Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

674 Cards in this Set

  • Front
  • Back
rbcs seen in csf as a result of subarachnoid hemorrhage/hemorrhagic encephalitis
presence of rbcs but no xanthochromasia in csf is indicative of...
traumatic tap, rbcs are not lysed (whereas in xanthocromia they are lysed)
significance of oligoclonal bands
ms (or any other demyelinating dz)
cns infx
non-infectious inflammatory proceess
what does a + ebv pcr from csf indicate
lymphoma in pts with aids or immunosuppression
what is the danger of performing a lp? how to avoid this?
cerebral/cbl herniation if there is a supra/infratentorial mass lesion
what protein is present in csf that can indicate cjd?
what is the best initial imaging study for HA, trauma, sz, subarachnoid hemorrhage, and stroke
when is an mri of the brain indicated
to examine posterior fossa and craniocervical junction (both regions are seen poorly on ct d/t artifact from surrounding bone)
what does a ct show that is relevant in strokes
fresh blood
where do alpha waves originate from? when are they seen?
posterior head
seen in relaxed, awake state with eyes closed
where do beta waves originate from
frontial region
when are theta waves seen normally?
if seen at other times, can indicate
during sleep
if seen during wakefulness, can indicate encephalopathy, esp if generalized, slow and arrhythmic)
why do pts have to hyperventilate during eeg
in order to provoke absence sz
how to induce myoclonic sz
interictal changes on eeg
seen only in minority
what should be given to all unconscious pts upon arrival in a hospital
why should thiamine be given before glucose
glucose alone can induce wernicke's encephalopathy
definition of pvs
pt has lost all awareness and cognitive fxn, but remain wiht eyes open, have sleep-wake cycles, and maintain respiration and other autonomic fxn
how is locked in syndrome different from pvs
in locked in syndrome, pt is awake and intact, with no altered consciousness
can only move eyes vertically and blink
what causes locked in syndrome
usually a large lesion at the base of the pons
definition of encephalopathy
inability fo carry out a coherent plan or thought or action
describe the visual pathway
light enters the retina, stimulating the rods and cones --> optic nerve --> optic chiasm --> optic tract --> LGN --> optic radiations --> occipital cortex
what is the visual defect if the right optic nerve is damaged
total right eye blindness
what is the visual defect if the optic chiasm is damaged?
bitemporal visual field deficit
what is the visual defect if the right optic tract is damaged
left homonymous hemianopia (can't see anything from the left-most regions of the visual field)
what is the visual defect if the right parietal optic radiation is damaged?
left inferior homonymous quadrantonopia
what is the visual defect if the right temporal optic radiation is damaged?
left superior homonymous quadrantonopia
what is the visual defect if both right optic radiations are damaged?
left homonymous hemianopia
what is the visual defect if the right occipital cortex is damaged
left homonymous hemianopia with macular sparing
what is the visual problem if the pinhole test improves vision
the problem is with refraction
marcus gunn pupil - how to test for it, what is it?
pt is in a dimly lit room, have them look in the distance
shine light in each eye
if the light is flashed in one eye and the ipsilateral pupil dilates, a relative afferent pupillary defect is present (aka marcus-gunn pupil); this pupil WILL constrict when light is shows into contralateral eye
unequal pupils
edinger-westphal nuclei
what is the pathway
midbrain nuclei that regulates pupil size
it has efferent parasympathetic fibers that travel with CN III, then synapse on the ciliary ganglion
this will lead to constriction of the pupil

light enters and travels via cn ii and synapses in pretectum, and travels to b/l edinger-westphal nucleus, which synapses with cn iii (carries parasymp fibers) --> synapses in ciliary ganglion and goes to retina
how does the pupil dilate?
there are sympathetic fibers that start in the ipsilateral posterolateral hypothalamus and project down the brainstem at the C8-T1 spinal level, where they synapse.
2nd order neurons then synapse in superior cervical ganglion and the post-ganglionic (3rd order) neurons travel a;ong internal carotid artery into cavernous sinus into the orbit to the pupillodilaotr muscles
how to distinguish physiologic anisocoria from pathologic?
if it is physiologic, then the degree of anisocoria will not change with different illumination
how to determine if anasocoria is caused by horner's syndrome
cocaine drops will fail to dilate the affected pupil
if cocaine test for anasocoria is negative, what can be used to distinguish a preganglionic from a post-ganglionic horner's syndrome
hydroxyamphetamine - if post-ganglionic, then horner's syndrome is post-ganglionic
sx of CN III palsy
"down and out with a 3rd nerve palsy"
dilated pupil
transverse myelitis
inflammatory demylenation in spinal cord with certain spinal tracts affected
--> b/l or u/l weakness below lesion -> bowel/bladder loss, hyperreflexia, + babinski
uhthoff's phenomenon
worsening of ms sx in heat
prognosis for ms
1/3 make great recovery, 1/3 can't work, 1/3 are wheelchair bound;
young women with rapid remission adn mild relapses have best prognosis
what do new ms lesions look like on mri

what do old lesions look like?
T2 shows hyperintense areas in white matter

T1 shows hypodense (looks like black hole)
most common locations for ms lesions
periventricular white matter
juxtacortical regions
corpus callosum
cbl peduncles
dawson's fingers
in ms, there is demyelination spreading from corpus callossum
what are oligoclonal bnads
IgG AB from plasma cells, seen in ms
how to evaluate old optic neuritis in ms
visual evoked potential... can be used to show how fast signals travel down optic nerve
chronic tx of ms
interferons B-1a/1b, glatiramer, metoxantrone--> decreased rate of relapses
tx for acute relapses of ms
corticosteroids (shortens duration of relapse)
what can be used if ms doesn't respond to traditional tx
aka Guillan Barre
rapid ascending areflexic motor paralysis; no sensory problems
starts with pins/needles in feet
ADEM and how can it be distinguished from ms
acute diisseminating encephaolmyelitis
usually follows viral infx or vaccine, but similar presentation to ms, except that lesions are in posterior cerebral hemispheres (white matter; in ms its periventricular) and there are behavior and cognitive changes (usually only seen in late ms)
csf of adem
lymphocytic pleiocytosis with increased protein
oligoclonal bands rarely occcur
prognosis of adem
neuro recovery is usually complete
steroids decrease duration of episode
where does corticospinal tract cross
clinical manifestations if there is a lesion here
crosses in medulla

umn signs and weakness
where does spinothalamic tract cross
1-2 levels above the lesion, anterior commissure
where do dorsal columns cross
sx of brown-sequard syndrome
ipsilateral weakness, umn signs (from corticospinal tract)
ipsilateral decrease in vibration/position sense
contralateral decrease in pain/temp
where is the lesion in polio
clinical features
anterior horns
flaccid paralysis, lmn sx
where is the lesion in als
clinical features
anterior horns and corticospinal tracts
combined umn and lmn sx; cramps, dysphagia, weakness, ataxia, common; respiratory muscles affected late in dz; death in 5 yrs
clinical features if there is an occlusion of anterior spinal artery
corticospinal tract, anterior horns, and spinothalamic tract are all affected

dorsal columns are spared
where is the lesion in tabes dorsalis
clinical features
dorsal columns and dorsal roots
impaired proprioception and sensory ataxia
where is the lesion in syringomyelia
clinical features
at crossing fibers of of anterior commissure

loss of pain and temp and lmn signs (in a cape like distribution if lesion is in c spine)
how do fibers of corticospinal tract travel
start in motor cortex, pass through basal ganglia, cross in medulla, travel down spinal cord via corticospinal tract, synapse in anterior horn, to muscle
what other condition is associated with syringomyelia
chiari syndrome
chiari syndrome I

chiary syndrome ii
cbl tonsils go down and put pressure on c-spine and brainstem

downward herniation of cbl tonsils and vermis and 4th ventricle; hydrocephalus is common, difficulty swallowing, choking
what bv supplies the dorsal columns
posterior spinal artery
where is the spinal cord lesion in b12 deficiency
dorsal columns and corticospinal tracts
csf in pt with adem
lymphocytic pleiocytosis and increased protein
oligoclonal bands are RARE
prognosis for adem
recovery is common and is usually complete
tx fo adem
steroids to decrease duration of episode
jc virus gets reactivated --> demylenation by infected oligodenrocytes, seen in immunocompromised
htn leukoencephalopathy
sudden increase in bp, p/w acute confusional states, sz, ha, vomiting,
papilladema, retinal hemorrhages
reversible but can lead to coma/death
what is required for the dx of narcolepsy
sleep latency <5 min in 2/5 naps measured in sleep study, and must have rapid rem onset
possible causes of restless leg syndrome
fe deficiency,
etoh, uremia
tx of restless leg syndrome
da agonists, BZ, fe (if deficient)
pathogenesis of ha
irritation of pain-sensitive structures in head (bv, meninges, cn), periosteum, muscles, eyes, ears, sinuses, mucous membranes
tumors and hydroceph --> pain by --> mass effect --> streches meninges/bv
what, if physically disturbed would not cause ha
brain parenchyma and bones
pathophysiology of ha pain
cn v adn uppercervical roots carry pain info to brain when pain sensitive structures are irritated
clinical finding of trigeminal neuralgia
pain in V2, V3
what body position can alleviate migraines? what can this be used to help differentiate?
laying down
if from increased icp, then it would be relieved by sitting up
what structure is involved in a cluster ha
superior pericarotid cavernous sinus plexus
"worst headache of my life"
subarachnoid hemorrhage
clinical features of subarachnoid hemorrhage
sudden, severe ha, with vomiting, neck stiffness, cessation of activity, and loc
dx of subarachnoid hemorrhage via lp
heme breakdown in csf
tx of trigeminal neuralgia
if that doesn't work, rf ablation
risk factors for pseudotumor cerebri
obesity, women,
neuro findings in pseudotumor cerebri
b/l visual sx + ha
scotomas, dbl vision, papilledema, otherwise nml neuro exam
ct/mri nml
tx for pseudotumor cerebri
acetazolamide, furosemide, steroids, **weight loss**
most common cause for low pressure ha
caffeine or a blood patch (periph blood injected into lp site, and causes clots (on purpose), to seal of puncture site adn
slowly evolving weakness starting in legs
widespread areflexia
loss of vibration sense
weakness in neck flexors
tx fo cidp
steroids (aidp has no response to steroids)
plasmapheresis and ivig are also useful
mechanism behind etoh intoxication - which receptors are involved?
inhibits glutamate nmda (excitatory) receptors
agonizes gaba
inhibits reticular activating system (--> sedation) and impaired hand-eye coordination (parietal association cortex)
long term effects of etoh on receptors
down reg of gaba neurotransmission and upregulation of glutamate neurotransmission --> tolerance
which cranial nerves have autonomic function
what cranial foramen does CN I travel through
cribriform plate
what cranial foramen does CN II travel through
optic foramen
what cranial foramen does CN III travel through
superior orbital fissure
what cranial foramen does CN IV travel through
superior orbital fissure
what cranial foramen does CN V1 travel through
superior orbital fissure
what cranial foramen does CN V2 travel through
foramen rotundum
what cranial foramen does CN V3 travel through
foramen ovale
what cranial foramen does CN VI travel through
superior orbital fissure
what cranial foramen does CN VII travel through
internal auditory meatus
what cranial foramen does CN VIII travel through
internal auditory meatus
what cranial foramen does CN IX travel through
jugular foramen
what cranial foramen does CN X travel through
jugular foramen
what cranial foramen does CN XI travel through
jugular foramen
what cranial foramen does CN XII travel through
hypoglossal foramen
which CNs travel through superior orbital fissure
which CNs travel through jugular foramen
which CNs travel through the internal auditory meatus
olfactory pathway
olfactory sensory neurons are w/i epithelium of dosrsal posterior nasal cavity
they project into neurons of olfactory bulb , which rest on cribriform plate (on ethmoid bone)
what can meningiomas compress if they primarily affect olfactory bulb
visual impaiarment -> blindness
frontal lobes and anterior cerebral arteries
where do meningiomas affecting smell most commonly occur
olfactory bulbs adn primary olfactory fibers that project to them from olfactory epithelium
mechanism behind anosmia following trauam
sheering of olfactory bulbs passing through cribriform plate
or bilateral contusion of orbitofrontal cortex
if pituitary tumor compresses optic chiasm from the side or posteriorly, what visual defect in visual fields would there be
homonymous hemianopia
pathophysiology of ha 2/2 pituitary tumor
stretching of diaphrama sella and other pain sensitive structures
they are frontal b/c these structures are innervated by V1
why do non-secretory pituitary tumors sometimes cause amenorrhea, elevated gh, fsh, lh, and prl
pituitary stalk compression and interruption of da fibers that normally inhibit prl release
explain macular sparing as is seen when there is occipital pole damage
there is anastomotic blood supply to occipital pole, where foveal vision is represented; when posterior cerebral artery is occluded, collaterals from mca take over blood supply

also, more than 1/2 of visual cortex is devoted to representing foveal vision
is visual acuity affected in occipital pole damage
should be spared as long as the postchiasmal lesion is unilateral
when is optic atrophy seen?
what does it look like?
glaucoma, neurotoxins, optic nerve compression from neoplasms, infarction, trauma, ms, degen dz, long-standing papilledema

pale optic disk
optic neuritis findings on mri
t2 shows abnormally increased signal w/i optic nerve (= demyelination)
t1 shows nml scan, unless there is gadolinium, then it shows the lesion (= breakdown of bbb)
what type of visual defect is normally seen in optic neuritis and why
central scotoma
demyelinating lesions from optic neuritis are deep within the nerve, so affect fibers traveling from macular area of retina, representing central vision

also there may be impaired color vision b/c teh fovea contains many cones
prognosis of optic neuritis
depends on severity of attack, and if pt has ms
if lesion is mild, axons are mostly undamaged, and when axons get remyelinated, axonal fxn returns
tx of optic neuritis
residua following recovery from optic neuritis
decreased visual acuity, afferent pupillary defect
nodes of ranvier are closer together than before so saltatory conduction is slower
slower velocity seen in evoked potential
what is seen in papilledema on eye exam
disk margins become blurred
optic disk becomes less evident
disk color darkens and is almost the same color as the retina
in icp, ratio of diamter of retinal veins:arteries increaes
retinal hemorrhages and whitish exudates
what drug will decrease frequency of tias and likelihood of cerebral infarction
define myoclonus
when is it physiologic
when is it pathologic
sudden involuntary jerk of muscle/muscle group
sleep myoclonus and hiccups are not pathological

early sx in subacute sclerosing panencephalitis and a late sx in cjd, early sign in renal failure, gaucher's dz, segmental myoclonus can occur if there is a spinal cord lesion
defining features of a tremor
involuntary and it oscillates, can be regular/irregular, distal or proximal and intermittent/continuous
physiologic tremor
tremor in fingers of outstretched arms
irregular rhythm, accentuated by nervousness
what dzs accentuate phsyiologic tremor
etoh w/d
renal/liver failure
features of essential tremor
induced by intentional activity
tremor improves with etoh
distorted handwriting is present
intention tremor
structure involved
tremor that increases as target is approached
cbl and cbl outflow tracts (cbl peduncle), red nucleus may be damaged as well
what types of dzs --> intention tremor
ms (may be seen esp when walking)
wilson's dz (large amplitue flapping as finger approaches nose, then arm may flail in a way similar to chorea - cbl and basal ganglia may both be involved)
describe tremor seen in parkinson's dz
regular rhythm (5hz)
usually decreases or disappears with voluntary mov't
see to and fro movt's of thumb across fingertips, and flexion dystonia of mcp (--> pill rolling tremor)
difference between asterixis and myoclonus
myoclonus is an active muscle contraction (seen in renal failure only)
asterixis is a relaxation of contracted muscle (seen in hepatic and renal failure)
how to evoke chorea during exam
continuous, but increase w intention or anxiety, dampened with relaxation
pt should hold arms above head with palms facing forward, or they should protrude tongue (neither position can be maintained for very long)
can also look for resp irregularities and hyperextension of fingers when arms are prone
describe athetosis
when is it seen?
similar to chorea, but is slower and leads to writhing movt's of fingers, hands, feet, or face
often seen in fetal/perinatal birth injury - one form of cp
describe dystonia
similar to athetosis, and positions tend to be held for a long time (torticollis and tortipelvis are examples)
often dependent on posture
describe ballism
which area of the brain is involved
proximal continuous flinging movt of arm
acute lesions of subthalamic nucleus (usually from occlusive ro hemorrhagic stroke)
myerson's sign
tapping of glabelllar area on forehead --> uncontrollable blinking
common physical findings in parkinsons' pt
spontaneous movt
masked facies
infrequent blinking
soft voice, syllables run together
how would a lesion in occipital lobe present
loss of ability to perceive motion, or selective loss of depth or color vision
term given to lack of any color vision, from absence of 2 or 3 cone types
where in the retina would be damaged if there was a loss of blue color discrimination?
loss of red discrimination?
outer retinal dz
inner retinal dz
fortification scotoma (scotoma in a string of connected z's) pathognomonic for migraines

comes from spontaneous firing of complex ro hypercomplex cells w/i visual cortex
pathophys of migraine ha
2 phases:
1. central transmission to spinal trigeminal nucleus from cortex --> pain
2. stimulated spinal trigeminal neurons fire antidromically DOWN axons to nerve endings on BV of brain and meninges; this wrong way firing --> vasoactive peptide release --> vasodilation, plasma protein extravastation and release of other substances that sensitize nerve endings sustain pain
moa of ergotamine
increase threshold for cortical spreading depression and abort migraine attacks
moa triptans
5-ht agonists; don't affect cortical spreading depression but may decrease cortical input to spinal trigeminal nucleus
what role does NO play in migraines
activation of NO-cGMP pathway precipitates migraine attacks
most common cause of unilateral miosis
lung ca that affects sypathetic cervical ganglia
what causes the ptosis in horner's syndrome
denervation of smooth tarsal muscles w/i eyelid
explain why cocaine has the result it does in horner's syndrome
cocaine blocks the presynaptic reuptake of norE, if neuron hasn't fired, there is no synaptic NT to block
describe why hydroxyamphetamine has the results it does in horner's syndrome
hydroxyampthetamine acts as an adrenergic agonist by releasing norE from nerve endings; if the nerve in contact with the iris is damaged, it doesn't matter if the norE is there or not, it won't work --> no dilation

if the preganglionic nerve is affected, there will be a dilation of the pupil
if a pt can't elevate the eye when it is abducted where is the problem
either superior rectus or CN III
if a pt can't lower the eye when it is adducted where is the lesion
superior oblique or CN IV
if a pt can't lower the eye when it is abducted, where is the lesion
inf rectus or CN III
if a pt can't elevate eye when it is adducted, where is the problem
inf oblique or CN III
what is seen in 4th nerve palsy
head tilt away from the side of the lesion
gaze palsy
from certain cns lesions
eyes remain conjugate adn there is no diplopia but neither eye moves fully in a particular direction
what triggers saccadic movements
frontal eye fields, ant to motor cortex on cerebral convexity
stimulation of this area (as is seen in szs) --> conjugate horizontal eye movts in direction CONTRALATERAL to the side of the stimulus
if the area is destroyed, there is a conjugate deviation of the eyes towards the side f the lesion and an inability to move them voluntarily to the opposite side
physical findings that would suggest that a horizontal gaze palsy is from cerebral vs brain stem lesion
frontal lesions spare reflexive pursuit (pt fixates n a target and then doesn't lose fixation when head is passively moved)

smooth pursuit is controlled by posterior temproal lobes (projections go from posterior limb of internal capsule to cbl/vestiblar structures - no pprf involvment)
what happens if there is destruction of the pprf
contralateral deviation and inability to move eyes conjugately in the direction of the lesion
what is pprf
area adjacent to CN VI nucleus, involved in horizontal gaze
what does the mlf do
connects CN VI with contraolateral CN III nucleus
what causes one and a half syndrome
damage to pprf and ipsilateral mlf --> ipsilateral gaze palsy and ino on contralateral side
clinical features of right sided ino (internuclear ophthalmoplegia)
inability to adduct right eye in left lateral gaze, convergence is preserved
where (brainstem or cortex) would you expect a lesion if a pt can't gaze leftward and also has a left hemiparesis
where (brainstem or cortex) would you expect a lesion if a pt can't gaze leftward and also has a right hemiparesis
what disturbance in eye movement would you expect if there was an injury to the left frontal cortex
impaired gaze to the right
what disturbance in eye movement would you expect if there was an injury to the left mlf
impaired adduction of left eye during rightward gaze
adduction during convergence is intact
what disturbance in eye movement would you expect if there was an injury to left CN III
left eye goes down and out
what disturbance in eye movement would you expect if there was an injury to right abducens nerve
inability to fully abduct right eye
what disturbance in eye movement would you expect if there was an injury to left CN VIII
horizontal rightward jerking nystagmus
how would a pineal tumor affect vision
can --> impaired upward gaze, with intact downward gaze
features of pendular nystagmus
what causes it
nystagmus with equal velocity b/l
result of severe visual impairment during childhood
features of jerk nystagmus
WHAT causes it
slow drift in one direction and a rapid corrective mov't in the other, accentuated by ocular deviation; fast component is in the direction of the gaze
most common causes of horizontal and rotary nystgmus
vestibular lesions (either periph or central)
mlf lesion
causes of vertical nystagmus
brain stem lesion (ms/syringobulbia if intrinsic) or (cbl tumor/chiari malformation if extrinsic)
type of nystagmus seen in barbiturates and phenytoin
how to test for nystagmus
use tape with vertical stripes (tape measurer, ex) and pass it horizontally in front of eyes
fast component is in direction opposite to the direction the tape is moving; this happens b/c visual stimulus of tape --> reflexic pursuit eye mov't in the same diection, which is corrected by the saccades in opposite direction (this is called opticokinetic testing)
when does opticokinetic testing fail to produce nystagmus
anterior cerebral lesions b/c there are no corrective saccades
posterior cerebral lesions b/c there is no initial pursuit
what type of sz does phenytoin treat
simple/complex partial
what type of sz does carbamazepine treat
simple/complex partial
what type of sz does lamotrigine treat
simple/complex partial
what type of sz does gabapentin treat
simple/complex partial
what type of sz does topirimate treat
simpile/complex partial
what type of sz does topiramate treat
simple/complex partial
what type of sz does phenobarbital treat
simple/complex partial
what type of sz does valproic acid treat
simple/complex partial
what type of sz does ethosuximide treat
what role do bz play in sz
1st line for acute status epilepticus
what is used for status epilepticus proph
MOA phenytoin
increased na channel inactivation
MOA carbamazepine
increased na channel inactivation
MOA lamotrigine
blocks voltage gated na channels
MOA gabapentin
increased GABA release
MOA topirimate
blocks na channels
increased GABA action
MOA phenobarbital
increased GABA-A action
MOA valproic acid
increased na channel inactivation and increased GABA concentration
MOA ethosuximide
blocks thalamic t-type Ca channels
increased GABA action
adverse effects of phenytoin
gingival hyperplasia
megaloblastic anemia (prob with folate metabolism)
teratogenic in pregnancy
hepatotoxic diplopia
sle like syndrome
tx for trigeminal neuralgia
toxicity of carbamazepine
aplastic anemia
toxicity of ethosuximide
gi distress
steven's-johnson syndrome
toxicity of valproic acid
rare, but fatal hepatotoxicity
NTDs in pregnancy
gi distress
toxicity of lamotrigine
stevens-johnson syndrome
toxicity of gabapentin
sedation, ataxia
toxicity of topiramate
mental dulling
kidney stones
weight loss
which epilepsy med should be used in pregancy and children
which epilepsy drug should be used in sz during eclampsia
what can be used to prevent sz of eclampsia
difference between umn lesion of facial nerve and lmn lesion
umn lesion: contralateral lower face weakness
lmn lesion: ipsilateral upper and lower facial weakness
things that could cause a lmn cn vii lesion
cerebellopontine angle neoplasm
bell's palsy
what type of dz can cause an umn cn vii lesion
suprasegmental stroke or brain tumor
what type of facial weakness is seen if there is a lesion of the motor cortex
facial movements associated with emotion are preserved but not preserved when asked to do a facial movement on command, there will be weakness
what type of facial weakness is seen if there is a lesion in the amygdala
facial muscle strenght is normal but an emotionally produced smile is crooked
what can occur following peripheral nerve injury (bell palsy/trauma) upon reinnervation

why does this occur
synkinesis - eye closure --> involuntary elevation of the angle of the mouth on affected side
baring teeth --> ipsilateral eye closure

this can be caused by aberrant regeneration (damaged axons regrow distally, but make wrong turns) and there is also cross talk so that damaged axons make nonsynaptic electrical contact with each other
what causes hyperacusis
denervation of the stapedius muscle of middle ear, so can't dampen the ossicles during loud noise
pathophysiology behind crocodile tears
lacrimal-salivatory synkinesis with ipsilateral lacrimation stimulated by eating following a bell palsy

(lacrimation and salivation are both mediated by cn vii)
what autonomic functions are mediated by cn vii
intermedius portion of cn vii --> innervation of lacrimal gland (via pterygopalatine ganglion) and the chorda tympani (via submandibular ganglion) innervates the submandibular ganglion and submaxillary salivary glands

(chorda tympani also innervates the ant 2/3 of tongue)
where is the lesion if there is unilateral facial weakness that spares the forehead (esp if ipsilateral limb weakness)
contralateral motor cortex
where is the lesion if there is unilateral facial weakness of forehead, as well as ipsilateral abducens weakness
(and if there is hemiparesis, it will be contralateral)
where is the lesion if there is unilateral facial weakness in forehead, and if taste, salivation, and lacrimation are affectd
facial nerve before the take off of the greater superficial petrosal and chorda tympani branches (i.e.: geniculate ganglion)

if v, vii, viii are all affected, then it is at the cerebellopontine angle
where is the lesion if there is unilateral facial weakness in the forehead, that is unaccompanied by other abnormalities
lesion is either of the facial nucleus in th epons or the nerve distal to the chorda tympani
if a person can unilaterally raise one eyebrow voluntarily, what does that mean about their innervation
there is mostly contralateral facial representation in teh motor cortex
describe the innervation of the tongue
the motor cortex sends fibers bilaterally to the hypoglossal nucleus in the medial medulla
what type of lesion does atrophy of the tongue indicate
lmn lesion (either centrally or peripherally)
bulbar palsy
b/l weakness of muscles innervated by cn in the lower brainstem,(to less of an extent if the cerebrum or upper brainstem lesions are unilateral)

no movt of palate or pharynx with phonation
gag reflex is absent
pseudobulbar palsy
b/l lesions of cerebrum or upper brainstem --> severe dysarthria and dysphagia
tongue is paralyzed, but is not atrophic and doesn't fasciculate
gag reflex is hyperactive
extremely labile emotional response
progressive supranuclear palsy
degen d/o --> d/o eye mov't, pseudobulbar palsy, dystonia, dementia, pyramidal and cbl dysfxn
what nerve carries info from the barorecpetors in carotid body and aortic arch
cn x
which nerves comprise the nucleus solitarius
what kind of info does this carry
vii, ix, x
visceral sensory info taste, baroreeptors, gut distention)
which nerves are through the nucleus ambiguous
what info does this carry
ix, x, xi

motor innervation of pharynx, larynx, and upper esophagus
what info is carried in the dorsal motor nucleus
cn x, that sense parasymp fibers to the heart, lungs, adn upper gi
what type of lesion is suggested if a pt has a nasal voice
palatal weakness
what type of lesion is suggested if a pt has h/o nasal regurg of fluids
palatal weakness
what type of lesion is suggested if a pt has hoarseness or reduced cough
laryngeal weakness
what type of lesion is suggested if a pt chokes on saliva while talking
pharyngeal weakness
what type of lesion is suggested if a pt has dysphagia to solid foods only
mechanical obstruction (carcinoma)
what type of lesion is suggested if a pt has dysphagia to solids and liquids
neurological dysfxn
to what side dose the uvula deviate if it does not rise symmetrically
towards the normal side (away from the side of the lesion)
when testing the gag reflex, what is suggested by b/l weakness with preserved sensation
motor neuron dz (als, polio), neuromuscular junction dz (ex - mg) or myopathy
when testing the gag reflex, what is suggested by u/l motor and sensory loss
ipsilateral lesion of lower brainstem (eg- lat medullary infarction or combined lesions of cn xii and x either in posterior fossa or as they exit through jugular foramen)
when testing the gag reflex, what is suggested by b/l motor and sensory loss in posterior pharynx
intraparenchymal medullary lesion where other cn and long tracts are probably present
when testing the gag reflex, what is suggested by b/l sensory loss with nml movement on phoation
psychiatric dz... very rare
if there is weakness in the right scm, where is the lesion
RIGHT cortex (the only muscle with ipsilateral muscle innervation from cortex)
if there is weakness in the right trapezius, where is the lesion
LEFT cortex
jugular foramen syndrome
affects cn ix, x, xi
loss of sensation over palate and pharynx
loss of general sensation over palate and pharynx
loss of general sensaton and tasste over posterior third of tongue
paralysis of palate, pharynx, and larynx
weakness of scm and trapezius
the hypglossal foramen is adjacent to jugular foramen --> weakness of tongue with atrophy and fasciculations
causes of central spinal cord compression
neck flexion-extension injury
intrinsic tumor
si and sx of foramen magnum lesion
spastic quadriparesis
neck pain and stiffness
c2-c4 and upper facial numbness
ipsilateral horner's ysndroem
ipsilateral tongue and trapezius muscle weakness
si and sx of conus medullaris lesion
lower sacral saddle sensory loss (s2-s5)
sphincter dysfxn
aching back
rectal pain
l5 and s1 motor probs (ankle and foot weakness)
si and sx of cauda equina syndrome
sphincter dysfxn
paraparesis with weakness in multiple nerve roots
sensory loss in multiple bilateral dermatomes
what does contrast enhancement mean in a ct
presence of a disrupted bbb
when should contrast be used in ct
suspected neoplasm, abscess, vascular malformation, new onset sz
what things appear black in a ct
what things appear white in a ct
acute hemorrhage
iv contrast
what are t1 mris used for
to detect anatomy
most pathologic processes are associated w increased water content and appear darker than normal brain
what are t2 mris used for
to detect pathology (they will look white to reflect increased water content)
what color are fat and subacute blood in t1 mri
what things are white in t2 mri
when is diffusion weighted imaging used
to detect hyperacute ischemia in pts with acute stroke

changes are seen w/i minutes
when is mr angiography used (mra)
used to detect large scale lesions (carotids or large aneurysms) not good for smaller lesions, must use conventional angiography
what can standard angiography detect
arterial dissection
vasculitic narrowing
dural venous sinus thrombosis
most impt complication of angiography test
1-2% --> stroke secondary to emboli generated by the catheter (seen mostly in elderly with atherosclerotic dz)
how do simple szs affect consciousness
simple partial sz have no impairment in consciousness

complex partial sz has alteration in consciousness
how do complex szs affect consciousness
complete loss of consciousness
definition of status epilepticus
10+ minutes of continuous szs where pt fails to fully awaken
differential dx of sz
Autoimmune (seen in sle, vasculitis, ms)
Neoplasm (most common way for neoplasm to present if it is in brain)
what are things to be concerned for in pt actively seizing, or prolonged szs
aspiration of gastric contents if airway is not protected
head injury
lactic acidosis
cerebral edema
tx for status epilepticus
full dose of bz, followed by fosphenytoin, but risk of recurrence is very high
what is the best way to secure the airway in coma
endotracheal intubation
why should you give thiamine before dextrose
hyperglycemia promotes the consumption of thiamine and will acutely worsen wernicke's
what does naloxone do
reverses opiate intoxication
what does flumazenil do
reverse come from bz intox
top 3 causes (in order) for coma/stupor
toxic/metabolic d/o (66%)
structural intracranal d/o (33%)
psychiatric d/o (1%)
role of unilateral hemispheric lesion in producing stupor or coma
doesn't usually cause it, unless there is a mass effect sufficient to raise icp or compress either the contralateral hemisphere or brainstem, or compresses the contralateral hemisphere/brainstem
how do focal brainstem lesons --> coma
disrupting the reticular activating system
3 common, treatable causes that can rapidly --> coma/death
increased icp
herniation and brainstem compression
tx of herniation and brainstem compression
neurosurgery (it's an emergency1)
tx of increased icp
1. elevate head of bed
2. intubation and hyperventilation (this will cause cerebral vasoconstriction and lowering of intracranial volume)
3. sedation if pt is agitated
4. osmotic diuresis with mannitol
all of these things will be used to buy time before neurosurg
urgent ct of the head should also be obtained
why is increased icp so dangerous
--> impaired cerebral perfusion and global hypoxic-ischemic injury
bladder fxn in als
spared until final stages of illness
why does muscle cramping occur in als
irritability of denervate muscles
mode of inheritance of als
5-10% are familial, autosomal inheritance
SOD1 deficiency is involved, coded for in q21 arm of chromosome 21
relationship between SOD1 and als
there is a mutant variation of SOD1 in als; it is not the loss of fxn of SOD1 that leads to sx, but the toxicity of the altered SOD1 (gain of fxn d/O)
SOD1 is not affected in sporadic (non-familial) cases of als
what is the difference between dominantly inherited als compared w sporadic als
clinical features are identical, but familial develops 10 yrs earlier
hypothesis of pathogenesis in sporadic als
glutamate excitotoxicity (acts on nmda, ampa, and kainate receptors) --> selective neuronal damage

in other pts there are abs to voltage gated ca channels

other pts have monoclonal and polyclonal abs to gm1
tx for als
riluzole (a glutamate antagonist) may slow progression of dz

ivig may also be helpful
what causes waddling gait
describe waddling gait
weakness of gluteus medius muscle
pts pelvis drops with each step
describe gower's sign
to rise from sitting position, pt puts his hands on his knees, pushes his trunk back and works his hands up thighs
what is seen on muscle biopsy in muscular dystrophy
degeneration and regeneration of muscle fibers of varying sizes
there is no inflammation or storage of a metabolic product
replacement of muscle by fat and ct --> pseudohypertrophy of gastroc
which gene is involved in duchenne's muscular dystrophy
X chromosome, 21p --> dystrophin
what does dystrophin do
links actin within the muscle fiber and laminin on muscle fiber's external surface

in DMD, no dystrophin is produced
types of hypertonicity
spasticity: from lesions in frontal lobe, or descending corticospinal projections --> resistance to passive movements that increases with speed of movement; tends to affect flexor muscles in arms and extensor muscles in legs

rigidity: associated with parkinsons and other basal ganglion d/o --> plastic resistnace (lead pipe rigidity) that is not dependent on velocity and is constant throughout the rom
describe cogwheel rigidity
rapidly alternating contractions of agonist and antagonist muscles (seen in parkinson's)
what happens to tone following severe spinal cord injury
flaccid areflexia (aka spinal shock), followed by spastic hyperreflexia (cause of this change is unknown)
describe spinal shock
results from the removal of suprasegmental descending systems that facilitate spinal motor neurons
there is flaccid areflexia
what effect does noxious stimuli cause below level of complete spinal transection
called "mass reflex"
full flexion + urination + sweating and piloerection below the level of injury

this occurs secondary to disinhibition of sympathetic response that relesase norE and epi released from adrenal glands
describe dichotomous findings with sweating seen in complete spinal cord transection
noxious stimuli --> sweating, but warm environment does not
moa baclofen
gaba agonist that likely acts at substance p synapses in dorsal horn
describe pain seen in spinal cord transection that is present below the lesion
not well understood, usually clears spontaneously over several months

may be from sympathetic splanchnic nerves that enter the spinal cord above the level of the injury
what is cushing's response
respiratory depression

they all occur as a consequence of increased icp
cerebral perfusion pressure
cpp = mabp - icp
the goal is to keep cpp constant, so if icp increases, then mabp will increase
what is the acceptable range of cpp
70-120 mm hg
if it is above that --> cerebral edema
if it is below that --> hypoxic injury
how does jvp relate to icp
csf is reabsorbed across meninges into venous circulation, so if jvp is elevated, then csf can't get out --> increased icp
what are the 3 components w/i the cranium that contribute to volume
what are the clinical signs of herniation
(all occurring from brainstem compression)
1. loss of pupillary reactivity
2. impairment of eye movements
3. hyperventilation
4. motor posturing (flexion/extension)
when should increased icp be suspected
in pts with known or suspected intracranial pathology (stroke, trauma, neoplasm) and have depressed level of consciousness, htn w/ or w/o bradycardia
most common causes of increased intracranial volume
extrinsic mass lesions
cerebral edema
describe the cerebral autoregulation curve
in nml pts, cbf can remain constant with bp between ~60-160 mmHg
in htn pts, cbf will remain constant between ~75-180
in pts with vasospasm and/or ischemia, autoregulation is not possible, so there is an upward linear line that increases as the arterial bp increases
what fibers are carried in the internal capsule
posterior limb carries corticospinal fibers and sensory fibers

genu carries corticobulbar fibers

anterior limb carries frontopointine and spinothalamic fibers
blood supply of the internal capsule
striate arteries that come off of the mca
csf in guillain-barre
high protein count mild wbc (pleocytosis usually <10 lymphos/dL)

albumin/cytologic protein dissociation
charcot-marie-tooth dz
progressive muscular atrophy that starts in feet and then spreads to hands; sensation affected less or not at all
aka peroneal muscular atrophy
mode of inheritance of charcot-marie-tooth
x linked
which dz that causes elevated gamma-globulins (M-proteins) will also --> senosorimotor periopheral neuropathy
the M proteins act as antibodies anda can bind to epitopes within peripheral nerves --> peripheral neuropathy

ex: IgM can bind to myelin associated glycoprotein --> segmental demyelination and secondary axonal degeneration

IgM autoantibodies --> combined motor and sensory loss and can progress over many years
explain why long nerves tend to be more affected in demyelinating processes, compared to short nerves
stocking and glove distribution is common; statistically, anything that is going to affect a long nerve has more of a chance to do it than a short nerve
also, when compensatory sprouting of fibers from short nerves occurs, they are more likely to reach their end-targets, compared to the sprouts from long nerves
what is an easy way to distinguish between a myopathic motor problem and a neuropathic motor problem
myopathic problems will usually affect proximal muscles (with a few exceptions)
neuropathic problems will usually affect distal muscles
signs of denervation on emg
fibrillations, positive waves, polyphasic potentials of increased duration and amplitude
spinal muscular atrophy
hereditary progressive degeneration of motor neurons in anterior horn of spinal cord
type of gait seen with cbl dz
broad based gait
fall towards side of lesion
if a pt is standing with their feet together, what is seen in cbl vermal lesions or b/l vestibular lesions
they will fall backward or fall inconsistently in any direction
what is circumduction and when is it seen
dragging of contralateral foot, leg may swing outward from the hip \; if lesion is above c-spine, the ipsilateral arm swing may be reduced

u/l umn lesions
what causes a stiff spastic gait
describe the gait
b/l umn lesions
dragging o fboth feet, and scissoring (both feet will cross over each other)
if there is preserved gastroc power, --> toe walking and eventual contracture in plantar flexion
what findings of gait are there in a pt with impaired proprioception
they watch their feet as they walk
leg(s) may move randomly in different directions
what are the main differences between bulbar and pseudobulbar palsy
bulbar: b/l lmn dz --> fasciculations in tongue (not seen in pseudobulbar), no mov't of pharynx or palate with phonation, absent gag reflex (hyper-reflexive in pseudobulbar)

pseudobulbar: b/l umn lesions --> hyper-reflexive gag, NO tongue fasiculations, and absence of mov't of pharynx and palate with phonation
what happens when a parkinsons pt tries to rise from sitting
they can't, unless they use their arms
what is magnetic gait and when is it seen
legs are broad based adn feet never leave the ground, takes tiny steps,
cause by b/l frontal lobe dz, seen in chronic nph
what is titubation and when is it seen
coarse tremor of head and neck
seen in cbl dz
describe jacksonian march
focal motor sz that has a clonic jerking that rapidly spreads proximally from one or more digits, up a limb
what way do eyes deviate during a sz
deviated away from the lesion
what is todd paresis
transient postictal focal weakness, signifying functional unresponsiveness of neurons in the area of maximal discharge, could be from excessive glutamate neurotransmission
what is the difference seen in electrical activity in a pt with partial szs who generalizes, compared to a pt with primary generalized szs
secondary generalization: cortical focus that spreads via corpus callosum to contralateral hemisphere; then projects to thalamus; widespread thalamocortical projections activate both cerebral hemispherse --> generalization

in primary generalized szs, activity begins in the thalamocortical discharge and spreads to b/l cerebral hemispheres
most common cause of a tia
usually they are embolic
less common cause for a tia
transient hypotension in the presence of severe carotid stenosis (>75%)
most common etiology of cva
infarction from embolic strokes - most common origin of embolus is secondary to embolization of mural thrombus in pts with a-fib
what are the 3 most common causes of stroke
infarction (embolus, atherothrombotic, lacunar)
intracerebral hemorrhage
subarachnoid hemorrhage
misc causes
when should htn be treated immediately following a stroke
if there is a htn emergency
if bp >220/120
bp can be lowered if there is evidence of a hemorrhagic stroke on ct
major threats to life following stroke
transtentorial herniation
cbl infarction or hemorrhage (need neurosurg evaluation)
aspiration pna (v common cause of death; consider pt to have impaired swallowing until proven otherwise)
presentation of SAH
sudden, severe ha (drom ruptured cerebral aneurysm)
stiff neck and photophobia reported (must r/o meningitis)
chaged in ms
focal signs are not as common as in other stroke types
why is sah so dangerous
50% fatality if not treated, the majority of which are from hemorrhage, but there is significant risk for re-rupture as well
aneurysm must be surgically clipped!
what will a ct scan of sah show
hyperdensity in sulci, major fissures, and around brainstem
if the ct is negative for sah, but clinical suspicion is still high, what is the next step in dx
lp - csf will show xanthochromia; can also r/o meningitis
after sah is dx, what is the next diagnostic step
catheter angiography to r/o additional unruptured aneurysms
difference in presentation of sah vs other stroke types
other stroke types don't prsent wiht any pain, and they have focal neurologic findings
sah has ha with focal findings rare
sah presents with meningeal signs
stroke sx that are suggestive of cardioembolic strokes
sudden deficit, maximal at onset
hemianopia w/o hemiparesis, pure wernicke's aaphasia, and top of the basilar syndrome
most common location for aneurysms
pca, aca, mca
what presentation is likely to suggest large-vessel stenosis as basis for stroke
fractional weakness (shoulder weaker than the hand, hip weaker than the ankle)
risk factors commonly associated with large vessel stenosis
presentation of lacunar stroke
no cortical signs/sx
clumsy hand dysarthria, pure motor hemiparesis, ataxic hemiparesis, sensorimotor syndrome
management of ischemic stroke
if stroke sx <3 hrs and ct shows no hemorrhage, give tpa
presentation of intracerebral hemorrhage
higher incdidence of ha and severe htn c/w ischemic stroke
otherwise caan be identical
pathogenesis of intercerebral hemorrhage
chronic htn
results from rupture of smallest penetrating arteries
most common sites for intercerebral hemorrhage
most commonly in basal ganglia and thalamus (70%)
management of hemorrhagic stroke
correction of coagulopathy - give ffp if there is coag d/o
control bp: systolic between 160-180 to help prevent recurrent bleeding
hyperventilation to control increased icp
when should CEA be considered to prevent stroke
sx pts: carotid stenosis >70%
asx pts: no surgery; just lower atherosclerotic rsk factors and give asa
ha that can can cause major threat to life
herniation from intracranial mass lesion
preventive measures for cluster ha
prednisone + verapamil and lithium (prednisone use is not long term, should be tapered over a couple of weekS)
triad of sx in pseudotumor cerebri
ha, increased icp, papilledema in absence of mass or hydrocephalus
what type of intracranial pathology is likely to be seen in trigeminal neuralgia
vascular compression of the pons , although it might not be seen on imaging
what are the 2 most common causes for acute paralysis + ventilator failure

myasthenia gravis
guillan barre

c-spine correction
transverse myelitis
diphtheritic polyneuropathy
organophosphate intox
poor prognostic factors in guillan barre
advanced age
low distal motor amplitudes
rapidly progressive weakness over the first week
resp failure --> intubation
in aidp, which is more affected, proximal or distal muscles
csf in guillan barre
cytologic-albumin dissociation
eleated protein
mild pleocytosis
what is seen on emg of a pt with aidp
reduced conduction velocities
occ reduced amplitude
aside from ascending paralysis and areflexia, what other clinical signs/symptoms are seen in aidp
pain (from meningeal inflammation or neuropathic mechanisms)
dysautonomia (htn or tachycardia)
pathophysiology behind myasthenia gravis
auto-ab directed against nicotinic ach receptors --> defect in nm transmission
most common muscles affectd by myasthenia gravis
remission of myasthenia gravis
can occur within 2 years of onset
30% remit
what tumor is associated with myasthenia gravis
malignant thymoma (assoc with more severe dz)
myasthenic crisis
resp failure requiring intubation and mechanical ventilation
provoked by infection, but can also occur spontaneously
70% recover by 1 month
30% likely to experience it again
dx of myasthenia gravis
edrophonium testing (shows transient improvment of sx)
repetitive nerve stimulation --> >10% decrement in amplitude between the first and fifth stimulation
ACh antibodies
single fiber emg: see jitter variation (95% sensitive)
anti-muSK abx (seen in those who are lacking the ACh abx)
what is anti-musk
associated with myasthenia gravis, seen in pts w/o the ach ab
anti-muscle specific tyrosine kinase
usualy seen in females with predominant neck and oropharyngeal weakness
tx for myasthenia gravis
symptomatic tx: acetylcolinesterase inhibitors (pyridostigmine)
s-t dz suppression: plasmapheresis and ivig
long-term immunosuppresion: thymectomy, steroids, azathioprine, chemotherapy
tx for botulism
botulism trivalent antitoxin
guanidine hydrochloride (ACh agonist that counteracts the presynaptic blockade caused by the toxin)
why does botulism toxin --> weakness
inhibits presynaptic ACh release
sx of botulism
gi complaints
dilated and nonreactive pupils
blurred vision
weakness (beginning in extraocular and oropharyngeal muscles, then --> generalized)
urinary retention
dry mouth

(impaired parasympathetics)
what differentiates guillan barre from polio
polio has fever, headache, mental status change, asymmetric weakness
neutrophils on csf

otherwise, both are flaccid areflexic paralysis
medical tx of tetanus
assist ventilation
immune globulin
procaine penicillin to eradicate the soft-tissue infection
what triad of sx should always be treated as a cns infection
neurologic signs/sx
(any 2/3 require lp, with ct prior)
pathogenesis of acute bacterial meningitis
seeding of leptomeninges occurs from hematogenous spread of infecting organisms
can also spread form parameningeal infection (otitis media) or following trauma, cochlear implants, o neurosurgery
common tx for community acquired meningitis for adults, children
ceftriaxone and vanco until cx return
+ dexamethasone
common tx for community acquired meningitis in infants, immunosuppressed, and older
ampicillin should be added to cover listeria
presentation of viral meningitis
neurologic dysfxn is not seen, otherwise similar to bacterial meningitis
how to treat viral meningitis
it is self-limited
most common viruses --> viral meningitis
arthropod born (WNV)
(meds can do it too)
definition of chronic meningitis
develops over 2 wks
physical sx of tuberculosis meningitis
cn palsies
vasculitic small vessel infarction
obstructive hydrocephalus

all result from severe granulomatous inflammation of the basal meninges

all occur from severe granulomatous inflammation fo basal meninges --> tuberculoma

evidence of active pulm dz present in 30% of pts
late complications of tb meningitis
cognitive impairment
dx of tb meningitis
csf shows lymphocytic pleocytosis, increased protein level, moderately reduced glucose level
acid-fast mycobacteria in csf

ppd not reliable in th meningitis wu
tx of tb meningitis

dexamethasone can be given in severe cases to limit inflammation and damage
manifestations of tertiary neurosyphilis
general paresis (from chronic, diffuse encephalitis --> dementia w psychiatric features and b/l umn signs)
tabes dorsalis (from chronic spinal polyradiculitis with secondary dorsal root and column degeneration)
argyll-robertson pupils (react to accomodation but not to light --> blindness from optic atrophy)
what is the difference in presentation btwn hiv + pts and nonimmunosuppressed pts with neurosyphilis
in most ppl, it takes 10-15 yrs of asx syphilis before tertiary neurosyphilis develops;
in hiv + it is accelerated and meningitis and meningovasculitis predominate
tx of neurosyphilis
penicillin G
dx fo cns lyme dz
evidence of intrathecal production of igg ab to borrelia
in csf, see lymphocytic pleocytosis with mildly elevated protein
sx of cns lyme
early: mild meningitis/meningoencephalitis
cranial neuropathy

lyme encephalopathy (immune mediated)
recurrent/chronic meningoencephalitis
chronic myelitis
causes of chronic fungal meningitis
dx of fungal meningitis
demonstrates the organism by wet smear
stain used to dx cryptococcus
india ink
tx of fungal meningitis
fluconazole for mild cases
amphotericin b for severe cases
presentation of bacterial abscess
subacute progression of ha, altered ms, focal neurologic signs and fever
how are most brain abscesses formed
contiguous spread from a parameningeal infection (aom, osteomyelitis, sinusitis) or hematogenous spread in pts with endocarditis, bronchiectasis, congenital cyanotic heart dz
what are the most common orgs seen in brain abscesses
b fragilis
dx fo brain abscess
ring enhancing lesion on ct/mri
perform blood cultures and lp if etiology is not known
tx of brain abscess
broad spectrum tx:
vanco (if pt is post-surgical or post-traumatic and staph is a concern)
tx of subdural empyema
surgical drainage
what setting are cranial/spinal abscesses normally seen
often seen with osteomyelitis
presentation of cranial epidural abscess
localized pain and tenderness --> cn defects
sx of spinal epidural abscess `
intense local pain and tenderness
local root pain irritation with referred pain
cord compression
what are the most common organisms sen in spinal epidural abscess
gram -
tb (pott's dz)
tx of spinal epidural abscess
surgical drainage to prevent cord compression
vanco + ceftriaxone
most common cause of sporadic viral encephalitis
presentation of hsv-1 encephalitis
altered ms
pathogenesis of hsv-1 encephalitis
reactivation of dormant hsv-1 within trigeminal ganglion with viral spread via sensory pathways to brain
dx of hsv-1 encephalitis
intrathecal hsv ab
+ hsv pcr from csf
what is seen on hsv-1 encephalitis imaging
focal necrotizing lesions of inferior frontal and temporal lobes
tx of hsv-1 encephalitis
wnv encephalitis - how common is it?
clinical sx
20% with wnv are sx, and 1% of those --> neuroinvasive wnv

usually presents as meningoencephalitis characterized by altered ms, focal neuro deficitis, tremor,

can also present as meningitis
dx of neuroinvasive wnv
based on clinical suspicion + wnv igm in blood/csf
tx of neuroinvasive wnv
difference between bacterial and viral meningitis
in viral meningitis the neurologic dysfxn doesn't occur, it's only ha and fever
features of tb meningitis
severe granulomatous inflammation of basal meninges
vasculitic small vessel infarction
obstructive hydrocephalus
spinal arachnoiditis
tx of tb meningitis
features of neurosyphilis
general paresis- dementia with psych features and b/l umn signs
tabes dorsalis
argyll-robertson pupils
dx of neurosyphilis
vdrl is specific but not very sensitive, so use:
csf fta-abs (very sensitive, but not as specific)
if both are - then can definitely r/o syphilis
which hsv virus --> encephalitis
hsv is w/i trigeminal ganglion, gets reactivated and then there is viral spread via sensory pathways into the brain
tx of hsv encephalitis
phenytoin to prevent sz
tx of wnv encephalitis
opportunistic complication of AIDS
cns toxo
primary cns lymphoma
hiv meningitis
proph of toxo in hiv +
tx of toxo
sulfadiazine and pyrimethamine
proph of mac
tx of mac
clarithromycin and ethambutol
proph of cryptococcus
tx of cryptococcus
presentation of toxo
subatue encephalopathy
focal neurologic deficits
presentation of cryptococcus
suspect in any hiv + pt with a ha
fever is usually present
presentation of pml
subacute onset of focal neurologic deficits and dementia
peripheral ns is spared
mri of pml
striking white matter hyperintensities
tx of pml
presentation of cmv retinitis
slowly progressive, painless loss of vision
dx of cmv
pcr is highly sensitive
what does mri show in cmv
ependymal enchancement (area around ventricles and spinal cord)
tx of cmv
neuro complications of shingles
cns vasculopathy, presenting with stroke-like sx or myelopathy
sx of hiv myelopathy
insidious onset of spastic paraparesis, sensory ataxia, and bowel/bladder/erectile dysfxn (looks similar to b12 deficiency)
nonopportunistic infections associated with hiv
distal sensory polyneuropathy
neuromuscular weakness syndrome
features of distal sensory polyneuropathy
most common hiv related neuro complication
caused by immune mediated pathway or antiretroviral toxicity
presentation of distal sensory polyneuropathy
symmetric, painful paresthesias
sensory loss
allodynnia in a stocking/glove distribution
loss of ankel jersks
tx of distal sensory polyneuropathy
better control with haart
pathogenesis of hiv asssociated dimentia
hiv infects non-neuronal cells shortly after primary viremia
wiht immune failure, chronic encephalitis ensues
presentation of hiv associated dementia
motor slowing
behavioral change
tx of hiv associated dementia
haart can arrest and sometimes reverse dementing process
major causes of syncope
reflex vasodilation
neurologic causes
psych causes
different reflex vasodilation disturbances --> syncope
hypersensitive carotid body
situational syncope
cardiac causes of syncope
flow/pump failure (outflow obstructions - stenosis, hocm, dissection, myxoma, mi, cardiac tamponade)
orthostatic causes of syncope
volume depletion
dru induced
autonomic dysfunction (shy-drager is a central dysfxn, autonomic neuropathy is a peripheral cause)
neuro causes for syncope
brainstem ischemia (vertebrobasilar stenosis/occlusion) or subclavian steal syndrome
vilateral hemispheric ischemia from carotic artery stenosis/occlusion
sah, space occupying lesion (both secondary to icp)
how long is a pt unconscious before it is considered a coma
15 mins
what sx would suggest it's from cardiac arrhythmia
no prodromal sx
what sx would suggest it's from vasovagal causes
dizziness, lightheadedness, pallor, diaphoresis, dimming vision
what sx would suggest it's from carotid sinus
during turning head to one side
what sx would suggest it's from
vertebrobasilar insuff
1+ episodes of vertigo, diplopia, dysarthria, numbness, weakness, ataxia
what normally happens to bp in syncope? what is the exception
usually it drops, unless it's from sah, then pt is htn
tx for vasovagal syncope
if table tilt test is +, beta blocker or paroxetine
subclavian steal syndrome
--> vertebrobasliar insuff
1 subclavian artery is occluded proximal to the vertebral art
distal subclavian art is supplied by retrograde flow from ipsilateral vert art that "steals" from basilar and contralateral vertebral arteries
tx of autonomic dysfxn --> orthostatics
fludrocortisone, support stockings
how does hypervent --> syncope
hypocapnia decreases cbf 2ndary to cerebral vasoconstriction
what part of the spine normally is affected by mets
thoracic spine
there is the most drainage from visceral organs through the spinal extardural venous plexuses
intrinsic cord tumors that mimc extra axial compressive lesions
what is the difference between how cervical disks herniate and lumbar disks herniate
cervical disks herniate centrally

lumbar herniates laterally and --> radicular sx
where is the herniation in an acute cauda equina syndrome
what types of sx can be associated with arnold-chiari malformation
spastic diplegia of legs
cervical myelopathy
(pts are predisposed to subluxation or dislocation)
how should an acute traumatic sci be treated
1. methylprednisolone
2. blood tests in case surgery is needed
3. imaging, if stable
anti-inflamm tx for spinal neoplasm
what does an anterior cord compression of c-spine suggest
cervical disk herniation
what does a posterior cord syndrome in t-spine suggest
bony mets
can tendderness in lumbar/sacral spine --> cord compression
no, the spinal cord stops at l1
features of anterior cod syndrome
b/l spinothalamic tract
umn paralysis below lesion
lmn paralysis at lesion
sphincter dysfxn
preserved dorsal column sensation
mononeuritis multiplex
multiple, asymmetric regions of sensory loss, corresponding to multiple peripheral nerves
sx of spinal muscular atrophy
lmn degen
infantile or chiildhood onset; adult forms are rarer
pathophys of multifocal motor neuropathy
immune mediated motor neuropathy; conduction block present on nerve conduction studies
tx multifocal motor neuropathy
parsonage-turner syndrome
idiopathic brachial neuritis (sudden onset of pain in shoulder and arm; weakness and muscle wasting become evident after 2-4 wks)
ramsay hunt syndrome
herpes zoster infection of ipsilateral geniculate ganglion
when to suspect neurosarcoidosis
interstitial lung dz with hilar adenopathy, uveitis, or parotitis
what is suggested by decreased hearing or a decreased afferent corneal reflex
cerebellopontine angle tumor
tx of idiopathic bell's palsy
tx of ramsay hunt syndrome
differential for mononeuropathy multiplex
vasculitis (esp PAN)
different types of neuropathy caused by dm
distal axonal sensorimotor neuropathy
autonomic neuropathy
mononeuropathy multiplex
diabetic amytrophy
what is diabetic amytrophy
asymmetric proximal leg wekaness and wasting, not limited to a root, plexus or nerve territory
paraprotein associated neuropathy
demyelinating or axonal sensorimotor neuropathy

can be seen in plasma cell dyscrasia, mm, amyloidosis, lymphoma, leukemia, waldenstroms'
tx of paraprotein associated neuropathy
plasmapheresis, ivig, azathioprine
lambert-eaton myasthenic syndrome
ab vs ca channels of presynaptic nerve terminals --> impaired neuromuscular transmission (usually neoplastic cause)

see proximal limb weakness, lower extremity areflexia, dry mouth, myalgias, and impotence
dx of lambert-eaton
incremental response on repeated nerve stimulation
tx of lambert-eaton
dx of polymyositis
ck levels elevated
emg shhhows myopathic findings with denervation
bx shows endomesial lyphocytic infiltrates, necrotic and atrophic muscles fibers and ct deposition
tx of polymyositis
sx of dermatomyositis
same as polymyositis, but with heliotropic rash on eyelids, erythematous rash on face and trunk
violaceous scaly eruptions on knuckles
subcutaneous calcifications
gottron's papules
violaceous scaly eruptions on knuckles
assoc with dermatomyositis
dx of dermatomyositis
different findings on bx (c/w polymyositis)
shows perivascular inflammation adn perifascicular atrophy
tx of dermatomyositis
sx of inclusion body myositis
different from polymyositis b/c it prodcues distal and asymmetric weakness
poor response to steroids
endocrine dz that can --> myopathy
thyroid dz
sx of myotonic dystrophy
distal myopathy
ptosis, frontal balding, cataracts, cardiac conduction defects, gonadal atrophy and mental impairment
periodic paralysis
genetic abnormalities in ion channels , pts are nml between attacks of severe weakness
sx of mitochondrial myopathy
high serum lactate levels
most common type of primary brain tumor
most common type of glioma
most common type of astrocytoma
dx of gbm
mri with gad
shows ring enhancing lesions
can show butterfly glioma if it grows along white matter tracts like corpus callosum
presentation of gbm
ms changes
focal motor deficits
sz are less common
presentation of anaplastic astrocytoma
focal deficit
dx of anaplastic astrocytoma
gad-enhanced mri
bx is needed to make definitive dx
most common presentation of low-grade astrocytoma
imaging of low grade astrocytoma
mri (no gad)
see very little mass effect
bx for confirmation of dx
pathologic appearance (under microscope) of oligodendroglioma
fried egg appearance
presentation of oligodendroglioma
behavioral changes
cognitive changes
mri of oligodendroglioma
mri shows tumor with indistinct margins and variable amounts of contrast enhancement
what age group is ependymoma most coommon in
children and young adults
where do ependymomas usually occur
in children, on the floor of the 4th ventricle
presentation of ependymoma
noncommunicating hydrocephalus --> increased icp with ha, vomiting, ataxia
dx of ependymoma
mri with gad
will fill subarachnoid space through foramina of luschka and magendie
drop metastases
results from seeding via csf
primitive neuroectodermal tumor
highly malignant
seen exclusively in children and adolescents
presentation of pnet
depends on location
extraneural mets occur more often with pnet c/w any other cns neoplasm
dx of primary cns lymphoma (pcnsl)
mri (will appear isointense on ct)
seen periventricularly and enhances uniformly with gad
what type of lymphoma is a pcnsl
presentation if there is a meningioma in the hemisphere
focal sx
presentation if there is a meningioma in the sphenoid wing
visual loss
presentation if there is a meningioma in the olfactory groove
ipsilateral optic atrophy and c/l papilledema
presentation if there is a meningioma in the suprasella
bitemporal hemianopia
sometimes hypothalamic dysfxn
presentation if there is a meningioma in the posterior fossa
cn efects
sx of brainstem compression
dx of meningioma
dural tail on mri
see braod based dural attachment
what dz is associated with acoustic neuroma
neurofibromatosis type 2
pathophys of acoustic neuroma
arises within internal acoustic canal, follows path of least resistance, growing into cerebellopontine angle
presentation of acoustic neuroma
tinnitus or hearing loss u/l
dx of acoustic neuroma
gad enchanced mri shows small intracanalicular tumors
tx of prolactinoma
da agonist (bromocriptine) first, otherwise if it doesn't work, then operate
most common malignant tumor of childhood/adolescence
where does medulloblastoma arise
cbl, and can present with signs of increased icp when mass effect causes obstruction
dx fo medulloblastoma
mri/ct shows contrast enhancing tumor, usually midline and distorts or obliterates 4th ventricle
sx of thalamic pain syndrome
spontaneous contralateral pain and dysesthesia is areas of impaired sensation
pathophys of thalamic pain syndrome
hemisensory loss from interruption of spinothalamic and dorsal column system at level of ventral posterior nucelus of thalamus

dorsal column --> severe contraolateral ataxia
path of dorsal columns from spinal cord
dorsal colums go to dorsal column nuclei, x midline at medial lemniscus --> ventral posterior lateral nucelus of thalamu and posterior nuclei of thalamus

vpln -->primary sensory crtex --> posterior parietal cortex and secondary sensory cortex
what would happen if there is a lesion in the primary sensory cortex
severe impairment of discriminative sensations, but only modest impairment of affective sensations such as pain (b/c of the dual projection of the spinothalamic tract)
cause of wallenberg's syndrome
occlusion of lateral medullary branches of vertebral artery and pica
(posteriolateral region of brainstem)
what neurologic injury (in brain) can hiccups be attributed to
lateral medullary infarction
what does pica supply
dorsolateral medulla
posterior inferior cbl
what is preserved in wallenberg's syndrome and why?
tongue fxn
pyramidal signs
contralateral loss of proprioception and discriminative touch
path of anterolateral system starting at spinal cord
dorsal horn --> x midline --> brainstem and intralaminar nuclei of thalamus --> praimary seonsry and association cortex
sx of vertebral artery dissection
neck or posterior head pain
horner's syndrome
decreased pain and temp of face, contralateral body
how to dx a vertebral artery dissection
mri and mra of neck
juvenile myoclonic epilepsy
myoclonic jerks that lead to generalized tonic clonic sz (suspect when all things on exam and imaging are nml)
what sized symptomatic meningioma should not be operated on
<3 cm, should give radiation
causes familial alzheimer's dz
clinical features of frontotemporal dementia
personality change
lost initiaitve
slowing though
recent memory is preserved
imaging for frontotemporal dementia
see disproportionate atrophy of anterior frontal and temporal lobes
difference between activity levels of pts with migraines vs cluster ha
migraines: lay down
cluster: mobile b/c laying down makes their ha worse
transverse myelitis
bilateral sensory and motor dysfunction
autonomic dysfxn
umn signs
sx present acutely or subacutely
tx of transverse myelitis
high dose corticosteroids
if a pt has afib and is s/p stroke, but it is after the 3 hr window for tx with tpa, how to tx the pt?
post-ictal confusion in simple partial sz
not present
spinal muscular atrophy
motor neuron dz NOT associated with any sensory abnormalities
generally presents with symetric proximal muscle weakness and atrophy
limb-girdle muscular dystrophy
symmetric proximal muscle weakness
nml sensation
what is commonly associated with cervical dystonia
cervical spondylosis
common tx for cervical dystonia
course of tias over time
they would worsen in severity over time
what does lermitte's sign mean
indicates the presence of cervical spinal cord problem
features of cervical spondylosis
chronic degenerative and hypertrophic changes of vertebrae, ligaments, and disks --> narrowing of spinal cord
in a pt with stroke >3 hrs ago, how to tx
early admin of asa --> modest reduction of risk of recurrent stroke in short term and less death and disability in the long term
dz associated with mononeuritis multiplex
sx of mononeuritis multiplex
asymmetric weakness
sensory loss
severe pain
sx of lewy body dementia
fluctuating encephalopathy
visual hallucinations
what is deficient in pts with lewy body dementia
central cholinergic activity
tx of lewy body dementia
centrally actiing anticholinesterase agent (donezepil, galantamine, rivastigmine)
what would happen to a pt w lewy body dementia who took a da agonist
exacerbation of encephalopathy
what would happen to a pt w lewy body dementia who took a nueroleptic agent
increased risk for neuroleptic malignant syndrome and increased mortality
risk to fetus if mother is on interferon or glatiramer acetate for ms
increased risk of spontaneous abortion and lbw
how to handle pregnancy in a woman with ms who is on disease modifying meds for ms
discontinue interferon or glatiramer several months before wishing to conceive
what effect does pregnancy have on a woman with ms
decreased frequency of relapse in the 3rd trimester
rebound increase in relapse during the first 6 months post-partum
hereditary component of ms
1st degree relatives have a 20-50x increase of having ms compared w general population
how does wilson's dz differ from huntington's dz
in huntington's dz, there are cognitive deficits
in wilson's dz ,the deficits are more psychiatric
mov't d/o associated with frontotemporal dementia
paroxysmal hemicrania
u/l ha of seconds-minutes that can be very disabling despite its brevity
in a pt with suspected vascular dementia, with nml head ct, what should be done
f/u imaging
sx of optic neuritis
smudging of central vision, graudually worsening so pt can read with affected eye
central scotoma present
rapd preseent
fundoscopic exam nml
deficiency sometimes associated w restless leg syndrome
if low ferritin levels, iron supplementation can improve sx
meds associated with development of pseudotumor cerebri
oral contraceptives
how sensitive is ct scan in picking up sah
90%, but it is most likely to be missed if there is a delay in pt presentation, so lp must be done instead
how long is lp able to detect xanthochromia following a hemorrhagic event
14 days
who is most likely to remain sz free after being taken off epilepsy meds
those with no structural brain lesion
no epileptiform or focal abnormalities on eeg
sustained sz free pd
no abnormalities on neuro exam
csf in critical illness polyneuropathy
sx of critical illness polyneuropathy
same as guillan barre but follos admission to icu (predisposed by sepsis and/or multi-organ failure)
which structures are implicated in short term memory fxn
dorsomedial thalamus
dorsolateral prerontal cortex
how do pts with alzheimers react to their memory loss
they lack insight into their condition
abnml physical findings in alzheimers pts
paratoni a
extrapyramidal rigidity
are scans necessary in dx alzheimers
they are required in order to r/o any other etiology causing memory problems
meds for alzheimers
in late stages: memantine
use of antipsychotic meds in pts with alzheimers
can be used to treat behavioral probs in ad but should bge used with caution b/c of risk of sedation and extrapyramidal sx
another name for frontotemporal dementia
pick's dz
sx of frontotemporal dementia
behavior dominant or language dominant sx
memory and spatial ability are spared early on
sx of behavioral frontotemporal dementia
early progressive personality changes and early decline in social interpersonal contact
lack of insight into these features
decreased spontaneous speech = and language
primary progressive aphasia
form of frontotemporal dementia
loss of speech fluency
inappropriate word order and simplified sentence structure
oral apraxia
impaired repetition
eventually become mute and behavioral changes can occur
semantic dementia
form of frontotemporal dementia
fluent but empty spontaneous speech with loss of word meaning
What region of the brain is affected in semantic dementia
left anterior temporal lobe is usually affected
what region of the brain is affected in primary progressive aphasia
left perisylvian atrophy, usually more anterior than posterior
sx of cortical basal ganglionic degeneration
form of frontotemporal dementia
progressive cognitive impairment with associated asymmetric rigidity, apraxia, cortical sensory loss, and pyramidal dysfxn
limb dystonia
tx of frontotemporal dementia
sx of lewy body dementia
early dementia
fluctuations in cognition and consciousness
visual hallucinations
subsequent development of parkinsonism
action tremor
autonomic dysfxn
form of dementia where pts won't recognize their own reflection
lewy body dementia
form of dementia where capgras syndrome can occur
lewy body dementia
tx for lewy body dementia
cholinesterase inhibitors can be helpful but don't modify dz
what drugs are contraindicated in lewy body dementia
typical neuroloeptics b/c it can --> irreversible parkinsonism
atypicals can be used cautiously
which form of dementia is associated with rem-behavioral d/o
lewy body
tx of rem behavioral d/o
clonazepam qhs
parkinson's dementia
similar to lewy body dementia
how is lewy body dementia different from parkinsons dementia
the time course is different (early in lewy body and late or not at all in parkinsons)
dementia seen in huntington's dz
forgetfulness and concentration difficulty early on
later there is more severe memory decline, difficulty learning, language decline, adn apraxia
meds used in huntington's dementia
antipsychotics to help with the psychosis
ssris for any ocd or depression that may develop
pathyophysiology of nph
communicating hydrocephalus develops in elderly pts w/o clear obstruction to csf outflow
what does imaging show in nph
enlarged ventricles out of proportion to brain atrophy
dx of nph
lp which should improve gait substantially and should be reproducible; they should then be referred for a shunt
sx transient global amnesia
during a stressful situation, there is profound anterograde and retrograde amnesia
self limiting condition
in pt with pcnsl what is the first step in dx
do an eye exam; some pts have vitreal/uveal involvement and dx can be made w vitrectomy, so no need for brain bx
is resection recommended in pcnsl
no, it is prone to hemorrhage and doesn't improve survival
tx of pcnsl
once dx is made, mtx is tx of choice
adverse effects of donezepil
increased vagal tone
av block
adverse effects of memantine
secondary progressive ms
begins as relapsing/remitting ms, 85% become 2dary progressive
recurrent progression of neuro sx
primary progressive ms
starts with spinal cord dysfxn or ataxia
no acute exacerbations
fewer cerebral lesions
more common in men
why does metoclopramide --> parkinsonism
it is a da antagonist
when to refer an epileptic for surgery
after pt has failed on 3 aeds
correct sequence of dx and treating pseudotumor cerebri
do imaging to r/o organic brain dz
perform lp
confirm dx and tx w acetazolamide
sleep-wake cycles are maintained
brainstem and hypothalamic fxn is preserved
pathology of ms lesions
demyelinated areas surrounded by macrophages and lymphocytes
how does ms differ from leukodystrophies
ms has focal demyelination
sx of optic neuritis
periorbital pain with eye movements
subtle loss of vision
red desaturation
if there is tremor in ms, where would you expect the lesion
plaques affecting cbl afferent/efferent pathways
adverse effects of glatirimer acetate
chest tightness
moa mitoxantrone
topo II inhibitor
moa natalizumab
blocks interaction between vla4 and vcan 1 which is needed for adherence to vascular endothelium
sx of acute transverse myelitis
b/l le weakness
loss of sphincter tone
sensory loss at a spinal cord level
tx of acute transverse myelitis
steroids + acyclovir
plasma exchange if above not successful
sx of acute ms
rare, fulminant demylenation dz
large edematous contrast enhancing lesions with mass effect

entire brainstem demyelination --> death
tx of acute ms
plasma exchange + steroids
if pt survives acute attack, put pt on immunosuppressents
sx of ADEM
seen in children commonly after vaccination or infection
monophasic, multifocal inflammation and demylenation
can be associated with sz and loc
tx of adem
plasma exchange and ivig
add steroids if necessary
sx of neurosarcoidosis
chronic meningitis
sx depend on location of granulomata
blood test findings in neurosarcoidosis
increased ACE increased serum globulin
tx of neurosarcoidosis
steroids + azathioprine
behcet's dz
relapsing iritis/uveitis + oral/genital aphthous ulcers
can have abrupt onset of meningoencephalitis + cn palsies
central pontine myelinolysis
symmetric destruction of the white matter in the pons
who is more prone to developing central pontine myelinolysis
EtOH abusers
ppl with multiorgan failrue
presentation of central pontine myelinolysis
rapidly progressive spastic quadriplegia
facial, glottal, pharyngeal paralysis
--> locked in syndrome
where is cmV localized to in brain?

myotonic dystrophy
can't release grip
cardiac problems
--> parkinsonism in drug users
can be treated with amantadine
eye deviation in stroke of
if in cortex, eyes will deviate towards lesion
if in pons, eyes will deviate away from lesion and look at affected limbs
in putamen, eyes deviate towards lesion
in cbl, eyes deviate away from lesion
describe CN III neuropathy in dm
it is ischemic in dm
there are 2 blood sources to the nerve fibers in cn iii, and in dm only the somatic fibers are affected, so accomadation and light response is ok
side effects of riluzole
weight loss
increased lfts
moa riluzole
glutamate inhibitor
when is hemineglect seen
lesion in non-dominant parietal lobe
describe tremor seen in wilson's dz
wing beating tremor
eeg findings in cjd
triphasic synchronous waves
neurologic uses of amantadine
parkinsons dz
tx of ms related fatigue
where is the lesion that causes locked-in syndrome
lesion at base of the pons
vertebro-basilar artery
spinal muscular atrophy
affects anterior horn cells (sim to polio)
persistent vegitative state
awake but not aware
caused by cortical anoxia
brainstem still fxns and there are brainstem reflexes present
cortex doesn't work
when should berry aneurysms be repaired
what is the main cause of morbidity and mortality in huntington's pts
what does mri of hd show
bilateral atrophy in cerebral hemispheres, corpus callosum, brainstem
sx of cerebral venous thrombosis
ha --> change in ms, somnolence, death