OMS 2 - Fall - Block 3 - MSN

What color is pathology on a T2 weighted MRI

white.

CT Units?

x-rays in all directions. Hounsfield units. Bone is white (most units) air is black (least, negative value). Water is set to zero hounsfield.

6) Become familiar with the post-concussive syndrome, its symptoms, and its treatment.

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7) Become familiar with post-concussive seizures , how they are treated, and their prognosis.

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8) Become familiar with traumatic coma and the basic principles in how it is treated

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Be able to recognize epidural hematomas and subdural hematomas, and understand their clinical importance and treatment.

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Become familiar with subarachnoid hemorrhages - both traumatic and non-traumatic - their causes, manifestations, and treatment.

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Understand how Contusions, Brain Hemorrhage, and Axonal Shearing lesions manifest in brain injuries

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Dizziness cause by Brainstem Ischemia Signs/Symptoms:

"Frequent and sudden episodes of vertigo lasting a minute or so may be consistent with transient brainstem ischemia" A.R./M.S. Principles of Neurology Internal auditory artery occlusion (usual origin = AICA) Vertigo, nystagmus and unilateral hearing loss Other brainstem signs may not be present Lateral medullary infarction (Wallenberg syndrome) affecting vestibular nuclei and connections Rarely other vascular syndromes (e.g. superior cerebellar artery occlusion)

Three Major vertigo treatment med classes?

(1) Antihistamines/Anticholinergics Can use stimulants to treat drowsiness: methylphenidate or modafinil; Action is to suppress the undiseased vestibular apparatus Use only for short-term (up to one month) Prolonged used inhibits recovery from vestibular injury and leads to vestibular de-afferentation with chronic vertigo and gait disorder (2) Promethazine (3) Belladonna Alkaloids: Scopolamine

For CPA tumors, what test is needed?

brainstem audiometry.

Aneurysm: how to treat?

clip or coil

drug for acute vestibular neuritis?

methylprednisolone (must be started within 3 days of onset)

Hairdresser: 38 year old woman Difficulty climbing stairs & blow drying her own hair No sensory disturbance =WEAKNESS ALONE CK: 3400u/l (HIGH) So you think of?

weakness alone-->more NMJ or muscle. could be neuron. High CK means MUSCLE usually. NCS/EMG: Myopathic (confirms it) Muscle Biopsy: Dermatomyositis Treatment: immunosuppressive therapy, often for many years

Chronic Onset dizziness: Multiple sensory deficits.

"Multiple sensory deficits" syndrome Abnormalities in sensory proprioceptive systems Typical patient is elderly with: Vision disorder (cataracts, macular degeneration, etc.) Auditory disorder (presbycusis, etc.) Myelopathy (cervical spondylosis, B12 deficiency, etc.) Peripheral neuropathy (diabetes, alcohol, etc.) Complains of ***dizziness at night (dim lights), may fall when no visual cues (as in shower)*** Treatment is to correct modifiable conditions and make any safety modifications (lights on at night) **Do not treat for vertigo—medications for vertigo may sedate patients and exacerbate the situation**

How to TREAT a skull Fracture IMPORTANT...STARRED in PPT

***NON-CONTRAST CT*** Admit to neurosurgery *Anticonvulsants* are often given to reduce risk of seizures, though few studies exist to support this *Tetanus status* must be addressed *Prophylactic antibiotics* are usually given for about a week to reduce risk of CNS infection If the fracture is depressed more than the thickness of the cranium, or the wound is contaminated, or there is an underlying hematoma, or there is a dural tear --> then it needs to be dealt with in the Operating Room

Dix-Hallpike Epley Maneuver WHAT ARE THEY USED FOR?

***benign positional vertigo = BPV*** or BPPV (benign positional paroxysmal vertigo) Dix Hallpike to test (see NYSTAGMUS), Epley Maneuver to treat.

List disorders which may cause disequilibrium

--Cerebellar hemorrhage (ACUTE EMERGENCY) --Drug intoxications (think of alcohol as model) --Wernicke's Encephalopathy --MS --Bilateral Vestibular Hypoperfusion --Chronic Cerebellar Disorders --Posterior fossa tumors --Sensory ataxias and Multiple sensory deficits syndrome --Extrapyramidal disorders --Other ataxic disorders --Chronic Drug Intoxications

List disorders which may cause vertigo (including both peripheral and central disorders)

--Physiologic = motion sickness. (peripheral) --Benign Positional Vertigo (peripheral) --Labyrinthitis (peripheral) --Meniere's Disease (peripheral) --CPA Tumors (cerebellopontine angle = vestibular schwannoma) (peripheral) --Post Traumatic Vertigo (peripheral) --Toxic Vestibulopathies (peripheral) --Brainstem ischemia ***EMERGENCY*** Central --Posterior fossa tumors ***EMERGENCY*** Central --Cerebellar Hemorrhage (central) --Multiple Sclerosis (Central) --Migrainous vertigo (Central) --Basilar-Type Migraine

Causes of CTS?

--Repetitive Motion such as extreme grasping in cold environment --Pregnancy/menopause/breast feeding --Trauma to the wrist --Small stature --Diabetes Mellitus --Hypothyroidism --What about keyboarding and mousing? ----Literature shows exacerbations but not causation!

List disorders which may cause syncope/pre-syncope.

--Vasovagal Syncope (Cardiac) --Arrhythmias (Cardiac, may be emergency) --Obstructive --Orthostatic HTN (Drug-Induced, Volume depletion, Autonomic insufficiency

One of these five bones is involved in a BASILAR FRACTURE:

1) cribiform plate of the ethmoid bone 2) orbital plate of the frontal bone 3) petrous and squamous portion of the temporal bone (most common location) 4) sphenoid bone 5) occipital bone

Signs of an MTBI

= concussion. A vacant stare (befuddled facial expression), Delayed verbal expression (slow to answer), Inability to focus attention, Disorientation (e.g. walking in wrong direction), Slurred or incoherent speech, Emotionality out of proportion to situation, Gross observable uncoordination (stumbling, etc), Memory deficits (asking the same questions repeatedly,, unable to recall 3 objects for five minutes), Any period of Loss of consciousness Additional Signs Hx of a brief convulsion or autonomic signs such as pallor, bradycardia, faintness with mild hypotension, or sluggish pupillary reactions CT and MRI scans are usually normal, but 3% of patients have intracranial hemorrhage of some type Sequela A single uncomplicated head injury will only infrequently cause permanent neurobehavioral changes in those previously free of psychiatric problems and substance abuse Minor problems in memory and concentration may be anatomically correlated to small shearing or other microscopic lesions.

May have already been covered, but what's a DTI (imaging).

=Diffusion Tensor Imaging = Diffusion MRI (or dMRI) is a magnetic resonance imaging (MRI) that allows visualization of the diffusion process of molecules, mainly water, in biological tissues, in vivo and non-invasively. Molecular diffusion in tissues is not free, but reflects interactions with many obstacles, such as macromolecules, fibers, membranes, etc. Water molecule diffusion patterns can therefore reveal microscopic details about tissue architecture, either normal or in a diseased state. USE: great for finding a mass or figuring out how to ENTER a brain to do the least amount of damage.

How to treat AIDP (Acute Inflammatory Demyelinating Polyradiculoneuropathy):

=Guillain-Barre IVIG, plasmapheresis

What is a complicated skull fracture?

A complicated skull fracture is one that is open, or depressed, or involves a sinus, or has resulted in air somehow entering the skull (pneumocephalus...pictured)

Prefrontal association areas: main deficits seen with damage (2 classes, with some additional distinctions)

A distinction can be made between lesions affecting the lateral aspect or the orbitofrotal cortex Lateral frontal lesions - patients tend to be apathetic, abulic (can't make independent decisions), passive with little spontaneous activity Orbitofrontal lesions - patients tend to exhibit impulsive, disinhibited behavior with poor judgment Left frontal lesions - associated with more depressive-like disorders Right frontal lesions - more commonly associated with maniac-like disorders In clinical practice many exceptions to this traditional view are observed

Know the Glasgow Coma Scale and how it is used.

A neurological scale which is aimed at giving a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. Was initially only used to evaluate trauma, but is now used for grading and monitoring most neurologically compromised patients. The range of scoring is from 3 (deeply unconscious) to 15.

what is a mononeuropathy?

A simple mononeuropathy involving only a single nerve most commonly is the result of traumatic injury or entrapment (e.g., carpal tunnel syndrome).

Describe the location of the language centers and identify typical language deficits

About 12-14 is when tongue flexibility/language ends, so you develop your accents from then on out! Language is concerned with the use of a system of arbitrary symbols for the purpose of communication. There is a set of rules for using these symbols that we call grammar. The symbols have to be ordered in a particular way that we call syntax. We need to provide these symbols with appropriate emotional valence, we call this PROSODY. ***Aphasia*** is the partial or complete loss of the ability to produce or comprehend language after a lesion of the cerebral cortex. Most of the time this occurs without a loss of cognitive abilities or the loss of motor function to the muscles of speech. ***BROCA'S***: frontal, left side. Producing Language. Can't talk. ***WERNICKE'S***: parietotemporal. Understanding Language. Can't Stop talking! Word Salad. Two other types: Global—stem MCA stroke = both brocas and wernickes; Conduction, pathway of communication between the two. Nearly all lateral fissure brain areas play a role in language. Should TEST: Fluency, Comprehension, Repetition (none in brocas, often a little messed up in Wernicke's), Severity of disorder PLEASE READ: Blumenthal Ch 19 885-891 She had this in red on the slide. Probably should do it.

Botulism: Onset? Acquired? Signs/Symptoms? Diagnosis? Treatment? Treatement?

Acute onset of bilateral cranial neuropathies associated with symmetric descending weakness, resulting from neuroparalytic toxin from Clostridium botulinum bacteria. May be food-borne, wound, inhaled (bioterror agent). Presents with: descending weakness, dipoplia. Infant botulism usually constipation and weakness. Diagnose by: history of ingestion of suspect foods, clinical syndrome, serum botulin toxin assay, stool for botulin spores or toxin Treat with botulism antitoxin Respiratory Support, typical hospital stay 1-3 months.

Identify relevant diagnostic tests in the evaluation of these disorders

Again will be mentioned on a case by case basis.

Most common Epidemiology of neuro emergencies?

Alcohol withdrawal- SUPER common (12% prevalence alcohol abuse) CVA/Stroke- 795,000 new strokes per year (in USA) Guillain Barre syndrome- 6000-9000 cases/year Tetanus- about 40 cases a year in USA, 213,000 worldwide in 2002, most in children under 5 y.o. Botulism 110 cases a year in USA (72% infant!).

Aphasia chart (on it's own) & other language related deficits (main text content): Alexia Agraphia Apraxia Gerstmann's Syndrome

Alexia - Reading impairment without sensory or motor deficits. This is an acquired reading deficit. Dyslexia is a developmental reading disorder Agraphia - Writing impairment without sensory or motor deficits. It is always present in patients with aphasia Apraxia - The inability to perform an action in response to a verbal command in the absence of any motor, comprehension, or coordination deficits Gerstmann's Syndrome - The lesion is in the angular gyrus of the parietal lobe. Patients present with: agraphia, acalculia (acquired impairment in which patients have difficulty performing simple mathematical tasks), right - left disorientation, finger agnosia (loss of recognition).

Four Toxic Vestibulopathies?

Aminoglycosides Salicylates Quinine and Quinidine Cis-Platinum

Neuroleptic Malignant Syndrome What is it? Presentation? Dx? Tx?

An idiosyncratic reaction to dopaminergic medications such as neuroleptics haloperidol or chlorpromazine resulting in fever, mental status change, dysautonomia, stiffness Presents with: altered LOC, fever, diaphoresis, rigidity, tachycardia, hypertension Diagnose by: Think of it! Exclude other causes, elevated creatine kinase and WBC, electrolyte abnormalities* Treat with: Cooling, immediate supportive care, withdrawal of offending medication, Dantrolene controversial for recalcitrant hyperthermia

Vertigo symptoms? location of disturbance? How to tell if it's central or peripheral?

An illusion or hallucination of movement. Patient or environment: tilting, rocking, falling, spinning, or any other words suggesting motion. Disturbance in the vestibular system Is it in the PERIPHERAL nervous system? (end-organ or nerve) Clues: More severe vertigo and possible hearing loss Is it in the CENTRAL nervous system? (brainstem, including cerebellar pathways, or temporal lobe) Clues: Symptoms indicating other CNS dysfunction

Neuropathic Pain drug treatments (3)

Anti-convulsants Antidepressants --Tricyclics --SNRIs Analgesics, including opioids

General class of drugs listed for motion sickness?

Antihistamines: Meclizine Dimenhydrinate Promethazine Benzos also listed (diazepam, clonazepam)

Name the 3 other (not vasovagal) cardiogenic causes of syncope:

Arrhythmia: EMERGENCY!!! Potentially life-threatening May occur in context of cardiac ischemia and myocardial infarction Obstructive cardiac disease: Characterized by low cardiac output (e.g. aortic stenosis, asymmetric septal hypertrophy) Hypersensitive carotid sinus (=carotid sinus syndrome)

How to treat CTS?

Avoidance of offending behaviors Night splints (volar, neutral) Glucocorticoid injection into the carpal tunnel NSAIDs (when acute) Treat the underlying condition Surgical decompression

Describe the concept of lateralization and hemispheric dominance

Each side is specialized in performing certain functions and collaborate via corpus callosum. The left hemisphere is particularly good with analytical functions (language) Right is better on spatial and musical perception. Handedness (Right-handed people excel in more logical, analytical thinking; Left-handed people are more creative and artistic) Language (left) Attention (right)

UMN Involvement Most likely cause? Pt Presentation?

B12 deficiency is most likely cause. Can also be due to copper deficiency, HIV, hepatic disease SYMMETRIC DISTAL SENSORY systems. signs of distal sensory neuropathy. Your patient may present with any of these (or a combination of them): --Loss of sensation (numbness) --Altered sensation to touch --Hyperpathia (exaggerated subjective response to painful stimuli) --Allodynia (pain caused by something that does not normally cause pain) --Uncomfortable spontaneous sensations (tingling, burning, aching) --Can be dull in nature and poorly localized --May be a challenge if you are dealing with possible substance use/abuse issues

Subdural Hemorrhage what is it/caused by? Presentation? Dx? Tx?

Bleeding under the dura mater lining the skull and above the arachnoid mater surrounding the brain. Acute (highest mortality), subacute, and chronic types. Caused by: Head trauma, ranging from minor to severe. Presents with: Loss of consciousness, headache, ALOC, focal neurological findings. Diagnose by: Hx of trauma, exam, CT. Treat with: surgical decompression, sometimes observation if minor.

Understand Pattern recognition for peripheral nerve disorders (PND)

Motor weakness only-->think motor neuropathy, nmj junction, myopathy. Sensory--neuropathy mostly. Can have autonomic or combinations too. Think about location. Root/plexus/nerves: Length dependent, Multifocal, diffuse? NMJ, Muscle. Distal/proximal? Both? Asymmetric?

Benign Positional Vertigo Symptoms? KEY EXAM FINDING? most common cause? common pathology?

Brief episodes of severe vertigo. May have nausea and vomiting. May occur with any change in position. May continue for several weeks. Resolves spontaneously. No hearing loss EXAM FINDING: ***Dix-Hallpike maneuver***. Positional nystagmus always present in benign vertigo of peripheral cause. Unidirectional, rotatory, delayed in onset Sudden head movement and trauma is the most common cause. Pathology: Canalolithiasis (debris in semicircular canal). OR Fistulae between inner and middle ear. May be able to reproduce the symptoms w/otoscope plus balloon. TREATMENT maneuver: ***EPLEY MANEUVER***

Describe the concept of Brodmann's areas

Brodmann area = a region of cortex w/a characteristic cytoarchitecture or cell organization. Different fiber tracts: --Association fibers: connect different cortical areas in same hemisphere --Commissural fibers: connects homologous cortical areas in diff. hemispheres (corpus callosum) --Projection Fibers: connect cortical areas w/ other brain areas like brainstem/cerebellum. Brodmann is responsible for establishing the basis upon which the present day science of comparative cytoarchitectonics of the mammalian cortex rests. All confusion of brain area nomenclature disappeared with Brodmann's contribution. (worked with Drs. vogt and alzheimer)

Raccoon Eyes = ?

Bruising around the eyes

Guillain Barre Syndrome Cause? Presentation? Dx w/? Tx?

Caused by: Immune mediated acute polyneuropathy, thought to occur after infection such as Campylobacter (most common) or influenza virus exposure. Presents with: ***Ascending*** paralysis. Progressive muscle weakness with decreased deep tendon reflexes. Dysautonomia. Diagnose by: Lumbar puncture with elevated protein in CSF. Polyneuropathy on electomyography and nerve conduction studies. Treat with: Supportive care, ventilatory support as needed. Plasmaphoresis, Intravenous Immune globulin It has a huge DDx list. I didn't even bother.

Skull fracture symptoms!

Otorrhea Rhinorrhea Hemotympanum Bruising around the eyes Bruising over the mastoids Recurrent meningitis (less common) ***Skull X-rays can miss a basilar skull fracture, so must be alert for the above signs!***

Exam of choice for an acute bleed?

CT

Vertebral Artery Dissection: Presentation? Dx w/? Tx?

Can occur after minor trauma to the vertebral artery, causing an intimal tear --> dissection --> occlusion. Example 'Beauty Parlor Stroke' frp, excessive hyperextension and rotation. Presents with: Facial dysthesias, vertigo, diplopia, other focal neurologic symptoms Diagnose by: MRI, Magnetic Resonance Angiography, traditional angiography. Treat by: observation, consider anticoagulation if CT of head is negative for intracranial hemorrhage Current OMM methods taught at American Osteopathic medical schools minimize the risk of vertebral artery injury by appropriate use of HVLA techniques.

2. Know the utilization of Ultrasound in the evaluation of the patient at risk for stroke

Can use doppler to see stoppage of flow. Can get a quick sense of hemorrhaging. Especially useful for neonates. The external carotid is the one with the bifurcation (shown in pic). A plaque would show turbulence and you would see uneven coloration. Get an idea of velocity and turbulence. With velocity you can get a sense of narrowing (if it's same volume passing through). 70% occlusion requires immediate opening.

Differentiation tree for syncope dizziness

Cardiac Orthostatic HTN

3. Know the indications and the method of Angiography

Carotid stenosis. Area of most strokes Vascular Ultrasound CT angiography (CTA) Magnetic Resonance Angiography (MRA) Angiography (catheter angiography (interventional)): Usually reserved for therapeutic procedures, or problem solving for inadequate CTA or MRA.

What disease do these three signs point towards: Weakness of thumb opposition and abduction Thenar muscle atrophy NCS is positive

Carpal Tunnel. Median nerve issue. They were the less obvious ones.

Tetanus What is it? Presentation? Dx? Tx? Prevention?

Caused by a toxin from Clostridium tetani bacteria, usually from wound contamination Presentation: ***prolonged painful contraction of skeletal muscles*** often starting in the jaw (lockjaw) progressing to opisthotonus (extreme torso hyperextension). Also see stiff neck, risus sardonicus, rigid abdomen, apnea, dysphagia.Autonomic overactivity (irritability, restlessness, sweating, cardiac AR, labile BP, fever) Diagnose by: clinical diagnosis, there are currently no blood tests Treat with: ICU admission, antitoxin (anti-tetanus IgG) and antibiotics, wound management/debridement. Prevention: Tetanus vaccine, wound care, hygiene, education.

Spinal Injury/Acute Myelopathy Cause? Presentation? Dx? Tx?

Caused by acute trauma, compression, or inflammation Presents with: absent reflexes, urine retention, absent plantar reflexes, (depending on timing and degree of injury, hyperreflexia and plantar reflexes may be present) Diagnose by: clinical history and exam. CT/MRI. Treat with: early stabilization for trauma. Administer corticosteroids. Early surgical treatment-decompression or treatment of underlying cause.

Hepatic Encephalopathy Cause? Presentation? Dx w/? Tx?

Caused by high ammonia levels from hepatic insufficiency, typically from cirrhosis Presents with: altered mental status ranging from mild confusion to coma Diagnose by: clinical signs and ammonia level Treat with: lactulose (inhibits intestinal ammonia formation)

Rabies: Acquired via? Presentation? Dx via? Tx?

Caused by infection with the rabies virus via animal bite (most commonly bat in USA; dog elsewhere). Very deadly. Until 2005, no known unvaccinated survivors. Kills 55,000 people yearly worldwide, mainly in Africa and Asia Presents with: partial paralysis, anxiety, confusion, agitation, difficulty swallowing. Diagnosis: testing multiple body fluids for rabies virus RNA, antibodies. Treatment: Early Post-exposure vaccination. For clinical rabies, consider Milwaukee Protocol- induced coma.

Examples of Toxic Peripheral Neuropathies:

Over the counter vitamin preparations: Most common B6 (B6 can be recommended for Carpal Tunnel Syndrome (a peripheral neuropathy)) **Consider B6 for either Toxicity OR Deficiency** Medications Denture adhesives( Containing zinc, which can lead to copper deficiency)

4 red flag neuroemergencies?

Pain ALOC Abnormal Movements Specific Deficits

Describe the differential diagnosis for common signs and symptoms of neurologic emergencies including: Altered level of consciousness (ALOC) - including confusion, delirium, somnolence, obtundation, stupor, syncope and coma

Causes: Medications, Intoxicants, Intracranial tumor, Stroke, Concussion or other trauma, Toxic ingestion or exposure, Hypoxia, Glucose or Electrolyte abnormality, Seizure, Hypotension, CNS Infections: viral, bacterial, Less common infections- Trypanosomiasis, Yellow fever, malaria, typhoid fever. Hypo/hyperthermia. SIGNS/SYMPTOMS: Confusion - impaired, slowed thinking and responses to questions and commands. Delirium - restless, disoriented, inattentive. Somnolence - excessively drowsy, verbal responses incoherent, motor responses disorganized. Obtundation - decreased alertness, slowed psychomotor responses. Stupor - sleeplike state, withdraw to painful stimuli, but little/no spontaneous activity. Syncope - transient loss of consciousness Coma - cannot be aroused, no response to stimuli. No corneal, gag or pupillary reflexes.

Sort the following lesion locations into the these three categories: Increased Reflexes, Decreased reflexes, Very Decreased/Unobtainable reflexes, Moderately decreased Reflexes Central Peripheral Roots Plexus Nerves Sensory Nerves Only Motor Nerves Only NMJ Muscle

Central - Increased Peripheral - Decreased Roots/Plexus/Nerves/Sensory nerves - Very Decreased/Unobtainable reflexes Motor Nerves Only/NMJ/Muscle-Moderately Decreased.

Cerebellar Disorders Symptoms and signs, general.

Cerebellar disorders Look for wide-based gait, falling to one side, intention tremor Cerebellar and other posterior fossa tumors or malformations Alcoholic cerebellar degeneration

Cerebellar Hemorrhage

Cerebellar hemorrhage: Sudden onset, often with nausea, brainstem signs EMERGENCY!!! May be life-threatening Immediate CT, coagulation studies Etiology: Hypertension (most common), Anticoagulation Blood dyscrasia, Tumor, Trauma

To be able to recognize the various types of skull fractures, be familiar with their possible physical manifestations.

Classified by LOCATION: basilar vs. skull convexity by PATTERN: linear or depressed or comminuted and by whether it is open or closed. Skull fractures are usually due to direct trauma focused at a small area. Fragments of bone can disrupt the dura and create portals of entry to the CSF. PHYSICAL MANIFESTATIONS: Nerve issues, : Occulomotor palsies, Battle Sign (=mastoid ecchymosis (bruising) after 1-3 days), Raccoon Eyes (also develop later, bruising around eyes), clear rhinorrhea or otorrhea (in up to 20%), and hemotympanum (which is common) ***DO NON-CONTRAST CT***

Key components to making the diagnosis of PNS disorders

Common presentations: Sensory Disturbance +/- weakness. Asymmetric weakness, or Pure weakness (could also be muscle here). Of the above, B is the only pure PNS distribution. The other could be either or.

Aneurysm imaging?

Computed Tomography Angiogram (CTA) IV contrast (Iodine) injected and CT scan of the area of interest Magnetic Resonance Angiogram (MRA) IV injection of contrast (Gadolinium) and MRI scan of the area of interest Catheter angiogram (Invasive), (Fluoroscopy)

To become familiar with 'concussions' (Mild Traumatic Brain Injuries), including the mechanisms by which they develop, their clinical manifestations, and their epidemiology.

Concussion' is a term commonly used for what in the medical literature is now termed 'mild traumatic brain injury' (MTBI) "a trauma-induced alteration in mental status that may or may not involve loss of consciousness" Concussion may be caused by a direct blow to the head, or elsewhere on the body, with an 'impulsive' force transmitted to the head In ***rotational movement***, the head turns around its center of gravity - this is the primary mechanism causing concussion. There is a transient electro-physiologic dysfunction of the reticular activating system in the upper midbrain caused by rotation of the cerebral hemispheres on the fixed brainstem SYMPTOMS: ***Feeling dazed or star struck***, often after a blunt forward impact that caused sudden deceleration of the cranium and a movement of the brain within the skull. ***Amnesia*** - if only a few moments of unresponsiveness is reported, then the amnesia will only last for a brief time. It will respond quickly once the patient is alert. The memory loss can vary from only moments before the injury, to even several weeks prior to the trauma (retrograde amnesia). Again, this lasts longer, the more severe the injury. ***Anterograde amnesia***, if present, is usually brief. This is the inability to form new memories. Also, Dizziness, Disorientation and confusion, Nausea and vomiting, Loss of balance, Headache - the most common symptom, Lack of motor coordination, Light sensitivity, Blurred vision, Tinnitus

Chronic onset disorders (dizziness) just a list, read it.

Paraneoplastic cerebellar degeneration Autosomal dominant spinocerebellar ataxias Autosomal recessive cerebellar ataxias Friedreich's Ataxia Autosomal recessive, chromosome 9 Ataxia-telangiectasia (Louis-Bar syndrome) Autosomal recessive, chromosome 11 Wilson's disease Autosomal recessive, chromosome 13 Creutzfeldt-Jakob (prion) disease

What does DSP stand for? What labs do you run?

Dependent symmetric pattern (length). so SENSORY > MOTOR. HbA1c, B12, SPEP (Serum protein electrophoresis--to look for amyloidosis???) & immunofixation.

Peripheral Nerve Medical Disorders?

Diabetes Mellitus Systemic Lupus Erythematosis (SLE) Infections (recently past or on-going) Surgeries Medications Alcohol intake Dietary habits Use of dentures

Earliest and most sensitive method of detecting an ischemic stroke?

DIFFUSION WEIGHTED IMAGING. Ischemic stroke: Profound restriction in water diffusion. With ischemia there is inhibition of the Na/K pump and therefore a net movement of water into the cells. (This causes cytotoxic edema). There is less overall movement of water in the cell compared to the extracellular space.) This lack of movement gives an area of brightness in the image within 30minutes of an event causing ischemia. Earliest and most sensitive manner of recognizing ischemia. This is presumed area of cell death (infarction) and not reversible.

Carotid Artery Dissection

Definition: A separation in the layers of an arterial wall leading to altered blood flow. May occur after traumatic neck hyperextension, flexion, or rotation such as in a motor vehicle accident, or as a result of an inherited disorder such as Ehlers Danlos syndrome Presentation: headache, amaurosis fugax (loss of vision in one eye due to a temporary lack of blood flow to the retina), neck swelling, localized neurological findings Diagnosis: Helical CT Angiography, MR Angiography, carotid doppler ultrasound. Treatment: Systemic anticoagulation, monitoring, surgical and radiologist consults

What are the two other (not length dependent) patterns of root/plexus/nerve loss? + examples.

Diffuse (Motor > or >> Sensory): Acute Inflammatory Demyelinating Polyneuropathy (=AIDP, Guillain Barre), CIDP (Chronic inflammatory demyelinating polyneuropathy), Osteosclerotic myeloma, Drugs and toxins (amiodarone, gold, arsenic, lead), Inherited [i.e. Charcot-Marie-Tooth (CMT)], Diphtheria ---------------------------------- Multifocal (Motor and sensory): Immune-Mediated, Vasculitis, Sarcoidosis, Brachial Neuritis, Multifocal CIDP, Multifocal mononeuropathy, Infectious, Lyme, HIV-Associated CMV, Leprosy, Zoster, Infiltrative, Amyloidosis, Lymphomatous Infiltration, Hereditary, Rare versions of CMT

Answer these questions for CENTRAL Vertigo: Direction of associated nystagmus? Purely Horizontal nystagmus w/o torisional component present? Purely vertical or purely torsional nysagmus present? Visual fixation results in? Tinnitus or deafness present? Associated CNS abnormalities? Common causes?

Direction of associated nystagmus? BIDIRECTIONAL OR UNIDIRECTIONAL Purely Horizontal nystagmus w/o torisional component present? MAY BE PRESENT Purely vertical or purely torsional nysagmus present? MAY BE PRESENT Visual fixation results in? NO INHIBITION (of nystagmus)! Tinnitus or deafness present? usually ABSENT Associated CNS abnormalities? EXTREMELY COMMON--diplopia, hiccups, cranial neuropathies, dysarthria Common causes? vascular, demyelinating, neoplasm

Answer these questions for PERIPHERAL Vertigo: Direction of associated nystagmus? Purely Horizontal nystagmus w/o torisional component present? Purely vertical or purely torsional nysagmus present? Visual fixation results in? Tinnitus or deafness present? Associated CNS abnormalities?

Direction of associated nystagmus? UNIDIRECTIONAL; FAST PHASE OPPOSITE LESION Purely Horizontal nystagmus w/o torisional component present? UNCOMMON Purely vertical or purely torsional nysagmus present? UNCOMMON Visual fixation results in? INHIBITION OF NYSTAGMUS Tinnitus or deafness present? OFTEN PRESENT Associated CNS abnormalities? NONE Common Causes? Benign paroxysmal positional vertigo, infection (labyrinthitis), vestibular neuritis, Meniere's disease, labyrinthe ischemia, trauma, toxin

Meniere's disease drug?

Diuretics/low sodium diet

Drug Intoxication (Equilibrium disorder)

Drug intoxications Prominent features: Nystagmus (present in therapeutic dosing as well). Dysarthria. Limb and gait ataxia Common drugs: ***Alcohol***, sedative-hypnotics, anticonvulsants and hallucinogens Severity is dose related Confusional state is common General supportive care is sufficient

Basilar skull fracture cause?

Dural tears and leakage of CSF

Describe the differential diagnosis for common signs and symptoms of neurologic emergencies including: Abnormal movements - Abnormal movements - such as dystonias, abnormal posturing, or seizures

Dystonias - sustained muscle contractions causing repetitive, usually twisting movements, abnormal postures. CAUSES: Hypoxic brain injury (drug overdose, seizure), Encephalitis, infectious and post-infectious (PANDAS, Sydenham's chorea), Head trauma, Pontine myelinolysis, Stroke, Tumor, Cervical cord injury or lesion, Drugs - DA receptor blockers, agonists, Toxins Seizures Status epilepticus Abnormal posturing - decerebrate v decorticate v opisthotonus (is a state of severe hyperextension)

Extrapyramidal disorders that deal with dizziness (main one)

Extrapyramidal disorders Parkinson's disease and "parkinsonism plus" (multiple system degeneration) neurodegenerative disorders Truncal ataxia Difficulty with turning Autonomic neuropathies commonly accompany these disorders so postural hypotension may also contribute to "dizziness"

Vestibular Schannoma Family Hx? Gold standard test? Treatment?

Family Hx of neurofibromatosis MRI w/gadolinium Gamma Knife radiation or surgery.

Know the elements of the relevant history by listing and describing the four common sensations that patients may call "dizziness" and what features characterize each sensation

Features of "dizziness" (1) Vertigo--Disturbances of vestibular function (50%). Imbalance in vestibular input. (2) Syncope/pre-syncope--CV disturbances = WOOZY. decreased cerebral blood flow (3) Disequilibrium--Neurologic disorders. Decreased proprioceptive input or impaired extrapyramidal or cerebellar function. (4) Lightheadedness other than above--psychological disorders.

Disequilibrium What is the common sign you see?

Feeling as if s/he might fall Ask, "Do you fall?" 50% say yes 50% report staggering Indicates gait/balance disorder (ataxia)

Wernicke's Aphasia details:

Fluent but "nonsense" speech with a marked loss of language comprehension in "heard" speech Grammar and syntax are adequate but the ability to appropriately link speech to meaning is lost - frequent use of "nonsense" words, paraphrasic errors and words similar to the correct word. The patients have difficulty understanding simple commands.

what is FMRI?

Functional magnetic resonance imaging or functional MRI (fMRI) ***measures brain activity by detecting associated changes in blood flow.*** This technique relies on the fact that cerebral blood flow and neuronal activation are coupled. When an area of the brain is in use, blood flow to that region also increases.

Temporal Arteritis What is it? Presentation? Dx? Tx?

Giant Cell Arteritis- inflammation affecting medium to large arteries (vasculitis) -unknown cause Presents with: headache, temporal tenderness, fever, abrupt onset of visual disturbances, jaw claudication. Risk of vision loss. Diagnose by: clinical pattern, elevated C-reactive protein and/or erythrocyte sedimentation rate. Consider MRI with contrast. Definitive diagnosis by temporal artery biopsy if needed. Treat by: Prednisone, typically 40-60mg /day

My Feet are Burning 35 year old female with burning pain and weakness in feet 2 weeks ago: pain & numbness over the lateral aspect of right leg and lateral foot, behind ankle 10 days ago: entire foot burning, foot dragging and "rolled her ankle" Yesterday, lateral aspect foot and distal lower leg.left started with symptoms. Pattern: Asymmetric Proximal or Distal Sensory & Motor NOT Length-Dependent What can you gather from this? WHAT TESTS DO YOU DO?

Guillain Barre Syndrome. Mononeuritis Multiplex pattern (doesnt fit a particular pattern). PNS (hyporeflexive--though I don't see where this is mentioned) WHAT TEST TO DO: Elevated CRP and ESR ANCA+ NCS: multifocal polyneuropathy with features suggestive of ***VASCULITIS*** Sural Nerve Biopsy confirms Vascutlitis diagnosis

Describe the differential diagnosis for common signs and symptoms of neurologic emergencies including: Pain - Headache, Back Pain

HEADACHE (Vascular event such as aneurysm, intracranial or epidural hemorrhage or thrombosis, internal carotid or vertebral artery dissection, pituitary apoplexy, Brain tumor, Malignant hypertension, Temporal arteritis, Glaucoma, Intracranial infection (meningitis, encephalitis, abscess)) Neck Pain, Thoracic Back Pain, Low Back Pain = ACUTE AXIAL PAIN: (Spinal cord compression due to fracture, neoplasm, stenosis, disc pathology, Neck/Suboccipital pain: Subarachnoid hemorrhage, meningitis/encephalitis, spinal stenosis, Epidural abscess, Cauda equina syndrome)

The College Professor: Left foot "dragging" ~ 4 months, getting weaker Left leg thinner than the right Right foot "catches" recently Cramps Exam: Asymmetric weakness in legs Atrophy in the weakest muscles Fasciculations in the calves Toe tapping slow Reflexes: 3+ with spreading Hoffman and Babinski present Is this LMN or UMN?

Has signs of BOTH UMN (Hyperreflexia, Babinski and Hoffman signs, Increased tone/spasticity, Slowness of movement) and LMN (Hyporeflexia, Atrophy, Fasciculations, Cramps) Dx: ALS Clues: Upper and lower motor neuron dysfunction Insidious, asymmetric onset No sensory disturbance No bowel or bladder dysfunction Note: Be sure to exclude other UMN + LMN issues. Particularly combo of cervical and lumbosacral spinal stenosis.

The wobbly grad student, 28 3 days of uncomfortable tingling in feet and hands. Over the past 24 hours having difficulty walking, climbing stairs and getting weaker. 10 days ago, experienced several days of diarrhea, assumed to be a viral gastroenteritis. Exam: Tactile paresthesias in hands and feet Diffuse (proximal and distal) weakness Reflexes unobtainable Pattern: Symmetric Proximal and distal Motor>sensory

Hyporeflexia --> Peripheral Proximal and Distal weakness with MOTOR > SENSORY means this is a DIFFUSE DISTRIBUTION DDx Includes: Acute Inflammatory Demyelinating Polyneuropathy (=AIDP, Guillain Barre) CIDP (Chronic inflammatory demyelinating polyneuropathy) Osteosclerotic myeloma Drugs and toxins (amiodarone, gold, arsenic, lead) Inherited [i.e. Charcot-Marie-Tooth (CMT)] Diphtheria So you gotta do labs: EMG/NCS (nerve conduction study), Spinal Fluid, FBS (fasting blood sugar), HbA1c, B12, Thyroid, LFTs (liver function tests), HBV, HCV, ESR, ANA RF, Lyme antibodies, Anti-Neutrophil Cytoplasmic Antibodies (ANCA), Cryoglobulins, HIV - if +, CMV titer

A 50 yo patient presents with episodes of spinning vertigo, severe tinnitus and a sensation of a stuffed ear well as progressive sensorineural hearing loss. The proposed etiology for this condition is: Progressive demyelination of both parts of CN VIII Idiopathic distention (hydrops) of the endolymphatic system Microinfarcts in semicircular canals and cochlea Formation of amyloid plaques and tangles in vestibular and auditory nuclei + How to treat? + What is the prognosis of this disorder?

Idiopathic distention (hydrops) of the endolymphatic system --Diuretics, salt restriction, nerve section if severe --Hearing loss progresses and severity of vertigo diminishes

Causes of MONONEURITIS MULTIPLEX (non-symmetric, doesn't fit a pattern)

Immune-Mediated: Vasculitis, Sarcoidosis, Brachial Neuritis, Multifocal CIDP, Multifocal mononeuropathy Infectious: Lyme, HIV-Assocated CMV, Leprosy, Zoster,, Infiltrative, Amyloidosis, Lymphomatous Infiltration Hereditary: Rare versions of CMT

Describe the relevant findings in the general physical and neurological examinations for these disorders

Important and emphasized ones will be mentioned later on.

Broca's Aphasia in more detail:

In these patients the speech is characterized by its telegraphic style with use of mainly content words and verbs not conjugated. The patients have difficulty repeating words spoken to them and they substitute sounds for incorrect ones: paraphrasic errors. The speech lacks emotionality (monotone), with anomia but comprehension is largely intact. Patient's become very frustrated by their inability to communicate. Motor or Expressive aphasia: loss of the ability to produce language. The organizational aspects of language such as grammar and syntax are disrupted.

Meningitis/Encephalitis Cause? Presentation? Dx w/? Tx?

Inflammation of the meninges or brain parenchyma. May be viral, bacterial, parasitic, or even autoimmune. Presents with: headache, fever, confusion, neck stiffness. Diagnose by: CT to r/o other pathology, Lumbar puncture, (brudzinski and kernig's signs). CSF studies, serology. Check HIV antibody test Treat with: Supportive care. Antiviral treatment, i.e. acyclovir for HSV until cause known; antibiotics until bacterial cultures are negative x 48hr. Supportive care and pain management.

Skull fracture facts!

Intracranial lesions are evident in 2/3 of skull fracture patients. A skull fracture increases the likelihood of a subdural or epidural hematoma by many times. A skull fracture can be considered as a marker for the severity of the injury. Most fractures are linear, extending from the point of impact toward the base of the skull. About 15% of skull fracture pts have a cervical spine fracture in addition to the skull fracture

Two Headaches Mentioned in West's Lecture. Provide quick info about these two: Migrainous vertigo: Basilar-type migraine:

MIGRAINOUS VERTIGO: Dx in about 10% of patients with vertigo Most migraineurs have ***hx of motion sickness*** (physiologic vertigo) May need therapeutic trial of anti-migraine medication to make dx BASILAR TYPE MIGRAINE: Rare, onset before age 50 ***Two or more aura symptoms indicating brainstem or bihemispheral involvement but without motor weakness*** Use of typical anti-migraine meds still controversial

Clinical patterns of PURE WEAKNESS Motor Nerve findings? NMJ findings? Muscle finding? Describe the above three in terms of symmetry, location (distal/proximal), any specific diseases, CK/NCS/EMG findings.

MOTOR NERVE: Usually asymmetric; Usually distal; Atrophy, *fasciculations*, cramps. NORMAL/MILDLY elevated CK. **Reduced** amplitude & conduction velocity NCS. EMG: Fibrillations, Positive Sharp Waves, Giant motor unit action potentials (MUP). NMJ: Usually fluctuating and fatiguable. --Myasthenia gravis (Bulbar, ocular involvement common); --Lambert-Eaton Myasthenic Syndrome (paraneoplastic, Usually proximal and symmetric. Bulbar involvement rare.). NORMAL CK. ***DECREMENTAL DECREASE IN NCS w/REPETITION*** Jitter w/single fiber EMG. MUSCLE: Usually proximal, Usually symmetrical, Usually painless, Usually non-fluctuating. ***ELEVATED CK***. Normal NCS, *Short Duration (potentials)* for EMG.

4. Know about the utilization of Neuro Neonatal Ultrasound

Main thing you see is a sub-ependymal hemorrhage.

Hypertensive emergency/Malignant HTN what is it? presentation? dx? tx?

Markedly elevated BP, PLUS end organ damage either to CNS, cardiovascular or renal system. Papilledema necessary for diagnosis. (Presentation) Symptoms: headache, vision changes, chest pain, epistaxis (nose bleed), retinal findings. (Dx) Signs: Systolic BP >180, Diastolic BP typically >120, renal insufficiency, stroke, myocardial ischemia, artery dissection, retinopathy. 'Hypertensive Urgency' if severe BP elevation (DBP >120) and potential for damage Treat with: steadily reduce BP over 2-6 hr, identify and treat underlying causes.

Other common neuropathies

Meralgia Paresthetica: Lateral femoral cutaneous neuropathy S/s parasthesias, numbness and occasionally pain at lateral thigh Worse with standing/walking; relieved by sitting Strength and motor not affected Diagnosed clinically - no further tests needed Ulnar neuropathy at the elbow: Cubital tunnel syndrome Parasthesias, tingling & numbness medial hand, half of 4th finger and 5th finger Pain at elbow or forearm and weakness Positive Tinel's sign Radial neuropathy Femoral neuropathy Peroneal nerve neuropathy

Glasgow Coma Scale...what the number mean?

Mild Brain Injury ... GCS 13 - 15 Moderate ... GCS 9 - 12 Severe ... GCS 8 and below

Linear Skull fractures?

Most are full thickness Most have ***minimal clinical significance*** (in and of themselves) - UNLESS - the fracture crosses the middle meningeal groove in the temporal bone, or a major venous dural sinus. Then there is the potential for significant bleeding inside the skull (but outside the brain parenchyma) Usually presents without neurologic symptoms (if it is a simple, closed fracture).

Myasthenic Crisis What is it? Presentation? Dx? Tx?

Myasthenia Gravis- autoimmune production of antibodies to postsynaptic acetylcholine receptors, blocking transmission of motor impulses, resulting in descending weakness. A myasthenic crisis is an acute, life-threatening exacerbation of weakness involving the bulbar (facial, oropharyngeal) and respiratory muscles resulting in dysphagia with aspiration and/or respiratory failure (needs intubation and mechanical ventilation) Presentation: Ptosis, respiratory distress, in the setting of infection, surgery, pregnancy or other stressor. May also occur spontaneously. Diagnose by: tracking respiratory status (vital capacity or maximum inspiratory force). Arterial blood gas analysis changes occur late and are less helpful. Treat by: Elective intubation, Plasmaphoresis or IV immunoglobulins, high dose corticosteroids or other immunomodulator.

Explain the anatomical organization of the cerebral cortex into layers of neurons and white fiber tracts

Neocortex - 6 layer cortex - 90% of all cortex in humans, and it has a laminated structure and a columnar organization (discovered by Vernon Mountcastle). We've seen this w/ocular dominance columns where one point in space is represented by a column from one eye, then right next to it the same point from the other eye. Pia at the top. Info comes to Layer 4. Layer 3 distributes info. Each layer of the neocortex is composed of cells that based on their sizes and shapes are classified either as PYRAMIDAL (seen in the motor cortex a lot) or non- pyramidal cells. Non- pyramidal cells are called stellate or GRANULE cells (fusiform is also in there, along w/pyramidal are the main outputs). "Older" (evolutionarily) cortical areas: Paleocortex - 3 layer cortex - Olfactory areas Archicortex - 3 layer cortex - Hyppocampus

Discuss management of the patient with ill-defined lightheadedness

Often "dizziness" is a metaphor for anxiety or depression Important to recognize anxiety and affective disorders How do you feel when you are with the patient? Making an appropriate diagnosis is key Treatments for vertigo may exacerbate psychological disorders Appropriate treatment for the underlying disorder will usually relieve the "dizziness"

Know the indications for a CT of the brain following mild traumatic brain injury (MTBL). also discussed here, low, medium and high risk categories.

Often benign, but carries a high risk of serious short and long-term sequela Occurs with a head injury due to contact and/or acceleration/deceleration forces Typically defined as 'mild' by a Glasgow Coma Scale (GCS) score of 13 to 15, measured about 30 minutes after the injury (some argue that score of '13' should be included within "moderate" brain injury [GCS 9-12]] 'Low risk' = GCS 15 and NO Hx of LOC, amnesia, vomiting or diffuse headache. 'Medium risk' = GCS 15, but with a + hx of LOC, amnesia, vomiting or diffuse headache. These pts have a 1-3% risk of having an intracranial hematoma requiring surgical evacuation. Obtain a CT. If CT not available, get skull x-rays and transfer to a facility with neurosurgery if positive. 'High risk' = mild head-injury patients are those with a GCS of 14 or 15 with a skull fracture and/or neurological deficits. About 10% of these 'high risk group' patients will require surgical evacuation of intracranial hematomas. Patients with a coagulopathy, drug or alcohol consumption, previous neurosurgical procedures, epilepsy, or age greater than 60 years are included in the high-risk group, regardless of their clinical presentation. 40% of patients with GCS 13 will have a positive brain CT!!

Drug Related Dystonia Cause/description? Presentation? Dx? Tx?

Parkinsonism or movement disorder caused by a medication, typically a dopamine antagonist such as a phenothiazine Presentation: oculogyric crisis, torticollis, jaw/mouth movements, torso movements, akasthesia Diagnosis: clinical history and exam Treatment: Withdraw/taper offending medication. Consider anticholinergic such as diphenhydramine or benztropine.

Discuss the concept of "dizziness" as metaphor for anxiety or depression (ill-defined lightheadedness)

Patient persists with term "dizzy" despite optimum history-taking. Called "true dizziness". Usually arises as part of a psychological disorder: --Hyperventilation syndrome --Anxiety disorders --Affective disorders --Somatization --Obsessive compulsive disorder

Hyponatremic Encephalopathy What is it? Presentation? Dx w/? Tx?

Patients can develop hyponatremia from many causes. If especially acute and severe, cerebral edema ensues. Presents with: headache, nausea and vomiting, confusion, lethargy, fatigue, loss of appetite, restlessness, irritability, muscle weakness, spasms, or cramps, seizures and ALOC, even coma. Symptoms may start with sodium <130 and be severe with sodium <115. Diagnose by: serum sodium, urine sodium. Treat with: Treat underlying cause, ***slow*** correction of the serum sodium. Rapid correction can cause osmotic demyelination (central pontine myelinolysis) = next card

Basilar Skull fracture MGMT?

Patients diagnosed with a basilar fracture should be admitted for observation If bloody drainage, check for a 'halo sign' - but cannot exclude saliva or other clear fluid. In nursing, the halo sign is the result of a test to see if drainage from a head injury contains cerebrospinal fluid. When a Dextrostix or Tes-Tape test gives a positive reading for glucose, the drainage must be further tested because glucose is also found in the blood. To perform the test, the leaking fluid is dripped onto a 4x4 gauze or towel. The blood should coalesce into the center, leaving a ring if cerebrospinal fluid is present. Most leaks resolve spontaneously within a week 3% risk of meningitis in first week - but routine treatment with antibiotics is unnecessary. If leak last more than 7 days, start antibiotics Cranial nerve palsies are a delayed complication, due to swelling from compression, starting 2-3 days after the injury. May use steroids, obtain consult

The Inebriated Man 43 year old man with long history of heavy alcohol ingestion comes in to ER with alcohol on his breath and stating "I think I had a stroke" Awoke unable to extend his wrist What do you want to know? Exam With right arm extended, the hand dropped and he could not extend the fingers of the hand When examiner straightened the wrist and held it, adduction and abduction of the fingers, wrist flexion and grip were all normal. Small patch of sensory loss over dorsum of the right thumb Remainder of neurologic exam normal What's the Pattern?

Pattern: Asymmetric, Distal, Sensory and motor, NOT length-dependent. He has: SATURDAY NIGHT PALSY Humeral radial neuropathy Compression of the radial nerve, as it spirals around the humerus in the spiral groove on medial side in axilla Direct Pressure to the area: Axillary crutches, sleeping on arm along back of chair or underneath you Signs: Wrist drop (weakness of wrist extensors and weak finger extensors; Sensory loss of back of hand at base of thumb: Triceps is spared - innervation comes off the radial above the level of compression

Vestibular Rehabilititation. In what kind of injury? Describe some of it's purposes/benefits etc.

Peripheral Promotes recovery in patients with peripheral vestibular injury Forces patient to perform challenging balance exercises Promotes adaptation Facilitates strategic substitution Reduces the negative impact of inactivity

The TINGLY GRANDMOTHER 65 year old woman with several years of gradually worsening numbness and tingling in her feet Exam: Light touch produces some tingling and "isn't quite as strong," up to ankles Vibratory sense reduced at toes, ankles Toes are a little weak Ankle jerks unobtainable Pes cavus: mild. More severe, with hammer toes Indicates weakness of the intrinsic foot muscles ("small muscles of the feet") Pattern Symmetric Distal/ascending Sensory and motor "stocking-glove" Sensory before motor & loss of reflexes

Pes Cavus and Stocking Glove distribution shown. Hyporeflexia-->Lower Motor Neuron/Peripheral. Sensory changes indicate it's Roots/Plexus/Nerve area. It appears to be Length Dependent (Sensory>Motor); the opposite would be (Diffuse = Motor>Sensory). Common causes: Alcohol/Diabetes/Idiopathic. Also, B12 def, Toxic, amyloidosis

Explain the function of the prefrontal association areas.

Planning and enabling humans to function as effective and social beings. Integrates information from all brain regions and is also involved in the generation of our ***concept of "self"*** = Personality. Also involved in short term memory storage and utilization. EXECUTIVE FUNCTIONS. control and sequencing of other cognitive functions important in: Selection of the appropriate strategies to solve problems Motivation for productive and positive activities -Initiative The inhibition of incorrect responses mostly in relation to social behavior - Restrain The ability to deal with changes in focus (dealing with different things at the same time) and sequential tasks - Order Being able to apply previously learned experience to new situations Working memory - Hold a limited amount of information for a short time while a number of cognitive operations are performed. Integration of information from multimodal association cortices and limbic cortex in decision making. Blumenthal CH 19 pg. 906

What is Polyneuritis Multiplex?

Polyneuritis multiplex, in which the damage randomly affects portions of individual nerves, resulting (for example) in a right radial nerve palsy and wrist drop together with loss of sensation in the left foot

What is a Polyneuropathy?

Polyneuropathies usually affect peripheral nerves in a symmetric, length-dependent fashion. Axonal loss is typically diffuse and more pronounced in the distal segments of the longest nerves. Patients commonly present with loss of sensation and paresthesias that start in the toes and spread upward to the knees and then involve the hands in a "stocking-and-glove" distribution.

Coma Presentation? Dx? Tx? Recognize decordicate v decerebrate postures.

Presentation: Unconsciousness and unresponsive to external stimuli. Typically caused by damage to the reticular formation or both cerebral hemispheres Diagnosis: Neuro exam, CT scan, metabolic panel, tox screen. Look for the underlying cause. Treatment: Manage airway, circulation. Supportive care. Correct underlying causes. Don't forget: Skin care, nutrition Family support

Alcohol Withdrawal Presentation? Dx? Tx?

Presents with: anxiety, autonomic hyperactivity (vitals go up and down), tremor, generalized seizures. Diagnosis: history and exam. Treatment: Manage withdrawal symptoms early to avoid potentially life threatening delirium tremens. ***Benzodiazepines*** are the mainstay of treating alcohol withdrawal. Diazepam and chlordiazepoxide are typical choices. Supportive care- fluids, thiamine, folic acid, magnesium. Alcoholism treatment.

Discuss the concept of primary, secondary and association cortical areas

Primary SENSORY - sensory inputs coming from periphery are FIRST RECOGNIZED (Primary Somatosensory = Brodmann's 1, 2, 3; P. visual = 17, P. auditory = 41) Primary MOTOR -- UMNs that descend and influence LMNs (Primary motor area = Brodmann 4) --------- Secondary = UNIMODAL association areas. Places receiving input from primary areas, or from thalamus. Extract more info from the input they receive. Ex: shape, texture, object, color, light, direction etc. Secondary Motor areas = supplementary and premotor: function w/primary motor cortex and basal ganglia to genereate patterns of motor movements. --------- Heteromodal Association Areas: Association areas that receive and analyze SIMULTANEOUS input coming from motor and sensory cortices. Bidirectional communication w/thalamus, cerebellum, basal ganglia, limbic system, and brainstem areas. Highest, most complex mental functions = COGNITION basically. = PREFRONTAL ASSOCIATION AREA, PARIETO-OCCIPITOTEMPORAL JXN and LIMBIC ASSOCIATION AREA.

Meniere's Disease:

Reccurent attacks, episodic vertigo. Audiometry: low freq, unilateral sensorineural hearing impairment. Progressive sensorineural hearing loss. Aural FULLNESS (ears feel stuffed)

Peripheral Nerve Infectious causes?

Recent illness with significant diarrheal component Can Precede Guillain Barre (GBS) Syndrome

Benign Paroxismal positional treatment?

Repositioning maneuvers vestibular rehabilitation.

Attention and Spacial Processing

Right side: Attention is the ability of selectively process simultaneous sources of information coming to the brain and be able to separate one from the others Attention depends on the activation of many different areas of the CNS. At cortical levels the posterior parietal, frontal and limbic areas of the right hemisphere are the most important for attention mechanisms The parietal association areas of the non-dominant hemisphere are particularly important in the processing of spatiotemporal information and is becoming increasingly clear that the cortical eye movement systems are extremely important in directing attention.

How to treat ALS:

Riluzole

Describe the differential diagnosis for common signs and symptoms of neurologic emergencies including: Neurological deficits including impairment in cognition, motor, sensory or autonomic function

SPECIFIC NEUROLOGICAL SYMPTOMS: Vascular events such as TIA, RIND, Stroke (hemorrhagic, thrombotic), spinal cord infarct, Infections, including CNS bacterial, viral, parasitic infections, peripheral toxins such as tetanus, HIV, Prion disease, Intracranial or spinal cord tumors, Guillain Barre Syndrome, Increased intracranial pressure of any etiology, Spinal cord or nerve root compression. Reduced motor function, especially focal deficits, including muscles for respiration Altered speech/language Trouble with vision, eye movement, swallowing Ataxia, vertigo Memory problems Altered sensation such as Paresthesias, Numbness

psychosomatic vertigo drug treatment?

SSRIs.

Labyrinthitis Key signs: Tests to run?

SUDDEN UNILATERAL LOSS. HEARING LOSS (mild/moderate in higher freq) SEVERE SPINNING VERTIGO NAUSEA AND VOMITING May persist for 3-6 weeks but does not result n permanent impairment. HEARING TESTS (yes, that vague).

Berry Aneurysm Presentation? Dx? Tx?

Saccular aneurysm leading to sub-arachnoid hemorrhage Presents with: acute headache, ALOC, collapse. Sudden ***"thunderclap" headache is classic "worst headache ever".*** Diagnosis: MRA. For bleeding, head CT without contrast; lumbar puncture Treatment: ICU admission, nimodipine (control BP and vascular spasm), intracranial pressure monitoring, surgical repair (clip placement)

What disease state are these symptoms describing? Complicate hip arthroplasties, pelvic procedures (with prolonged position in lithotomy position), trauma, hematomas, tumor infiltration and vasculitis. Seen in Low back pain patients Many are idiopathic Weakness may be at all motion of ankles and toes, flexion of leg at the knee. Hip is generally spared Sensory loss in the entire foot and distal lateral leg Ankle Jerk typically absent or diminished Can be misdiagnosed as peroneal neuropathy

Sciatic Neuropathy.

Chronic onset dizziness: Sensory ataxias.

Sensory ataxias: Impaired proprioceptive sensation at any level, Polyneuropathies, Diabetes mellitus, Drugs (chemotherapeutic agents esp. cisplatin and paclitaxel, isoniazid, pyridoxine, amiodarone, others), Myelopathies, Acute transverse myelitis, Multiple sclerosis, Mixed, Vitamin deficiencies (B-12, E), Neurosyphilis (tabes dorsalis).

Peripheral Nerve Vitamin Deficiencies. Most common causes?

Surgeries: Gastric Bypass - very common Most common is Vit B12 and folic acid Dietary habits (Socioeconomic, Poor intake, Lack of access) Alcohol Intake (Thiamine)

Vasovagal: Classification? Main content here describes the common triggers. What's the PRODROME of symptoms?

Syncope that is cardiogenic. "Neurocardiogenic syncope" Very common Typical triggers include: Prolonged standing, Stress/extreme emotions, Painful or unpleasant stimuli, High ambient temperature and hyperthermia, Urination or defecation, Vasodilators (including alcohol) Often recurrent Prodrome of symptoms (early symptoms, or before they happen): Lightheadedness, nausea, sweating, ringing in the ears, and visual disturbances Overactivity of baroreceoptor reflex Simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone.

Explain hemineglect syndrome and identify the cortical area involved in producing this deficit. 4 important evaluations to make:

The left hemisphere responds to stimuli on the right space The right hemisphere respond to stimuli on both left and right spaces with more emphasis on the left Lesions of the right posterior parietal cortex produces hemineglect on the LEFT. EVALUATIONS: (1) Sensory neglect - patients tend to ignore visual, tactile, or auditory stimuli on the contralateral side. (2) Motor neglect - patients perform fewer movements on the contralateral space (3) Visual neglect (4) Conceptual neglect - the patient exhibit lack of internal representation of the body or the external world contralaterally. ANOSOGNOSIA - Patients are not aware of the disease Patients frequently present APRAXIA (person is unable to perform tasks or movements when asked, even though: The request or command is understood; They are willing to perform the task; The muscles needed to perform the task work) ***TEST w/DRAWING*** Blumenthal CH 19 898-901

Cavernous Sinus Thrombosis Presentation? Dx? Tx?

Thrombosis of the cavernous sinus veins with ***concurrent infection.*** Rare but life threatening. A potential complication of sinusitis. Presents with: headache, cranial nerve signs, and proptosis. Periorbital edema. Death from CNS infection. Diagnosis: clinical history and exam. CT of head. Treatment: early and aggressive antibiotics ***covering S. aureus.*** Possible role for corticosteroids. Drainage of primary infection if applicable

CVA Ischemic Stroke Presentation? Dx? Tx?

Thrombotic (aka ischemic) stroke, typically caused by a blood clot blocking blood flow in an artery to the brain Presentation: focal deficit like weakness, speech problems, dizziness, confusion, numbness, etc Diagnosis: history and neuro exam, head CT. Treatment: if under 3-4.5 hours since confirmed start, and no contraindications*, may use tissue plasminogen activator to potentially restore patency of thrombosed artery Contraindications include recent bleeding, uncontrolled BP, greater than 3-4.5 hours since start of stroke, recent MI.

osmotic demyelination (central pontine myelinolysis) What is it? Presentation? Dx? Tx?

Too rapid correction of hyponatremia causes demyelination of brain stem neurons. Presentation: 2-6 days after you corrected the sodium, patient develops dysarthria, dysphagia, paraparesis or quadriparesis, behavioral disturbances, lethargy, confusion, disorientation, obtundation, and coma; seizures, locked in syndrome. Diagnose by: MRI, but sometimes delayed 4 weeks Treat with: consider relowering Na, supportive care, often damage is irreversible. DON'T CAUSE IT - always correct Na slowly (post hyponatremic encephalopathy)

Depressed skull fracture: Mortality rate? What to assume?

Trauma was of significant force to drive a segment of skull below the level of adjacent skull. These often involve brain injury with significant risk for CNS infection, seizures, and death - if not identified early High mortality rate in patients who present with a significant decline in mental status and a depressed skull fracture. May be open (most are), or closed ASSUME EVERY DEPRESSED SKULL FRACTURE IS OPEN UNTIL PROVEN OTHERWISE

Opioid OD Presentation? Dx? Tx?

Typically occurs when heroin users inject more than usual, inject after a period of abstinence, or accidentally inject higher purity heroin or fentanyl. Also with 'body packers' and 'body stuffers.' Can occur with other high potency opiates or polysubstance abuse. Accidental ingestion. Presents with coma. Diagnose by: coma and signs or history of drug use. Respiratory depression. Miosis. Treat by: IV naloxone in small increments, repeatedly (t ½ ~20'). Airway management.

SLOWLY PROGRESSIVE TINGLING IN BOTH FEET In 48 year old male, who is 6 months post gastric bypass for weight loss Exam: Patchy hypopigmentation of arms, neck and trunk Reduced vibratory & position sense Normal pinprick and temperature sensation Good strength Brisk reflexes 3+ Plantar response is extensor Pattern: Symmetric Distal Sensory Position & vibratory only REFLEXES BABINSKI LOCALIZATION????

UMN, Dorsal Column

Status Epilepticus What is it? Presentation? Dx? Tx?

Uninterrupted seizure longer than 5-10 minutes. Problematic due to both underlying causes and complications such as hypoxia, lactic acidosis, and rhabdomyolysis Causes: sub-therapeutic seizure med dosing, infection, hypoglycemia, toxins, hypoxia. Presents with persistent: 1) altered level of consciousness 2) automatic movements 3) focal neurological findings Diagnose by: Clinical history and exam. Check blood glucose, O2 saturation, electrolytes. Consider EEG, CT. Initial treatment with IV/IM/PR/nasal ***benzodiazepine*** such as diazepam, lorazepam, or midazolam (parenteral routes) and oxygen. Route depends on specific benzodiazepine. Subsequent phenytoin or fosphenytoin administration.

Tell the location and function of the main areas for visual perception and the deficits produced by damage to those areas 3 VISUAL CORTEX 3 DORSAL 3 VENTRAL

VISUAL CORTEX DAMAGE: Blindsight - Awareness of movement or light in the lost visual field (unilateral deficit) Cortical Blindness or Anton's Syndrome. Damage of the visual cortex ***bilaterally***: (1) Complete visual loss (2) Anosognosia (pt is unaware of their deficit) (3) Lack of blink to threat -------------------------- VENTRAL PATHWAY (what?): Cortical color blindness or achromatopsia: Produced by damage to area V4 on the ventral temporal lobe. Visual agnosia - Produced by lesions of the ventral object area. Prosopagnosia - Lesion of the face recognition area this deficit occurs mostly with bilateral lesions -------------------------- DORSAL PATHWAY (where?): Motion Blindness - Produced by lesion of the area MT and surrounding areas Visual neglect - Produced by damage to the posterior parietal cortex. Balint's syndrome - Produced by a bilateral lesion of the parieto-occipito cortex. Patients have difficulty to scan a complex visual scene or identify moving objects. They are able to perceive small regions of the visual field at a time. Patients have optic ataxia, ocular apraxia and simultanagnosia. -----OPTIC ATAXIA - Inability to reach an object in space under visual guidance or point to a target -----OCULAR APRAXIA - Difficulty in directing the gaze towards an object through saccades -----SIMULTANAGNOSIA - Inability to perceive more than one object in the visual field simultaneously Blumenthal CH 19 913 - 917

Brain edema kinds (2)

Vasogentic vs Cytotoxic Vasogentic has BBB breakdown, influx of water into interstitium, intravascular protein and fluid-->extracellular space, ***mostly white matter***, sparing the GREY matter. Cytotoxic: intact BBB, Ischemia with lactic acidosis and breakdown of Na/ K ion pump. Influx of water into cells and not moved out by ion pump. Mostly involves the ***gray matter***, but then extends into the white matter.

A patient presents with sudden unilateral moderate loss of mainly high frequency hearing, incapacitating vertigo, nausea and vomiting. The most likely etiology of this disorder is: Occlusion of PICA or vertebral artery (Infarction) Viral infection (Labrynthitis) Demyelination (Multiple sclerosis) Idiopathic (Meniere's disease) + Prognosis?

Viral infection (Labrynthitis) Resolution in 3-6 weeks

Orthostatic HTN What to rule out?

Volume depletion: Rule out hemorrhage! Also vomiting, hyperglycemia, (drug-induced: diuretics). Drug-induced: Antihypertensives, vasodilators, Tricyclic antidepressants, phenothiazines, opioids, EtOH. Autonomic failure--Primary: CNS and PNS disorders; or isolated (PAF) PAF: Endocrine, electrolytes, surgical sympathectomy. Secondary: Diabetes, amyloidosis May affect 20% of pts over 65 years of age. Decreased baroreceptor sensitivity common. Milder form. Diagnosis of exclusion.

1. Recognize the differences of hemorrhagic vs. ischemic stroke and imaging work-up

Want to give a CT to distinguish. Non-Hemorrhagic: --Hyperacute -- <6hrs normal CT or. Cytotoxic edema- (30 minutes) failure of cellular ion pumps - causing Cytotoxic edema. Imaging- ***loss of gray white junction***, loss of cortical sulci and Compression of ventricular system. --Acute - 6 to 48 hrs: More of above --Subacute -- 48hrs to weeks: Mass effect progressively decreasing, May develop secondary hemorrhage --Chronic - weeks to months: Encephalomalacia and atrophy depending on size of the area of infarction. In ischemic we may have a diffusion/perfusion mismatch and thus a penumbra. ------------------------------------- Hemorrhagic Stroke: Computed Tomography CT. Acute bleed - hyperdense (white). May have surrounding edema (dark)—fluid density Severe anemia bleed maybe isodense—may look like grey/right matter. So if someone is severely anemic, they may not show a stroke. Sub acute (weeks) - isodense: Chronic hypodense and surrounding encephalomalacia (atrophy) MRI: Dependent on time of bleed and resolution of hemosiderin

Wernicke's CLASSIC TRIAD How to confirm a diagnosis?

Wernicke's Classic triad: ataxia, ophthalmoplegia, confusion BUT triad seen only in one-third of patients. Thiamine (Vit B1) deficiency Chronic alcoholics and malnourished. Diagnosis confirmed by response to ***thiamine***. Administer BEFORE glucose Ocular palsies resolve within hours but nystagmus persists in 60%. Vestibular function and ataxia may take weeks to resolve; about 60% have persistent gait disturbance or are unable to walk at all.

A 55 yo woman presents with progressive unilateral hearing loss and more recent onset of tinnitus and vertigo. What office-based test will provide an important clue to the diagnosis? Pneumatic otoscopy Finger rub hearing test Whisper hearing test Caloric testing of vestibular function

Whisper hearing test We are worried about a vestibular schwannoma. Hearing loss and vestibular issues.

Vestibular Migraine drug?

antimigrainous drugs is all that was listed (helpful!)

What can skull x-rays miss? so what do you do?

basilar fractures! so you need to know the symptoms of skull fractures!

Battle sign = ?

bruising behind the ears.

Pneumoencephalopathy

can see the ventricles

Temporal bone fractures are at high risk for?

extra-axial hematomas, especially ***subdurals***

What imaging method was used here?

fluoroscopy.

which one is vasogenic edema and which is cytotoxic (see pics)

left is cytotoxic, right is vasogenic.

MRI of hemorrhage?

looks hyper white

Synesthesia is an example of?

multisystem integration and processing. SYNESTHESIA is a phenomenon by which people experience 2 or more perceptions blend together (syn= together and aisthesis=perception) Seeing blue when the note C sharp is played on the piano. Seeing printed black numbers in colors: 3s are green, 5s are red!!!!!

If perfusion scan matches the diffusion scan then do you do you give thrombolytic agent?

no. if diffusion is smaller compared to perfusion, then mismatch = penumbra and you give therapy. Diffusion bit is non-salvageable (cytotoxic edema), rest is salvageable (that isn't being perfused, but the proton pumps are still working basically, so they arent dead).

What line is used to standardize CT images?

orbitmeatal line.

Motion sickness drug?

scopolamine

How do you confirm a diagnosis of vasculitis?

sural nerve biopsy

How to treat Myasthenia Gravis:

pyridostigmine, immunosuppressive Rx, thymectomy

How to treat Vasculitis and dermatomyositis-

steroids, IVIG, immunosuppressive drugs

With perfusion imaging, which area is at risk?

the one that does NOT light up. IV contrast injected with immediate imaging being performed. The area of contrast enhancement is normal. Area with no contrast enhancement is at risk (no flow) ***If the perfusion scan is matching the diffusion then no penumbra is present and no thrombolytic is needed.*** If the diffusion is smaller compared to the perfusion then the area of mismatch is the penumbra and therapy is needed to attempt to salvage this area.

Location of an ACA infarct?

there.

MCA stroke locations

there.

PCA stroke

there.

Hemotympanum = ?

this---hard to say what's going on here.

What is opisthotonus?

this. (hyperextension) Seen in tetanus.

When to use CT vs. MRI

use MRI for detail basically. CT is cheaper, faster and better for recent bleeds.

Salesman: 68 year old man Difficulty walking long distances, climbing stairs, getting in and out of the car No sensory disturbances =WEAKNESS ALONE CK: 128u/l (normal/minimal) NCS/EMG: evidence of a NMJ disorder So you think of?

weakness alone-->more NMJ or muscle. could be neuron. CK/NCS/EMG suggests MG or Lamber-Eaton. Turns out to be Lambert-Eaton Myasthenic Syndrome Work up - revealed lung cancer