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Neuro USMLE

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Question
Answer
CN I innervates? Syndrome to look for and its cause?   smell; Kallman's syndrome=anosmia and hypogonadism due to gonadotropin rel hormone defic  
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CN8 innerv? Defic causes?   (vestibulocochlear nerve) for hearing and balance; defic: deafness, tinnitus, vertigo  
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CN9 innerv? Defic causes?   (glossopharyngeal) pharyngeal mscles, afferent gag reflex, parotid, taste in P 1/3 tongue, skin external ear; defic: loss of gag and loss of taste P 1/3 tongue  
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CN10 innerv? Defic?   (vagus) palate, pharynx, larynx, abd viscera, skin of ext ear; defic: hoarseness, dysphagia, loss of gag or cough  
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CN 11 innerv? Defic?   (spinal access nerve) sternocleidomastoid, trapezius; defic: can't turn head to side opp to lesion, shoulder droop  
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CN 12 innerv? Defic?   (hypoglossal) innervates tongue; defic: tongue on protrusion deviates ipsi  
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name 3 spinal tracts and their fxns   corticospinal=mvmt contra limbs, dorsal column=tactile, vibration, sensation; spinothalamic=pain, temp  
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CNV innervates   (aka trigeminal nerve) mastication and facial sensation, afferent limb corneal reflex  
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characteristics trigeminal neuralgia, treatment, rule out other diagnoses   (CN V) unilateral shooting pains in face, incl w brushing teeth, tx: carbamazepine [could be MS, or if bilateral could be stroke]  
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CN3 fxn   eye mvmt, pupil constriction, accomodation, eyelid open  
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CN4 fxn   eye mvmt  
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pneumonic for which CN are sensory, motor   Some say marry money but my brother says big brains matter most  
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pneumonic for eye mvmt mscls innerv   LR6SO4R3-lateral rectus=VI, superior oblique=IV, rest=III  
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how differentiate CNIII, IV, V, VI, and VII problems wrt to eye exam   III: eye is down and out and can only move laterally, IV: can't look down when medial, V/VII: blink reflex, VI: can't look lateral  
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nerves involved in pupillary reflex; 2 types of reflexes   CN II to sense light, III to constrict pupil; direct reflex if light was in that eye, consensual reflex if light was in other eye  
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nerves involved in blink reflex   ophthalmic branch (V1) of CN V to feel stimulus, CNVII to close eyelid  
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if L optic n damaged, what see on pupillary reflex   stimulating L eye causes no response in either eye, stimulating R causes both to respond  
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if L occulomotor n damaged, what see on pupillary reflex   stimulating L eye causes R to respond, stimulating R eye causes R to respond  
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characteristics CN7 UMN? LMN? MC cause for each?   UMN=contralateral lower facial paralysis **forehead is spared, usu cause is stroke; LMN=ipsi upper and lower facial paralysis, **forehead is involved on affected side, usu due to Bell's palsy or tumor  
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Bell's palsy-- how can be difft from CNVII LMN? Causes?   can also have hyperacusis (noises loud) bc stapedius muscle is paralyzed; MC causes: AIDs, Lyme, sarcoid, tumor, DM  
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how difft UMN from LMN   UMN have incrsd tone, spastic, and DTR (although initially may be decrsd for ea) + Babinski's; LMN has decrsd tone, flaccid and DTR, atrophy, fasciculations  
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nerve for ea DTR   achilles=S1,2; knee=L3,4; biceps=C5,6; triceps=C7,8 [just count up]  
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what number cause of death is stroke? % isch v hemorrh   number3, 85% isch  
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how define TIA; usu cause/type   neuro deficit for <24hrs, (usu <30min). Usu embolic and high risk of stroke in next mos.  
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characteristics of carotid stroke/TIA   loss speech, paralysis/paresthesia/clumsy contra extremity; can have amaurosis fugax (chol emboli to retinal/ophthalmic artery causes ipsi vision loss)  
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define amaurosis fugax   chol emboli to retinal/ophthalmic artery causes ipsi vision loss  
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characteristics of vertebrobasilar stroke/TIA   dizziness, dbl vision, vertigo, numb ipsi face & contra limb, dysarthria, hoarseness, dysphagia, HA, projectile vomitting, drop attacks  
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what paradoxial stroke   venous clot goes through ASD/VSD/PFO and into head  
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4 causes/types stroke/TIA   embolic (MC, usu from heart), thrombotic (usu atheroscl), lacunar (small vessels), non vascular (anoxic injury, low CO)  
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describe subclavian steal and sympt   stenosis of subclavian before vertebral, so retrograde down vertebral artery to back fill subclavian; BP less in that arm and claudication when exercise that arm  
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causes of stroke in younger pts   OCP, preg, hypercoag (prot C, S), cocaine, amphet, polycythemia, SC  
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risk factors for stroke, which most impt   Age, HTN most impt; smoking, DM, hyperlipid, A Fib, CAD, prev stroke, Fm Hx, carotid bruits  
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MC embolic stroke site   MCA  
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sympt MCA stroke   aphasia (if L (dominant)), neglect/apraxia/confusion (if R), contra paresis face and arm, gaze twd lesion, homo hemianopia  
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stroke a cerebral artery causes   contra paresis and sensory loss in leg (incl foot drop, gait dysfunction), amnesia, personality changes, cognitive changes [this artery also supplies frontal lobes]  
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stroke posterior cerebral artery causes   homo hemianopia, memory deficits, dyslexia/alexia  
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stroke basilar artery   coma, locked in syndrome, CN palsies, apnea, visual symptoms, dysphagia, dysarthia, drop attacks, **crossed weakness/sensory affecting ipsi face and contra body  
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MC site circle of willis aneur   anterior communicating  
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anterior communicating artery aneur sympt   bitemp hemianopsia + frontal lobe  
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posterior communicating artery aneur sympt   CNIII (often see first impaired pupillary light reflex, unlike isch CNIII where that is spared until late]  
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cerebral v subcortical strokes   cerebral: contra motor or sensory face, arms, trunk not usu legs (interhemisph), aphasia if L, visual/spatial more if R; subcortical: hemiparesis is complete (tracks all run together thru internal capsule)  
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key plegias from brainstem   crossed, ipsi face, contra body  
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how to differentiate peripheral neuropathy from myopathy   peripheral neuro: usu asymm, weakness more distal, can have sensory; myopathy: symm w weakness prox>distal, nml sensation  
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how difft NMJ v peripheral neuro or myopathy   NMJ: fatigability, nml sensation  
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general features of spinal cord injury, that are unique to these lesions   decrsd sensation below a sharp band  
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general features of radiculopathy   pain! Affects muscles supplied by that root (myotome), and sensory area supplied by that root (dermatome) Weakness, atrophy, sensory deficit in a dermatomal pattern  
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general features Cb lesion   incoord, intention tremor, ataxia  
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general features of brainstem lesion   cranial nerve and spinal cord findings; ipsi face and contra body hemiplegia  
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fxn radial nerve lesion   no supination, no extension (radial is SUPER), w wrist drop, sensation back hand finger 1-3  
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fxn ulnar nerve lesion   can't cross fingers or V sign, sensation 1/2 of ring finger and pinkie  
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fxn median nerve lesion   can't flex fingers of wrist, thenar eminence atrophied (ie carpal tunnel), sensation 2,3,1/2 of ring from underside to nails, loss pronation. Thumb's up, all's ok when you flex yr nail polish w carpal tunnel  
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axillary n lesion   innerv deltoid, can't abduct to horiz  
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long thoracic n injury (metastetcomy)   serratus anterior, winged scapula, can't abduct past horiz  
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common peroneal n lesion   foot drop, anterolateral sensation leg  
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femoral n lesion   paralysis of quad, can't extend leg and loss of knee jerk, sensation anterior thigh  
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upper brachial plexus lesion   Erbs palsy, arm by side, rotated inward, waiter's tip. Can't abduct arm, felx elbow or supinate  
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lower brachial plexus lesion   Klumpke, median/ulnar n; clawed hand and Horners  
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fxn of interosseus   palmar adduct, dorsal abduct PAD DAB  
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how long might it take for isch stroke to show by non contrast CT   24-48hrs  
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what order if present s/s acute stroke   non contrast CT, ECG, CXR, CBC, PT/PTT, Lytes, Glu, caortid U/S, Echo  
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when to tx acute stroke w tPA   <3hrs no contraindications, incl: prior hemorrh stroke, sz w onset stroke, stroke or head trauma w/in 3mos, HTN BP>185/110, BG<50 or >400, age <18, bleeding (GI, urinary <21d), plt <100K, INR>1.7 or elev PTT, surg<14d, recent MI, think TIA (rapid improve)  
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tx of acute stroke other than maybe tPA   1) ASA (don't give if tPA), 2) tx HTN only if >220/110, 3) treat F, hyperglu  
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once give tPA what must control   BP <185/110  
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longterm tx s/p stroke   ASA if sm vessel dz, manage risk factors (HTN most impt, also DM, hyperlipid, etc), carotid endartectomy if nec  
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epidural bleed: describe clinical present and anatomy (where blood is, how appears on imaging)   lucid interval, often temporal bone fx m. meningeal artery; biconvex blood bw dura and skull  
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subarachnoid hemorr: describe clinical present and anatomy (where blood is, how appears on imaging)   worst headache, ruptured berry aneurysm (MC A. commun artery, blood in CSF, blood bw pia and arachnoid)  
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subdural bleed: describe clinical present and anatomy (where blood is, how appears on imaging)   elderly pts, EtOH, may not remember fall, bridging veins, blood bw dura and arachnoid, crescent moon shaped on imaging  
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order of compartments for cranial bleeds moving from brain surface outwards   pia-[subarachnoid space]-arachnoid-[subdural space]-dura-[epidural space]-skull  
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clinical signs transtentorial (central) herniation   bilateral small and reactive pupils, Cheyne-Stokes respirations, flexor or extensor posturing  
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clinical signs uncal herniation   CNIII gets entrapped, fixed and dilated ipsilateral pupil [from mass in middle fossa]  
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clinical signs cerebellar tonsillar herniation   compression medulla, respiratory arrest, usu rapidly fatal [from mass in posterior fossa]  
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describe Cushing triad   from incrsd ICP: HTN, bradycardia, repir irreg  
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cerebral perfusion is determined by   MAP-ICP (nml ICP 5-15)  
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MC location intracranial hemorrh   BG (66%), then Pons and Cb ea 10%  
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key clinical factors suggesting intracranial hemorrh   focal neuro deficit that WORSENS over next 30-90min, AMS, signs incrsd ICP  
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how pupils help differentiate place of intracranial hemorrh   pin point=pons, poorly reactive=thal, dilated=putamen  
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tx intracranial hemorrh (after CT confirms)   control BP if >16-180/105, but slowly, if elevated ICP give mannitol and diuretics…surgery maybe for Cb hematomas, otherwise no  
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if CT in suspected SAH is negative, what do   LP, diagnostic if xanthochromic (yellow CSF) bc means RBC have been there for a while (v traumatic tap)  
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once SAH diagnosed, what do   cerebral angiography and call neurosurg; quiet rest in dark room w head elevated and stool softeners, nifedipine for vasospasm, control HTN  
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name 5 key adult brain tumors   glioblastoma (type IV astrocytoma), meningioma, schwannoma, oligodendroglioma, pit adenoma  
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name 5 key pediatric brain tumors   pilocytic atrocytoma, medulloblastoma, ependymoma, hemangioblastoma, craniophrangioma  
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name where ea of 5 pediatric tumors occur: pilocytic atrocytoma, medulloblastoma, ependymoma, hemangioblastoma, craniophrangioma   pilocytic atrocytoma=P fossa, medulloblastoma=Cb, ependymoma=4th ventricle, hemangioblastoma=Cb, craniophrangioma=supratentorial  
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what are the 3 MC primary adult brain tumors, in order   1) glioblastoma, 2) meningioma, 3) schwannoma  
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which primary brain tumor is found in the cerebral hemispheres and can cross the corpus callosum   glioblastoma  
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majority of adult primary brain tumors are supra or infratentorial? Pediatric?   adult are usu supratentorial, pediatric are infratentorial  
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what brain tumors suspect for hydrocephalus in kids   ependymoma (4th ventricle), medulloblastoma (Cb but can compress 4th v)  
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what brain tumor assoc w von Hippel Lindau   hemangioblastoma in Cb  
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what brain tumor can cause bitemporal hemianopia (so confused w pituitary adenoma)   craniopharyngioma (benign childhood tumor, MC childhood supratentorial tumor)  
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supratentorial tumor in kid--think what? Benign or malignant?   craniopharyngioma, benign  
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diffusely infiltrating brain tumor in P fossa in child, dx? Benign or malignant?   pilocytic astrocytoma, benign  
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MC primary CNS neoplasm, characteristics   astrocytoma (ie glioblastoma), arise IN cerebral hemispheres, infiltrate brain w indistinct boundaries and can cross corpus callosum  
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besides astrocytomas, what cancers appear in parenchyma?   mets (50%)-in order of freq: Lung, breast, melanoma, kidney, GI  
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differential for ring enhancing lesion   met, brain abscess, glioblastoma multiform, lymphoma, toxo  
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name 2 extraparenchymal brain tumors   meningioma, scwhannoma  
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are schwannomas unliateral or bilateral? Assoc?   always unilateral, if bilateral then its NF II  
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describe population that get meningiomas   usu 40-50, females >2x than males  
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how do meningiomas appear on imaging   extracerebral, rounded w well-defined dural bases that compress underlying brain  
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schwannomas--malignant or benign?   benign (no malignant potl)  
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where schwannoma arise? Presenting symptom?   cerebellopontine angle, involved 8th cranial; first present w hearing loss (+/- tinnitus, loss of balance, nystagmus)  
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schwannoma and meningioma--surg excision?   yes, although meningiomas have high recurrence rate  
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calcified lesion external to brain parenchyma in adult--think what?   meningioma  
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4 types of MS   1)clinically silent/stable/benign (may progress late), 2) relapsing and remitting (MC), 3) 2ry progressing (relaps/remit gradually worsens), 4) 1ry progressive  
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key clinical features MS   white matter plaques; scanning speech, intention tremor/INO/incontinence, nystagmus. Also optic neuritis w sudden vision loss  
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describe INO, where injury is   injury medial longitudinal fasculus (MLF), If R MLF is affected and pt looks L, the R eye can't adduct and stays midline while the L abducts and start nystagmus (pt also sees dbl looking L)  
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tx acute MS attack   hi dose IV steroids can shorten but won't alter overall progression dz, most attacks resolve <6wks  
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disease modifying MS tx   INF, can cause flu-like sympt. Only use cyclophosphamide and other non specific immunomodulators in rapidly progressive bc many SE  
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Rx for mscl spasticity in MS   baclofen (deriv of GABA)  
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neurpathic pain tx   carbamazepine (Na channel) or gabapentin (neurontin, GABA analog)  
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describe Guillan Barre clinical progression   infxn (often URI) or immun 1 wk before, symmetric distal weakness starts in legs w loss DTR **sensation intact, ascending paralysis, watch for respir paralysis (use spirometry to monitor)  
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treatment Guillan Barre   usu stops spontaneously, plasmaphoresis reduces severity and length **don't give steroids, could make it worse!  
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mech MG   autoantibodies Ach R at NMJ  
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key characteristics MG clinically   mscl fatigue, esp extraocular, often asymm prox mscl wknss at end of day  
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compare Lambert-Eatn Myasthenic syn to MG   Lambert-Eaton is often w SCLC, Ab to Ca++, sympt get better with use  
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test for MG   1) auto Ab (20% neg), 2) edrophonium (Tensilon, anticholinesterase) improves sympt  
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what extra diagnostic need MG   CT to evaluate thymoma (10-15% on scan), but histol abnl ~75%  
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tx MG longterm   pyridostigmine, steroids if not responding  
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vit B12 and Friedrich ataxia damages which neural tracts, signs on exam?   demyelin of dorsal columns, corticospinal, and spinoCb; ataxic gait, hyperreflexia, impaired position/vibration sense  
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describe Friedrich's ataxia (genes, pathophys, clinical)   AR triple repeat expansion dz of mitochondria; leads to demyelin of dorsal columns, corticospinal, and spinoCb; ataxic gait, hyperreflexia, impaired position/vibration sense  
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describe syringomyelia (pathophys and clinical)   (basically a cyst of CSF) crossing fibers of [spinothal tract I think] are damaged; leads to bilateral loss of pain and temp sensation in shoulders (capelike distrib), +/- muscle atrophy hands  
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what leads to destruction of anterior horns spinal column? Cause? Symptoms?   polio and werdnig-Hoffman; flaccid paralysis (LMN)  
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occlusion ventral spinal artiery causes what? Clinical?   damages everything except dorsal columns, so only have tactile, vibration, sensation  
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3 syphillis, aka? Damages?   tabes dorsalis damages dorsal roots and columns; impaired propioception and locomotor ataxia  
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symptoms of ALS (amyotrophic lateral sclerosis=Lou Gehrigs)?   asymmetric, progressive weakness, UMN and LMN signs (spasticity, hyperreflex, + Babinski AND fascicul, atrophy, flaccidity); treatment is supportive  
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pyramidal tract aka   corticospinal=mvmt contra limbs  
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Pseudotumor cerebri-describe what it is and how it presents   incrsd ICP papilledema, daily headaches worse in am +/- N/V; young obese women  
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Pseudotumor cerebri-describe how diagnose and treat   CT, MRI negative; concern about vision loss; treatment supportive w wgt loss and lumbar puncture or CSF shunt  
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Pseudotumor cerebri-potl causes   large doses vit A, tetracyclines, wdrawal from corticosteroids can cause  
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differentiate resting tremor, intention tremor, and hemiballsimus as to causes   hemiballismus (involuntary, unilateral flailing limbs) from subthalamic nucleus, intention tremor due to Cerebellar dz, resting tremor due to basal ganglia  
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Brown-Sequard syndrome--distrib of lesion and clinical findings   hemisection of spinal cord; contra pain and temp, ipsi hemiparesis and ipsi loss of position/vibration (dorsal columns)  
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what Rx may help extend life ALS   rituzole (glutamine blocking agent)  
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2 main types of sz, which more common   partial (70%), generalized  
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subtypes of partial sz   1) partial; simple partial (consciousness intact), complex=LOC, postictal, may have automatisms, olfactory or gustatory halluc  
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subtypes of generalized sz   tonic-clonic, absence (45% of these can have minor clonic, ie eye blinking)  
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what's name of paralysis s/p seizure   Todd's paralysis, can last hrs-days  
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tx generalized tonic clonic or partial sz   phenytoin and carbamzepine  
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tx for absence sz   ethosuximide and valproate  
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describe Rinne test   vibrating tuning fork on mastoid until they can’t hear it, then move to outside ear—they should be able to hear (+ test).  
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describe Weber test   tuning fork on forehead, which side is louder  
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outcomeof Weber/Rinne if conductive loss   abnl (-) Rinne (bone conduction>air); Weber louder in affected (think of cotton in yr ear)  
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outcome Weber, Rinne if sensorineural loss   nml (+) Rinne (air >bone conduction); Weber louder in unaffected (good) side  
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types of Vertigo (4)   1) Peripheral: benign positional, Meniere's, labyrinthitis; 2) central (tumor, CVA, MS)  
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how test for benign positional vertigo in the office   have pt go rapidly from sitting to laying while turning head->should reproduce  
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describe Meniere's dz and px   thgt 2/2 fluid retention, recurrent severe vertigo, tinnitus, hearing loss lasting for hrs to days; recur mos-yrs later and hearing loss eventually permanent  
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tx Meniere's   low Na diet, diuretics, maybe also anti chol and anti His [meclizine]  
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when pt falls w vertigo, which side do they fall to   same side as lesion  
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dominant lesion in R handed person? L handed?   95% R handed are L dominant, 50% of L handed are L dominant  
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describe location of lesion and clinical presentation of Wernicke's aphasia   Posterior superior temporal gyrus, wordy receptive/sensory/fluent aphasia, use wrong or nonsensical words; they don't comprehend written or spoken language; can't follow commands or repeat  
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describe location of lesion and clinical presentation of Broca's aphasia   expressive/nonfluent broken, short sentences but meaningful. Comprehension intact. Impaired repetition. Posterior inferior frontal gyrus  
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describe conduction aphasia   can't repeat bc no cxn bw Broca's and Wernicke's  
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defect causing L homo hemianopia w macula sparing   R visual cortex  
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defect causing L homo hemianopsia   R optic tract  
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defect causing L upper quad anopsia   R optic radiations in R temporal lobe  
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defect causing L lower quad anopsia   R optic radiations in R parietal lobe  
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defect causing L homo hemianopsia w macular sparing   R occipital lobe, from P cerebral artery occlusion  
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lesion causing bitemporal hemianopsia   optic chiasm (usu pit tumor)  
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define difft types of glaucoma, general features   open angle (90%): painless, incrsd intraocular P 20-30mmHg, progressive visual field loss, incsrd cup-to-disk on fundo exam; closed-angle: sudden ocular pain, see halos around light, intraocular P >30, N/V, sudden decrsd vision, fixed, mid-dilated pupil  
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tx closed angle glaucoma   pilocarpine, oral glycerin and/or acetazolamide  
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tx open angle glaucoma   can include b-blockers, a agonist, prostaglandins (latanoprost), acetazolamide  
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types of macular degeneration   exudative wet=neovascular w sudden vision loss; atrophic/non exudative/ dry (90%)=yellow-white dposits drusen  
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findings on fundo exam: cotton wool   HTN  
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findings on fundo exam: dot blot hemorr   DM  
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findings on fundo exam: neo vascul   DM  
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findings on fundo exam: pale fundus, cherry spot   central retinal artery occlusion  
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findings on fundo exam: tortorous retinal veins   retinal vein occlusion  
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findings on fundo exam: focal yellow-white deposits   macula drusen (macula degeneration)  
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findings on fundo exam: incrsd cup to disk ratio   glaucoma  
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findings on fundo exam: blurred optic disk margins   papilledema or papillitis  
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differentiate fundo changes see with DM, HTN   DM: dot-blot hemorrhages, neovasc retina; HTN: ateriolar narrowing and cotton-wool spots and may see papilledema in severe HTN/HTN emergency  
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common causes blindness in US, infxs causes (3)   DM in younger adults, macular degen in >55; river blindness (onch volvulus, a helminth, give ivermectin), chl trachomatis, toxo carnis (if granuloma)  
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what's river blindness? What's the treatment   river blindness (onch volvulus, a helminth, give ivermectin),  
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how recognize central retinal artery occlusion? Tx? Assoc?   sudden, painless, unilateral loss of vision; most common due to emboli (carotid, heart), but also temporal arteritis; no tx exc temporal arteritis give corticosteroids  
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3 causes of sudden, unilateral vision loss, painless   1) central artery occlusion (pale fundus, cherry red spot), 2) central vein occlusion (distended retinal veins, retinal hemorrhages), 3) retinal detach (pt reports floaters, flashes of light, curtain coming down)  
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describe Sturge Weber   neurocutaneous dz; SKIN: congenital port wine stain (hemangioma), NEURO: leptomeningeal angio, glaucoma, sz, hemiparesis, MR  
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describe tuberous sclerosis   neurocutaneous dz; hamartomas in skin, CNS, organs; astrocytoma, MR, sz **facial lesions with ash leaf spots, shagreen patches (thickened skin)  
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describe neurofibromatosis   neurocutaneous dz; café au lait, axillary freckling, Lisch nodule (iris), neurofibromas in skin, neural tumors (meningiomas, acoustic neuromas), optic path glioma, Pheorenovascular HTN, scoliosis, sz  
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NF1 v NF2   NF1:café au lait, Lisch nodule (iris), gliomas, meningiomas, pheo, scoliosis; NF2: bilateral acoustic neuroma, juvenile cataracts (Step 1 pdf)  
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von Hippel Lindau   neurocutaneous dz; **renal cell carcinoma, hemangioblastoma cerebellum, retinal angiomas, cysts in kidney and liver, pheochromocytomas, polycythemia,  
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name 4 neurocutaneous dzs   Sturge Weber, tuberous sclerosis, NF, von Hippel Lindau  
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NF2? Chromosome? Gene?   bilateral acoustic scwhannoma, juvenile cataracts; chrom 22, gene NF2  
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Lisch nodules are charact of?   (found in iris) Neurofibromatosis  
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NF1 aka? Chromosome?   von Recklinghausen's disease=NF type 1; chrom 17  
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café au lait spots with normal IQ? With MR? with anemia?   nml IQ:NF; MR: McCUne Albright or tuberous sclerosis; anemia: Fanconi's anemia  
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which neurocut has hamartomas (incl skin)? skin hemangioma? Skin neurofibromas?   hamartomas: tuberous sclerosis; skin hemangiomas: Sturge Weber and von Hippel-Lindau; skin neurofibroma: NF  
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which neurocut has MR?   tuberous sclerosis, Sturge Weber  
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describe corticospinal tract path and where decussates   Start in motor cortex, cross over in medulla, become LMN in anterior horn of spinal cord at that level.  
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describe dorsal/posterior column tract path and where decussates   Start in mscl spindles, golgi tendon organs, Pacini&Meissner’s disks, signal through dorsal root ganglion up fasciculus gracilus and cuneatus (upper body), cross in medulla  
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describe spinothal tract path and where decussates   Afferent/ascending. Start free nerve endings, pain fibers, cross at level of spinal cord (anterior/ventral white commissure), then go the length of the spinal cord to thalamus.  
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