept

9) Blood supply of the cerebellum**

1) Superior cerebellar artery (SCA) -supplies the superior cerebellum, superior cerbellar peduncle, and part of the middle cerebellar peduncle 2) Anterior inferior cerebellar artery (AICA) -supplies the ventral and inferior cerebellum and middle cerebellar peduncle 3) Posterior cerebellar artery (PICA_) -supplies the inferior and posterior cerebellum and inferior cerebellar peduncle

6) List the brainstem upper motor neurons projections**

1) Superior colliculus (midbrain) = tectospinal tract (seeing something out of the corner of your eye) 2) Red nucleus (midbrain) = rubrospinal tract 3) Vestibular nuclei (pons &medulla) = vestibulospinal tract 4) Retricular formation (pons&medulla) = reticulospinal tract

4) Identify the ocular manifestations of communicable disease in the eye***

1) Syphilis: (Neurosyphilis) -great imitator -due to priochete treponema pallidum -can effect all layers of eye -Tx: IV pencillin 2) CMV retinitis -CD4<50 and IS pts -hemorrhage, necrosis, vasculitis (whitening sheat) -Tx: systemic and inject ganciclovir into eye 3) Toxoplasmosis -headlight in fog -seen in AIDs pts -Tx: pyrimethamine, sulfadiazine, folinic acid, +/- predinison and must scan brain to check for more 4) Endophthalmitis A) Exogenous -due to trauma, or post catract surgery -Staph usually -Tx: inject, surgery depedning on severity B) Endogenous -sepsis, infected prosthetic, candidemia

2) Taste pathway**

1) Taste buds 2) Solitary nucleus and tract: -solitary tract contains axons from the ganglion cells in the PNS and terminate on the solitary nucleus -solitary tract runs inside the nucleus 3) Neurons in solitary nucleus project to the VPM in the diencephalon via the central tegemental tract 4) VPM projets to the insula and postcentral gyrus

Brain Development regions $$$TEP

1) Telenencephal -> cerebral hemispheres and lateral ventricles 2) Diencephalon (Di= 2) -> thalamus, hypothalamus and 3rd ventricle Rest are in alphabetical order 3) Mesencephalon-> midbrain and cerebral aqueduct 4) Metencephalon-> pons and cerebellum and upper part of 4th ventricle 5) Myelencaphlon-> medulla and lower part of 4th ventricle 1) Forebrain(prosencephalon) -> telencephalon and diencephalon 2) Midbrain(mesencephalon) -> mesencephalon 3) Hindbrain(rhombencephalon) -> Metencephalon and myelencepahalin

Wallerian Degeneration and regeneration**

1) Uninjured nerve 2) Initial reaction to injury (within 24 hrs) 3) Macrophage recruitment; Wallerian degeneration (weeks) 4) Schwann cell alignment; axon regeneration (weeks - months) 5) Sucessful target reinnervation (weeks to years)

1) Common medical causes of psychiatric symptoms**

1) Vascular Dementia = ischemic or hemorrhagic brain injury due to CV disease 2) Frontotemporal dementia (Pick's Disease) = slow onset, no brakes, fontal lobe exuctive deficts, personality cahnge 3) Metabolic causes = hypothyroidism, DM, hypercalcemia, kidney disease, wilson disease (copper accumulates in brain and other organs) 4) Substance/Meds (there are a lot) 5) Infection= neurosyphilis, herpes encephalitis, chronic mengitis, SLE 6) Wernicke-Korsakoff = Wernicke: chronic alcohol abuse, prevalence 2%, usually reversible, ophthalmoplegia, ataxia, confusion, thiamine B1 defiency Korsakoff: continued chronic alcohol misuse, recovery less, amnesia, and confabulation 7) Structural problems - tumors, subdural hematoma, compression of neurons, disruption of BBB, disruption of cerebral blood flow, normal pressure hydrocephalus (NPH) -causing cognitive impairment

3) Localize neuro-anatomy of lesions which produce vertical and horizontal gaze palsy**

1) Vertical gaze Palsy: -acute ischemic stroke of the medial thalamus and medial midbrain -occlusion of artery of percheron -involment of the riMLF/Interstial nucleus of cahall(INC) 2) Dorsal midbrain syndrome -upgaze palsy (can't go up) with intact downgaze -convergence retraction nystagmus -lid retraction -light near dissociation -classically from a glioma 3) Progressive supranuclear palsy -parkinsonism -supranuclear vertical gaze palsy -unstable primary gaze-square wave jerks -slow inaccurate sarcaddes intrusions due to loss of sarcadde gate-keeper(due to parkinsons cuz of the substantia nigra decomposing) -intact VOR

10) Function of 3 main subdivisions of the cerebellum**

1) Vestibulocerebellum: -flocculonodular lobe and adjacent vermis -Input = bestibular ganglion, vestibular nuclei, inferior olive -Output= fastigial nucleus, vestibular nuclei -Function= eye movement and neck and trunk movement -Lesion = impaired balance, wide-based gait, involuntary eye movement (nystagmus) 2) Spinocerebellum: - vermis and paravermis -Input = uncounscious proprioception from DRGs via the spinocerebellar tracts; inferior olive -Output = Fastigial nucleus, globose and emboliform nuclei -Function=Axial and lower extremity movement-gait and station -Lesion= stomping gait, lack of propropioceptive info 3) Cerebrocerebellum: -lateral portion of the cerebellar hemispheres -Input: pontine nuclei, inferior olive -Output: denate nucleus -Function: precise, coordinate movements of the extremities, especially upper extremities -Lesion= intention tremor = amplitude of tremor increases during voluntary movement as you get closer to the target (shaky towards finger), difficulty with skilled movements, subtle (nystagmus)

2) Inputs to the cerebellum**

1) Via superior cerebellar peduncle = mossy fibers from anterior spinocerebellar tract 2) Via middle cerebellar peduncle = mossy fibers from the pontine nuclei (pontocerebellar tract) 3) Via inferior cerebellar peduncle = climbing fibers from the inferior olivary nuclei, mossy fibers from posterior spinocerebellar tract (PSCT), cuneocerebellar tract (CCT), vestibular nuclei and reticular nuclei 4) Pons mediates communication from cerebral cortex to the cerebellum -via the corticopontine fibers, -axons orginating from the frontal cerebral cortex travel within the medial 1/3 of the cerebral peduncle -pontine nuclei project to the contralateral cerebellum via the pontocerebellar tract. thus left cerebral cortex conveys info to the right cerebellar cortex -the cerebellar cortex receives input from the spinal cord, vestibular nuclei, pons, and infererior olive. -Purkinje cells in the cerebellar cortex project to the deep nuclei

Neurologic Diagnosis****

1) WHERE? Where is lesion = LOCALIZATION -focal, multifocal, or diffuse -the evaluation process that leads to finding where is the lesion -localization allows you to predict the level of the lesion, right, left, midline, multifocal, or diffuse 1) Can be suprtentorial, infratentorial (posterior fossa), spinal, or peripheral 2) Level- 2) WHAT -what is the lesion or disease -temporal profile -specific sign, symptom or laboratory finding

2) Describe a technique to obtain history details in chronological order**

1) What is not working right? (moving, feeling, thinking, etc) 2) What is it like? What is harder to do? = Details & When did it happen 3) Time of onset (hyperacute, acute, subacute, subacute to chronic, chronic) 4) Tragjectory (progressive, paroxysmal, fluctuating)

Building a great DDx************ GOOD FOR LIFE

1) What should it be 2) What could it be, but less likely 3) What you can't miss, but isn't impossible

Hemiballismus**

1) What would be the effect of a lesion on a patient's movement be after a lesion of the subthalamic nucleaus in the diencephalon? -MORE MOVEMENT (hyperkinetic disorder)

Cluster C personality disorders (worried) (SAD) **

1) avoidant PD: shyness and fear of rejection (might stay in same situation despite wanting change) 2) dependent PD: continuous need for reassurance, intense discomfort with being alone, exaggerated fears of being helpless when alone 3) Obsessive-compulsive PD: perfectionist and inflexible, detailed schedules, orderliness, stubborn -anxious and fearful disorders, inability to make decisions which interferes with their medical care

1) Describe the clinical presentations of coordination disorders**

1) cerebellar hemisphere syndrome (ipsilateral) = whole left or right side 2) Rostral vermis syndrome = everything but the head 3) Caudal vermis syndrome = affects only the trunk

1) Explain the dopamine hypothesis for schizophenria and describe evidence and relation to MOA**

1) excess of mesolimbic DA activity causes positive symptoms 2) Deficit of mesocortical DA activity causes negative symptoms and cognitive dysfunction -Mesolimbic mesocortical DA pathway = emotion and congition -Nigrostriatal DA pathway = coordination of movement -Tuberoinfundibular DA pathway = prolactin secretion -Medullary-periventricular = eating behavior

Mcmillian Objectives**

1) identify agents that are associated with malignant hyperthermia: -rare syndrome that can be triggered in genetically-susceptible patients exposed to halogenated inhalation anesthetics (all GAs except NO2) and/or succinylcholine (SUCK) -DEFECTIVE RYAN = DEFECT IN RYR RECEPTORS, RELEASE MASSIVE AMOUNTS OF CA+ AFTER EXPOSED TO ANESTHETICS CAUSES LOTS OF ATP UPTAKE LEADING TO HEAT AND THEN RHABDOMYOLYSIS (EATING CHICKEN LEG) -TREAT WITH DANTROLENE TRAMPOLENE -MAN BLOCKS RYAN= DANTROLENE BLOCKS RYANODINE RECEPTORS -Presents as a hypercatabolic state: hypercapnia and acidosis are intial signs, severe muscle rigidity, tachycardia, hyperthermia, hyperkalemia, frequently fatal if not treated -Tx: stop administration of trigger, aminister 100% 02, administer antidote-dantrolene, treat hyperkalemia

Cluster A personality disorders (weird) (MAD)*8

1) paranoid personality disorder: pervasive mistrust of others and suspicions regarding their motives 2) Schizotypal PD: pattern of odd or eccentric thinking - may of ideas of reference and magical thinking (superstitiousness), 3) Schizoid PD: pervasive pattern of detachment from social relationships and a restricted range of emotional expression, the LONER, lifelong social withdrawal -Odd and eccentric behaviors

Assesment of afferent system

1) psychophysical tests a) visual acuity b) Color vision c) contrast sensitivity d) stereo-acutiy e) Visual field 2) Imaging = structural integrity = OCT, MRI 3) Electrophysilogy = functional integrity = VEP, ERG

Stages of Sex

1. Excitement 2. Plateau 3. Orgasm 4. Resolution

Anterior spinal artery stroke $$$TEP

1. Lateral corticospinal tract-> contralateral hemiparesis of upper/lower limbs 2. Menial leminicus-> decreased contralateral proprioception 3. Caudal medulla -> ipsilateral hypoglossal dysfunction *MEDIAL MEDULLAR SYNDROME

Ischemic brain disease/stroke timeline $$$TEP

12-48 hours: eosinophilic cytoplasm +pyknotic nuclei (red neurons) 24-72 hours: necrosis and neutrophil 3-5 days: macrophages (microglia) 1-2 weeks: reactive gliosis and vascular proliferation >2 weeks: glial scar

Palatine Bone**

2) Horizontal plate 3) Cruciform suture 4) Greater and lesser palatine foramina (greater and lesser palatine n) 5) Posterior nasal spine

Frontotemporal Dementia (FTD)**8

3 Syndromes: 1) Behavioral variant 2) Semantic dementia 3) Primary progressive aphasia (non-fluent type) -disinhibited and impuslive behaviors, lack of initative and indecisveness, lack of empathy, and socially inappropriate behaviors -Dx supportied with neurological testing and imaging -Labs: see bilateral atrophy offrontal lobes, and temporal lobe (milder) along with severe reduction of glucose in frontal lobes and milder reduction in temporal -Pathology = abnormal tau (MAPT) or TDP-43 Pick's Disease:

4) Rostral-caudal development of the CNS**

3 vesicle stage: 1) Forebrain (prosencephalon) -cavities will form the lateral ventricles and 3rd ventricle 2) Midbrain (mesencephalon) -cavity will form the cerabral aqueduct, will narrow 3) Hindbrain (rhombencephalon) -cavity will form the 4th ventricle -walls of the vesicle formed by the neuroepithelium -Hox and Pax genes play a role 5 vesicle stage: 1) Telencephalon - derived from prosencephalon 2) Diencephalon - derived from prosencephalon 3) Mesencephalon 4) Metenceohaon -derived from hindbrain 5) Myelencephalon - derived from rhombencephalon

Conjuctiva

3 zones: 1) Palpebral 2) Bulbar 3) Fornix -rich in lymphatics -lot of golbet cells Pinguecula /Ptergium: -localized yellow-white plaques -nasal, bilateral, interpalpebral -sun-induced,adults -Pterygium go on CORNEA ONLY DIFFERENCE** -Solar elastosis

Spinal Nerves $$$TEP

31 pairs of nerves arising from the spinal cordexit -8 cervical -12 thoracic -5 lumbar -5 sacral -1 coccygeal -Nerves C1-C7 exit above vertebra - Nerves C8 and on exit below corresponding vertebra

Brain Stem-ventral view $$$TEP

4 CN are in above pons (I, II, III, IV). 4 CN are in pons (V, VI, VII, VIII). 4 CN are in medulla (IX, X, XI, XII). 4 CN nuclei are medial (III, IV, VI, XII). "Factors of 12, except 1 and 2."

Signs of alcohol withdrawal**

4 S's and avoid the 5th 1) Dec Sleep 2) no Sweating 3) Stomach issues (N/V) 4) Shakes - tremors 5) Grand Mal Seizures -50% mortality -along with high BP

grading reflexes on 0-4+ scale**

4+ = hyperactive w/ clonus, consistent repetitive movement on a joint when stretched 3+ = hyperactive reflexes - brisker than average, spreads to more than one joint 2+ = normal response, movement across a single joint 1+ = diminished reflex, flicker of movement in muscle (no movement on a joint) 0 = no response

Sexual History Taking

5 Ps Partners Prevention of Pregnancy Protection Practices Past STI -Know gender id, sexual orientation, sexual practices/behaviors -Mental Status Exam = General, appearance, mood, affect, *

4) EMG/NCS differentiating features between neuropathic or myopathic diseases**

7) Myopathic disorders -less muscle fibers = smaller, shorter, polyphasic -clicking sound, crisper -SMALL AND SHORT -fibrillation potential -polyphasia -recruitment -normal activation of motor unit 8) Neuropathic disorders (LMN) Acute = recruitment decreased Chromic = decreased recrutiment, polyphasic, large ampiltude - LONG MUAP length AND LARGE MUAP amplitde -fasciculations -fibrillation potentials -polyphasia -recuriment -normal activation of motor unit 10) UMN -reduced activation of motor unit

Fundus

= Retina, macula, optic nerve

hippocampal formation

A forebrain structure of the temporal lobe, constituting an important part of the limbic system; includes the hippocampus proper (Ammon's horn), dentate gyrus, and subiculum -lies within the inferior horn of the lateral ventricle -located deep to the parahippocampal gyrus near the temporal horn of the lateral ventricle, caudal to the amygdala -includes the subiculum (transition cortex), dentate gyrus (archicortex), and hippocampus proper (archicortex) -Subiculum = number of layers vary from 3-6 -Dentate gyrus and hippocampus proper are 3 -Cholinergic neurons in the septal nuclei project to the hippocampal formation, the hippocampus proper projects to the septal area via the precommissural fibers of the fornix

Blow-out Fracture

A fracture of the orbit floor or medial wall or of the bones that support the floor of the orbit.

Fragile X Syndrome

A genetic disorder involving an abnormality in the X chromosome, which becomes constricted and often breaks. -usually male -FMR1 gene -associated with trinucleotide repeats on X chromosome, increased symptoms with longer repeats -2nd most common cause of retardation -most common inherited cause of mental handicap -elongated face, prominent chin, speech problems

Myelin $$$TEP

A layer of fatty tissue segmentally encasing the fibers of many neurons; -enables vastly greater transmission speed of neural impulses as the impulse hops from one node to the next (saltatory conduction of AP at nodes of Ranvier, where there are high conc of Na+ channels -increases space constant and conduction velocity

sexual sadism disorder**

A paraphilic disorder characterized by repeated and intense sexual urges, fantasies, or behaviors that involve inflicting suffering on others causing distress/impairment for more than 6 months

suprachiasmatic nucleus (SCN)

A small brain structure that uses input from the retina to synchronize its own rhythm with the daily cycle of light and dark; the body's way of monitoring the change from day to night. -receive input from photosensitive ganglion cells which have their own photopigment; melanopsin

4) Triazolam** (PASSED OUT KID, ONLY RIDE TRICYCLE FOR SHORT PERIOD OF LIFE)

ALL A.M. = OLAM ending only last in the morning = SHORT ACTING ADDICTIVE FLAVOR= SHORT ACTING MORE COMMON TO CAUSE ADDITICTION - Uses: -insomnia = short-acting , patient that cant fall asleep but stays asleep

Psychiatric Diseases Dendrites and Synapses

ASD (autism) = more dendrites Rett syndrome = less dendrites Szhizophrenia = very few dendrites, overactive pruining plays a role may also be decreased dendrites to start Alzheimers disease = very few dendrites Stress and anxiety = less dendrites Downs= very few dendrites Fragile X= normal number of dendrites but long and thin Treatment may include pharmacotherapy and behavioral intervention, including psychotherapy

3) Proper technique for strength, tone, and muscle bulk testing**

ATROPHY -primarily assesed by inspection -measurements can be made (asymmetry, changes over time) -symmetry is important, with consideration given to handedness and overall body habitus -Atrophy takes weeks to develop Strength: -poor effort is different then weakness. -Poor effort= good initial contraction followed by collapse (giveaway or collapsing weakness (not real weakness) -Grading Scale 0 = no movement 1= only trace or flicker of movement 2= active movement with gravity eliminated 3= active movement against gravity w/out resistance 4= active movement against graity with resistance 5= normal power Axial Muscle testing = neck flexion/extension, respiratory, paraspinal, abdominal wall Trunk Muscle testing = Can you turn in bed Functioning Testing = pronator drift, getting off chair, walking on heels and tip toes, squatting

Inferior Oblique

Abducts, elevates, and laterally rotates (extorsion) eyeball -Inferior division of CN III

Clinical reflexes $$TEP

Achilles = S1, S2 buckle my shoe Patella = L3, L4 (kick the door) Biceps and brachioradialis= C5, C6 (pick up sticks) Triceps = C7, C8 (lay them straight) Cemasteric reflex = L1, L2 (testsicles move) Anal wink reflex = S3, S4 (winks galore)

PTSD and acute anxiety disorder (Tx, risk factors)

Acute Stress Disorder -Less than one month following the trauma PTSD -onset 1-3 months after trauma -an anxiety disorder characterized by haunting memories, nightmares, social withdrawal, jumpy anxiety, and/or insomnia that lingers for four weeks or more after a traumatic experience -Risk factors: increased metabolic amygdala activity, smaller hippocampus volume , baseline low cortisol levels, childhood adversity and exposure, lower SES, gentics, personality, severity, cultural -DSM 5 : 1) Exposure to trauma 2) Intrusion symptoms 2.5) Persistent avoidance 3) Negative alterations in cognitions and mood 4) Alterations in arousal and reactivity 5) Duration > 1 month 6) Clinically significant distress or impairment Tx: SSRIs and SNRI for mood and anxiety Atypical antipsychotics and anticonvulsants for impuslivity and aggression Pscyhotherpay by exposure to trauma narrative to lead to desensitization, the GOLD STANDARD is Prolonged exposure therapy

1) Inddications and contraindications for the treatment of acute ischemic strokes***

Acute Stroke Care: 1) Id stroke yes or no 2) Stroke type ischemic or hemmorhagic 3) Eligible for acute stroke therapy 4) determine sizing, location, and vascular territory 5) Plan for management and discharge 6) Stablization and prevention of complications 7) Determine etiology and mechanism 9) initiate rehab assessment and therapy Emergent Stoke Care 1) Airway, vent support, supplemental O2 2) Accurate time of onset, 3) Mnitiore basiline and neurologic changes 4) Check all 4 limb pulses 5) Vital signs 15 mins in ED 6) Avoid aggressive control of HTN with exception to thrombolysis 7) Hypotension treated almost always 8) Monitor Cardiac rhythm and 12-lead ECG Biggest questions to ask: 1) time of onset 2) Is it a real stroke 3) Is the patient at risk for bleeding 4) Does patient have large vessel occlusion 5) Do benefits outweigh risk (bleeding) 6) Is final infarct too large and may cause herniation? Types of Care** -Supportive: -Antithrombotic(ischemic strokes):minor strokes and TIA condon dual antiplatelet therapy, clot buster = tPA -Throbolytic -Mechanical thromboectomy:stent retrivers -Neruoprotective -Surgical : only indicated for patient with massive infarct and less then 70, remove part of skull to allow for edema

Ischemic Stroke $$$TEP

Acute blockage of vessels-> disruption of blood flow and subsequent ischemia -> liquidefactive necorsis. 3 types: 1) Thrombotic - due to a clot forming directly at site of infarction (commonly MCA) usually over an atherosclerotic plaque 2) Embolic - embolus from another part of the body obstructs vessel. can affect mutiple vascular terrioties. Example A fib, carotid artery stenosis, DVT with patent foramen ovale. 3) Hypoxic- due to hypoperfusion or hypoxemia. Common during cardiovascular durgeries, tends to affect watershed areas Tx: tPA (if withing 3-4.5 hours of onset and no hemorrhage/risk of hemmorhage) Reduce risk with medical therapy (aspirin, clopidogrel), optimum control of BP, blood sugars, lipids, and treat conditions that increase risk (A fib and carotid artery stenosis )

6) Vision loss patterns

Acute vs Chronic: Monocular vs. Binocular: Transient vs. Permanent Partial vs. complete

3) Descrbie the pathophys and managment of HTN retionopathy***

Acute: -due to HTN emergency BP >180/110 and impending end organ damge -leads to optic disc edema, diffuse retinal hemorrhages, cotton wool spots, macular star, bilateral -bilateral, acute, declined visision = must check BP -admit, slowly reduce BP, vision will return if properly treated Chronic: -leads to retinal arteriosclerosis and predisposes to vascular occlusions, macular edema, and macroaneuryms -tx: tight control of BP

Lenticulostriate artery stroke $$$TEP

Affects striatum, internal capsule-> contralateral hemiparesis, hemiplegia -common location of lacunar infarcts

Gag Reflex $$$TEP

Afferent - IX Efferent - X

pupillary reflex $$$TEP

Afferent- II Efferent- III

Lacrimation reflex $$$TEP

Afferent- V1 (loss of reflex does not preclude emotional tears) Efferent- VII

corneal reflex $$$TEP

Afferent- V1 (opthalmic- nasociliary branch, levator palpebrae) Efferent- VII (Temporal Branch, Orbicularis Oculi)

jaw jerk reflex $$$TEP

Afferent:V3 (sensory- muscle spindle from masseter) Efferent: V3 (motor-masseter)

5) Dorsal-ventral regionalization of the CNS**

Alar plates - form dorsally ** -give rise to sensory structures -derivatives are the sensory cranial nuclei of the medulla and pons, the cerebellum, the tecta of the midbrain, and the thalmus and cerebral cortex -rostral hypothalmus related to alar plates Basal plates - form ventrally** -gives rise motor structures** -derivatives are the motor cranial nuclei of the medulla, pons and midbrain, -related to caudal hypothalmus -The plates are seperated by the sulcus limitans -BMP (Bone morphogenic protein) secreted by the roof plate cells induce dorsal sturctures -SHH (sonic hedgehog) secreted by floor plate and notochord cells induce ventral structures

Chemical injury**

Alkali solutions: -results in suponification = turns fat into soap and will erode the cornea and get into uveua Acidic Compounds: -not as dangerous as less alkali Tx: Copious irrigation with water for 15-20 minutes

2) Histo changes seen with alzheimer's and lewy body disease (parkinsons)**

Alzheimers -tau become hyperphosphorylated and unactive then you see neurofibrillary tangles (NFT) -amyloid precursor protein (APP) is cleaved inside neurons to form beta-amyloid which is released into Extracellular space -Plaques of beta amyloid from outside neurons Lewy Body Disease (Parkinson's) -concentration of alpha-synuclein in lewy bodies leading to neurodegeneration in the substantia nigra -Mutautions in SNCA and SNCB genes can deform the shape of alpha-synucein leading to lewy body formation

Visual Axis

An imaginary line passing from the midpoint of the visual field to the fovea centralis. -Macula lutea dense cones, with the fovea being the densest portion

6) etiology of anisocoria and localiz lesions of the sympathetic and parasympathetic innervation**

Aniscocoria = unequal pupils Physiologic aniscoria: -normal, 20% of population -both pupils react normally Aniscocria more in light: -large pupil is abnormal -if ptosis = thrid nerve palsy -if sluggish to light and large pupil contriscts = adie's toxic pupil (senstive to pilocarpine), light near dissociation, usually benign -if sluggish to light and large pupil doesnt constrict = Pharmacologic anisocoria, Hx of eye drops, very big pupil -Iris sphincter trauma: big pupil history of trauma Aniscoria more in dark -small pupil abnormal -if smal pupil doesnt dilate = horner's syndrome -if both pupil dilate = physologic aniscoria -argyll-robertson pupil (bilateral, reacts to near target not light) -pharmacologic due to pilocarpine

Cerebral arteries-cortical distribution $$TEP

Anterior cerebral artery - supplies anteromedial surface Middle cerebral artery - supplies lateral surface Posterior cerebral artery - supplies posterior and inferior surfaces~

Hippocampus (bilateral) lesion $$$TEP

Anterograde amnesia - inability to make new memories

Dysarthria vs Aphasia $$$TEP

Aphasia = higher order language deficity ( inabilityh to uderstand/produce/use language appropriately ) caused by pathology in dominant cerebral hemisphere (usually left) Dysarthria = motor inability to speak (movement deficit)

Spinothalamic $$$TEP

Ascending tract Function: [Lateral] pain and temperature, [Anterior] Crude touch and pressure 1st Order Neuron = -- Sensory nerve endings [Aδ and C Fibers]→ by pass pseudounipolar cell body in dorsal root ganglion -- Enters spinal cord, SYNAPSES IN IPSILATERAL GRAY MATTER [Spinal cord] → 2nd Order Neuron -- Decussates at ANTERIOR WHITE COMMISSURE → Ascends CONTRALATERALLY → Synapses in the VPL [Thalamus] 3rd Order Neuron Sensory cortex

Dorsal Column $$$TEP

Ascending tract Function: Pressure, vibration, fine touch, proprioception 1st order neuron: Sensory nerve ending bypasses pseudounipolar cell body in DRG, enters spinal cord and ascends ipsilaterally in dorsal columns Synapse 1: Nucleus graciLis (Lower body, legs) OR Nucles cUneatus(Upper body, arms) 2nd order neuron: Decussates in medulla, ascends as the medial lemniscus Synapse 2: VPL (thalamus) then goes to sensory cortex

Spinal tract anatomy and functions $$$TEP

Ascending tracts synapse and then cross Ascending tracts: 1) Dorsal column 2) Spinothalamic tract Descending tract: 1) Lateral corticospinal tracct

T10 Dermatome $$$TEP

At the level of the umbilicus (belly butTEN) -important point of referred pain in early appendicitis

L1 Dermatome $$TEP

At the the Inguinal Ligament (L1 at IL)

1) Normal sleep $$TEP

Awake (eyes open) = Alert and active mental concentration, Beta wave (highest frequency and lowest amplitude Awake (eyes closed) = Alpha wae Stage 1 NREM1 -N1 -transition from sleep to wake -hypneic jerks -slow, rolling eye movement -5% of sleep -Theta waves Stage 2 NREM2- N2 -most common stage of sleep (45%) -no eye movements -sleep spindles and K-complexes -Bruxism (teeth gridning occurs) Stage 3 Sleep -NREM 3-N3 -slow wave sleep -deep sleep -Delta waves -25% -dreaming can occur -most parsomnias occur during this stage -happens more during first half of night -sleepwalking, night terrors, bedwetting REM sleep -occurs in later half of night -relative paralysis -rapid eye movements -autonomic actication -desychronized EEG rhytm -loss of muscle tone -Ach is primary REM-on neurotransmitter** -Extraocular movements due to PPRF -Occurs every 90 minutes, and duration increases throughout the night -Beta waves at night BATS Drink Blood

Benzodiazapienes**

BDZS: -BIND TO ALLOSTERIC SITE ON THE GABA-A CAB =ENHANCING GABA, BUT OVERALL REDUCE CNS -CHLO-RIDER = GABA-A RECEPTOR IS A CL CHANNEL -NOW OPEN MORE FREQUENTY = OPENS CL CHANNELS MORE OFTEN -DRINKER= ALCOHOL BINDS TO GABA-A AT SEPERATE ALLOSTERIC SITE -BDZS USED TO TREAT ALCOHOL WITHDRAWAL LONG ACTING ONES -LIVER SPONT ON OX = ALL METABLOIZED BY LIVER -TOLERANCE AND DEPENDENCE OCCURS -WITHDRAWAL = ATAXIA, SEIZURES, SWEATING, IRRITABILITY -SE: ? MARK CAP = ANTERGRADE AMNESIA AND TROUBLE WITH LONG-TERM MEMORY AND LEARNING SLEEPING PATRONS = DROWISNESS CONFUSED ELDERLY = MORE IMPACTFUL ON OLD LEANING TOWER OF PAMCAKES = ATAXIA USES; ANXIOUS YOUNG LAD, INSOMNIA, SURGERY, WITHDRAWAL -Benzos lock channel into a conformation that increases receptor affinity for GABA**, BZDs must have GABAs with them or do not do anything -Benzos can bind to 3 isoforms of different alpha subunits 1) Alpha -1 = sedation, amnesia, ataxia 2) Alpha-2,3 = anti-anxiety, muscle relaxant 3) Alpha-5 = long-term memory and learning Uses: -Anxiety, but have been replaced by SSRI/SNRI -Insomnia* -Sedation and antergrade amnesia* -Status epilepticus termination -muscle releaxation -drug/alchohol withdrawal symptoms Tolerance/Dependence: -Tolerance develops to anti-seizure and hyponotic effects but develops slowly to anti-anxiety effecs -Dependence there is little tendency to inc dose, but there is a tendency to continue use, with discontinuation can see symptom recurrence, rebound, or withdrawal -Withdrawal symptoms vary on drug shorter acting have shorter withdrawal but more severe, long acting longer withdrawal but not as severe SE: -Drowsiness and sedation the next day -ataxia, resp suppression, confusion, anterograde amnesia -paradoxical reactions - hyperactivity and aggression -Pregnancy = chronic use is contraindicated -cant OD on these due to GABA needs to be present and their wont be enough -Toxicity signs/OD signs = severe drowisnes, ataxia, and vital signs usually normal, only fatal when combined with alcohol or other CNS effects

Ventral Amygdalofugal Pathway

BIDIRECTIONAL interconnects the amygdala especially the central amygdaloid nucleus with the septal region and the preoptic areas of the hypothalamus

Prognosis of Comas*

Bad signs: -myoclonic status eplipticucs within a day -absent of pupil or corneal reflexes by day 3 -absent or extensor motor responce by day 3 -SSEP absent N20 response by day 3 -Serum NSE > 33 micrograms/L day 1-3

Id + and - prognostic factors of schizo***

Better prognosis: -later and acute onset,with fewer relapses -female -good social support -positive symtoms and mood symptoms -good premorbid function Worse prognosis: -early, gradual onset, with more relapses -poor support -egative symptoms -males with family history -poor premorbid function -cormorbid substance abuse

Watershed zones $$TEP

Between 1. Anterior/middle cerebral 2. Posterior/Middle cerebral 3. Internal border zones between superficial and deep vascular terrritories of the middle cerbral artery DAMAGE IN SEVERE HYPOTENSION 1. Upper arm/leg weakness if internal border zone stroke 2. Defects in higher-order visual processing if posterior cerebral/middle cerebral cortical border zone stroke

2) Identify the cells of the dorsal root and trigeminal ganglia and their projections to the spinal cord and brainstem**

Body = somatosensation with Dorsal root ganglion (DRG) -pseudounipolar neurons Face = somatosensation with trigeminal ganglion (TG) -pseudounipolar neuron

3) Palliative care vs hospice**

Both: -interdisciplinary team -focus on quality of life -the patient is both the person with illness and their family -treats symptoms, help with coping, do advance care plannin, legacy work Hospice: -Less than 6 months to live -no other disese directed treatments available or forego disease directed treatments Palliative Care: Any stage of illness -can be delivered with curative or disease directed therapies

Cerebral Perfusion $$TEP

Brain perfusion relies on tight autoregulation. -Cerebral perfusion is primarily driven by PC02 -Cerebral perfusion relies on a pressure gradient between mean arterial pressure (MAP) and ICP. -Dec Blood Pressure or Inc ICP => Dec cerebral perfusion pressure -Therapeutic hyperventilation => decrease PC02=> Vasoconstriction=> decrease cerebral blood flow => decrease intracranial pressure . It maybe used to treat acute cerebral edema (2nd to a stroke) unresponsive to other interventions CPP (Cerebral Perfusion Pressure) = MAP-ICP. If CPP = 0 there is no cerebral perfusion = brain death -Hypoxemia increases CPP only if PC02 <50 mmHg -CPP is directly proportional to PC02 until PC02 >90 mmHg

7) Describe the effects of lesions at different levels of the somatosensory system**

Brown Sequard Syndrome: -Ipsilateral loss of fine touch and consciou proprioception due to damage to the dorsal columns which consit of ipsilateral axons from the DRGs -Contralateral loss of pain and temp is due to damage to the spinothalamic tracts which consist of axons which orignate in the dorsal horns but have crossed in the anterior commissure of the spinal cord -these losses are oftentimes seen 2-3 segments below the lesion -may see ipsilateral loss of both fine touch and pain and temp at level of the lesion due to damage to the dorsal roots Dejerine Syndrome : -damage to the ventral-medial medulla on one side causes loss of fine touch and conscious proprioception for the body contralateral to the lesion. The face is spared -anterior spinal artery infarct -medial medullary syndrome Wallenberg syndrome: -lateral medullary syndrome -vetebral artery infarct (sometimes PICA) -damage to the lateral half of the rostral medulla causes loss of pain temperature for the face ipsilaterally and loss of pain and temp for the body contralaterally -Lesion in medulla wont affect fine touch of the face

1) Cranial nerve screening exam*

CN 1: Smell intact to coffee in each nostri CN II, III, IV, VI: No visual field deficts are demonstrated. The pupils are symetrically round and reactive to light. Eye movements appear normal, symmetric, and full. No ptosis. No nystagamus CN II: visual acuity, fields, color vision, pupil exam, in charge of afferent pupillary light response CN III: pupillary response, ptosis, eye movement, Palsy = down and out position CN IV: superior oblique down from medial position Palsy= vertical diplopia, corrected by chin tuck and tilting the head away from affected eye, eye will be up, extorted, and adducted if palsy CN V chewing (masseter, temporalis, lateral and medial pterygoid) *and facial touch/pain/temp normal CN VI: loss of lateral rotation Palsy = double vision that is horizontal, eye rests intorted CN VII: facial expression muscles, anterior 2/3 of taste***, submandibular/sublingual gland, lacrimal (tears), ear pain CN VIII hearing is normal, no nystagmus CN IX: Gag reflex is normal , palate elevates in midline. No horseness, POSTERIOR 1/3 CN X: Gag reflex is normal , palate elevates in midline. No horseness CN XI: Trapezius and SCM strength normal bilateral CN XII: Tongue protrudes in the midline. No tongue atrophy or fasciculations are noted

9) Parasympathetic Nuclei**

CN 3 (constrict pupil) -preganglionic parasympathetic neuron located in Edinger-Westphal nucleus (MIDBRAIN) -Postganglionic parasympathetic neurons located in the ciliary ganglion which syapse on the iris sphincter and ciliary muscel Superior Salivatory Nuclei System (Lacrimation and salivation): -Pregangliongic parasympathetic neurons are located in superior salivatory nucleus in the PONS -Postganglionic parasympathetic neurons are located in the pterygopalatine and submandibular ganglia which terminate in lacrimal and submandibular glands -Hypothalamic control= emotional experieces can lead to lacrimation(crying) in absence of sensory stimuli to the eye Inferior Salivatory Nucleus (Salivation) -Preganglionic parasympathetic neurons located in the inferior salivatory nuclues found in the medulla, the axons are found in CN IX -Postganglionic parasympathetic are located in the otic ganglia and terminate in the parotid gland' -Hypothalamic control = food can trigger salivation via the hypothalamic projections to the inferior salivatory nucleus Dorsal Motor Nucleus of the Vagus: -preganglionic parsympathetic neurons are located in the dorsal motor nucleus in the vagus in the MEDULLA, their axons are found in CN X -postganglionic parasympathetic neurons are located in ganglia close association with may structures including the lung, heart, and GI -hypothalamic control = emotional stimuli can affect cardiac, lung, and GI functioning

4) Dx 3rd, 4th, 6th CN palsies and when to be concerned for life-threatening etiology*

CN 3: -ptosis, adduction, elecation, depression motility deficits -results in exptropia (eyes going out) and hypotropia (one eye going down) -pupil involvment may mean aneurysm, trauma, brain tumor, microvascular ischemia must do MRA or CTA -pupil involved CN3 palsy = posterior communication a. aneurysm until proven otherwise CN 4 -hyertropia in primary, worse in contralateral gaze and ipsilateral head tilt -often due to traumatic, congenital, or ischemic -longest intracranial course so can be due to trauma -innervates superior oblique muscles CN 6 -abduction deficity with incomitant esotropia (one eye going in) long intracranial course -causes is brain tumore (30%), trauma, small-vessel diease,viral, inc intracranial pressure

Superior orbital fissure

CN III, IV, V1, VI and the superior ophthalmic vein

Primitive Reflexes $$$TEP

CNS reflexes that are present in healthy infant, but are absent in neurologically intact adult Normally disappear w/in the first year of life Primitive reflexes are inhibited by a mature developing frontal lobe May reemerge in an adult following FRONTAL LOBE LESIONS → loss of inhibition of this reflex

2) Describe general principles of MRI and CT imaging of the spine, roots, and plexi**

CT -better for detecting All Fractures -first line for imaging for spine trauma -hardware complications MRI -further characterizing trauma beyond fracture -ligamentous injury -cord injury -epidural hematoma -degenerative disease -Infection -MS

3) General facts about MRI and CT**

CT: Computed Tomography -3D x-ray -fast -hyperattuneuated = bright = hyperdense -typical HU values: 0=Water, air negative, bone + -really good at picking up bones -can inject contrast = CTAngiography (CTA) -Contrast is nephrotoxic MRI: -magnet is always on -uses magnetism of hydrogen, NO RADIATION -slower -Bright = hyperintensive, high signal -better for soft tissue = Brain -Contrast is not nephrotoxic as long as normal kidney function (don't give if GFR <30) MRI Sequences: T1-Weighted Sequence = CSF/fluid is dark, fat is bright, gray matter is gray, white matter is white T1 Post-Contrast = Gadolinium is bright on T1, brain doesnt usually enhance unless something breaks down BBB like tumor, subacute stroke, infection T2 (inverted one) = inverse of T1, Gray matter = white, white matter = grey, CSF = bright, fat is still bright -good for looking at fluid cuz edema is frequently pathologic Fat-Saturation = Often used on a T2 sequence, gets rid of the fat (cuts the fat) by making it dark so can see fluid better Fluid-Attunated Inversion Recovery (FLAIR) = T2 BUT with dark CSF, grey matter = white, white matter = grey T2*-Gradeint-Recalled Echo (GRE) = able to see blood and calcium better Diffusion-Weighted Image = used for stroke imaging - most acute way to diagnosis acute stroke (immediate) becomes bright on imaging, all path is bright Magnetic Resonance Angiography (MRA) = look at blood, but doesnt need to inject contrast

Organ Effects during General Anesthsia

CV: -dec in MAP due to systemic vasodilation, myocardial suppresion, blunted baroreceptor reflex, reduced sympathetic tone Respiratory: -reduced ventilatory drive leads to need for assisted ventilation, Hypothermia

1) Most common cause of perioheral and central dizziness**

Central: -coming from the brain (cerebellum or brainstem) -worried about stroke Acute: -Cerebellar dysuction = infection, inflammation, demylination, autoimmue, Meds, ETOH tocisity -Stroke -Vestibular migraine Chronic: -stroke or demylinating Peripheral: -comes from problems in the Ears Acute: -BPPV -Menieres disease -vestibular neuritis -Labrynthitis Chronic: -bilateral vestibulopathy

Posterior Cranial Fossa

Cerebellum and brain stem 1) Clivus (Basilar part of occipital/sphenoid) 2) Petrous temporal bone -superior petrosal sinus -inferior petrosal sinus -sigmoid sinus -Internal auditiry meatus (CN VII, VIII) -Jugular foramen (CN IX, X, XI, jugular bulb) 3) Occipital bone -foramen magnum (medulla, meninges, vertebral a. CN XI, spinal a., dural v.) -Anterior condylar canals/Hypoglossal canal (CN XII) -Internal occipital protuberance -Groove for transverse sinus -Groove for sigmoid sinus -Groove for confluence sinus

1) Cerbral edema**

Cerebral Edema: Cytotoxic: -intracellular fluid accumulation -BBB intact -response to ischemia or hypoxia Vasogenic: -extracellular fluid accumulation -BBB disrupted -response to trauma or tumor

2) Most common CNS tumors in adults and children*8

Children -CNS tumors are second most common type of malignant tumor of childhood, but are most common type of solid tumors -most common is medulloblastoma if less than 4, 5-19 most common is pilocytic astrocytoma, 20-24 is pituitary -majority occur in the posterior fossa (infratentorial) -can be pilocystic astrocytoma, medulloblastoma, ependymoma, brainstem astrocytoma in the infratentorial OR craniopharyngioma in supratentorial Adults -more commonly found in the supratentorial -Most common is meningioma from 35-85+

Trisomy 21**

Chromosomal disorder -Intellectual disability may be due to inhibition of SNX27, which is normally inhibited by micro RNA on Chromosome 21 -Increased risk of early onset alzheimers may be due to amyloid precursor protein (APP) gene

Overview of Caverzagie **

Communication Techniques: -SBAR -Callout -Checkback -Handoff Communication Strategies (Team) -breif -huddle -debreif Communication Strategies (indvidual) -task assistance -feedback -advocacy -assertion

1) Explain the importance of communication, language skills, and adaptive behaviors***

Communication: -verbal and non verbal Language skills Adaptive behavior is an important component in measuring intellectual ability and furthermore ability to function on own

1) Explain key features of conventional and electrical synapses***

Conventional: -chemical -typically unidirectional -neurotransmitter release is quantal= produces small postsynaptic signal (excitatory or inhibitory) -Synapitc transmission is 10,000 X slower than transmission of same distance on axon -Key proteins: vesicle proteins, cytomatrix and vesicle docking proteins, proteins in exocytosis, and endocytosis Electrical: -FAST -Known as gap junctions -AKA the heart -connexons form hydrophilic channel = gap junction

Vomiting Center $$TEP

Coordinated by nucleus tractus solitarius (NTS) in the medulla, which recieves info from the chemoreceptor trigger zone (located in area postrema in 4th ventricle), GI tract (via Vagus), vestibular system, and CNS -CTZ and adjacent vomiting center nuclei recieve input from 5 major receptors: Muscarinic (M1), Dopamine (D2), Histamine (H1), Serotonin (5-HT), and neurokinin (NK-1) receotors -5-HT, D2, and NK-1 antagonists used to treat chemotherapy-induced vomiting -M1 and H1 antagonists used to treat motion sickness and hyperemesis gravidarum

3) List the degenerative and dystrophic conditions that affect conjunctiva and cornea and describe their clinical and pathologic findings**

Cornea: 1) Ulcers/Keratitis: -defense breakdown lose epithelium and or tears -organisms gain acess to stroma -can be due to bacteria, fungi, viruses (herpes) , parasistes (acanthomeoba) -cultures/stains are important to diagnose cause 2) Keratoconus: -bilateral degeneration, progressive astigmatism due to coning of eye, onset in puberty -central thining/ectasia, breaks in bowman's membrane, iron in epithelium, decement's disruption leading to hydrops 3) Fuchs Endothelial dystrophy -bilateral, elderly females -common indication for transplant -blurred vision -endothelium abnormal = thickened descement's, guttae, corneal edema, bullous change, subepithelial fibrosis 4) Band Keratophathy -Interpalpebral A) Calcific band keratopathy -Ca++ in bowmans layer -uveatits, inc PTH, Vit D, uremia B) Actinic (Climatic Droplet) Keratopathy -proteinaceous accumulation -solar damage

3) Neuronal Plasticity**

Cortical Remodeling 1) Short term changes- strengthening of existing synapses, activation of second messenger system 2) Long term changes- forming and changing synapses, neuronal gene expression changes

5) Bipolar disorder in youth** (Pathophys, tx, and DSM-5 dx)

Criterion A -Mania= lasting at least 1 week or (any duration if hospitalized) -Hypomania = lasting at least 4 consecutive days Criterion B Defining Mania: -7+ days of elevated (+3 symptoms) or irritable mood (+4 sysmtoms) OR mood requiring hospitalization* -DIG FAST for symptoms -Distractibility -I excessive involvment in pleasurable activities -G inflated self-esteem or grandiosity -F flight of ideas -A increase in goal-directed activity or psychomotor agitiation -S decreased need for sleep (less than 3) -T more talkative Over diagnosies -40x increas of bipolar disorder dx in 10 years -medicaid use of antipsyhcotics nearly tripled in 10 years -may be due to parental/caregiver misinformation, lack of training, diagnostic confusion, industry influences, and satisfaction of search Ddx: -externalizing disorders (ADHD), internalizing disorders, substance abuse, normal development, prepubertal children S/S: -post puberty usually -most have onset 14-19 years -most common symptom is minor or major depressive disorder Tx: -Meds remains the primary tx usually atypical antipsyhchotics are now 1st line tx (SE is weight-gain) -limited support for lithium and divalproex sodium -antidepressants are not typically

Two general categories of dopamine receptors in striatum

D1=Direct pathway = facilitates movement D2= indirect pathway = inhibits movement Net effect causes an increase in movement

Corticospinal tract**

DRAW THIS OUT ON PAPER -Axons from pyramidal neurons in layer 5 of primary motor cortex give rise to corticopsinal and corticobulbar tracts

1) Midazolam** (PASSED OUT DRUNK WITH STRAW IN MOUTH DOESNT END IN PAM)

DRUNK ASLEEP AT THE BOOTH OPEN MOUTH WITH STRAW (TUBE) WAITING FOR PANCAKES (SURGERY Uses: -proceduarl sedation/anxiety

2) Illness anxiety disorder ***

DSM 5: -Preoccupation with having or acquiring a serious illness -no somatic symptoms are not present or are very mild -bunch of anxiety -present for at least 6 months -are either care-seeking or care-avoidant (cuz so scared) Risk Factors: -major life stress -threat of a serious illness in past -hx of abuse -serious childhood illness -1:1 M:F ratio, early onset rarely onsets after 50 years -persits in 40-70% of patients -high rate of at least one comorbid psychiatric disorder Tx: -regular visits with PCP -establish collaborative therapeutic alliance -acknowlege health fears -limit dx testing and referrals -make sure assure dont have serious medical disorders -may need referral to psychiatrist for pharm or psychotherapy -explicititly make functional improvement the goal of tx

4) Factitious Disorder***

DSM-5: -falsification of physical or psychological symptoms or indication of injury, associated with identifed deception -individual presents himself or herself to others as ill, impaired, or injured -deceptive behavior is evident in absence of obvious external rewards -DO THIS FOR THE ATTENTION, absence of secondary gain Risk Factors: -Women, single, previous health care background, 3rd-4th decade, cormorbid substance disorders, trauma and sexual abuse, -poor prognosis Most common Falsified Symtoms: -ab px, arthraligia, chest px, hematuria, hypoglycemia, skin wounds (non-healing) Most common factitious psychiatric symptoms: -bereavement, depression, psychosis, suicdial ideation/behavior When to suspect: -high rates of healtcare utilization, jump states, -evasiveness in providing hx -refuse to allow team to obtain collateral info -numerous drug allergies -inconsistencies in the hx, exam, and lab tests -tests and procedures are eagerly accepted -strong opposition to consultig psychiatry -few vistiors -appears more comfortable than expected -tell you how symptoms will go -course of illness is unusal -new symptoms right before discharge Tx: -management should be seen by one clinician -psychotherapy is standard tx, meds less helpful -consult psychiatry will probably wont see them -careful with procedures -TEND NOT TO BE AS DISTRESSED AS THEY SHOULD BE

Neurocognitive Disorder Due to another medical condition**

DSM-5: -impairment of at least one: 1) Learning 2) Memory 3) Language 4) Perceptual-motor skills 5) Complex attention (processing speed) 6) Executive function 7) Social cognition

3) Conversion Disorder*** (Functional Neurological Symptom Disorder)

DSM-5: -one or more symptom of altered voluntary motor or sensory function -symptoms are real, but not intentially produced -no organic etiology -Blind guy in WWII Risk Factors: -female, hx of conversion disorder, hx of mental health disorders, hx of trauma, lower SCS, lower education -Acute onset, most common in age 10-35 yoa, short duration, recurrance is common Tx: -education, reassurance, referral, therapy

Autosomal Recessive Mutations**

Deafness- GJB2 -many genes involved in hearing loss (meaning two deaf parents may have a kid that can hear)

Red Nucleus lesion $$$TEP

Decorticate (flexor) posturing: -lesion above red nucleus, presents with flexion of upper extremities and extension of lower extremities Decerebrate (extension) postuing -lesion at or below red nucleus -worse prognosis -extension of upper and lower extremeties

Lateral Corticospinal tract $$$TEP

Descending Tract Function: Voluntary movement of contralateral limbs 1st Order Neuron: UMN: Cell body in 1° motor cortex → Descends ipsilaterally through INTERNAL CAPSULE, most fibers decussate at CAUDAL MEDULLA [Pyramidal decussation] → Descends CONTRALATERALLY 1st Synapse: 1. Cell body of ANTERIOR HORN LMN: Leaves spinal cord Synapse II: NMJ-> muscle fibers

Iris

Sphincter pupillae: -innervated by parasympathetic fibers of CN III, synapse in ciliary ganglion -narrows aperture of pupil Dilator pupillae: -innervated by ympathetic fibers from internal carotid plexus (synapsed in superior cervical ganglion) -widens aperture of pupil

3) Importance of EEG for evaluation of seizure, status epilepticus, and non-convulsive status epilepticus**

Status Epilepticus: -active part of tonic-clonic seizure lasts 5 mins or longer -person goes into a second seizure without recoving consciousness from the 1st one -a person has repeated seizure for 30 mins or longer - life threatening emergency Non Convulsive status epilepticus (NCSE) -more difficulat to dx -altered mental status = may be confused, aphasic or comatose -subtle signs such as facial twitiching, hand twitches, eye deviation -strongly suspect NCSE in a comatase pt who presents after prolonged generalized tonic-clonic seizures

8) Distinguish and adjustment disorder from ASD or PTSD and other major disorders such as MDD and GAD**

Step 1) Did a stressor occur that triggered onset of symptoms? If yes move one Step 2) Is the stressor a truama IF YES How long did that truama occur less than a month = acute stress disorder More than a month = PTSD IF NO Step 3) Does the patient meet full criteria for another condition (MDD, GAD) IF YES Diagnose with a primary mood or anxiety disorder IF NO = Adjustment disorder

Endocrine myopathies**

Steriod Myopathy: -Women more common, direct catoblic effect on muscle, predinosone more than 30 mg, Fluorinated steriods are worse -proximal muscle weaknes -Normal CK is hallmark -Need to be on steriod for 1-2 months -More likely to affect type 2 fibers (dark brown) white cells Hyperthyroidism: -proximal weakenss -peroidic paralysis*** -CPK is usually nomral -type 1 and 2 fibers Hypothyroidism: -proximal weakness -muscle hypertrophy -cramps, myalgia, ankle jerks, myoedema -CPK usually elevated

Galant Reflex $$$TEP

Stroking along one side of the spine while newborn is in ventral suspension (face down) causes lateral flexion of lower body toward stimulated side

Red Flags of acute red eye**

Subjective: 1) Blurred Vision 2) Severe pain = keratitis, ulcer, iridocyclitis, scleritis, or acute glaucoma 3) Photophobia = iritis and corneal inflammation 4) Colored Halos = indicate corneal edema, abrupt increases in IOP, glaucoma Objective: 1) Reduced VA = keratitis, iridocyclitis, or glaucoma. never seen in simple conjuctivitis** 2) Ciliary flush-injected deep conj and episcleral vessels, faint violaceous ring, prominent at the corneal limbus, indicates ciliary and or iris involvement 3) Corneal opacification = keratic precipitates 4) Pupillary abnormalities 5) Elevated IOP = iridocyclitis, glaucoma 6) Proptosis = orbital or cavernous sinus disease 7) Strabismus = eye going the wrong way

Moro reflex (startle reflex)

Sudden loud noise will cause symmetric abduction and extension of the arms followed by adduction and flexion of the arms over the body. Disappears by 3 to 4 months. (Hang on for life relex)

Anatomical Localization

Supratentorial- higher brain functions -contraleral side -vision, olfaction, cognition, ememory, intelligence, behavior ,seazurs -if face involved on opposite side**** Posterior Fossa/Infratentorial- things to keep us alive -hearing, vertigo, diplopia, dysarthria, dysphagia -if face involved on same side*** Spinal -neck or back pain, mengieal signs Peripheral -limb pain, sensory or motor deficit confind to single nerve distribution -confined to a single root or nerve

4) Describe the role of the reticular formaton in visceral control**

Swallowing: -swallowing is controlled by swallowing centers in the reticular formation -Dorsal swallowing group (DSG) is in the nucleus of solitary tract (NTS) -cerebral cortex projections to NTS DSG gives us voluntary control of swallowing -The NTS projects to the LMNs of motor CN V and VII, the nucleus ambiguus and the spinal cord Emesis: -controlled by the vomiting center in the reticular formation in the MEDULLA -gets input from strong emotion (limbic system) , vertigo (vestibular system) , chemicals from blood (chemorecptor), visceral afferents (from the vagus) -Sends projections to the pharynx, larynx, and glottis closure (via nucleus ambiguus), GI (via dorsal motor vagus), respiratory (via ventral respiratory group) Micturition: -controlled by a center in the reticular formation in the PONS -don't have control over urinating until 3-5 -frontal lobe recieves sensory info from thalamus about state of bladder -reticular formation in the PONS receives input fro cerebral cortex and communives via the spinal cord to the bladder to empty or hold it Respiration and Cardiac function -reticular formation center plays key role -Nucleus of the soliatary tract (NTS) receives info abotu the cardiac and respiratory function -Projections from the NTS go to the rostral vental lateral medulla for the heart, to the nucleus ambiguus effect on heart, and to the rostral vental respiratory group which projects to phrenic nucleus Chewing center in reticular formation is in PONS Coughing center in reticular fromation is in the MEDULLA

6) Axons for the preganglionic and postganglioic sympathetic and parasympthetic nervous system**8

Sympathetic: -Preganglion= Short axons myelinated -Postganglion = long axons unmyelinated Parasympathetic: -Preganlion = long axons myelinated -Postganglion = short axons unmyelinated -myelinated axons of the preganglion neuron exit the ventral root and travel in hte white ramus and terminates in paravertebral or prevetebral ganglia. -postgagnlionic nuerons axons travel from the paravetebral ganglia travel within the gray ramus and are primarly unmyelinated

8) Neurotransmitters released related to the sympathetic and parasympathetic nervous system**

Sympathetics: -Preganglion = ACh -Postganglionic = NE unless its sweat glands than its ACh -Adrenal medulla just has one axon and uses ACh Parasympathetics: -Preganglion = ACh -Postganglionic = ACh

Supraoptic and paraventricular nuclei $$$TEP (part of the hypothalamus)

Synthesize ADH and oxytocin -stored in the posterior pitutary where they are released

Monitoring neuromuscular blockade

TOF-4 successive situmuli applied at 2 Hz Nondepolarizing block = will drop to 0.4 see fade Depolarzing block = phase 1 drops response but no fade, unless gets to phase II then drop TOF-R to 0.4 and yo see fade (need high doses) -Phase 1 block is usually sufficient for uses

2) Phenytoin** (Tow Truck)

TOW TRUCK = PHENYTOIN -CHIP CLIPS = BLOCKS NA CHANNELS -SE: FALLING HAMBURGER PATTIES,= ATAXIA, DIPLOPIA = HEADLIGHTS, DROP IN FOLATE LEVELS = DROPPED FOLAGE, EXPANDING BUBBLE GUM = GINGIVA HYPERPLASAI , HIRSUTISM = COOL BEARD, CAN INDUCE LUPUS = WOLF, SJS MASK (HLA-B15 ALLELE) , TARANTULA JACKET -ORDER STATUS 30 MINS = USED TO TREAT STATUS EPLIPTUS -tradiational -Main MOA is Na+ channel blocking PK: Its a b*tch, rapid and extneded release -hard to reach target blood level due to variable absorption and non-linear kinetics -must do plasma blood drug sampling Uses: -Focal and tonic-clonic seizures, status eplicus (most severe seizure, they lose consciousness) -not efective against absence seizures (doesnt effect T-type Ca + channels) SE: -CNS = systagmus, ataxia, sedation -CV= blocked warming = sever arrhythmias -Rash and SJS -Hirsutism in females (hair growth) -Blood dyscrasias -Teratogenic - FHS, and reduces affects of BC -Gingival hyperplasia

Brain stem **

Tectum = roof , behind cerebral aqueduct, special Tegmentum = floor , inbetween the two , motor and sensory Basis = foundations- all motor pathways -anterior = pure motor

Middle Cranial Fossa**

Temporal lobe of brain 1) Body of sphenoid bone -Tuberculum sellae -Hypophyseal fossa (pituitary gland) -Dorsum sellae -Posterior clinoid processes 2) Greater wing of sphenoid bone -superior orbitial fissure -Foramen rotundum (CN V2) -Foramen ovale (CN V3) -Foramen spinosum(middle meningeal a.) 3) Squama of temporal bone -Groove - middle meningeal a. 4) Petrous part of temporal bone -hiatus for greater petrosal n. 5) Foramen lacerum 6) Carotid canal (int. carotid a. and plexus) 7) Arcuate eminence-ant. semicircular canal 8) tegmen tympani-roof of middle ear

8) Location of thalamus and hypothalamus **

Thalmus: -in dorsal diencephalon -dorsal to hypothalmus -involved in sensory and motor processing Hypothalamus: -in ventral diencephalon -involved in memory formation, regulation of autonmic system and neuroendocrine system -The hypothalamic sulcus divides the two

3) Identify the visual field deficits produced by lesions of the occipital lobe**

The importance of the primary visual cortex is shown by the prescence of: 1) Cortical magnification 2) Dual Blood Supply- posterior cerebral artery (calcarine a.) and middle cerebral artery 3) Ocular dominance columns Lesions/Problems with Occiptial lobe show these symptoms 1) congruous = exact same spot of VF in both eyes 2) Macular sparing -can selectively spare or involve the macula 3) Temporal crescent = -Causes a large impact on life 1) Reading skills = hemianopic dyslexia 2) Impact on driving = dec visual field

Preoptic Nucleus $$$TEP (part of the hypothalamus)

Thermoregulation, sexual behavior. Releases GnRH -Failure of GnRH-producing neurons to migrate from the olfactory pit = Kallmann syndrome

Tectospinal Pathway

This pathway (from the superior colliculus) mediates head and body orientation in response to localized visual, auditory and tactile stimuli, often from the same source. -in the midbrain -travels in the ventral funiculus -the axons do not descend past cervical levels and primarily influences medial LMNs

C6 Dermatome $$$TEP

Thumbs Thumbs up sign on left hand looks like a 6

Fragile X**

Trinucleotide repates -6-45 = normal -46-55 repeats is the grey zone, ** likely unaffected -56-200 = premutation= see premature ovarian failure in women, and tremors and ataxia in men ->200 = full mutation = intellectual disabiloty, autism is more common and more severe in men -Repeats in the 5' UTR portion of FMR1 gene affect expression

Paraventricular Nucleus and Supraoptic Nucleus histo

Two regions of the hypothalamus that are associated with the posterior pituitary and are where vasopressin and oxytocin are produced

Chiari Malformation** $$$TEP

Type 1 = malformation see vermis of cerebellum protrudes more than 6 mm into the foramen magnum, ectopia of cerebellar tonsils -congenital and asymptomatic in childhood -manifests in adulthood with headaches and cerebellar symptoms -associated with spinal cavitations (syringomyelia) Type 2 = cerebellulum with both tonsils and vermis protrud into foramen magnum aqueductal stenosis leading hydrocephalus. Usually associated with lumbosacral menigomyelocele (which may present as paralysis/sensory loss at and below the level of the lesion )

5) Histologic difference between type II (pompe disease) and other types of glycogenoses**

Type II (Pompe disease) -defiency of lysosomal a1,4-glucosidase (acid maltase) Type V (McArdle disease) -defiency of myophosphorylase (not lysosomal)

Primary progressive aphasia**

Types: 1) Non-fluent/agrammatic variant = looks like brocas and is progressive 2) Semantic variant = mirrors wernkicke's, trouble with word meaning, like not speaking language 3) Logopenic variant=naming objects, and losing nouns 4) Mixed variant=

2) Explain the difference and similiarities between typical and atypical antipsychotics**

Typical: -old -D2 antagonists (decrease DA) -will block H1, a1 receptor, M receptor -psychotic disorders, antimetic, sedative Atypical: -newer -D2 antagonists (dec DA) -serotonin effects (treat - symptoms) antagonist 5-HT2A -will block H1, a1 receptor, M receptor -psychotic disorders, mania, MDD, anxiety, OCD, PTSD, delusional parasitosis, antiemetic, sedative PK: oral, rapid onset takes 2 weeks for Max, metabolized by CYP2D6, 3A4 -usually given as a monotherapy trial for 4-6 weeks for a typical SE: -EPSE = akathesia (restlessness) , Parkinsonism, dystonias (acute muscle spasms), tardive dyskinesia (irreversible**[only one] repetitive movements (grimacing) -hyperprolactinemia = hypogonadism, infertility -Neuroleptic malignant syndrome = typical drugs, TETRAD (mental status, hyperthermia, muscle rigidity, ANS dysfunction) life-threatening must withdraw drug, -QT interval prolongation -Adverse metabolic effects = dyslipidemia and diabetes (ATYPICAL) -Boxed warning = inc mortality in elderly w/ dementia-related psychosis -ANS effects = anticholinergic, anti-adrenergic, and anti-histaminergic

Facial Palsy

UMN lesion --> corticobulbar tract. C/L lower face paralysis, upper forehead unaffected LMN lesion --> facial nucleus. I/L upper and lower face paralysis + can't close eyelid, ant 2/3 taste, salivation, lacrimation, facial movt.

UMN and LMN**

UMN: -indicate that the lesion is above the anterior horn -Weakness, hyperreflexia, spastic muscle tone, babinski sign + (plantar response) -myotatic (stretch) reflex is exaggerated LMN: -indicate that the lesion is either in the anterior horn cell or distal to the anterior horn cell -Weakness, atrophy, hyporeflexia, fasciculations, flaccid muscle tone,

Disulfiram*

Used in tx of alcohol cessation. Inhibits acetaldehyde dehydrogenase (ALDH)_-->increased acetaldehyde (EtOH) when drinking (toxic)-->N/V, headache-->incentive not to drink -Makes you sick -SE: hepatotoxicity, contraindicated with CV disease -MUST BE HIGHLY MOTIVATED PTS

3) Flurazepam** (PASSED OUT KID FOR LONG TIME, YOU SLEEP A LONG TIME WITH THE FLU ENDING IN PAM)

Uses: -Insomnia = long acting

1) Be able to read an ophthalmologist's note**

VA= visual acuity OD = right eye OS= left eye OU= both eyes SC= uncorrected CC=with correction ph=pinhole MRx: manifest refraction 1st number = sphere (round lens) 2nd number = cylonder and axis (lens is oval) I would assume someone without astygmatism would just have 1 number -3.5x2.0x90 = near-sighted with 2.0 of astygmatism, at a 90 degree

Muscle Actions of eye

Vertical axis = abduction and adduction A-P axis = lateral -medial rotation Transverse axis = elevation - depression

2) Id vertical and horizontal gaze palsy**8

Vertical eye movement = Midbrain (mesencephalon) Horizontal eye movement = Pons (Metencephalon) Holding = medulla (myelencephalon) Horizontal Gaze: -pons -Pulse command happens at PPRF-> move to the abducens nucleus -> go to contralateral CN III (medial rectus) and goes to lateral rectus of ipsilateral side -Medial vestibular nucleus and nucleus prepositus hypoglossi do the HOLD integrator Vertical Gaze: -midbrain -pulse comand by riMLF (rostral interstital MLF), -Hold command by the interstial nucleus of cahall -signals go to CN III and CN IV ipsilateral and contralateral

2) Examine vibration sense of proprioception**

Vibration: apply vibration to a bony prominence Joint Position sense: evaluates the proprecipetion

1) Exam characteristics of LMN syndrome**

Weakness -anterior horn = asymmetric, proximal and distal (myotomal) -Peripheral nerve: symmetric distal -Radiculoneuropathy (roots) = symmetric proximal and distal -Plexus = usally limited to limb Syndrome Hypo-reflexia / areflexia Flaccid Paralysis Muscle Wasting Fasciculations, Fibrillations -atrophy is prominent*

2) Exam characteristics of UMN syndrome**

Weakness: -affects anti-gracity muscles, generally flexors weaker than extensors in the legs and the reverse in the arms = pyramidal pattern of weakness -Affect large areas of body below lesion -loss of performance of fine-skilled voluntary movement especially at the distal end of limbs -Paresis (weakness) vs plegia (complete weakness) Acute Damage of UMN: -contralateral paralysis of distal limb movement and proximal limb movement severally weakened -muscle tone initially depressed, deep-tendon reflexes likely absent, recovery over time to normal or hyperactive, the superifical relexes opposite lesion are depressed/absent -babinski on affected side -Proximal strength restores over weeks-months, distal = poor revovery -Shock duration is longer for spinal cord than cortical lesions -Progressive UMN lesions not associated with shock Syndrome: Hyperreflexia Babiski Urine Retention Sexual Dysfunctions Ipsilateral if below pyramid decussation in medulla Contralateral if above -disuse atrophy due to inactivity and immobilization

mammillary bodies (bilateral) lesion $$$TEP

Wernicke Korsakoff Syndrome (Confusion, Ataxia, Nystagmus, Opthalmoplegia), Korsakoff- memory loss (retro and anterograde) confabulation, personality changes, come from CAN O' beer

2) When is EMG/NCS indicated**

When to do NCS: 1) compression neuropathies (sensory affected before motor) -most common is median nerve (carpal tunnel) will see prolonged latency, prolonged F-waves 2) Peripheral neuropathies (DM) -absent sural sensory response -reduction in median, ulnarm radial sensory amplitude respnse -reduction in amplitude of tibial and peroneal motor with perserved latency and conduction velocity -needle exam showed no active denervaton, When to do EMG: -New onset of MG crisis -botulism -Infectious anterior horn disease (West Nile) -Guiran-Burrae -Rhabdomyloysis/ severe inflammatory myopathies -Critical illness myopathy

Olfactory trigone

Where olfactory tract meets medial and lateral olfactory stria Medial olfactory stria = fibers from the ant. olfactory nucleus cross in the rostral portion of the ant. commissure and then to the ant. olfactory nuclues on the other side Lateral olfactory stria= contains most of the olfactory fibers from the olfactory tract, contains axons from the mitral cells and terminate on the piriform cortex, entorhinal cortex and amygdaka

Axis of movement

Yaw axis = produces horizontal movement Pitch axis = produces vertical movement Roll axis = produces torsional movement Donder's Law= the eye position will always be the same regardless of where it came from or how it got there

Transient ischemic attack $$$TEP

a brief episode of neurological dysfunction resulting from an interruption in the blood supply to the brain or the eye, sometimes as a precursor to a stroke. (MRI negative) -usually resolves in less than 15 minutes, -deficits due to focal ischemia

Circle of Willis $$$TEP

a circulatory anastomosis that supplies blood to the brain and surrounding structures

Down Syndrome

a condition of intellectual disability and associated physical disorders caused by an extra copy of chromosome 21 with translocation of 21 &15 -Most common genetic cause of mental retardation -

Kluver-Bucy syndrome

a condition, brought about by bilateral amygdala damage, that is characterized by dramatic emotional changes including reduction in fear and anxiety, hypersexuality, hyperphagia, hypermetamorphosis (tendency to recognize what an object is) -Causes: herpes simplex encephalitis, brain surgery, trauma, stroke, and neurodegenerative disease

stria terminalis

a limbic pathway connecting the amygdala and hypothalamus

pedophilic disorder***

a paraphilia in which an adult's preferred or exclusive sexual partner is a prepubertal child causing impairment/distress for more than 6 months

Glasgow Coma Scale (GCS)**

a scale used to assess the consciousness of a patient upon physical examination, typically in patients with neurological concerns or complaints -Glasgow Coma Scores Mild TBI 13-15 Moderate 9-12 Severe 3-8 Eyes: 1= no opening 2= open w/ painful stimulation 3= open with verbal stimulation 4= open spontaneously Verbal 1= no sound 2= incorheint 3= inappropriate words 4= confusion 5= normal Motor 1 = no movement 2= extensor posturing (decerbrate) 3= flexor posturing (decorticate) 4= withdrawal to painful stimuli 5= localization of painful stimuli 6= follows commands

Extraocular Muscles

a set of six muscles innervated by the cranial nerves that move the eyes in a conjugate (parallel) manner, movement of which is tested by a number of physical-examination techniques including the cover/uncover test and the corneal light reflex test -Superior rectus -Lateral rectus = CN VI -Medial rectus

reticulospinal tract

a tract of axons arising from the brainstem reticular formation and descending to the spinal cord to modulate movement -Neurons in the reticular formation project to the spinal cord via the reticulospinal tracts, which travel in the ventral funiculas 1) The cerebral cortex projects to the reticular formation of the pons and medulla 2) Neurons in the pontine reticular formation give rise to axons that descend ipsilaterally in the medial reticulospinal tracts to influence medial LMNs. this pathway facilitates antigravity muslces 3) Neurons in the medullary reticular formation gives rise to axons that descend bilaterally in the lateral reticulospinal tract to influence both medial and lateral LMNs. This tract inhibits spinal segemntal reflexes

Superior Oblique

abducts, depresses and internally rotates (intorsion) the eye -CN IV

Saccades

acheieve fixation by bring images of new objects into the fovea -goals= rapid gaze shift to new image -fast, brief, accuritye -slows down with age -cortical planning = volitional -reflexive -spontaneous -scanning -quick phases Neuroanatomy= single decussation-contralateral deficit***w{"

Vergence

acheive and maintain fixation of images at varying distance from eye; dis-conjuigate movements -goal= binocularity and avoid diplopia -stimulus= image blur and image disparity -slower, convergence is faster than divergence -usually accompanied by dysconjugate saccades-producing oscillations -neural substrates= posterior temporal, peristriate, and dorsal prefrontal

4) Differentiate between the clinical features of lesions involving the WHAT visual pathways **

agnosia= inabilty to recognize visual cues Cerebral achromatopsia: -deficient/altered perception of color 1) Complet achromatopsia BL area V4 2) Color anomia = cannot name colors, lesion of left lingual gyrus 3) Color agnosia = cannot name colors for objects, left occiptotemoral lesions Prosopagnosia -often seen with cerebral achromatopsia -impaired abilityh to recognize previously familary faces or to learn new faces -aware of defect -BL lingual and fusiform gyri of medial occiptiotemporal cortex Topographagnosia: -inability to naviagate routes using familary landmarks -right lingual gyrus Alexia without agraphia -inability to read in previously literate individuals -ability to write is preserved -lesion of left medial and inferior occipito temporal region Anosognosia: -deficit of self-awareness of existance of neurological disability -visual anosognosia (anton's syndrome) denial of blindness in blind patients. If bluntyly confronted, response is indifferent -caused by lesions to bilateral retrogeniculate pathways

Dominant parietal cortex lesion $$$TEP

agraphia, acalculia, finger agnosia, left-right disorientation -Gerstmann syndrome

Ataxia telangiectasia

an AR disease due to defect in DNA repair enzymes. The DNA of these patients is hypersensitive to ionizing radiation. Manifestations include cerebella ataxia (and atrophy, telangiectasias, repeated sinopulmonary infections, and an inreased incidence of malignancy. Defect in the ATM gene on chromosome 11, leads to disabled DNA repair, and increased susceptability to ionized radiation CNS affects: -normal at birth -lose cerebellar function starting at age 2 -truncal and gait ataxia then extemitias more common in vermus hence location of ataxia

Ataxia Telangiectasia

an AR disease due to defect in DNA repair enzymes. The DNA of these patients is hypersensitive to ionizing radiation. Manifestations include cerebellar ataxia (and atrophy, telangiectasias, repeated sinopulmonary infections, and an inreased incidence of malignancy. -Purkinje cells began to degenerate shortly after birth, ataxia becomes worse and worse -Life expectancy limited due to recurrent infections of the lungs -Symtoms: problems with balance, hand coordination, eye movements, and slurred speech Defect in the ATM gene.

Korsakoff's syndrome

an alcohol related disorder marked by extreme confusion, memory impairment, and other neurological symptoms -due to thiamin deficiency following chronic alcoholism damages to several structures including mamillary bodies impairs acquistion of new memories

generalized anxiety disorder

an anxiety disorder in which a person is continually tense, apprehensive, and in a state of autonomic nervous system arousal due to general worry about everything -last more than 6 months -worry is difficult to control -risk factors: trauma, intolerance of uncertainity, cognitive distortions -Tx: SSRI, SNRI, TCA, Hydroxyzine, Buspirone, CBT, and benzo (start only with a plan to stop)

2) Anisocoria and recognize physiologic anisocoria**

anisocoria = unequal pupils 20% of the population has some anisocoria -both pupils act the same Adie's Tonic pupil -affected pupil usually larger -dilute pilocarpine supersensitivity (abnormally large pupil dilates the normal eye doesnt -light-near dissociation -irregular pupil -vermiform movements of iris, sector palsy -benign usually

Aphasia***

any of a number of linguistic disorders caused by injury to or malformation of the brain causing impairment of language** (oral, reading, writing) -stoke is the leading cause -right handed people 95% dominant at left hemisphere -Left handed people 70% dominant at left hemisphere Tx: -speecha and language therapy -no meds currently -compensatory approaches (Ipads etc)

C2 dermatome $$$TEP

back of head

Infratentorial

below the tentorium cerebelli

subarachnoid hemorrhage $$$TEP

bleeding due to trauma or rupture of an aneurysm or arteriovenous malformation. -"Worst headache of my life" -Need to run to the hospital -bloody or yellow (xanthochromic) spinal tap -vasospasm can occur due to blood breakdown or rebleed 3-10 days after hemorrhage -> ischemic infarct -nimodipine used to prevent/ reduce vasospasm -increased risk of developing communicating and/or obstructive hydrocephalus

Neonatal intraventricular hemorrhage $$$TEP

bleeding into the germinal matrix with extension into ventricles and beyond; Germinal matrix is a source of nerve cells in embryo and fetuses (up to 33 weeks of gestation), richly vascular areas with many thin walled capillaries that are very sensitive to anoxia -increased risk in premature and low birth weight infants -due to reduced glial fibers support and impaired autoregulation of BP in premature infants -can present with altered level of consciousneess, buldging fontanelle, hypotension, seizures, coma

diffuse axonal injury $$$TEP

caused by traumatic shearing forces during rapid acceleration and or deceleration of brain (MVA) -usually causes devasting neurologic injury often causing coma or persistent vegative state

Tonsillar Herniation**

cerebellar tonsils herniate into foramen magnum; compression of brainstem produces cardirespiratory arrest; "coning" of cerebellar tonsils and coma -may be secondary to posterior fossa mass (child mengioblastoma) or edema -may occur without supratentorial herniation syndrome -may occur as the natural progession of transtentorial hernination (uncal herniation) -Kid gets sedated then decrease breathing causing respiratory distress in the MRI

Anterior Cerebral artery stroke $$$TEP

contralateral motor and or sensory loss more in lower than upper limbs, urinary incontinence -motor and sensory cortices -lower limb lesion

transvestic fetishism***

cross-dressing for a period of 6 months causing impairment/distress -heterosexual male is most common

Syringomyelia $$$TEP

cystic cavity (syrinx) within SC (if central canal-->hydromelia) crossing anterior spinal commisural fibers damaged 1st "cape-like" bilateral loss of pain, temp sensation in upper extremities (fine touch sensation preserved) most common at C8-T1 -associated with chiari malformations -can be congenital or acquired due to trauma and tumors syrinx = tube

amyotrophic lateral sclerosis

degenerative disorder of motor neurons in the spinal cord and brainstem

Inferior rectus

depression, adduction, extorsion -inferior division of CN III

Selective Mutism

developmental disorder characterized by a consistent failure to speak in specific social situations despite speaking in other situations

Myopathy***

disease of the muscle (skeletal) -Muscle weakness is number one complaint, followed by cramps, stifness, -S/S: generally symetric, generaly proximal, may impair cardiac and respirorty muscles Labs: -CK will be increased -Aldolase increased -AST, ALT will be increased -Gamma GT is for liver -EMG (electromiography) Risk Factors: -age, female, thyroid disease, ICU stay, alcohol abuse, statins, steriods, FHX

Radiculopathy**

disease of the nerve roots

Mitochondrial Encephalomyothies

disorders or oxidative phophorylation from nuclear or mitoconfrial genoume mutantionwhich effect grey matter and muscles

female orgasmic disorder**

distress due to infrequently or never experiencing orgasm

levator palpebrae superioris

elevates upper eyelid 2 components: 1) Skeletal muscle = CN III (superior division) (faster firing but tires) 2) Smooth muscle (superior tarsal muscle) - sympathetic (works longer but fires slower) ptosis = dropping of eye

Vestibulospinal Tract

extrapyramidal motor tract for ipsilateral gross postural adjustments subsequent to head movements -vestibular nuclein project to the spinal cord via the vestibulospinal tract which travels in ventral funiculus 1) Medial vestibulospinal tract projects bilaterally from the medial vestibular nuclei to the medial LMNs, mostly end at cervical levels 2) The lateral vestibulospinal tract projects ipsilaterally from the lateral vestibular nucleus orimarily to the lateral LMNs -Limb extensors

Frontal eye field lesion $$$TEP

eyes look toward (destructive) side of lesion. In seizures (irrative) eyes looks away from side of the lesion

Orbital Septum**

fibrous membrane forming the anterior border of the eye, extending from orbital margins to the tarsi and palpebral ligaments

Conduction aphasia $$$$TEP

fluent aphasia Lesion: supramarginal gyrus, arcuate fasiculus Severe impairment with repetition intact fluency, good comprehension, repitition impaired speech interrupted by word finding difficulty reading intact writing impaired

Wernicke's aphasia

fluent speech, impaired repetition and comprehension, wordy but meaningless speech -superior temporal gyrus of temporal lobe

Bones that make up the orbit

frontal, sphenoid, zygomatic, maxilla, lacrimal, ethmoid, palatine

Keratitis **

inflammation of the cornea

Anterior Uveitis**

inflammation of the iris and ciliary body

VPL Ventral Posterolateral Nucleus $$$TEP

input: spinothalamic and dorsal columns/medial lemniscus. Info: Pain, temperature; pressure virbation proprioception (VPPPL) destination: primary somatosensory cortex Just think, brings information from the lateral (arms and legs) part of body

VPM Ventral Posteromedial nucleus $$$TEP

input: tigeminal and gustatory pathway INfo: Face sensation, taste destination: pimary somatosensory cortex just think that VPM is for Makeup on the Face (or medial part of body)

Medial longitudinal fasciculus lesion $$$TEP

internuclear ophthalmoplegia (impaired adduction of ipsilateral eye; nystagmus of contralateral eye with abduction) Seen in MS

Pretectal area

involved in pupillary, consensual and accommodation reflexes -receive direct retinal input and projects to the accessory oculomotor nucleus -Projection from retinal ganglion cells to the pretectal area is the AFFERENT limb of the reflex -Projection from the nuclues of Edinger-Westphal to the ciliarly ganglion via CN III is the EFFERENT LIMB -Ciliary ganglion innervates the cilarly muslce and can cause pupil to constrict -Pretectal area projects both ipsilateral and contralateral edinger-westphal nuclei resulting in constriction of both pupils

Optokinetic

maintain fixation durin sustained head rotations or translations -goal= prevent image slippage during prolonged head movements -Physiologic nystagmus**** (able to look at new things) slow phase-smooth pursuit quick pahse- saccadic system -Neural pathways-similar to pursuit

Vestibular

maintain fixation during breif head rotations or translations -Goal is to prevent slipping of an image during brief head movement -stimulus: brief head position changes -occurs withing 15 ms 2 types: 1) Rotational VOR (angular) = mediated by Semicircular canals 2) Translational VOR (linear) = mediated by urticle /saccule Neural centers: 1) Horizontal = MVN/NPH 2) Vertical/Torsional = riMLF

Visual fixation

maintaining focus on an stationary objects minimizing ocular drifts -Goal = keep images on fovea and prevent habituation -3 involuntary normal fixation movements to avoid habituation and drifts 1) Microtremors 2) Microsaccades 3) Microdrift -occurs at the PEF, SEF, and the substantia nigra Pr is the gatekeeper for saccadic signals from cortex to brainstem (if have a defect in the sunstantia nigra cant fixate) Abnormalities of fixation are saccadic intrusions and nystagmus -

Smooth Pursuit

maintains fixation of small moving target -goal = hold slowly moving image stationary on fovea -latency 100-130 ms Neuroanatomy: -same as VOR -manocellular stream -double decussation* -ipisilateral deficit**

Hypothalamus $$$TEP

maintains homeostasis by regulating Thurst and water balance, controlling Adenohypophysis (posterior pitutary) release hormones and produced in the hypothalamus, regulating Hunger, Autonomic nervous system, Temperature, and Sexual urges (TAN HATS) -Inputs (area not protected by BBB) : OVLT (sense change in osmolarity), area posterma (found in medulla, responds to emetics)

Mastication muscles $$$TEP

masseters, temporal muscles, pterygoid muscles Medial, masseter, temporal all close Lateral pterygoid open All innervated by trigeminal nerve (V3) Lateral Lowers M's Munch

Intraparenchymal hemorrhage $$$TEP

most commonly caused by hypertension but also amyloid angiopathy, vasculitis, neoplasm. Typically occurs in basal ganglia and internal capsule, but can be lobar. -may be secondary to reperfusion injury in ischemic storke

Lateral Rectus

moves eye laterally {abduction} (VI abducens)

Medial Rectus

moves eye medially {adduction} (III oculomotor Inferior division )

Diabetic neuropathy ***

nerve damage from impoverished blood flow can lead to -erectile dysfunction, incontinence (ANS problems) -poor wound healing (blood flow) -loss of sensation from area (sensory) -High cholesterol and smoking will worsen -Does not differentiate between small nerves and large nerves -can affect sensory, motor, and autonomics -Spreads distal to proximal Tx: -no cure -if you fix blood sugar they will get better and will not get worse -Gabapentin is 1st line therapy for pain and symptoms

Neural development $$$TEP

notochord induces ectoderm into neuroectoderm --> neural plate --> neural tube + neural crest cells -notochord becomes nucleus pulposus of intervertebral disc in adults -Alar plate (dorsal) = sensory -Basal plate (ventral) = motor

Inclusion Body Myositis (IBM)**

older patients, usually >50 years of age, and affects men more than women more gradual onset of weakness (years). more refractory to therapy. distal muscle groups can also be affected, and asymmetry of involvement is characteristic CK: 600-800 OR NORMAL; lymphocytes are found predominantly within the fascicles, made up of CD8+ T lymphocytes. Vacuoles, amyloid deposits -more common to affect distal muscle

Optic Canal

optic nerve and ophthalmic artery

Lamina Papyracea

paper thin plates of vertical bone part of the ethmoid to which middle and superior nasal conchae are attached

Voyeruism ***

peeping tom on unsuspecting victims, often trespasser, don't escalate to contact for 6+ months -causes distress/impairment to them or someone else

Venous sinus thrombosis $$TEP

presents with signs/symptoms of increased ICP (eg, headache, seizures, focal neurologic deficits). May lead to venous hemorrhage. Associated with hypercoagulable states (eg, pregnancy, OCP use, factor V Leiden).

Horner's Syndrome

ptosis, miosis, anhidrosis -anisocoria greater in dim light -damage in sympathetic pathway -3 orders of neurons -topical cocaine test confirms (no dilatation is abnormal = horners -topical apraclonidine test confrims (abnormal pupil dilates = horners) -topical hydroxyamphetamine localizes 1st/2nd vs 3rd neuron 1/2 = dilates the pupil to an equal to greater extent 3= does not dilate as well as the normal pupil -Congenital = affected eye may be lighter in color -Acquired= carotid dissection, carotid aneurysm, pancoast tumor, occult neuroblastoma, goiter, surgery mishap

Frotteruism**

recurrent fantasies/urges/behaviors involving touching/rubbing against a noncensenting person causing distress/impairment for more than 6 months

cillary muscle

relaxes and contracts to control the eye's focus -relaxed muscles = flattened lens for distant vision -contraction = reduced tension on zonal fibers and lens returns to spherical shape for close vision (elasticity)

delayed ejaculation disorder**

retarded ejaculation, or the inability to ejaculate following a normal sexual excitement phase

1) Explain the term psychosis and common presentation of patients with psychotic symptoms***

schizo = split from reality phrenia= mind

Fetishism**

sexual attraction to nonliving things causing significant distress or impairment for more than 6 months

Becker muscular dystrophy**

similar to, but less severe than, Duchenne muscular dystrophy -ewakness onset variable from 5/6- to 50/60 -respiratory dysfunction tends to be milder -tx is supportive and life expentency is shorter depending on severity of cardiomyopathy, prednisone NOT USED

gender dysphoria**

the condition of feeling one's emotional and psychological identity as male or female to be opposite to one's biological sex. -childhood onset -may result in mood disorders, anxiety disorders, substance use disorders, suicidality

Accommodation

the process by which the eye's lens changes shape to focus near or far objects on the retina 1) Lens thickens 2) Pupils constrict 3) Eyes converge *Parasympathetic nerves from CN III through cilary ganglion

Spinal epidural abscess

traid 1. fever 2. localized back pain 3. neurologic deficits - motor weakness I. i.e. motor weakness, paresthesias, bowl/bladder dysfunction -most common S. aureus

Basal Ganglia lesion $$$TEP

tremor at rest, chorea, or athetosis -Parkinsons and Huntington disease

Cerebellar vermis lesion $$TEP

truncal ataxia, dysarthria -wide base, drunken sailor ataxia - vermis is CENTRALly located affects central body. -degeneration associated with chronic alcohol use

Palmar Reflex $$$TEP

when you place your finger in an infant's palm, he will grasp it