Neurophysiology Exam 2

Neurological Examination - Headaches and Facial Pain Match the "red flag symptom" to what you should consider as pathology. 1. Thunderclap Headache 2. Posititonal Component 3. Headache on Awakening 4. Focal Neurological Signs 5. Neck rigidity 6. Older than 50 Years of Age A. Mass lesion, dissection B. Intracranial Pressure C. Temporal Arteritis D. Ruptured Aneurysm E. Meningeal Irritation F. Mass lesion, elevated pressure.

"Red Flag" symptom -> Consider: 1. "Thunderclap" Headache -> Ruptured aneurysm (D) 2. Positional Component -> Intracranial pressure (B) 3. Headache on awakening -> mass lesion, elevated pressure. (F) 4. Focal neurological signs -> mass lesion, dissection (A). 5. Neck rigidity -> meningeal irritation. (E) 6. Older 50 years of age -> Temporal Arteritis.(C)

What is an abortive treatment for a MIGRAINE?

Anti-emetics

Corneal Reflex - what mediates the sensory? motor? blinking needs what nerve's function, which controls what? How is this test performed?

SENSORY = CN5. MOTOR = CN7. BLINKING NEEDS CN7 FXN for eyelid CLOSURE. Have patient LOOK STRAIGHT AHEAD & gently BRUSH the SCLERA with a COTTON tip. This will make the patient BLINK (immediately).

Patient presents with paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes. Pain is intense, sharp, superficial, or stabbing. Pain precipitated from trigger areas or by trigger factors. 1) What is your diagnosis? 2) How do you treat them?

Trigeminal Neuralgia. Trigeminal Neuralgia is more common in V2, V3 (V1 relatively rare). Attacks are stereotyped in the individual patient. There is no clinically evident neurological deficit. Not attributed to another disorder. Treatment: 1. Antiepileptics: Carbamazepine, oxacarbamazepine, phenytoin; gabapentin. 2. Muscle relaxants: baclofen. 3.Surgical: Rhizotomy, Microvascular decompression, Gamma knife.

Sensory/afferents (for mastication) from trigeminal peripheral structures converge on the ______. * A. Facial brainstem complex B. Lateral Faniculate Nucleus C. Trigeminal Brainstem Complex

Trigeminal Brainstem Complex.

Commissure (spinal cord anatomy)

located in center of gray matter (circle). = corpus collosum = connects right and left hemispheres of cerebrum, fxns to relay information btwn them.

Do you understand phototransduction by rods and cones? (must know) Explain the overall process. Is there action potential? What GCPR is involved? State of Na+ channels at rest vs when activated by light; and what influences opening/closing?

"Retina: Optical Path" 1. Light (stimulus) enters eye => GRADED SHIFT IN PHOTORECEPTORS. NO APs! Uses RHODOPSIN = GPCR, 7 transmembrane = opsin protein containing retinal molecule. 2. Rest: Na+ channels kept open by high levels of cGMP. 3. Light activates signal transduction leading to decreased cGMP and closing of Na+ channels. FACTS: - System allows signal amplification via G-proteins. - Can scale with background illumination. - Has a large dynamic range. - Is extremely fast. 1. photochemical reaction activates rods and cones (the PHOTORECEPTORS cells) at back of retina** => chemical reaction activates BIPOLAR CELLS. - horizontal neurons (lateral pathway) associated. 2. => GANGLION CELLS => info sent to visual cortex (BRAIN) via thalamus. - amacrine neurons (lateral pathway) associated. **The activation can be different based on shape, motion, and color, and these differences in activation r picked up by the visual cortex which turns them into what we actually see.

The Reticular Formation - receives, projects, integrates what type of information? FUNCTIONS OF: 1. Midbrain / Pons 2. Pons 3. Medulla A) Breathing and lung function, maintain consciousness. B) Control HR, BP, Lung function. C) Modulate activity of cortex

"anatomically indistinct cell groups in the Brainstem" RECEIVE: multi-functional sensory, motor, somatic and visceral, ascending and descending, local circuits and long projection input from widespread regions of the neuraxis. PROJECT: to widespread regions of the neuraxis. One neuron may synapse on more than 25,000 neurons throughout the brain. INTEGRATE: functions of many different neurons. 1. Midbrain/pons: Modulate activity of cortex. 2. Pons: Control of breathing and lung function. Maintenance of consciousness. 3. Medulla: control of heart rate, blood pressure, and lung function.

Clonidine, Guanethidine - mechanisms of these drugs at the synapse / on the NT? - Clonidine acts on which receptors to do what and is used in tx of what?

"indirect-acting sympatholytics (block stimulation of sympathetic NS, dec. NT in synapse)" - Clonidine does FEEDBACK INHIBITION OF NE release. - Guanethidine REDUCES RELEASE of ne. ALPHA 2 AGONIST in pre- and post-synaptic CNS (and other tissues) = reduces sympathetic outflow from CNS. - Uses for HTN, ADHD, help manage during withdrawal. "to produce vasodilation and is used in the treatment of hypertension; also as adjunct in opioid or alcohol withdrawal treatments".

Phenylephrine (Neosynephrine, Sudafed PE)

"specific adrenergic alpha-1 receptor agonist useful in clearing stuffy noses (because alpha-1 agonists constrict precapillary arterioles so capillaries stop leaking into the swollen weaping extravascular tissue of the nasopharyngeal mucosa) - the PE in Sudafed PE" . alpha-1 agonist = vasoconstriction. - stimulation of alpha-1 receptors located in peripheral vascular smooth muscles. - used as a topic ophthalmic MYDRIASIS) agent to facilitate fundoycopic exam of retina (since A1 receptor DILATES the pupils, by contracting radial muscles of iris). Used as nasal decongestant, the "PE" in "Sudafed PE" -know.

Ritalin, Adderall, .... Concerta, Metadate, Focalin, & Attenade - used to tx what? How do they differ?

"used to treat ADHD, they basically differ in duration of action, with Concerta, Metadate, Focalin, Attenade having extended durations compared to Ritalin and Adderall."

Degrees of Injury to spinal cord 1) whats the difference between complete transection versus partial transection of spinal cord? Where do paraplegic and tetraplegic fall under? What about the cord syndromes? 2) What is paresis? What is Plegia (dif. btwn quadraplegia, paraplegia, hemiplegia)?

(1) Complete transection = Absolute paralysis and loss of sensory and motor function at the level of injury and below, nothing downstream is functional = Paraplegic or tetraplegic. Incomplete (partial transection) = Mixed loss of voluntary motor activity and sensation = Anterior Cord Syndrome, Posterior Cord Syndrome, Central Cord Syndrome, & Brown - Sequard Syndrome (2) Paresis = some muscle strength is preserved. Plegia/paralysis = complete loss of muscle function: -QUADRIPLEGIA (tetraplegic) = Injury of the cervical spinal cord. Affects anything above C8. All 4 extremities affected. Patient can usu STILL MOVE (so consider this as a weakness) his arms using segments above the injury (e.g. in a C7 injury, patient can still flex his forearms using the C5 segment). - PARAPLEGIA = Injury of the thoracic, lumbar, or sacral segments = lower extremities affected. T1 and Below! -HEMIPLEGIA = Paralysis of one half of the body; Usually in brain injuries (e.g., stroke).

(1) How do you examine the light reflex? (2) How do examine the pupillary response to light? (3) How do you examine the visual fields? What is this testing? (4) How would you test any problem with the eye muscles supplied cranial nerves 3, 4, and 6? 1. Defect with abducens nerve (CN6) would show? 3. A patient with oculomotor nerve (CN3) DEFECT would show?

(1) LIGHT REFLEX = CN2 (afferent/sensory) & CN3 (efferent/motor) - SIT IN FRONT of patient and have them LOOK STRAIGHT AHEAD. BRIDGE PATIENT'S nose with your left hand. SHINE LIGHT INTO ONE EYE (i.e. right eye, picked up by optic nerve, go to midbrain where impulses picked up by CN3 of same and opposite side) -> note pupillary constriction of both that (right) eye: DIRECT LIGHT REFLEX BY CN3. ALSO NOTE PUPIL CONSTRICTION IN OPPOSITE EYE (i.e left): indirect or CONSENSUAL LIGHT REFLEX by OPPOSITE CN3. CN3 is the efferent/motor. (2) PUPILLARY RESPONSE TO LIGHT = CN2 & CN3 = patient looks straight ahead. LIGHT BEAM DIRECTED AT AND AWAY FROM EYE & RXN is noted: observe if pupils constrict and dilate appropriately. (3) VISUAL FIELDS = SIT IN FRONT of ur patient with your ARMS STRETCHED. Patient LOOKS STRAIGHT AHEAD & head is steady. Gradually BRING IN UR INDEX FINGERS on both sides, patient lets you know when they SEE UR FINGERS. Test the entire "CARDINAL DIRECTIONS OF GAZE." (4) EYES: EXTRA OCULAR MOVEMENTS. - SIT IN FRONT of patient. Ask patient to FOCUS ON UR FINGER W THEIR FAZE. Patient does NOT MOVE THEIR HEAD. The patient follows ur finger as YOU TRACE A BROAD LETTER "H", ur finger will COVER the "CARDINAL DIRECTIONS OF GAZE" = TESTS THE ABILITY OF THE EYES TO FOLLOW YOUR FINGER: Remember *SO4 (down & out), LR6 (out), rest 3* 1. eyes don't look out, gaze center - no conjugate lateral gaze (lateral rectus defect; LR6). 3. Eyes look DOWN & OUT (defect w extra ocular muscles except SO and LR) and FIXED DILATED PUPIL (defect w pupillary constriction and accommodation of lens from ANS). - since CN3 does PNS pupillary constriction. Corticobulbar (upper motor) system.

SPINAL CORD INJURY AND REGENERATION: (1) Role of Glia in spinal cord injury and regeneration: Fxns of Schwann cells, Astroglial Cells, Oligodendrocytes - which do: "glia scar formation" "inhibit axon growth" "support axon growth" (2) Would a de-myelinating disease limit spinal cord regeneration capacity?

(1) Schwann cells - support axon growth in peripheral. Astroglial cells- glia scar, inhibit axon growth Oligodendrocytes - inhibit axon growth. (2) Limitations to Spinal cord Regeneration = INFLAMMATION (lymphocytes and macrophages invade, microglia are activated) & DAMAGE OF NEURONS and OLIGODENDROCYTES (demyelination; wallerian degeneration; loss of neuronal circuitry).

Examination of Cranial Nerve 7 (Facial Nerve) (1) is really examining what muscles / is it motor or sensory? (2) You'd ask patient to do what? (2) A motor neuron facial palsy that affects the lower face only such that the left forhead is still intact, but left nasolabial fold is lost - would be an upper or lower motor neuron facial palsy? Is it due to a peripheral lesion or central lesion?

(1) examination of MOTOR to FACIAL MUSCLES & MOTOR TO ANTERIOR TONGUE MUSCLES. (2) ASK PATIENT TO: blow, whistle, look up & shut eyes tight. (3) Paralysis of face muscles. 1. LOWER MOTOR NEURON (LMN) FACIAL PALSY: affects UPPER & LOWER face {Loss of left forehead wrinkles + Loss of left nasolabial fold + Inability to shut left eye}; PERIPHERAL LESION/INJURY; Bell's palsy. 2. UPPER MOTOR NEURON (UMN) FACIAL PALSY: affects LOWER FACE ONLY {Left Forehead intact + Left Nasolabial fold lost} ; CENTRAL LESION.

CORTICOSPINAL TRACTS / PATHWAY of axons - need to know this: (1) Neuronal projections (MOTOR) exit Primary Motor cortex via the ___. (2) They descend through the midbrain in the _______. (3) In the medulla about 75% CROSS in the _______. (4) Crossed axons descend spinal cord in ______ tract. Uncrossed axons descend spinal cord in the ____ tract. (5) Final locations of the axons in Lateral Corticospinal tract and Anterior/Ventral Corticospinal tract?

(2) internal capsule. (2) cerebral peduncles (3) pyramidal decussation (4) crossed - dorsolateral column (lateral corticospinal tracts). Uncrossed - ventral corticospinal tracts. (5) - Lateral Corticospinal tract then ends on: alpha-motor neurons, or on interneurons that regulate the alphas. - Ventral/Anterior Corticospinal tract then ends on: (at various levels) interneurons in the medial ventral horn of the spinal cord.

Atenolol (Metoprolol)

* cardioselective direct beta-1 blocker (antagonist) used to treat hypertension (also angina, MIA) that is relatively free of CNS related side effects (Unlike Propranolol, Atenolol does not pass through the BBB so it avoids CNS side effects). - IMP: propranolol is the NON-specific beta blocker so acts on Beta-1 ALSO, plus acts on Beta-2 (blocking NE or epi) @ lungs for bronchoconstriction.

Ophthalmological Effects of Adrenergic Agonists - read this over before test A1, A2, B1, B2 - which one dilates the pupils? - use of Phenylephrine and Atropine? - which one increases production of aqueous humor in the eye?

- A1 receptor (activation) DILATES the pupils = MYDRIASIS (by contracting radial muscles of the iris). = Phenylephrine (A1 agonist) used mydriatic agent for examination of retina. - A1 receptors work against strong PNS muscarinic effects. Atropine (muscarinic agonist) dilates pupils bc it leaves the a1 receptors unopposed. - B2 activation increases production of aqueous humor in the eye. Blocking B2 receptors {timolol (non-selective beta-blocker) eye drops} is way of tx open-angle glaucoma (w.o the impaired accommodation caused by cholinergic drugs e.g. pilocarpine).

Dental Use of Epinephrine (Adrenaline) problematic when patient has conditions involving altered sympathetic activity.

- Disease states with inc. sympathetic activity (e.g. uncontrolled HTN, hyperthyroidism; pheochromocytoma; cocaine or ephedrine abuse; TCA antidepressants; Asthma). - Disease states requiring drug-induced decreased sympathetic activity: patients taking alpha or beta-blockers to reduce BP.

Which divisions of trigeminal nerve are sensory, which are motor? What other signals does it end?

- Sensory = 1st, 2nd, 3rd divisions. - Motor = 3rd division -> muscles of mastication. - General proprioceptive

Cluster headaches - classic patient?

- Uncommon - M > F (4-5 to 1) - classic pt: male, 40's, heavy drinker/smoker. - Features: Unilateral, excurciating pounding/penetrating pain (Peri-orbital, temporal, scalp, maxilla). Ptosis, lacrimination. Come in clusters with periods of remission.

1) Which of the following is an Irreversible alpha blocker used in the treatment of pheochromocytoma? 2) Which is a Reversible alpha blocked used in diagnosis of pheochromocytoma? A. Phentolamine B. Phenoxybenzamine C. Prazosin D. Tyramine

1) B. Phenoxybenzamine = "irreversible non-selective alpha blocker vasodilator used in the TREATMENT of pheochromocytoma" = Noncompetitive, irreversible. used for pheochromocytoma-induced HTN TREATMENT. Lasts longer than phenol mine. 2) A. Phentolamine is REVERSIBLE non-selective alpha blocked used in diagnosis of pheochromocytoma (AKA pheochromocytoma-induced Hypertension Diagnosis).

DESCENDING MOTOR PATHWAYS can be divided into: 1) Lateral Pathways: LATERAL CORTICOSPINAL TRACT, and Rubrospinal Tract 2) Medial Pathways: VENTRAL/ANTERIOR CORTICOSPINAL TRACT, Tectospinal Tract, Reticulospinal Tract, and Vestibulospinal Tracts know: - what are the functions of Lateral Corticospinal Tract & Ventral (Anterior) Corticospinal Tract?

1) LATERAL CORTICOSPINAL TRACT, and Rubrospinal Tract - Distal limb movement; regulate fine, skilled voluntary movements 2) VENTRAL/ANTERIOR CORTICOSPINAL TRACT, Tectospinal Tract, Reticulospinal Tract, and Vestibulospinal Tracts - Axial and proximal limb movements, regulate balance and posture;

Dorsal Spinocerebellar/Cuneocerebellar (DSC) Must know: 1) Function of pathway 2) Locations of tracts in spinal cord & brainstem (of first, second, third order neurons)? 3) At which levels is pathway present? 4) If crosses midline where do fibers decussate?

1) conveys MUSCLE SENSORY INFORMATION, which is used by cerebellum to COORDINATE MOVEMENT AND POSTURE. It collects information about individual muscles. - from syl: Info doesn't reach consciousness. Information from caudal part of body, from spinal levels C8 and below, including lower limbs and distal muscles in upper limbs. FIRST ORDER SENSORY NEURON: located in DRG, afferent fibers enter spinal cord and stay in SAME SIDE in lateral part of lateral funiculus. SECOND ORDER SENSORY NEURON: afferent fibers project to the IPSILATERAL =< C8: Clearke's Nucleus (Nucleus Dorsalis) in Lamina VII. > C8: external Cuneatus, in the medulla, this tract is called Cuneocerebellar Output (fibers from 2nd order sensory neurons project to the cerebellum). DECUSSATION: fibers do not cross the midline and always stay in the same side. FINAL DESTINATION: Cerebellum.

know - in class question: 1. Alpha-1 Receptor 2. Alpha-2 Receptor 3. Beta-1 Receptor 4. Beta-2 Receptor A) Tissue where receptor is primarily found B) Specific direct acting agonist at this receptor C) Specific direct acting antagonist at this receptor D) Clinical use for an agonist at this receptor E) Clinical use for an antagonist at this receptor

1. a) Peripheral Vascular Smooth Muscle. b) Phenylephrine c) Prazosin d) clear stuffy nose (nasal decongestion). e) relief of urinary retention in BPH. 2. a) pre + post synaptic CNS b) Clonidine (can be direct and indirect). c) Yohimbine (not in lecture - online) d) adjunct in opioid or alcohol withdrawal treatment e) autonomic insufficiency 3. a) cardiac muscle b) dobutamine c) atenolol d) heart failure e) treat hypertension 4. A) bronchiolar tissue b) Albuterol c) none d) exercise induced asthma e) no use

What is involved in the "retinotopic organization" of visual input of the optic projection through to the cortex? (must know) 1. Central visual pathway creating our perception of the visual world? 2. What pathway/circuit allows the pupil to change its DIAMETER in response to light (pupillary light reflex)? 3. What pathway allows for synchronization of your biological clock? Synapses, nuclei, etc?

1. Axons leave retina via optic disc -> form optic nerve that goes to Optic Chiasm where 60% cross to contralateral {axons from Nasal Retina} & 40% remain ipsilateral {axons from Temporal retina} -> visual info flows to "Lateral Geniculate Nucleus" of THALAMUS {relay station on way to visual cortex} - RETINOL GANGLION CELLS (RGC) SYNAPSE on cell bodies in RGN of THALAMUS => RGN neurons project to Primary Visual Cortex, which converts signals into our perception of visual world. 2. RGCs Synapse on interneurons in EDINGER-WESTPHAL nucleus, in midbrain => neurons leave EWN and Synapse on motor neurons in CILLIARY GANGLION 3. RGCs synapse on GABAnergic cells in SUPERIOR-CHIASMATIC NUCLEUS (SCN) of Hypothalamus -> SCN is biological clock, day/night and sleep/wake cycles. [Individual with optic nerve disease are 20X more likely to have disruptions in their sleep cycle compared to normally sighted people.]

Neurological Examination of - Motor Status - Lower motor neuron injuries vs. Upper Motor Neuron injuries - which show atrophy? hypotonia? Fasciculations? Spasticity? - Babinksi sign? - Hoffman sign?

1. Bulk and tone - Hypotonia, fasciculations, atrophy = LMN - Spasticity, lack of atrophy = UMN = Arm flexion, leg extension. 2. Strength, Graded on scale 0-5 3. Reflexes, Graded on scale 0 (areflexic) to 4+ (clonus) 4. Babinski/Hoffman - babinksi is UMN injury; hoffman can be in normal person but is of worry, just means person is hyper-reflexive.

Neurological Examination of - Sensory . - How would you examine Dorsal Column Pathways? Spinothalamic pathways? (where do each "cross")

1. Dorsal Column pathways = Crosses at medulla; Light Touch; Proprioception/Vibration 2. Spinothalamic pathways = Crosses in spinal cord; Pain (pin prick); Temperature.

Important Brainstem Reflexes - which nerves responsible for which? 1. Pupillary reflexes 2. Oculocephalic reflex / "Doll's eyes" 3. Vestibulo-ocular reflex - Eyes deviate towards injected side - Nystagmus to opposite side 4. Corneal Reflex 5. Gag Reflex

1. II 2. III, VI, VIII 3. III, VI, VIII 4. V, VII 5. IX, X

Neurological Examination of - Coordination - is primarilly to assess function of what brain part? - what is Dysmetria?

1. Primarily assesses cerebellar function 2. Finger-to-nose/Heel-to-Shin - Dysmetria (lack of coordination; can't scale properly) - Intention tremor 3. Rapid Alternating Movements 4. Mirror movements

Neurological Examination of - Gait What does romberg testing assess (pathway)? What two functions (of gait) should you test?

1. Station/Balance - Getting up from a chair - Pull testing - Romberg testing: primarily assesses dorsal column pathways, NOT cerebellar function! 2. Propulsion (thrust) - Stride length, arm-swing - Speed - Turning - Heel/Toe/Tandem gait

What medications should you consider if patient has AT LEAST 2 DAYS OF HEADACHE EVERY MONTH?

1. Tricyclic antidepressants = amitriptyline, nortriptyline. 2. Beta blockers (non-selective) = propranolol. 3. Calcium channel blockers = verapamil. 4. Antiepileptics = Topiramate, valproic acid. 5. Botulinum Toxin aka Botox.

WHITE MATTER TRACT: 1. do most paths cross? 2. Most consist of a chain of how many neurons? (know min. number neurons in chain). 3. Most exhibit what type of organization in their space? 4. Are all pathways paired?

1. Yes, most pathways decussate (cross form X). 2. two or three neurons. 3. somatotopy = precise spacial relationships. 4. YES, all pathways are paired - one on each side of the spinal cord.

Match definitions to the FIVE BASIC FUNCTIONAL GROUPS of Myelinated Axons: 1. Efferent (motor) fibers 2. Afferent (sensory) fibers 3. Propriospinal fibers 4. Long Ascending Fibers 5. Long Descending Fibers a. motor fibers "top-down" from cortex, brainstem & destined to reach peripheral muscles b. commissural (transverse) fibers that cross to opposite side of the spinal cord. c. Incoming projections from dorsal root ganglion (DRG) to reach dorsal horn. d. sensory "bottom-up" projections from DRG destined to reach cortex, thalamus, and brainstem e. exit-ing projections from motor or autonomic neurons from ventral horn.

1. exit-ing projections from motor or autonomic neurons from ventral horn. 2. Incoming projections from dorsal root ganglion (DRG) to reach dorsal horn. 3. commissural (transverse) fibers that cross to opposite side of the spinal cord. 4. sensory "bottom-up" projections from DRG destined to reach cortex, thalamus, and brainstem = majority 1/2 u see in spinal cord. 5. motor fibers "top-down" from cortex, brainstem & destined to reach peripheral muscles = majority 2/2 "".

1. "Jaw jerk" reflex is: 2. Jaw opening is:

1. low threshold (masseter stretch reflex), monosynaptic (brainstem loop), and via mesencephalic nucleus. (recall jerk means closing) - note: its analogous to knee-jerk. 2. DIsynaptic (loop excites jaw openers; and crossed disynaptic loop inhibits jaw closers) and via nociceptive trigeminal subnucleus caudalis (caudal region). - noxious response reflex; "pain-evoked jaw opening e.g. dental pulp stimulation"

Trigeminal Nerve: 1. Pain and Temperature 2. Touch/Pressure/Vibration 3. Proprioception/Motor Tone Which neurons are for which: A-alpha, A-beta, A-delta and C fibers

1. pain and temperature = A-delta and C fibers -> spinal nucleus and tract of V -> spinothalamic tract. 2. Touch/Pressure/Vibration = A-beta -> trigeminal ganglion, main sensory nucleus -> medial lemniscus -> dif area of somatosensory cortex. 3. Proprioception = A-alpha, mesencephalic nucleus, motor nucleus of V,.

1. Nociceptive input for mastication is processed via the _______. 2. Non-noxious mechanical stimuli is processed via the _____ . *

1. subnucleus caudalis region (caudal region of brainstem complex). 2. Main Sensory Nucleus (higher up in the pons)

Sympatholytic drugs - must know 2 mechs of how indirect lytics work and specific examples of drugs for each

= Drugs that reduce or block stimulation of the sympathetic nervous system. 1. DIRECT sympatholytics = directly blocking adrenergic receptors = propranolol, prazosin. 2. INDIRECT "" = decrease amount of sympathetic NT in the synapse either by: (i) FEEDBACK INHIBITION OF NE RELEASE = CLONIDINE, used for hypertension. (ii) Reducing release of NE from postganglionic nerve terminals = Guanethidine, used for hypertension but not used commonly anymore.

Indirect-acting sympathomimetics - 3 examples and their mechanisms?

= mimic stimulation of SYMPATHETIC nervous system; indirect bc act by INCREASING amount of sympathetic NT in snapse by: - inc. releae of NT from post-ganglionic nerve terminals = Amphetamines. - DECREASING the RE-UPTAKE = TCAs (tricyclic antidepressants), Cocaine - DECREASING the METABOLISM of the NTs = MAOIs List of Indirect-acting sympathomimetics: Amphetamine, MAOI Antidepressants, Cocaine, & Tricyclic Antidepressants .

6. What is the correct order of structures for which axons of the "lateral corticospinal tract" travel through (i.e. start to finish)? Also, where does this tract (if it does) cross over? a. Primary motor cortex, internal capsule, cerebral peduncles, medullary pyramids, alpha motor neurons. b. Primary sensory cortex, medullary pyramids, cerebral peduncles, internal capsule, alpha motor neurons. c. Primary motor cortex, cerebral peduncles, internal capsule, medullary pyramids, alpha motor neurons. d. Primary motor cortex, internal capsule, medullary pyramids, cerebellum, alpha motor neurons.

A is answer. You need to know this tract! It is a major descending tract of motor output. I did not mention decussation in this question, but this tract DOES CROSS-OVER in the MEDULLARY PYRAMIDS (anterior/ventral corticospinal tract does not cross-over). In general I want you to know where the fibers of the lateral corticospinal tract are located on its way down to lower motor neuron in the spinal cords.

Second order neuron can either synapse or not synapse, whats the difference in destination?

A) Synapse on nucleus in dorsal horn and crosses midline => Ascends spinal cord in lateral funiculus. B) Dont synapse & don't cross midline => ascends in posterior funiculus. The second order neuron is located rostral in the spinal cord. - recall: ascending tracts formed by second order neurons except ascending tracts in posterior funiculus.

9. The retina is comprised of photoreceptor cells named rods and cones. Which of the following is NOT a characteristic of rods? a. Concentrated at the fovea b. Have low temporal resolution c. Responsible for low acuity vision d. Achromatic (has no photopigments

A. Cones are concentrated at the fovea rather than rods because cones are important for high acuity vision. Know the distinction between rods and cones.

Which of the following is TRUE about Amyotropic lateral sclerosis (ALS)? Go through all answers and say why the others aren't true! A. It is an inherited lesion. B. Only upper motor neurons degenerate. C. Muscle weakness and muscle atrophy both result from the damage. D. There is a loss of sensory function, as well as bladder and bowel function. E. Patients symptoms get better when there is a failure in innervation of the major respiratory muscles.

A. ACQUIRED lesion. Progressive neurodegenerative disease. B. Both upper and lower motor neurons degenerate (CORTICOSPINAL and CORTICOBULBAR tracts). C (TRUE). Results in muscle WEAKNESS (UMN-L) and ATROPHY (LMN-L). - UPPER MOTOR NEURON SYMPTOMS: Spasticity and hyperreflexia, difficulty speaking, inappropriate motor expression of emotions. - LOWER MOTOR NEURON SYMPTOMS: atrophy, fasciculation, difficulty chewing, swallowing, moving face and tongue D. Disease is limited to the somatic motor system - No loss of sensory function or bowel or bladder function. E. Patients die when innervation of the major respiratory muscles fails.

Statement 1: A patient with a lesion of the right optic nerve posterior to the optic chiasm will lose sight of their left visual field on both eyes. Statement 2: A lesion of CN V affects the motor control of muscles of facial expression and may be seen clinically by jaw deviation to the same side of the lesion. A. Statement 1 is true, statement 2 is false B. Statement 2 is true, statement 1 is false C. Both statements are true D. Both statements are false

A. Statement 1 is true. Statement 2 is false: CN5 controls muscles of mastication, NOT facial expression. KNOW: Optic N (CN2) function: visual fields, acuity (SSA), light reflex. 1. ANT. TO OPTIC CHIASM = Monocular visual defects = Primary ocular disease (retinal disease, glaucoma). 2. POSTERIOR to Optic Chiasm = Binocular Visual Defects (Homonymous Hemianopsia - absence of vision in one side of visual field in both eyes). 3. OPTIC CHIASM = Binocular Visual Defects (Bitemporal Hemianopsia). 4. OCCIPITAL CORTEX = Binocular visual defects (homonymous hemianopsia with macular sparing).

Blood Vessel Tone - alpha vs. beta receptors: which CONSTRICT BVs and inc BP? A1 receptors ______ BVS. B2 receptors ______ BVs. A1 agonists are used as ________.

A1 receptors CONSTRICT BVs (thus restrict blood flow, inc. BP). B2 receptors DILATE BVS (thus inc. blood flow in those vascular beds). - All blood vessels have a1 receptors, but some vascular beds (skeletal muscle BVs) also have B2 receptors. - A1 agonists (phenylephrine, etc.) are used as nasal decongestants, bc they constrict pre-capillary arterioles -> capillaries stop leaking into the swollen wearing extravascular tissue of nasopharyngeal mucosa.

An upper motor defect affecting both sides of body (all) will be a lesion where? Versus if it just affects half your body, will be where? - Why do we get either contralateral or ipsilateral affects?

ABOVE the pyramidal decussation (e.g. in head area; where the fibers cross) = All = CONTRALATERAL deficit in pathways that have crossed and ipsilateral deficit in pathways that haven't crossed. BELOW it (e.g. below shoulder)= Partial = IPSILATERAL deficit in pathways from the contralateral side that have crossed, and an ipsilateral deficit in pathways from the same side that haven't crossed. - Upper motor neuron axons cross the midline at the pyramids in the medulla.

Which cranial nerve is located in the pons?

Abducens (VI)

Migraine (Status Migrainosis). - women vs. men? - bilateral or unilateral? - how long does it last if left untreated?

About 18% of women > 6% of men (probably higher) Family history common. Migraine without aura ("Common"). Migraine with aura ("Classic"). Hemiplegic Migraine ("Complicated"). Headache features: UNILATERAL location, PULSATING quality, Moderate to severe pain "8/10", Avoidance of routine physical activity, Duration: 4-72 hours if untreated Associated features: Nausea/vomiting, Photophobia/phonophobia, Triggers (Foods: preservatives, MSG, chocolate, cheese, alcohol; Poor sleep; & Other environmental (smells, lights). Childhood migraine variants: - Cyclic vomiting - Abdominal pain, "colic"

May cause tremors in elderly patients A. Propranolol B. Pseudophedrine C. Clonidne D. Albuterol

Albuterol = "Selective beta-2 agonist used in aerosol inhalers as a bronchodilator in the treatment of exercise-induced asthma. May cause tremors in elderly patients."

Mastication - read this over before the exam

An intermittent, rhythmic process to mechanically break down solid food by way of the actions of the teeth and oral structures into smaller fragments that are mixed with saliva to form a cohesive bolus that can be easily swallowed. Greatly increases the surface area of the food for more efficient breakdown by digestive enzymes. Not a prerequisite of ingestion, because liquids DO NOT REQUIRE this pre-swallow step. -------------------------- ------------------------ Transport - food ingested as a bite-sized portion and positioned on the occlusal surfaces between the teeth for further breakdown, if necessary. Processing - trituration of the food. Oropharyngeal accumulation time - adequately prepared food, ready for bolus formation, is moved distally through the fauces to the oropharynx. Hypopharyngeal transit time - the bolus is swallowed.

Man who talked about Mastication

Andrew Combes Mastication: "The first important step in the complicated process of digestion, is that by which the food, after being received into the mouth, is mixed with the saliva, and broken down till it becomes of a uniform pulpy consistence, fit for being easily swallowed and acted upon by the gastric juice on its arrival in the stomach. The term mastication, or chewing, is used to denote this operation..."--Andrew Combes, 1837 "Man, being naturally omnivorous, or adapted for the digestion of both animal and vegetable substances, holds, as it were, an intermediate place in regard to the rapidity of mastication. He neither is obliged to ruminate like the cow, nor can beneficially bolt his food with the rapidity displayed by beasts of prey."

After a major car accident a 60-yr old woman suffered severe neck injury that led to the following results upon physical examination: bilateral lower motor neuron signs, bilateral loss of pain and temperature sensation, and normal function of discriminatory touch. What is the likely diagnosis? (two answers) A. Quadraplegia B. Anterior cord syndrome C. Brown-Sequard Syndrome D. Central cord syndrome

Answer is B or D -> Normal fine touch in either Anterior (B) or Central cord syndrome (D). CLASS NOTES: - discriminatory touch is our fine touch -> dorsal columns pathway (came in thru gray cilus and cuneatus). Means posterior columns r unharmed. - Bilateral loss of pain and temp (sensation) & Bilateral motor damage -> not a complete lesion (A is eliminated).

Sympathomimetic beta-1 agonist for HYPOTENSION, SHOCK - "specifically approved for use in heart failure patients"? A. Carvedilol B. Dobutamine

Answer is B. Dobutamine = Beta-1 AGONIST/stimulation, receptors found in cardiac muscle => inc. cardiac output, force of contraction => for hypotension and shock. NOT: Carvedilol for CONGESTIVE HEART FAILURE = alpha1 and nonselective beta1/beta2 antagonist => vasodilation via alpha1 block plus RED. CARDIAC OUTPUT via beta block. - "vasodilating beta-blocker".

Amphetamines alter the functioning of adrenergic neurons by? A. Decreasing enzymatic breakdown of NE. B. Decreasing presynaptic reuptake of NE. C. blocking postsynaptic receptor stimulation by NE. D. Blocking the release of NE. E. Increasing the release of NE.

Answer is E. know this sample exam question and reasons why others are wrong / what they would be right for. A would be MAOI. B would be tri-cyclic antidepressant (TCA) or cocaine. D would be clonidine.

Patient is taking Epinephrine alongside Propranolol (Beta Blockers), what would happen? WHY? A. Postural Hypotension B. Cardiac Failure C. Potential Hypertensive Crisis D. Increased Blood Pressure E. Reflex Bradycardia

Answers are C, D, E. DON'T RX Epinephrine if patient is taking Propranolol/Beta Blockers. POTENTIAL HYPERTENSIVE CRISIS = DUE TO *UNOPPOSED* Epi stimulating ALPHA-1 VASOCONSTRICTION => INC. BP, reflex bradycardia {red, see pic}. Recall Epi is alpha-1 agonist at high concentrations. *unopposed* Because Propranolol is non-specific B antagonist: Blocking B2 causes bronco constriction, Blocking B1 causes inc. HR/CO! AKA - EPI stimulates vasoconstriction; and PROPRANOLOL blocks vasodilation.

Ascending tracts are ____, Descending tracts are ____.

Ascending = sensory Descending = Motor

Postural Hypotension is a side-effect of blocking? A. Alpha-2 receptors with Phentolamine. B. Alpha-1 receptors with Prazosin C. Beta-2 receptors with Propranolol D. Beta-1 receptors with Atenolol

B and A are both answers. Adverse side effect of alpha -adrenergic receptor antagonists (Phentolamine, Phenoxybenzamine; & PRAZOSIN}. 1. POSTURAL HYPOTENSION is side-effect of blocking spcfcly ALPHA-1 receptors e.g. w. PRAZOSIN {selective alpha-1 blocker}. - aka when u stand up too quick and feel faint. 2. Others include: nasal congestion & Vertigo. Recall: Phentolamine & Phenoxybenzamine are non-selective alpha blockers.

Which of the following could be the result of a complete lesion at the level of T8? A. Loss of all sensory information in both lower limbs. B. Loss of all sensory and motor function in both lower limbs C. Loss of all sensory information and weakness in lower limb muscles. D. Loss of all sensory and motor information in one half of the body below T8

B is answer. complete lesion so assume everything is gone: - i.e. sensory AND motor information -> eliminate A. - Its gonna be ALL the body below T8 -> D is out. B or C? - weakness implies still some function, so answer is B. This is definition of parapalegia (anything that is below T1). Notes: quadriplegia (paralysis of all four limbs; tetraplegia) VS paraplegia (paralysis of the legs and lower body, typically caused by spinal injury or disease.)

Hemifacial spasm has which of the following types of movement disorders? I: Chorea II: Dystonia III: Tremor IV: Myoclous A. I and II B. II and IV C. III and IV D. IV only

B is answer. KNOW: Hemifacial Spasm = 1. Myoclonus/ dystonia of facial muscles (orbiculares oculi & lower face). 2. Idiopathic or structural/compressive lesion involving facial nerve: - Vascular, Mass, or Demyelinating lesion (MS). 3. Responds to botulinum toxin injections.

Used for reversal of local anesthesia (ORAVERSE)? A. Prazosin B. Phentolamine C. Phenoxybenzamine D. Epinephrine E. Clonidine

B is answer. its a competitive non-selective alpha adrenergic receptor antagonist/blocker. - Phentolamine = "non-selective reversible alpha-1 and alpha-2 blocker sympatholytic agent used to diagnosis frostbite, useful in the diagnosis of pheochromocytoma. Non-specific direct acting alpha blocker causes vasodilation" = competitive; used for REVERSAL OF dental LOCAL ANESTHESIA (is active ingredient in ORAVERSE), pheochromocytoma-induced HTN DIAGNOSIS, and frost bite. Wares of quicker then other.

Which of the following actions is the major mechanism of neurotransmitter inactivation in sympathetic neurons? A. Feedback inhibition B. Re-uptake into presynaptic terminals. C. Breakdown by COMT in the synaptic cleft. D. Release from storage vesicles. E. Breakdown by MAO.

B is the answer. know this sample exam question. - excess adrenergic (EPI, NE) termination mechanism is by both: re-uptake & enzymatic degradation (MAO breaks it down) in the synaptic cleft.

10. The lateral geniculate nucleus projects fibers to synapse in the _______________? a. Primary sensory cortex b. Primary visual cortex c. Primary auditory

B. Know the central visual pathway! Lateral geniculate nucleus is where the majority of visual input from the optic tract will synapse. These nuclei then send their fibers to reach the occipital lobe/primary visual cortex.

Which of the following is an antihypertensive agent that blocks both alpha1 and both beta1 and beta2 receptors to produce vasodilation. It is called a "vasodilating" beta blocker, used with heart failure patients? A. Dobutamine B. Carvedilol C. Methyldopa D. Atomexetine

B. Carvedilol = CONGESTIVE HEART FAILURE. - alpha1 and nonselective beta1/beta2 antagonist => vasodilation via alpha1 block plus reduced cardiac output via beta block. - "vasodilating beta-blocker" DOBUTAMINE AGONIST ONLY B1.

Drug that masks signs of hypoglycemia so avoid it in diabetic patients? A. Phentolamine B. Propranolol C. Albuterol E. Amphetamine

B. Propranolol = "non-selective sympatholytic beta-blocker used to treat hypertension, migraine, angina (chronically), myocardial infarction, speakers anxiety, glaucoma, hyperthyroidism; masks signs of hypoglycemia so should avoid in diabetics, also masks signs of asthmatics. MEMORIZE: PROPANE MASK.

Review of spinal cord gross anatomy - what is the main function of the spinal cord (duh), and therefore what three components must it contain?

Begins at base of medulla and ends at CONUS MEDULLARIS {btwn L1/L2}. Approx. 2cm diameter, 45cm long, and encased within vertebral canal. Although spinal cord is well protected, it can become Irreversibly damaged causing devastating consequences for patients with spinal cord injuries. Main Function = conduit for communication btwn brain and periphery & vice versa. THUS, spinal cord must contain the THREE FOLLOWING ELEMENTS: 1. Pathways = both Ascending sensory "bottom-up" & Descending motor "top-down" tracts. 2. Neurons (and Glia) - motor, sensory, interneurons, autonomic; needed for processing signals in the pathway. 3. Reflex Circuitry - Pre-processing of sensory signals & motor control (aka the motor responses to sensory stimuli). DIVISIONS: -31 spinal cord segments (and pairs of spinal nerves) = 8 cervical + 12 thoracic + 5 lumbar + 5 sacral + 1 coccygeal. - Each segment has dorsal and ventral roots that mix and become spinal nerve: DORSAL ROOT arises from DRG and breaks into rootlets that enter spinal cord, they are sensory (muscle and skin, distant assoc). VENTRAL ROOT arises from motor neurons in ventral horn and autonomic pre-ganglionic neurons on lateral horn of gray matter. - 30 vertebral bodies: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral & 1 coccygeal. - Two enlargements (more of spinal cord and more neural input and output here bc plexuses): Cervical Enlargement (C5-T1) & Lumbar Enlargement (L2-S3). - Cauda Equina = Origin of spinal nerves extending inferiorly from conus medullaris. - Spinal Cord is protected within the vertebral column = area of injury. - Blood supply to spinal cord = posterior spinal arteries & anterior spinal arteries = another area of ischemic injury.

Statement 1: Outer segments of retina are fully replaced every day. Statement 2: Retina Pigment Epithelium absorbs scattered light which: reduces the quality of visual system, and diminishes photo-oxidative stress. True/False?

Both False! Outer segments of retina are fully replaced every 12 days. Old membrane is shed and degraded by the pigment epithelium. - Regina Pigment epithelium absorbs scattered light which: 1.) Improves quality of visual system and 2.) Diminishes photo-oxidative stress.

Albuterol

Bronchodilator for asthma. specific Beta-2 agonist, receptors in bronchioles and skeletal muscle vascular beds => bronchodilation, vasodilation. - note: does opposite of beta-2 antagonists, which have no clinically useful action.

Which of the following ascending sensory pathways (tracts) contains secondary neurons that cross at the level of the medulla? A) lateral spinothalamic B) anterior spinothalamic C) dorsal-column/medial-lemniscal system D) posterior spinocerebellar

C - The dorsal-column/medial-lemniscal system contains secondary neurons that cross at the level of the medulla.

A 47 year-old Caucasian male comes to the dental clinic for his first visit. After taking a thorough medical history, you find that your patient has a history of pounding headaches and is currently taking triptans and gets periodic Botox injections. Which of the following conditions does your patient most likely suffer from? A. Trigeminal neuralgia B. Hemiplegic migraine C. Cluster headaches D. Tardive dyskinesia

C is answer. - TRIPTAN used to "Abort" a Headache & do NOT USE for Hemiplegic Migraine {migraine plus weakness on one side of body}.

3. The neospinothalamic tract is important in the relay of pain and temperature transmission from the body to the brain. Which of the following locations would not be a point of synapse for the "neospinothalamic tract"? a. Nuclei in the dorsal horn of the spinal cord b. Ventral nucleus of the thalamus c. Cuneate nucleus d. Primary somatosensory cortex

C is answer. Cuneate nucleus is specific site of synapse for the dorsal columns pathway. A, B,& D are all locations the neospinothalamic tract will synapse.

Which of the following is a Beta-adrenergic AGONIST that affects both beta-1 and beta-2 receptors? A. Atenolol B. Dobutamine C. Isoproterenol D. Propranolol E. Albuterol

C is answer. Isoproterenol = beta-1/beta-2 Non-Specific AGONIST = VASODILATION (beta-1 stimulation; inc CO) & BRONCHODILATION (Beta-2 stimulation). - Atenolol blocks Beta-1 (for HTN without CNS and bronchoconstriction). - Dobutamine agonist Beta-1 (hypotension, shock, heart failure). - Propranolol affects both but is an ANTAGONIST (for HTN, bronchoconstricts and CNS side effects). - Albuterol is B2 agonist.

Which of the following is an example of a "selective alpha-1 receptor blocker useful in the treatment of hypertension due to its vasodilatory actions"? A. Propranolol B. Atenolol C. Prazosin D. Clonidine

C is answer. Prazosin (minipress) / Terazosin - vasodilation (BP down, reduced peripheral resistance). - also does relief of urinary retention in BPH.

Trigeminal Nerve's Sensory nuclei are located where? The motor nuclei are located where? Answers are: "Sensory location", "Motor location" A. Dorsal Root Ganglion, Venral Horn. B. Trigeminal Sensory Nucleus, Motor Nucleus of LMN. C. Trigeminal Brainstem Nucleus, Trigeminal Motor Nucleus. D. Trigeminal Sensory Nucleus, Trigeminal Brainstem Nucleus. Nuclei (sensory vs motor)

C. 1. Somatosensory - trigeminal brainstem nucleus (spinal tract of V). 2. Motor - trigeminal motor nucleus.

Which of these spinal pathways carries information from the right side of the body to the right side of the brain? A) anterior spinothalamic system B) lateral spinothalamic system C) spinocerebellar system (dorsospinocerebellar/ cuneocerebellar) D) anterior corticospinal system E) medial lemniscal system

C. Doesn't decussate or cross midline.

Patient presents with partial blindness where vision is missing in the outer half of BOTH right and left visual fields. Where was the lesion of the optic nerve? A. Anterior to Optic Chiasm B. Posterior to Optic Chiasm C. Optic Chiasm D. Occipital Cortex

C. OPTIC CHIASM = Binocular Visual Defects (Bitemporal Hemianopsia). - immediately eliminate A because that would be monocular. KNOW: Optic N (CN2) function: visual fields, acuity (SSA), light reflex. 1. ANT. TO OPTIC CHIASM = Monocular visual defects = Primary ocular disease (retinal disease, glaucoma). 2. POSTERIOR to Optic Chiasm = Binocular Visual Defects (Homonymous Hemianopsia - absence of vision in one side of visual field in both eyes). 3. OPTIC CHIASM = Binocular Visual Defects (Bitemporal Hemianopsia). 4. OCCIPITAL CORTEX = Binocular visual defects (homonymous hemianopsia with macular sparing).

Which of the following is an example of an antihypertensive that may cause EPI-REVERSAL ? A. Propranolol B. Atenolol C. Prazosin D. Clonidine

C. Prazosin (minipress) / Terazosin. = A1 blocker causing inhibition of epinephrine's vasoconstriction effects. So, B2 vasodilation predominates -> results in dec. BP.

Sensory/Afferent nerve for vision? What happens with lesion to this nerve?

CN2, optic nerve. - responsible for direct & consensual pupillary light reflex. Optic N lesion = loss of Direct & Consensual responses. - google: Consensual response is any reflex observed on one side of the body when the other side has been stimulated.

Efferent/Motor for most* extraocular eye movements is via what nerve? What are the *exceptions?

CN3, oculomotor nerve. Exceptions: 1. Lateral Rectus by CN6 (Abducens) moves eye lateral/outward. 2. Superior Oblique by CN4 (Trochlear) moves eye down and in.

What is the role of Cerebellum, Basal Ganglia, Cerebral Cortex in VOLUNTARY RESPONSES (mastication)?

Cerebellum - receives all sensory input from joints/muscles, cordinates and relays instructions to produce precise movements = part of "brainstem centers" which r responsible for basic movements and postural control. Basal ganglia - plan and INITIATE complex MOVEMENTS, receive data from cerebellum and relay info to cerebral cortex = part of "motor cortex" which responsible for planning, initiating, and directing voluntary movements. Cerebral cortex - receives sensory data from cerebellum, compares it with "instructional" data from basal ganglia, an modifies output accordingly. - Note: recall involuntary responses are ANS.

Which injury would be worse: one in cervical or sacral section of Spinal Cord? (think about gray and white matter)

Cervical would have more consequences because more white matter in cervical. ***Going from sacral to cervical, we have more white matter being added onto the spinal cord => white matter to gray matter ratio increases from caudal to rostral. ** Reverse organization gray and white matter in spinal cord vs. cerebral cortex. Gray = darker, lots cell bodies so lots of activity, lot more blood supply going to neurons to supply that activity = inside the white matter. From cervical to sacral region, the gray matter shape is changing (white matter shaping a little bit).

What types of lesions (bilateral or unilateral lesion) will produce WEAKNESS? Which cause paralysis?

Characteristics of brainstem/cranial nerve lesions = motor nuclei. - Lesions above the nucleus produce upper motor neuron symptoms. - Innervation of cranial nerves is bilateral (with the exception of the lower facial muscles, which is contralateral only). - Consequently UNILATERAL LESIONS produce only WEAKNESS and not paralysis. Only bilateral lesions cause paralysis.

Statement 1: Receptive or Wernicke's aphasia results from damage in the temporal lobe and is the most common type of aphasia. Statement 2: Individuals with Broca's aphasia have difficulty in repeating phrases but improve with successive attempts. A. Statement 1 is true, statement 2 is false B. Statement 2 is true, statement 1 is false C. Both statements are true D. Both statements are false

Check answers later. Susan is saying answer is D. I think its C. Neurological Examination of - Mental Status: 1. Level of CONSCIOUSNESS/alertness 2. ATTENTION - Serial sevens, digit span, "world" backwards 3. MEMORY - Recent vs. remote memory; Anterograde vs. retrograde amnesia 4. LANGUAGE - Fluency, comprehension, naming, repetition, reading. - APHASIA (loss of ability to understand or express speech, caused by brain damage.) = Receptive ("WERNICKE'S Aphasia") of TEMPORAL lobe; Expressive ("BROCA'S APhasia") of FRONTAL lobe; Global; &Conduction. 5. CALCULATIONS and VISUAL-SPACIAL tasks: Simple calculations, Right/left discrimination, Finger identification, Reading/writing ability, Copying shapes/geometric figures, & Gnosis. 6. PARIETAL Lobe 7. FRONTAL Lobe function - Sequencing tasks; Set switching; "Clock drawing" test - Frontal Release signs: Grasp, Paratonia, Palmomental, Glabellar (unable to suppress blink reflex).

Fundamental organization of the visual cortex?

Columnar. Cells of all layers of the cortex along a line perpendicular to its surface will share characteristics. Types of columns: Ocular dominance, preferred orientation, color, motion,

Swallowing (Deglutition) - read this over before exam

Complex sensorimotor activity involving 26 muscles and 5 cranial nerves. Due in part to the common shared pathway between the respiratory and GI tracts - to avoid the threat of food or liquid entering the airway. -------------------------- 3 phases under volitional and reflex control: 1. Oral - mastication and the oral phase refer to the volitional transfer of ingested material, as a prepared bolus, from the mouth into the oropharynx. 2. Pharyngeal - the first semi-reflexive component triggered by activation of the cortical and subcortical brain. 3. Esophageal - this reflexive component begins following closure of the upper esophageal sphincter and serves the primary function of transporting food to the stomach by a sequential peristaltic contraction of the muscles of the pharynx and relaxation of the lower esophageal sphincter

Why synapse in the thalamus?

Contains a large number of nuclei that relay information to the cerebral cortex and subcortical structures. Helps modulate activity of the primary sensory cortex. notes: major relay nucleus in the brain. outgoing information is relayed here. bc it helps modulate and fien tune activity. think of this as a switchboard/operator who directs your call initially.

An adrenergic drug that acts as an agonist but actually results in decreased adrenergic activity is: A. Dobutamine B. Phenylephrine C. Epinephrine D. Clonidine E. Albuterol

D is answer CLONIDINE INFO: 1. Does feedback inhibition of NE release. Is INDIRECT Sympatholytics {all red} aka decreases mouth of sympathetic NT in the synapse by what it does. 2. Alpha-2 agonist/stimulation {red}. - Receptors found both pre and postsynaptic in CNS and other tissues. - Agonist effect = reduces sympathetic outflow from CNS. - Uses for HTN, ADHD, help manage during withdrawal.

Which ascending spinal pathway (tract) carries the sensations of two-point discrimination, proprioception, pressure and vibration? A) lateral spinothalamic B) posterior spinocerebellar C) anterior spinothalamic D) dorsal-column/medial-lemniscal system E) spinotectal

D is answer.

Which of the following is a sympatholytic drug that can cause bronchoconstriction? A. TCAs B. MAOI antidepressants C. Isoproterenol D. Propranolol E. Atenolol

D is answer. Propranolol = DEC. BP/HR/CO (Beta-1 blocking) & BRONCHOCONSTRICTION (beta-2 blocking). - TCAs and MAOI's are lytic, but don't do this. - Isoproterenol is beta (mixed) agonist so causes bronchodilation at B2. - Atenolol is specific B1 agonist.

Which of the following is a non-stimulant drug used to treated ADHD? A. Dexedrine B. Ritalin C. Focalin D. Atomexetine (Strattera) E. Vyvanse

D is answer. ADHD Drugs = indirect adrenergic agonists =: • Dexedrine: dextroamphetamine • Ritalin: methylphenidate - semi-synthetic derivative of dexedrine • Adderall: Dexedrine variant based on a mixture of 4 amphetamine salts- longer acting than Ritalin • Concerta: reformulated ritalin for sustained delivery • Metadate: another sustained delivery ritalin • Focalin: like Attenade, contains only active isomer of Ritalin • Attenade: contains only active isomer of ritalin • Strattera - Vyvanse = amphetamine-based drug, abuse less likely bc crushing up and snorting doesn't work (unless swallowed, it remains inactive). Gradually releases its active ingratiate, d-amphetamine, after drug has been swallowed and comes into contact w. enzymes in the digestive tract.

An accident leaves a 33yr. old male with a fracture to his neck. A CT scan reveals a bony fragment that penetrated the lateral portion of the DORSAL COLUMNS IN THE CERVICAL SPINAL CORD. Which of the following functions would most likely be affected by a lesion at this site? A. Fine motor control of the ipsilateral hand B. Motor control of the contralateral hand C. Vibratory sense from the contralateral hand D. Vibratory sense from the ipsilateral hand

D is answer. Dorsal Columns = Sensory (eliminate motor answers: A and B); Fibers cross once they have reached (remember ascending is sensory) medulla -> since they haven't synapsed/crossed yet, the damage will be Ipsilateral. Notes from class: In cervical spinal cord, so both pathways have joined at this point (dorcilus and cuneatus) -> shouldn't have loss of motor bc this is only affecting the sensory pathways via dorsal columns (A AND B ELIMINATED). -> Is that information synapsed? No bc it didn't reach caudal medulla yet (its on its way up there).

2. Which of the following pathways do not decussate? a. Lateral corticospinal tract b. Dorsal columns pathway c. Spinothalamic pathway d. Dorsal spinocerebellar pathway

D is answer. This particular sensory pathway does not decussate (cross the midline). Information coming in the left side of the spinal cord will terminate in the left lobe of the cerebellum with no crossing over to the opposite side of the CNS during its ascent.

Which of the following is a non-selective direct acting sympatholytic agent used to treat frostbite? A. Phenoxybenzamine B. Propranolol C. Prazosin D. Phentolamine E. Clonidine

D is answer. KNOW PHENTOLAMINE <-> FROST BITE.

Which of the following is a vasoconstrictor most commonly used in commercial cartridges of local anesthetics? A. Albuterol B. Cocaine C. Ephedrine D. Epinephrine

D is answer. Epinephrine (Adrenaline) used a lot in doc office. = Beta2 (at low doses) vasodilation + Alpha 1 vasoconstriction and inc. BP.

Takers of this type of drug have to worry about "wine and cheese" syndrome? A. TCAs B. Cocaine C. Prazosin D. MAOI Antidepressants

D is answer. This syndrome is hypertensive crisis from eating tyramine in food. Normally, MAO would break tyramine down, but is inhibited. Tyramine (found in fermented food / cheese) = indirect adrenergic agonist - releases NE from nerve terminals. Normally metabolized by MAO; but if patient taking MAO inhibitor => may produce hypertensive crisis in these patients!!

"presence in food can cause hypertensive crisis in patients taking MAO inhibitor. Mixed acting adrenergic agonist, causes release of NE from neuron and stimulates post synaptic receptor directly"? A. TCAs B. Cocaine C. Prazosin D. Tyramine

D is answer. Tyramine (found in fermented food / cheese) = indirect adrenergic agonist - releases NE from nerve terminals. Is found in fermented foods (e.g.cheese). Normally metabolized by MAO; but if patient taking MAO inhibitor => may produce hypertensive crisis in these patients!!

Which major ascending pathway (tract) is involved in the conscious perception of external stimuli? A) spinocerebellar B) spinoolivary C) spinotectal D) spinothalamic E) spinoreticular

D. Aka Neospinothalamic Tract / Anterolateral = conscious perception of external stimuli. Conscious (reaching our cerebral hemispheres) = 1. Dorsal columns/ Medial Lemniscal system 2. Anterolateral System - Neospinothalamic pathway. Unconscious (reaching only our cerebellum) = Spinocerebellar Systems = Posterior Spinocerebellar, Cuneocerebellar Pathway, Anterior spinocerebellar pathway. KNOW Spinocerebellar Pathways terminate in THE CEREBELLUM (we need info going here so u can stand up appropriately and not tumble over; primary motor cortex).

"indirect acting sympathomimetic, decreases intraneuronal metabolism of neurotransmitter." A. TCAs B. Cocaine C. Prazosin D. MAOI Antidepressants

D. is answer

Defect with vagus nerve (CN10) would show? What does CN10 supply? what motor nerve system is affected?

DEFECT => difficulty in swallowing (defect larynx and pharynx). corticobulbar system (upper motor) MOTOR TO THE: Palate, Larynx, Pharynx. SENSORY TO THE: Pharynx and Larynx. recall: CN9 & 10 tested together for palate rising equal on both sides when ask patient to say "ah".

WHITE MATTER ORGANIZATION into?

Dorsal, Lateral, Ventral Funiculi. notes from syl: - Funiculi = lg bundles of white matter tracts, which contain different fasciculi. The dif. fasciculi r composed of ascending or descending fiber tracts connecting with specific targets and carrying information for dif. functions. - The nerve fibers in these fascicule belong to one of the five categories of nerve fibers: 1. long range ascending fibers (neurons in gray matter spinal nuclei or DRG -> sensory towards brainstem, cerebellum or thalamus). 2. long range descending fibers (neurons in cortex or brainstem -> project axons down gray matter -> synapse w spinal cord interneurons or motor neurons). 3. motor neuron fibers (spinal motor neurons -> exit spinal cord via ventral rootlets and project to peripheral muscles). 4. sensory afferent fibers (neurons in DRG -> enter spinal cord thru dorsal rootlets). 5. short and long range propriospinal fibers (involved in intersegmental and intrasegmental connections).

Which is true of the corticospinal tract? A)descending, direct motor nerve tract B)consists of anterior and lateral corticospinal tracts C) 80% of upper motor neurons decussate at the level of the medulla D) involved in direct cortical control of movements below the head E) all of the above

E. The corticospinal tract is a descending, direct motor nerve tract, consists of the anterior and lateral corticospinal tracts, has 75-80% of its upper motor neurons decussating at the level of the medulla as the lateral corticospinal tract, and is involved in the direct cortical control of movements below the head.

Which of hte following is a "mixed acting sympathomimetic (direct & indirect agonist) = (timulates post synaptic receptors as well as stimulates release of neurotransmitter, used as an appetite suppressant and to treat hypotension associated with anesthesia - banned from sale. "? A. Vyvanse B. Ritalin C. Epinephrine D. Ephedrine (Ma Huang) E. Tyramine

Ephedrine (Ma Huang) = produced by various plants (Ma-huang). Releases catecholamines from nerve terminal; and also some direct stimulation of alpha and beta receptors. Penetrates brain to produce CNS stimulation. *Weight Loss Products Containing Ephedra/Ma Huang* = these are herbal supplements for weight loss that were killing people!! People started dying from it bc too much cardiac stimulation (soldiers jacked up on ephedrine containing workout supplements would die) => FDA took it out of these products, but other synthetic derivatives exist still.

Patient comes in with FOCAL motor movements that persist in sleep. He says symptoms have lasted for three years. He says previous therappy attempts haven't worked well. What is your diagnosis? A. turrets syndrome B. Trigeminal Neuralgia C. Epilepsia Partialis Continua

Epilepsia Partialis Continua Form of partial status epilepticus- Focal (partial) motor movements & Persists in sleep. Can have very long duration (up to years). Indicates a focal, structural lesion. Refractory (resistant) to medical therapy.

Antihypertensive most likely to cause orthostatic hypertension? A. Clonidine B. Atenolol C. Prazosin D. All of the Above E. Both A and C F. Both B and C

F. Atenolol/Prazosin is answer. Prazosin = Selective alpha1 blockers; treat hypertension (via vasodilation of peripheral vasculature) WOULDN'T BE CLONIDINE EVEN THO ORTHOSTATIC HTN IS CAUSED BY ALPHA 2 AGONISTS - NEED TO KNOW WHY : I think bc Atenolol is B1 antagonist and Prazosin is A1 antagonist -> so antagonists cause it more.

True or False: Periodontal-masseteric reflex is a very slow and protective jaw closing reflex. *

FALSE. Memorize -" Periodontal-masseteric reflex is a very RAPID PROTECTIVE jaw OPENING reflex."

Anterior / VENTRAL SPINOCEREBELLAR Tract (VSC) Must know: 1) Function of pathway 2) Locations of tracts in spinal cord & brainstem (of first, second, third order neurons)? 3) At which levels is pathway present? 4) If crosses midline where do fibers decussate?

FXN: conveys to the cerebellum integrated information about the behavior of a LIMB AS A WHOLE, from lower limbs. - from syl: conveys feedback info to cerebellum about effectiveness of descending motor pathway during motor execution or after an attempted movement. FIRST ORDER SENSORY NEURON: located at DRG, afferent fibers enter spinal cord. SECOND ORDER SENSORY NEURON: establish synapses with SPINAL BORDER cells at lateral edge of spinal laminae V-VII. DECUSSATION: at each spinal level cells send axons that cross the midline and ascend in the anterolateral fascicles up to the upper pons. In the upper pons, a majority of fibers cross the midline again to reach the cerebellum. Fibers cross the midline twice. FINAL DESTINATION: Cerebellum.

Patient presents with Hyperacusis & Taste Loss ipsilateral to the lesion. What Cranial nerve is damaged?

Facial N (VII). Also probably will see: Peripheral facial weakness (eyelid as well as mouth)

Central Pattern Generator - is for what? * Mastication CPG is located?

For sterotyped or rhythmic movements: locomtion, respiration, eye movements, MASTICATION. Coordinates mastication; within the central nervous system (know!) - drives repetitive motor activity of chewing. - organized => initiates & maintains motor acctivity thru Pattern & Rhythm generation. - also requires help for fine-tuning rhythmic jaw movements: by integration of influences from sensory inputs, such as those from muscle spindles, joint, mucosal, and dental (e.g., periodontal) receptors. 3. "Mastication CPG" = Nucleus Reticularis Gigantocellularis = Rhythmic pattern generator in the brainstem medullary reticular formation. - Many factors modulate the pattern of muscle activation = Cortex, Sensory feedback, Cerebellar control. 4. "Modulation of Mastication CPG" - Masticatory pattern is "optimistic," based on hard wiring and past experience. - Feedback and internal processing can adjust for changes and modify subsequent masticatory movement patterns. - The cerebellum is important in this type of learning for both locomotion and mastication. - "Can you walk and chew gum?" may be an important clinical question. 5. "Disorders of CPG?" (a) Maxillofacial movement Disorder - Dystonia. (b) TMD - myofascial pain dysfunction: sensitization of muscles w dysfunction and pain. (c) Bruxism (compulsive grinding/clenching): Nocturnal bruxism may be primary disorder of CPG activation during sleep. Rapid eye movements during sleep (REM sleep) may be similar but with significant differences.

Which cranial nerves are tested together? ("I'm going to repeat that")

Glossopharyngeal (IX), Vagus (X). - Motor control of laryngeal muscles. - Parasympathetic control of heart rate (X). - General visceral sensation (X). Ask patient to say a deep "Ah" while you look into patients mouth with flashlight. NOTE IF THE PALATE RISES EQUALLY ON BOTH SIDES. Lesions: - Dysarthria/dysphagia - Inability to elevate palate (contralateral uvulal deviation)

Which would be better choice for a hypertensive patient w. asthma - Atenolol or Propranolol?

Goal: you don't want to bronchoconstrict the asthmatic patient by blocking beta-2 receptors. Atenolol because its Specific Beta-1 blocker => blocks inc. CO and inc. HR = to treat HTN relatively free of CNS side effects (doesn't cross BBB). Propranolol is non-specific beta1/2 blocker (CNS side effects bc crosses BBB) => blocking beta-2's bronchodilation action would cause bronchoconstriction of the asthmatic patient (bad);

Examination of Cranial Nerve 8 (vestibulocochlear) - is actually examining for what movements? How do you do the test?

HEARING AND BALANCE. (Acoustic Nerve) with the EYES SHUT, click your nails in front of each ear. Have patient indicate when he/she hears the sound & on which side.

A "complicated migraine" involving motor weakness as part of aura is?

HEMIPLEGIC MIGRAINE = Motor weakness also part of aura. Aura otherwise the same. Diagnosis of exclusion. AKA migraine w. weakness associated. = avoid triptan medication.

Which of the following is an alpha-2 Agonist that acts in frontal cortex to treat ADHD. It is not a controlled substance like other ADHD medications due to LESS abuse potential? A. Vyvanse B. Guanfacine (Intuniv) C. Ritalin D. Concerta

Intuniv (Guanfacine) = not a controlled substance. No known mechanism for abuse or dependence. Although other ADHD medications work indirectly in the PRE FRONTAL cortex, it has been shown that guanfacine works directly by binding selectively to alpha-2A adrenergic cell receptors located in the prefrontal cortex. The prefrontal cortex is an area of the brain associated with executive functioning, ie, working memory, behavioral inhibition, regulation of attention, distractibility, impulsivity, and frustration tolerance. The selective alpha-2A agonist strengthens working memory and prefrontal cortex neuronal firing.

Which jaw reflex will help to prevent injury when biting through a hard object?

Jaw-Unloading Reflex: - Produced by rapid closing movement of the jaw during contraction of jaw closer muscles (large forces exerted). - Closer muscles inhibited within 20 ms. of biting fracture. Mandible continues to elevated for another 60 ms. (< 5 mm.). Then depressed by the jaw opener muscles

Which are signs of UPPER motor neuron damage? Which are signs of LOWER Motor neuron damage? 1. Fibrillation and fasciculation (irregular contractions). 2. Clonus (muscular spasm: often rhythmic contractions), Babinski's sign. 3. Muscle Atrophy 4. Spastic Paralysis 5. Decreased muscle stretch reflexes (deep tendon reflexes). (hypOreflexia) 6. Lack of precise motor control, most pronounced in fingers.

LOWER: - Fibrillation and fasciculation (irregular contractions). - Muscle atrophy. - Flaccid paralysis (reduced muscle tone, weakness). - Decreased muscle stretch reflexes (deep tendon reflexes). - muscle tone decreased and strength decreased. UPPER: - Clonus (muscular spasm: often rhythmic contractions), Babinski's sign. - Muscle weakness. - Spasticity (stiff muscle) / SPASTIC PARALYSIS. - Increased muscle stretch (deep tendon reflexes) reflexes (hyperreflexia). - Lack of precise motor control, most pronounced in fingers. - muscle tone increased but strength decreased.

Primary depressors and opening muscles of the mandible are? *

Lateral Pterygoid and submandibular, suprahyoid (strap muscles) chain.

Examination of Cranial Nerve 6 (Abducens Nerve)

Lateral movement of the eye: lateral rectus muscle.

Examination of Cranial Nerve 11 (Spinal Accessory) - What muscle(s) does it supply and how would you test that muscle(s)? Defect with spinal accessory nerve (CN11) would show? what motor nerve system is affected?

MOTOR NERVE TO THE: SCM muscle & Trapezius Muscle. TRAPEZIUS MUSCLE TESTING: stand BEHIND THE PATIENT and press down on both the shoulders with your hands. Ask the patient to SHRUG against pressure. TENSION SHOULD BE EQUAL ON BOTH SIDES. SCM MUSCLE TESTING: Place ur right palm on patients right cheek. Ask patient to turn his face to the right against pressure. Feel the tension in the left SCM. Check the left side of face to test the right SCM muscle. DEFECTS WITH CN11 => WEAKNESS in HEAD movement on OPPOSITE side. corticobulbar system (upper motor)

Motor Pathway final neuron is always a? Sensory Pathway first order neuron is always?

MOTOR PATHWAY = final neuron is lower motor neuron. SENSORY PATHWAY means first order neuron is always a dorsal root ganglion. Assoc. Defintiions: 1. Pathway = simple chain of synaptically-related neurons, that originate from the same nuclei, have the same course and termination. 2. Direction of signal: 1st order to 2nd order to 3rd order, etc. Chain depicts MINIMUM number of neurons. Cell body located in named nucleus. Many pathways named for sight of origin and termination.

Migraine with aura - is there motor weakness? - are symptoms reversible? how long do each last?

Migraine aura: - No motor weakness - at least one of the following: reversible visual symptoms, reversible sensory symptoms, reversible dysphasic speech disturbance, vertigo, each symptom lasts ≥5 and ≤60 minutes.

Examination of Cranial Nerve 12 (Hypoglossal Nerve) - When doing this, how do you know if CN12 is damaged and which side its damaged on?

Motor to the tongue. Ask patient to PROTRUDE his tongue. NORMAL = tongue should be in the midline with no tremors. DEFECT: - If one of the cranial nerves is damaged, it causes the tongue to DEVIATE TOWARD THE AFFECTED SIDE = Ipsilateral paralysis.

What is an abortive treatment for a TENSION headache?

Muscle Relaxants

What is the biggest concern with using abortive headache treatments like NSAIDs, Triptans, Muscle Relaxants, Anti-emetics, Corticosteroids, Oxygen?

Need to avoid analgesic rebound.

When examining/testing ANY of the sensory nerves (cranial nerves), should the patients eyes be opened?

No. Eyes must be closed - PATIENT SHOULD NOT B ABLE TO SEE WHEN U TEST A SENSORY NERVE. *EXCEPT for CN2 (optic nerve) bc shine light into eye*

What areas of the brain regulate mastication? *

Numerous areas of Cerebral Cortex, Subcortical Nuclei, Brainstem, and Peripheral Nerves (motor and sensory).

Gray matter of spinal cord - organized into? what does it contain?

ORGANIZATION (from lecture) = Nuclear Groups (cells similar morphology in same location gray matter) & 10 zones / lamina e.g. Rexed's laminae. - notes from syl: = into columns called "Nuclei" or "Rexed's Laminae" = numbered from dorsal to ventral in roman numerals from I-X(ten). Dorsal horn comprised of Rexed laminae I-VI, lateral horn within laminae VII, and ventral horn consists of Rexed laminae VIII-X. Other notes: H-shaped core in spinal cord sections, contains NEURONS & GLIA. Gray matter nuclei belong to one of three groups: Motor Neurons (visceral or somatic efferent in the ventral horn who's axons exit CNS via ventral roots); Tract or projection neurons (axons send fibers to brainstem regions); & Interneurons (usually smallest and for local cell-cell communication within spinal segment). Divided into dorsal and ventral horns. Special within segments of T1-L2/L3, lateral horn extends from intermediate zone that lies between ventral and dorsal horns.

What is an abortive treatment for a cluster headache? (know)

Oxygen

What are the cell types of the retina and the neural circuit they are from? (must know) Be able to decipher between rods and cones!!!

PHOTORECEPTOR cells (RODS AND CONES) in retina activated by light. MACULA = area of retina most densely packed w rods and cones = highest visual acuity. FOVEA = @ center of macula = center of the visual field = where CONES concentrate, and rods seen at greater distance from here. - note: larger areas in CORTEX are for fovea and macula bc visual space is mapped out in cortex. RODS: - High sensitivity; More photo-pigment; High amplification. Low temporal resolution, low acuity (sharpness) & Achromatic. CONES: - Low Sensitivity, Less photo-pigment, Low Amplification, High temporal resolution, High acuity, & Chromatic [3 photo-pigments]. Retina = part of CENTRAL NERVOUS SYSTEM - "Island in the periphery" (the eye is the peripheral sensory apparatus) = DEVELOPS from VENTRAL DIENCEPHALON during development. Neurons of Retina: GBAMHRC. G = Retinal Ganglion Cells B = bipolar cells A = Amacrine Cells M = Muller Glia Cell H = horizontal cells R = Rods, Photoreceptor C = Cones, Photoreceptor SIMPLE CELLS OF VISAL CORTEX: Respond best to stationary bars or edges & Derive information from a small sub-portion of the retina. Orientations (represented by dif. neurons) matters bc some cells fire action potentials preferentially to edges or bars in the visual field.

Patient presents with an involuntary, rhythmic movement of the palate that persists in their sleep. Diagnosis? Treatment? A. Pharyngeal Rhatoma B. Oral Rhatoma C. Palatal Diclonus D. Palatal Myoclonus

Palatal Myoclonus = Idiopathic, Brainstem lesion involving "triangle" of Guillain-Mollaret [Red nucleus, inferior olivary nuclues, dentate nucleus] Treatment: - Clonazepam - Valproic acid - Carbamazepine - Botulinum toxin

What "governs" mastication? (inputs) * A. The size and texture of the food/drink. B. Peripheral inputs only. C. Cenreal inputs only. D. No neural control. E. Peripheral and Central inputs in a complicated neural network.

Peripheral and Central inputs in a complicated neural network. Notes: - Masticatory muscle activities are integral components of: feeding, talking, oral respiration, and airway maintenance, facial expressions, and emotional reactions.

Masticatory Sequence (the three phases)?

Preparatory phase, Reduction phase, & Preswallowing phase

Which of the following is a mixed-acting sympathomimetic used as decongestant, and an be used to make methamphetamine? A. Phenylephrine B. Amphetamines C. TCAs D. Cocaine E. Pseudophedrine

Pseudoephedrine (Sudafed): - Mixed and Mimetic: direct acting agonist at post synaptic receptors as well as causes release of NT. - Decongestant = alpha vasoconstriction & beta1 increased contractility and HR. - can be used to make methamphetamine {=is pseudo ephedrine w one molecule chemically removed}. - HAS BEEN REMOVED FROM OTC SALES bc of methamphetamine conversion.

5. Electrical stimulation of WHICH cortical area would elicit contractions of the left hand muscles? a. Left pre-central gyrus b. Left post-central gyrus c. Right pre-central gyrus d. Right post-central gyrus e. Right pre-frontal lobe

Right Motor cortex of brain controlling this. Pre-frontal lobe will communicate with other cortices but will never directly control your muscles which is the sole job of the primary motor cortex so eliminate E. This is where you need to remember the central sulcus of the brain divides the primary motor and primary sensory cortices. Pre-central means anterior to the central sulcus, which is the motor cortex. Post-central is posterior to the central sulcus and this is the sensory cortex. So the correct answer here is C.

Examination of Cranial Nerve 1

Sense of smell (special sensory afferent). Olfactory Nerve. Have patient SHUT THE EYES & BLOCK ONE NOSTRIL (repeat on opp. nostril). Use PLEASANT SMELLS (coffee, lemon juice) bc noxious odors stimulate trigeminal nerve.

Examination of Cranial Nerve 9 (Glossopharyngeal Nerve) - what happens when you have a palsy of CN9 (shift goes which way)?

Sensory and Motor to the PHARYNX. & Posterior Tongue TASTE. LEFT CN9 PALSY: have patient say "ah": uvula goes towards RIGHT side = SHIFT TO OPPOSITE SIDE OF THE PALSY.

True or False: Mastication is an involuntary process generally for all animals that exist. *

So false. VOLUNTARY. UNIQUE TO HUMANS. notes: the masticatory cycle pattern is distinct in each species. Humans are unique. - The cortico-bulbar (brainstem) pathway that drives mastication seems to be a UNIQUE feature of the oro-facial motor system, since both locomotion and respiration cannot be triggered by electrical micro-stimulation of cortical motor areas.

Trigeminal Nerve Ganglion

Somatosensory - trigeminal ganglion.

Statement 1: Subacute combined degeneration is usually caused by vitamin B12 deficiency. Staement 2: Subacute combined degernation affects all motor and sensory pathways. Statement 3: SUbacute combined degeration patient will NOT lose cutaneous sensation, but will lose sense of position and vibratory sense in the legs. true/false?

Statment 1 is true - Usually caused by VITAMIN B12 DEFICIENCY. Statement 2 is false - Affects corticopsinal tracts and posterior (dorsal) columns. Spinothalamic tract not affected. Statemetn 3 is half false - Loss of cutaneous sensation. Peripheral nerves also degenerate. & Loss of position and vibratory sense in the legs. Gait disorder due to sensory ataxia.

Sensation of depth that arises from viewing nearby objects with two eyes is called? A. Perception B. Diapses C. Stereopsis D. Stereocognition E. Visualsepsis

Stereopsis. Visual Field Fxn of Binocularity. = Due to disparity in retinal position for the object relative to the fixation point. => Cells in cortex are wired to respond to these differences and create the perception of depth.

Motor function to the 4 major muscles of mastication is via ____. *

THIRD DIVISION of Trigeminal Nerve (CN5) - control masseter, temporalis, medial and lateral pterygoids.

Pathology caused by "chronic dopamine antagonist" use (Antipsychotics Anti-emetics)? How would you treat?

Tardive Dyskinesia = CHOREIC (jerky, involuntary) usu. orofacial/buccolingual distribution; DYSTONIA (sustained contractions) & TICS also seen. Epidemiology: - Up to 30% of patients on long-term neuroleptics. - More susceptible = young men (< 30), & older women (> 60). Pathophysiology unclear: Dopamine receptor hypersensitivity. Treatment: - Stop offending medication. - Dopamine blocking agents. - Benzodiazepines. - Dopamine depleting agents (tetrabenazine). - Botulinum toxin (if dystonic).

1. A 55yr. old patient had an ischemic cerebral stroke that resulted in paralysis of his right-sided lower limb. Where is the most likely region of the stroke? a. Most medial aspect of his left primary motor cortex b. Most lateral aspect of his left primary motor cortex c. Right internal capsule d. Most medial aspect of right primary somatosensory cortex

The answer is A. Know about the Homunculus: - includes Primary Motor Cortex & Somatosensory Cortex. - Medial aspects of either = lower limbs. - LATERAL aspects of either = UPPER limbs & Facial structures. "This is where you must have a general knowledge of the homunculus. The lower limb is located along the medial longitudinal fissure of the brain, so representation of the lower limb is medial along the strip of primary motor cortex. Also if there is paralysis of the right limb then the left side of the brain was damaged."

Tic disorder is called? How would you treat the tics, and how about the associated behavioral issues?

Tourette's Syndrome = Common (est as high as 1% of population), Childhood onset (mean age 7 years) = - Motor tics & Vocal tics Ranging from grunting to words/phrases; Coprolalia (i.e. swear randomly), Echolalia (meaningless repeating words). - Neurobehavioral symptoms: Attention deficit disorder, Obsessive compulsive behaviors, Learning disabilities. - Treatment: of Tics: DOPAMINE BLOCKERS/DEPLETERS. of behavioral: clonidine, methylphenidate, SSRI's

Spinal cord lesions = traumatic, inherited or acquired - Tumor or Metabolic disorder (or both) are examples of which type of lesion? - Contusion or compression are considered of which category? - First response of traumatic injury? - ALS is an example of which type of lesion?

Traumatic lesions (such as injury) are usually segmental: - Contusion or compression (transection is rare). - Lesions above C4 are not survivable. - First response is SPINAL SHOCK = flaccid paralysis and loss deep tendon reflexes. - Then spasticity, increased deep tendon reflexes, Babinski sign. - Complete or incomplete loss of function. Inherited lesions (such as ALS) are usually longitudinal Acquired lesions (tumor or metabolic disorder) could be both.

"indirect adrenergic receptor agonist, blocks the reuptake of catecholamines (dopamine, epinephrine, and norepinephrine) into presynaptic terminals, thus prolonging the action of catecholamines "

Tricyclic Antidepressants

examination of Cranial Nerve 5 - motor & sensory: How do you examine temporals muscle? masseter muscle? Sensory to the face?

Trigeminal Neve. 1. MOTOR = Temporalis (Clench teeth), Master (move jaw side-side). (i) TEMPORAL MUSCLE EXAMINATION = Stand in FRONT OR BEHIND the patient. Place ur palms on EITHER SIDE OF THE FOREHEAD. Have the patient CLENCH. Note the EQUALITY of TENSION on both sides. (ii) MASSETER MUSCLE EXAMINATION = stand in FRONT OR BEHIND the patient. Now place your PALMS ON PATIENT'S CHEEKS. Have the patient CLENCH. Note the equality of clenching on both sides. 2. SENSORY to the face = Ophthalmic (V1), Maxillary (V2), & Mandibular (V3) divisions => have patient SHUT THE EYES. Using cotton tip or sharp object, touch the 3 sensory areas. Have patient IDENTIFY each area touched.

Patient presents with affected eye ELEVATED (hypertropia) and slightly ABDUCTED. Overall, the affected eye appears "UP and OUT." and also "Vertical Diplopia" Which cranial nerve is damaged here?

Trochlear Nerve Palsy - CN4 (SO4)- eye is moving in direction of unopposed inferior oblique muscle. Since affected eye is abducted, visual axis of the two eyes is misaligned and patient has double vision (DIPLOPIA) - to correct for this, patient tilts crown of their head away from lesion and tucks their chin in to bring their head down in attempt to align the visual axis of both eyes and avoid the double vision.

True or False: NSAIDs and Corticosteroids can be used to abort ANY type of headache (as long as there are no concurrent medications w DDIS).

True.

8. Atrophy of the muscles in the hand resulted from damage to the recurrent median nerve. Major signs of atrophy are a sign of a lower motor neuron lesion. True or False?

True. Know the signs between upper and motor neuron lesions.

Types of Movement Disorders: Tics, Myoclonus, Dystonia, Chorea, Tremor 1. rhythmic, oscillatory, across a fixed axis 2. random, irregular 3. rapid, jerk-like movements 4. sustained contractions 5. "semi-voluntary", stereotyped.

Types of Movement Disorders: Tremor - rhythmic, oscillatory, across a fixed axis. Chorea - random, irregular Myoclonus - rapid, jerk-like movements. Dystonia - sustained contractions. Tics - "semi-voluntary", stereotyped.

Multiple sclerosis (MS) - upper or lower motor neuron disease? What causes this? What else is lost besides motor control? What part of brain is involved?

Upper motor neuron disease. Multi-focal de-myelination of brain and spinal cord. Also proprioceptive sensory loss. CEREBELLAR involvement - ATAXIA, arm TREMOR, EYE movement disorder. Many potential symptoms (read thru image)

Upper motor neurons (corticospinal and corticobulbar neurons) originate in _______. 1. Corticospinal neurons innervate _________. CorticoBulbar neurons innervate ______. 2. Both arise in ________. 3. The corticobulbar tracts in the ________ are anterior to the corticospinal tracts. Then, they are medial in the _______. Then, they are medial in the _______. 4. Both tracts terminate in the ________. 5. The corticobulbar system provides __________ control of the muscles and glands innervated by all cranial nerves except _____.

Upper motor neurons originate in the motor strip = corticospinal & corticobulbar neurons. 1. INNERVATE DIF: - CORTICOSPINAL NEURONS innervate spinal segments. - CORTICOBULBAR NEURONS innervate cranial nerve nuclei. 2. ARISE SAME: both of these tracts arise in cortex. 3. TRAVEL DIFF: The corticobulbar tracts in the internal capsule are anterior to the corticospinal tracts. The corticobulbar tracts in the midbrain are medial in the cerebral peduncles. The corticobulbar tracts in the medulla are medial in the medullary pyramids. 4. TERMINATE SAME: They terminate in the brainstem (picture of MIDBRAIN, PONS, MEDULLA). 5. SYSTEM OF CONTROL DIF: - *The corticobulbar system*: Voluntary and involuntary control of the muscles and glands innervated by:CN III, IV, V, VI, VII, CN IX, X, XI and XI. (all except CN1,2,8).

How is the sitmulation of reflexes involved in Jaw opening differ from that of Jaw Jerk & Unloading? What nerve is involved in jaw reflex function?

Vertical (primarily): 1. Reflexes evoked by stimulation of receptors within the muscles themselves (jaw jerk & jaw unloading) 2. Reflexes which are responses to external (noxious) stimuli (jaw opening). - note: Horizontal jaw reflexes exist and are similar, yet less well understood Jaw Reflexes: 1. closing ("Jaw Jerk") 2. opening 3. unloading [he said these three are the major TRIGEMINAL reflexes involved in jaw function). 4. Periodontal-Masseteric (more for generating force/power).

Patient presents with SENSORY HEARING LOSS and VERTIGO. This is most likely due to a lesion of which cranial nerve ?

Vestibulocochlear (VIII). vertigo = off balance.

Mastication involves _______ movements that are complicated ______ movement patterns, similar to ____________. *

Voluntary Movements. Complicated Rhythmic Movement patterns. Similar to Respiration, Locomotion, GI digestion. notes (read before exam): - Complex, rhythmic movements of the jaw (at the TMJ) and soft tissues. - Complex, coordinated activation of the muscles controlling the mandible.

Can prophylaxis be used for headache treatment?

Yes (was on the slides...)

Overall, control of mastication is via? *

a complex brainstem central pattern generator, and higher cortical and subcortical brain areas. Note: - Rhythmic pattern of jaw muscle movement of the mandible. - Controlled by the central pattern GENERATOR in the BRAINSTEM. - Modulated by sensory feedback: from receptors of: periodontal, TMJ, muscle, tendon, mucosal, skin, etc. - Augmented by jaw reflexes Supplemented by voluntary input from higher CORTICAL center. **Little conscious effort is required once mastication is initiated, with chewing largely occurring automatically.

DORSAL COLUMNS / Medial Leminiscus PATHWAY Must know: 1) Function of pathway 2) Locations of tracts in spinal cord & brainstem (of first, second, third order neurons)? 3) At which levels is pathway present? 4) If crosses midline where do fibers decussate?

ascending sensory pathway. FUNCTION: pressure, vibration, movement / position, and highly discriminative touch: highly localized. FIRST ORDER SENSORY NEURON: located at dorsal root ganglion (DRG), afferent fibers enter spinal cord. Ascend UNCROSSED in dorsal columns, in two different fasciculi 1. Fasciculus GRACilis: (sensory from T6 or lower) =< T6 or lower aka mainly lower limbs. 2. Fasciculus Cuneate: (sensory from above) > T6 aka mainly UPPER LIMBS. SECOND ORDER SENSORY NEURON: located in Gracilis nucleus and Cuneate nucleus in the caudal MEDULLA. DECUSSATION: fibers cross midline in medulla to form "medial leminiscus". THIRD ORDER SENSORY NEURON: ventral nucleus of THALAMUS, projects to primary sensory cortex (somatosensory cortex) in parietal lobe. FINAL DESTINATION: postcentral gyrus (primary sensory cortex), parietal lobe.

7. Where are the cell bodies of lower motor neurons located? a. Layer V of the primary motor cortex b. Ventral horn of the spinal cord c. Ventral nuclei of the thalamus d. Layer I of the primary motor cortex

b. Remember those large neurons I showed you in my first spinal cord lecture? Those are lower motor neurons that receive the synapse from the lateral corticospinal tract. These lower motor neurons and their outgoing axons create ventral rootlets/roots that emerge from the spinal cord to eventually make a spinal nerve. Lower motor neurons originate: - In the ventral horn of the spinal cord. - In cranial nerve nuclei.

Which of the following is an Alpha receptor Agonist originally thought to act as a false neurotransmitter that acts at alpha2 receptors in the CNS to produce vasodilation? A. Phenylephrine B. Clonidine C. Isoproterenol D. Methyldopa

boards exam. METHYLDOPA = Alpha-2 Agonist = Anti-hypertensive = used to be thought of as false NT but actually is bc its taken up by storage vesicle and converted to methyl NE that gets released like NE and actually stimulates postsynaptic A2 receptors to inhibit NE release in periphery. - phenylephrine is A1 agonist decongestant. - Clonidine is A2 agonist for HTN and withdrawl. - Isoproterenol is mixed beta agonist for broncohdilation and inc. HR.

4. Which of the following ascending pathways contains SECOND order neurons in the MEDULLA? a. Cuneocerebellar pathways b. Neospinothalamic pathways c. Dorsal columns system d. Posterior spinocerebellar pathway

c. The dorsal columns system/pathway synapses in the medulla on gracile nucleus and cuneate nucleus.

Which of the following does NOT correctly describe characteristics of trigeminal neuralgia? A. It is often precipitated by triggers such as cold air, brushing teeth, and talking. B. The attacks are sudden and of sharp, stabbing pain lasting from seconds to minutes. C. It can be treated with antiepileptics or muscle relaxants. D. Attacks are stereotyped and occur bilaterally.

check once answers posted - susan is saying D, but i think its A. KNOW - TRIGEMINAL NEURALGIA: The typical form results in episodes of severe, sudden, shock like pain in one side of the face that lasts for seconds to a few minutes. Trigeminal Neuralgia is more common in V2, V3 (V1 relatively rare). Attacks are stereotyped in the individual patient. There is no clinically evident neurological deficit. Not attributed to another disorder. Treatment: 1. Antiepileptics: Carbamazepine, oxacarbamazepine, phenytoin; gabapentin. 2. Muscle relaxants: baclofen. 3.Surgical: Rhizotomy, Microvascular decompression, Gamma knife.

Patient comes in for root canal showing signs of anxiety and sympathetic arousal. Which of the following describes some signs of SYMPATHETIC AROUSAL that you patient might be experiencing? A. Miosis, dry mouth, bronchoconstriction, inc BP. B. inc. salivation and HR, mitosis, bronchodilation. C. bronchodilation, mydriasis, sweating, elevated heart rate. D. mydriasis, bronchoconstriction, inc. hr and BP. E. salivation and lacrimation, blurred vision, facial flushing.

correct answer has to have at least 1 or both of: bronchodilation and inc. BP/HR. C is the answer. know below Adrenergic Stimulation results in: 1. Inc. HR & Contractility - B1 receptors in cardiac tissues. 2. Inc. Peripheral resistance - Alpha receptors -> vasoconstriction and inc. BP. 3. Inc. Bronchodilation - B2 receptors in bronchiolar tissue. 4. Inc. Pupillary dilation, mydriasis - A1 agonism in iris's radial muscles causing relaxation. 5. Urinary Retention - A1 agonism in bladder.

1) Anterior Cord Syndrome 2) Posterior Cord Syndrome 3) Central Cord Syndrome 4) Brown-Sequard Syndrome know: motor, fine (discriminatory) touch, pain/temp symptoms

incomplete lesions 1) Rare, only after occlusion of anterior spinal artery (br of vertebral artery); which lies over ventral medial sulcus. There is only one of these (there is two posterior spinal arteries). - MOTOR: BILATERAL PARALYSIS OR WEAKNESS. - FINE TOUCH: normal. - PAIN/TEMP: BILATERAL LOSS 2) rare, only after occlusion of Posterior spinal artery (there are two of these); which lay over posterolateral or over posterior intermediate sulci {only present at certain spinal cord levels}. - Motor: Normal. - Fine Touch: BILATERAL LOSS. - Pain/Temp: Normal. 3) Cavity in central cord canal that expands; it first damages crossing fibers. - Motor: PROGRESSIVE BILATERAL PARALYSIS by direct damage to motor neurons. - Fine Touch: Normal. - Pain/Temp: IMMEDIATE BILATERAL LOSS. 4) only affects limited part of half spinal cord. Below Lesion, spinal cord is NORMAL. Also called Lateral Spinal Hemisection. - Motor: IPSILESIONAL PARALYSIS (same side as lesion. - Fine Touch: IPSILESIONAL LOSS. - Pain/Temp: CONTRALESIONAL LOSS.

Sympathetic and Adrenergic Stimulation on Salivary Glands? Delete / add to sympathetic arousal fc

inhibits salivary secretion (sympathetic also dilates pupil, tear glands maintain eye moisture, accelerates heart rate and constricts arterioles, etc.) - This is opposite of cholinergic / parasympathetic actions.

Primary elevators of the mandible are? *

masseter, temporalis, medial pterygoid (3).

Where is oculomotor nerve (CN3) located?

midbrain

Where is the trochlear nerve (CN4) located in brain?

midbrain

Sympathomimetics - exam question: which (direct or indirect) drug would have more of a selective and specific effect? MUST KNOW - 3 mechanisms of mimetic indirect drugs examples of drugs for each?

mimetic = producing same effect as the NT of the SNS. 1. DIRECT effect = directly activating adrenergic receptors just like NTs = selective, specific! = prazosin (alpha-1 blocker -> vasodilation). 2. INDIRECT = increasing amount of sympathetic NT in the synapse; the NT produces the effect on the receptor, not the drug: - by INC RELEASE OF NT from postganglionic nerve terminals (AMPHETAMINES). - by DEC. RE-UPTAKE OF NT (TCAs or COCAINE). - By DEC. ENZYMATIC DESTRUCTION of NE (MAO-Inhibitors).

Anterolateral System (ALS) - Neospinothalamic Tract Must know: 1) Function of pathway 2) Locations of tracts in spinal cord & brainstem (of first, second, third order neurons)? 3) At which levels is pathway present? 4) If crosses midline where do fibers decussate? Might need to know: 5) There are dif. tracts of this system, where do each terminate? Neospinothalamic tract, Paleospinothalamic tract, Spinomesencephalic tract , Spinoreticular tract, Anterior Spinothalamic tract

sensory FXN: pain and temperature (thermal sense) & poorly localized touch. FIRST ORDER SENSORY NEURON: located at DRG. afferent fibers enter spinal cord and project to LAMINA II (Substantia Gelatinosa). SECOND ORDER SENSORY NEURON: tracts located in LAMINAE I (n. Posteromarginalis) & Laminae III-V (n. Proprius): collect "edited" signals from lamina II and generate output fibers. DECUSSATION: fibers cross the midline at each spinal segment and ascend in the anterolateral fasciculus. Terminates in the thalamus. THIRD ORDER SENSORY NEURON: located in ventral nucleus in thalamus, and projects to primary sensory cortex. (same as dorsal columns pathway) FINAL DESTINATION of NEOSPINOTHALAMIC TRACT: primary sensory cortex = postcentral gyrus, parietal lobe (same as dorsal columns pathway, both are for conscious perception). 1. Paleospinothalamic tract (ends in cingulate cortex). - Spinomesencephalic tract (ends in the midbrain) - Spinoreticular tract (ends in the brainstem). -Anterior Spinothalamic tract (ends in the thalamus). - note: All tracts are involved in relaying and modulating pain pathways

Sensory information comes into spinal cord via the _________. And visceral motor (ANS) + muscle movement exit through the ________.

spinal cord segment. Dorsal root ganglion = sensory information going in. Visceral motor (ANS)/muscle movement = exit thru ventral horn.

Most common headache type

tension headache. Lifetime prevalence of 69% in men < 88% in women. "dull", "pressure", "squeezing". Usually bilateral but can be unilateral. Non-pulsatile & No aura.

Patient presents with Facial sensory loss (anterior to ear) & Jaw deviation IPSILATERAL to lesion. What cranial nerve is damaged?

trigeminal (V) - Sensation to face, oral, and nasal mucosa. - Motor control of muscles of mastication.