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121 Cards in this Set

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What possible results can you get EMG and what do they mean?
electromyography can show issues with activation (how fast pulses come from the brain) and recruitment (pulling in other fibers).

activation problems = upper problem, recruitment = lower.

also, if nerve problem, insertional activity and spontaneous activity are increased.
generally, what has to be wrong to be unconscious? what does the cranial nerve exam tell you?
unconscious person - ABC's, look for causes, naloxone/thiamine/glucose, cranial nerve exam.

unconscious = either brain stem or both hemispheres affected.

all nerves the same = diffuse = possibilities are metabolic, toxic, infection, hypoxia, or seizure.

focal findings (one blown pupil) = get a scan fast, something structural is wrong.
what structures does visual information go through? what's the problem if the right half of both eyes is black?
cornea, retina, then the optic nerve, to the chiasm, to the optic tract, to the LGN, then radiations (through the temporal/parietal), then to the cortex (broadman's 17).

left hemonomous hemianopia could be damage to the right optic tract (so after the chiasm, before LGN) or to BOTH optic radiations.

remember black on top = opposite side's bottom problem (temporal = meynert).

black on bottom quarter = top part (parietal optic radiation).
what's the weird presentation of MLF problem?
talk about R eye: can't adduct eye if looking left (look towards nose).

but convergence (both eyes towards nose) is fine. this doesn't depend on the MLF.

the MLF connects the CN VI (abducens) to the contralateral CN III
tell between parkinsons and essential tremor:
essential tremor usually bilateral, starts in one hand though. can involve neck/voice eventually. NO other symptoms (no bradykinesia, no dementia, no shuffling). have cogweel EFFECT, no RIGIDITY. ET is usually intention tremor. beta blockers, thalamic stimulators work.
what are the drugs used for parkinsons?
levadopa becomes dopamine when crossing the BBB. give with carbidopa to prevent gut breakdown of levadopa.

tolcapone/entacapone = COMT inhibitors, keep levadopa around.

selegeline/rasigiline = MAO-B inhibitors help. Anticholinergics good.

Amantadine may help with levadopa-caused movement.
adult onset ataxia with affected family members is what?
ADCA - adult dominant cerebellar ataxia, aka SCA (spinal cerebellar ataxia) - there are tons of different kinds. Can see telltale effects on MRI.

note that a worse form of parkinsons is multisystem atrophy (MSA)
cluster headaches - who do they typically affect, why are they called cluster, what do you do?
typically middle aged men, wake you up from sleep/early morning, come in clusters for several weeks and then go away, treat with OXYGEN and tryptans.
meniere's disease - triad is what? treatment?
vertigo, tinnitus, and hearing loss. low salt, meclezine, cyclizine, dimenhydrinate.
wallenburg's = ?
lateral medullary = PICA infarct. ipsilateral facial sensory loss, contralateral body sensory loss, horner's, dysphagia/vertigo.
lacunar infarcts of the anterior limb of the internal capsule vs. posterior limb - what will you see?
capsule infarcts lack cortex signs = no visual, speech problems.

pure motor on cotralateral upper/lower body is posterior capsule.

anterior capsule causes pure motor also, but involves ataxia too.

can also have pure sensory?
botulism poisoning looks like what?
descending paralysis starting in the face/neck and going down. dilated pupils, diplopia, trouble swallowing, NO sensory defects, going down.
pain and temperature fibers - what kind are they, where do they synapse, where do they go?
they're not well myelinated, A-delta and C fibers, 1st neuron in the DRG, synapse and cross, ascend in the spinothalamic tract to the VPL of the thalamus.
proprioception/vibratory sense travel in what? what kinds of fibers?
well mylenated a-alpha and a-beta fibers.

DRG neuron ascends ipsilaterally to the medulla, synapse at gracilis/cuneatus, become medial leminiscus and go to VPL of thalamus.
what do you have to worry about in an IVDU with back pain? do what?
epidural abscess in the spine - have to get an MRI.
what do you see in lewy body disease?
VISUAL HALLUCINATIONS with EPS (tremor, rigidity, etc).

don't always see severely impaired recent memory.

remember that lewy bodies are what are found in the substantia nigra of parkinsons.
when talking about the cerebellar causes of ataxia, what two broad categories can you make?
vermis problem = gait/trunkal ataxia.

cerebellar hemispheric problem = ipsilateral limb problem
what kind of incontinence can a stroke cause?
hyper-reflexic bladder = small capacity, small PVR, and URGE.

lower motor neuron diseases lead to atonic bladder.
what's paroxysmal hemicrania?
lots of little sluter heaadaches that don't last very long and respond super well to indomethacin.

remember cluster headaches are unilateral and tend to appear in temporal clusters over weeks, then go away for awhile.
broca's aphasia - where is the region, what vessel, symptoms?
broken speech, words mostly correct but broken up, some subtle comprehension problems, KNOW they're screwed up and frustrated.

posterior part of the inferior frontal gyrus, hit by the superior division of the MCA.
wernike's aphasia? vessel?
inferior division of MCA. don't know they're screwed up, can't comprehend and have fluid word salad.
what's gertsmann's syndrome?
dominant hemisphere lesion in the angular gyrus causing alexia, acalculia, right/left confusion, and finger agnosia (don't recognize own hand).
other than stepwise worsening, how can you tell vascular dementia from alzheimer's?
alzheimers patients will be neurologically intact until very late in the disease (motor/sensory/gait) - people with lots of strokes tend to have some focal neural deficit.
what do you see in progressive supranuclear palsy?
problem up-gaze (it's posterior midbrain loss), dementia, falls, EPS. Subcortical motor dysfunction (dysarthria especially) - so slurred speech + EPS + dementia is likely PSP. (EPS also seen in lewy body, corticobasal degeneration, striatonigral degeneration, multiple system atrophy).
treatment of choice for RLS?
Dopamine agonists - ropinerole and pramipexol (don't use levadopa = more movement). associated with IRON DEFICIENCY
other than pure motor and pure sensory strokes, what are the other capsular syndromes?
dysarthria-clumsy hand = slurred speech and bum hand.

ataxia-hemiparesis = one half of body ataxic and weak.
partial generalized complex simple - what do they mean for seizures?
partial vs. general = sx arising from one part or the whole brain.

simple = awareness unaffected, complex = awareness affected
phenytoin side effects?
funny face and gums = gingival hyperplasia and coarsening of facial features.
what are some non-brain things that might happen acutely with subarahnoid hemorrhage?
can get weird pulmonary edema, hyponatremia from high ANP/cerebral salt wasting, and HEART PROBLEMS (long QT, t wave inversions, arrhythmias)
what's the treatment of subarachnoid hemorrhage?
after CT w/out to dx (if negative and strong suspicion, do LP), do angiogram to help the surgeons figure out where to coil.

then triple H therapy (hypertensive/hypervolemic hemodelution) to keep brain wet.

then Ca++ blockers.
how do you test for wilson's disease?
rememember it's one of the EPS causing guys. Normal/high serum copper, low ceruliplasmin usually but not always.

increased urinary copper secretion (24 hour collection) is most sensitive.

confirm = liver biopsy.
post trauma central brain herniation - what happens to the pupils first?

uncal herniation?
central herniation = diencephalon downwards.
sympathetics get disrupted, so have un-opposed parasympathetics = small, reactive pupils. goes with de-cordate posturing, then decerebrate, then blown pupils. tends to crush the ACA = leg weakness.

uncal: dilated pupil early.
what's the b12 deficiency that causes peripheral problems called?
subacute combined degeneration = loss of the posterior columns and later the corticospinal tracts = loss proprioception/vibratory sense, neuropathy, weakness.
neuro manifestations of lupus?
antiphospholipid syndrome can cause strokes.

affective problems (dementia) common.

seizures/psychosis also common.

also peripheral neuropathy.
what demylenating disease appears like MS? what do you do for it?
ADEM - acute demylenating encephalomyelitis. often after vaccines/viruses.

self limited, generally, can use steroids.

likes posterior-cerebrum, causes PERSONALITY/COGNATIVE changes (only seen in late MS).

NO oligoclonal bands on CSF. May have lymphocytes/increased protein, more than in MS.
how is TB meningitis different from other bacterial? CSF findings?
likes the basal meninges = inflammation of the cranial nerves = focal cranial nerve deficits.

course is CHRONIC instead of acute.

little strokes sometimes happen.

CSF = lots of LYMPHOCYTES (not PMN's), REALLY LOW GLUCOSE, high protein.
what does lyme disease do in neurology?
subacute meningitis with lymphocytes/high protein in CSF.

facial nerve paralysis

poly-radiculopathy (pain in lots of places, some weakness).
what's the viral encephalitis you have to watch out for, how does it present, CSF findings?
HSV-1: often base of the brain around the temporal region = partial complex seizures with olfactory hallucinations, MEMORY problems,

csf has RBC's in it, lymphocytes, normal glucose, there is a PCR for HSV.

treat with IV acyclovir.
CSF fungal infection? what do you see in fluid? how do you see cryptococcous?
LOW glucose, LYMPHOCYTES, high protein, india ink stain now replaced by latex agglutination.
what's the viral encephalitis you have to watch out for, how does it present, CSF findings?
HSV-1: often base of the brain around the temporal region = partial complex seizures with olfactory hallucinations, MEMORY problems,

csf has RBC's in it, lymphocytes, normal glucose, there is a PCR for HSV.

treat with IV acyclovir.
CSF fungal infection? what do you see in fluid? how do you see cryptococcous?
LOW glucose, LYMPHOCYTES, high protein, india ink stain now replaced by latex agglutination.
how are transverse myelitis and ADEM different?
very similar in presentation (and both are hard to tell apart from first MS diagnosis) - transverse myelitis happens in hours/a couple days, ADEM over a week or two.
someone has otto/rhinorea and you're worried it's CSF. what test?
quick/dirty = spot accucheck. should be normal brain glucose (60-100 or so), but may be false if meningitis present.

real test = BETA 2 TRANSFERRIN. specific for CSF.
lady in her 20's has conductive hearing loss, and the same thing happened in her family before. what is it?
otosclerosis = new little vascualrized bones appearing in the ear.

exacerbated by pregnancy. hearing aids, some surgery can help.
benign paroxysmal positional vertigo - what might it be mistaken for, what are the symptoms, fix?
benign paroxysmal positional vertigo is the little autoliths in the inner ear - the DIX HALLPIKE manuver fixes it. worse in the morning.

labyrinthitis = viral infection, vertigo acute onset and lasts weeks.

meniere's disease = tinnitus, vertigo, hearing loss.
what blood vessels feed the spinal cord?
anterior: mostly the ASA, formed from the vertebrals up in the brain stem.

inferior anterior = artery of Adamkiewicz, from penetrating aortic branches, meets up with the ASA in the mid-T's.

posterior = various plexuses.
what is guillan barre also known as, and what antibodies might be found?
AIDP = acute inflammatory dymelinating polyneuropathy.

Anti-Gm1 common, also anti-GQ1b, GD1a, GD1b.
someone's getting really sick from guillan barre. what do you do? how do you know when to intubate? treatment?
FVC <15 mL/kg = intubate.

IVIG and plasmapharesis are equally effective.

no role for steroids.
how does CIDP differ from AIDP?
chronic inflammatory demyelinating polyneuropathy is kinda like chronic GBS, but it RESPONDS TO STEROIDS.

more sensory findings, kinda like diabetes, possible.

CSF shows high protein, like GBS.

refractory cases require IVIG/plasmaphareisis.

note that many have other chronic condition (HIV, lymphoma).
what's multifocal motor neuropathy? Dx? treatment?
pure motor weakness, usually asymmetric. EMG shows conduction block.

Anti-GM1 commonly found. Often mistaken for ALS. Not usually UMN signs, but can have.

Note that there is TREATMENT: IVIG/immune suppressants effective.
treatment of myasthenia?
acetycholine esterase inhibitors (pyridiostigmine in particular) = fixes symptoms.

immune suppression (steroids, IVIG/plasmapharesis/methotrexate/cyclosporine) all used.

also removing the thymoma.
how is lambert eaton symptoms different from mg?
lambert eaton = better with repeat muscle use, eye problems don't happen, but do get anti-cholinergic effects (dry mouth/eyes).
describe myotonic dystrophy: caused by?
dystrophy in adults, caused by trinucleotide repeat, lots of weird stuff - cataracts, insulin resistance, arrhythmia, dysphagia, small balls.
what are the mitochondrial diseases?
MELAS = myopathy, encephalopathy, lactic acidosis, and stroke.

MERRF = myopathy, epilepsy, ragged red fibers.
what symptoms tell apart dermatomyositis and polymyositis? what do you see on biopsy?
dermato = heliotrope rash over eyelids and grotton papules (scaly shit on knuckles)

dermato = mostly vessel problem with antibodies attacking.

poly = CD8 t cells attacking endomesium of nerves, you see these on biopsy.

steroids in poly, DM.
paraneoplastic syndromes in neurology - what are possible? test for it?
cerebellar degeneration causing ataxia, peripheral neuropathy. Look for ANTI-HU antibodies (anti-neuronal).
why doesn't an MCA stroke cause weakness/sensory loss to the face, arm, and leg?
leg is ACA. face/arm = MCA.
HIV and neurology - other than brain stuff and peripheral neuropathy, what does it do?
CMV infection in the spine = radicular pain/weakness = pain in the legs/scral region, weakness, sphincter dysfunction.

CSF pcr titers, treat with gancyclovir/foscarnet.

Also, VACOULAR MYOPATHY = kinda looks like b12 deficiency in the spine.
hypertensive strokes happen in what 3 most common places?
go anterior to posterior: basal ganglia, thalamus, pons, then cerebellum.
which sensory fibers are small?
temperature/pinprick....positional/vibration are large. this is why the temp/pin are lost in diabetic small fiber neuropathy.
where do lesions happen that cause apraxia?
defect in learned motor movement comes from dominant (left) frontal or parietal lesion.
what brian/systemic neuro disorders are associated with REM disorder?
synnucleopathies = parkinsons, multiple system atrophy, lewy body diesase.
what symptoms are seen in neurosarcoidosis?
bilateral LMN facial weakness, sometimes with cranial nerve afferent problems (afferent pupilary dilation problem).

remember in young african americans this is the #1 cause of bilateral lower motor neuron facial palsy.
if someone does have otto/rhino CSF leakage, what bugs are you most worried about?
strep pneumo and h. flu meningitis.
if you have little brain bleeds in an old person without hypertension, what is it?
amyloid deposition - it's beta amyloid, same as in alzheimer's, called cerebral amyloid angiopathy.
port wine spot in the distribution of trigeminal = what disease? expect what in the brain?
sturge webber kids often get leptominengal angiomatosis. sometimes retarded. Also get GLAUCOMA in 1/3 of cases
what's the difference between a basilar migraine and a reuglar one? classic vs common?
classic has aura, common doesn't.

basilar migraine = super bad neuro signs (quadrapelegia, even coma)
trigeminal neuralgia in a lady makes you wonder about...?
often presenting sign of MS.
what can you use to prophylax against migraine?
propranolol, ace inhibitors, amitryptiline, valproic acid.
other than pseudotumor and actual tumors, what are some other random causes of increased ICP?
hypothyroidism, vitamin A toxicity, SLE, steroid withdrawal, tetracycline
what nerve controlls the biceps? if damaged, what else happens?
the musculocutaneous nerve.

also does sensation to a lot of the forearm (radial side)
what does schistosomiasis have to do with neurology?
little bugs end up draining through batston's plexus, end up near/above spinal cord, granulomas form and crush cord.
HIV patient has ring-enhancing lesions in brain. How do you diagnose?
either CNS lymphoma or toxo. CSF test for EBV is specific for CNS lymphoma.
What's SSPE? diagnosis?
subacute sclerosing pan encephalitis - this is the late complication of measles. never after age 18.

super brain problems (ataxia, seizures, umn lesions). CSF has OLIGOCLONAL bands, like in MS.
why is cat scratch interesting in neurology?
immunocompromised people: bartonella causes lymphadenopathy, then can spread to brain, give you PULVINAR (post-thalamus) lesions, cause STATUS EPILEPTICUS.

also bascillary angiomatosis.
what's the confirmatory test for myasthenia gravis?
electroMyography under repetative stress.

tensiolon test is sensitive, not specific.
how can you tell between pituitary adenomas and crainopharyngiomas?
crainopharyngiomas are often calcified and full of yellow crap.

pituitary adenomas aren't.
other than phlebotamy, what do you give to polycythemia vera people?
for some reason, hydroxyurea. it minimizes thrombotic events.
what is the difference in hydration/urine between cerebral salt wasting and SIADH?
both happen from brain pathology.

SIADH = intravascular volume increased (retaining water) and urine salt increased.

cerebral salt wasting = high ANP. end up dehydrated with high urine salt (low intravascular volume is the difference).
guy with lung caner becomes super lethargic, looses reflexes, nauseous/vomiting. what happened?
hypercalcemia.
what's pickwickian syndrome?
fat people who don't breathe enough, have obstructive sleep apnea, and are sleepy/fall asleep during the day.
what's neuromyelitis optica?
optic neurotis plus transverse myelitis - so often have weird bilateral lower body paralysis/bladder dysfunction, along with optic neuritis.

mistaken for MS.
spreading central vision problem - what might it be?
hx of alcohol/smoking = alcohol/tobacco ambliopia.

if family affected, likely leber's optic atrophy
guy can't release a door knob. what else is probably wrong with him?
little balls, baldness, cataracts, heart problems. myotonic dystrophy happens later in life. also diabetes.

may need pacer.
lead poisoning in an adult looks like what?
GI pain, lead lines in the gums, and EXTENSOR PALESIES (wrist drop).

drinking acidic fluid out of contaminated cups is a good way to get lead.
sensory reversal (hot things feel cold, etc) is a hint for what kind of poisoning?
siguatoxin, from reef fish (dinoflagelates). give mannitol.
what is adie's pupil?
random benign illness with dilated pupils bilaterally, perhaps absent body tendon reflexes. goes away.
cerebellar infarct make vertigo. what vessel is especially likely to have been blocked?
PICA - the middle branches of it especially, but also the laterals can do it.

if there's also Auditory loss = AICA
3, 4, and 6th CN nerve palsies - what do they look like?
3rd = down and out, mostly due to no more medial rectus.

4th = can't look down due to superior oblique problem, so can't go downstairs.

6th nerve palsy = no LR, so medially deviated.
cortical vs. subcortical dementia?
cortical = no focal deficits. speech may not make sense, but there's no dysarthria. subcortical may have other motor problems (increased tone).

note that cortical be separated into anterior (pick's frontotemporal) vs. posterior (alzheimer's).
B12 deficiency symptoms?
subacute combined degeneration = CNS and PNS involvement. Distal small neuronal neuropathy common (pins/needles), vibration/proprioception (romberg +), and affecting cortico-spinal tract (UMN spasticity/hyperreflexia)
neurosyphilis - what's there to know? diagnosis? signs? test?
almost always hypOreflexic. Tabes doraslis kinda looks like b12 deficiency with lots of sensory modalities in the cord messed up.

RPR is a good test, but negative doesn't rule out neurosyph...need FT-ABS for that.

RPR on CSF is a good test.
a pt with HTN has either a cerebellar, cerebral, or deep hematoma. what's different in management?
cerebellum hematomas need to be rapidly evacuated - pts can recover completely. signs are often nausea/vomiting.

deep structure hemorrhages (most typical - pons, BG, thalamus) = supportive care.

cerebral often cause LOC, get surgical consult.
guillan barre - what's the best test to confirm the diagnosis?
nerve conduction studies - this is better than CSF for finding demylenating diseases.

CSF is only going to show increased protein.

don't forget that reflexes tend to be absent.
spinal muscle atrophy - what are the signs, how do you diagnose?
floppy baby that's a couple months old, absent DTR's, fasiculating tongue.

comes from progressive deinnervation of LMN's. Biopsy will show this.

Note that conduction studies will be normal, not a demylenation problem.

autosomal recessive.
cauda equina syndrome - do the leg reflexes get stronger or weaker? babinski?
weaker, no babinski - these eliminate cauda equina syndrome from the differential.
old person has several recent falls. what's the first test to do?
get up and go - stand from a chair, walk around, come back sit down. weakness, etc can be seen.

all the expensive wokrup after this.
normal pressure hydroecephalus - what will you see on head imaging, what's the opening pressure, what do you do?
enlarged ventricles = hydrocephalus.

opening pressure = normal (normal pressure).

VP shunt = surgery to cure.
what's ramsay hunt syndrome?
occular zoster - see vessicles on the ear, FACIAL half paralyzed (including forehead = LMN), decreased sensio-neural hearing.
what do you expect to see in patients with CIDP, diagnosis, treatment?
peripheral neuropathy + weakness, perhaps absent reflexes, a bit like diabetes. can be cranial nerves. AIDP (gbs) does NOT respond to steroids. CIDP DOES.

CSF = high protein, few cells.

EMG studies show demylenation.

No perfect test - treat = IVIG/plasmapharesis/steroids.
what physical signs are you allowed to have with pseudotumor?
only blurry vision, papiledema, and 6th nerve palsy. anything more than this and it's not pseudotumor.
guy newly found to have brain mets - what do you do first?
steroids and anti-convulsants while you talk to rad/onc and surgery.

both are needed.
diabetic with 3rd nerve palsy and pupil issues - what happened?
this is an aneurysm, not typical diabetic nerve palsy.

any time the pupil gets blown, it's an emergency and should get an angiogram.
what does narrow angle glaucoma look like?
comes from DILATED pupil - so it'll be dilated, eye will be red, vision somehwat compromised.

kinda looks like temporal arteritis except for the big pupil.

may be taking sympathitic stimulating medications.
how can you tell apart partial complex and absence seizures?
absene typically are only a few seconds and have NO POST ICTAL CONFUSION.

complex partial = post ictal, rare findings on EEG (as opposed to the 3hz spike/wave in absence).
what are the different kinds of aphasia?
none can name.
motor = broca's = no repetition, not fluent, but do comprehend

sensory = wernike's = fluent, no comprehension, no repeating

transcortical motor = around broca's = repeat intact, not fluent, do comprehend.

transcortical sensory = around wernike's = repeat intact, but don't comprehend, are fluent.

note that if you hit the arcuate fasicilus (connection between wernike's and broca's) = NO repetition possible.
how do you diagnose cataplexy/nacrolepsy?
decreased CSF hypocretin levels (those are the neurons lost in the hypothalamus that cause), or MSLT (polysomnography with short naps) showing latency <8min or fast onset REM.

remember modafenil = treatment.
abetalioproteinemia - when does it occur, what are the symptoms?
inherited, usually 5-10 yrs, looks like fredreich's (spinal cord issues - posterior columns, pain/temp) - see lack of cholesterol/triglycerides in blood, ACANTHOCYTES, retinitis pigmentosum (also seen in fredreich's).
arnold chiari I vs II?
I = doesn't show up 'till later in life, herniation of the TONSILS.

II: early, both VERMIS herniation + spina biffida
what do you expect to see in people with multiple system atrophy?
shy drager = PARKINSONIANISM plus autonomic dysfunction (othostatic hypotension, dry mouth, etc)

can also have random other neuro findings (cerebellar, LMN findings, etc).
person in their 30's has a clear MCA territory infarct. no drugs, no vascuilitis, no heart conditions. what's most likely?
carotid dissection - you'd do a doppler on the carotids anyway, but make sure you do this early.
what are the principles of how to prescribe/dose anti seizure meds?
use a single drug if possible, and max it out if necessary. if it doesn't work, switch to a different single drug and max it out. Avoid double therapy if possible.

don't follow blood levels religiously - go on the patient's symptoms. If blood levels a bit high but no side effects, don't change anything.
what are the principles of how to prescribe/dose anti seizure meds?
use a single drug if possible, and max it out if necessary. if it doesn't work, switch to a different single drug and max it out. Avoid double therapy if possible.

don't follow blood levels religiously - go on the patient's symptoms. If blood levels a bit high but no side effects, don't change anything.
recurrent viral meningitis is usually which bug?
HSV-2, and often coincides with outbreaks, but not always.

the fecal/oral viruses, echo/coxackie are the normal causes of non-recurrent.

note that you don't give acyclovir for herpes-2 infections.
someone gets shingles on their face. what's the big concern months later?
contralateral facial paralysis from ipsilateral vasculitis. brain vascuilitis from reactivated VZV can be deadly. Acyclovir can help.
other than absence seizures, what's the kind of seizure with unique prescriptions?
simple partial = carbamazapine, lamotrigine, oxcarbazapine, keppra.

not the typical valproate answer.
remember that basal ganglia, pons, and cerebellum are the major sites of hypertensive bleeds. what are the different symptoms?
back to front - cerebellum causes typical ataxia/nausea/vomiting, but also GAZE PALSY, NO HEMIPARESIS.

pontine hemorrhage = unconscious, bad.

basal ganglia = often get capsule = weakness, often sensory problems, homonomous hemianopsia.

just remember that no weakness is a danger sign for cerebellar hemorrhage which needs evacuation.
what is diabetic amotrophy, and why do we care?
it's reversible with good glucose control. Now called proximal diabetic neuropathy = wasting, usually of thigh/butt.
what are the contraindications to TPA usage?
tPA no use: stroke of any kind in the last 3 months, ever having an intracranial bleed, any GI/GU bleeding in last 21 days, INR >1.7, platelets >100k, >185/110, really high/low blood glucose, rapidly improving symptoms (TIA), surgery in last 14 days.
what's the difference between a typical and atypical absence seizures?
typical = seconds, 3hz spike and wave with hypervent.

atypical = longer, but still no post-ictal state, <2.5 hz with hypervent.
What do you see in juvenile myoclonic epilepsy?
Seizures, myoclonus, sometimes progressing from absence seizures.

Exacerbated by LACK OF SLEEP (sometimes occuring in the morning)