Neurology Shelf And Usmle

Front 1

xanthochromia

Back 1

rbcs seen in csf as a result of subarachnoid hemorrhage/hemorrhagic encephalitis

Front 2

presence of rbcs but no xanthochromasia in csf is indicative of...

Back 2

traumatic tap, rbcs are not lysed (whereas in xanthocromia they are lysed)

Front 3

significance of oligoclonal bands

Back 3

ms (or any other demyelinating dz)
cns infx
non-infectious inflammatory proceess

Front 4

what does a + ebv pcr from csf indicate

Back 4

lymphoma in pts with aids or immunosuppression

Front 5

what is the danger of performing a lp? how to avoid this?

Back 5

cerebral/cbl herniation if there is a supra/infratentorial mass lesion
DO A CT BEFOREHAND UNLESS MENINGITIS IS SUSPECTED!!!!

Front 6

what protein is present in csf that can indicate cjd?

Back 6

14,3,3-protein

Front 7

what is the best initial imaging study for HA, trauma, sz, subarachnoid hemorrhage, and stroke

Back 7

ct

Front 8

when is an mri of the brain indicated

Back 8

to examine posterior fossa and craniocervical junction (both regions are seen poorly on ct d/t artifact from surrounding bone)

Front 9

what does a ct show that is relevant in strokes

Back 9

fresh blood

Front 10

where do alpha waves originate from? when are they seen?

Back 10

posterior head
seen in relaxed, awake state with eyes closed

Front 11

where do beta waves originate from

Back 11

frontial region

Front 12

when are theta waves seen normally?
if seen at other times, can indicate

Back 12

during sleep
if seen during wakefulness, can indicate encephalopathy, esp if generalized, slow and arrhythmic)

Front 13

why do pts have to hyperventilate during eeg

Back 13

in order to provoke absence sz

Front 14

how to induce myoclonic sz

Back 14

photostimulation

Front 15

interictal changes on eeg

Back 15

seen only in minority

Front 16

what should be given to all unconscious pts upon arrival in a hospital

Back 16

naloxone
thiamine
glucose

Front 17

why should thiamine be given before glucose

Back 17

glucose alone can induce wernicke's encephalopathy

Front 18

definition of pvs

Back 18

pt has lost all awareness and cognitive fxn, but remain wiht eyes open, have sleep-wake cycles, and maintain respiration and other autonomic fxn

Front 19

how is locked in syndrome different from pvs

Back 19

in locked in syndrome, pt is awake and intact, with no altered consciousness
can only move eyes vertically and blink

Front 20

what causes locked in syndrome

Back 20

usually a large lesion at the base of the pons

Front 21

definition of encephalopathy

Back 21

inability fo carry out a coherent plan or thought or action

Front 22

describe the visual pathway

Back 22

light enters the retina, stimulating the rods and cones --> optic nerve --> optic chiasm --> optic tract --> LGN --> optic radiations --> occipital cortex

Front 23

what is the visual defect if the right optic nerve is damaged

Back 23

total right eye blindness

Front 24

what is the visual defect if the optic chiasm is damaged?

Back 24

bitemporal visual field deficit

Front 25

what is the visual defect if the right optic tract is damaged

Back 25

left homonymous hemianopia (can't see anything from the left-most regions of the visual field)

Front 26

what is the visual defect if the right parietal optic radiation is damaged?

Back 26

left inferior homonymous quadrantonopia

Front 27

what is the visual defect if the right temporal optic radiation is damaged?

Back 27

left superior homonymous quadrantonopia

Front 28

what is the visual defect if both right optic radiations are damaged?

Back 28

left homonymous hemianopia

Front 29

what is the visual defect if the right occipital cortex is damaged

Back 29

left homonymous hemianopia with macular sparing

Front 30

what is the visual problem if the pinhole test improves vision

Back 30

the problem is with refraction

Front 31

marcus gunn pupil - how to test for it, what is it?

Back 31

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

Front 32

anisocoria

Back 32

unequal pupils

Front 33

edinger-westphal nuclei
what is the pathway

Back 33

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

Front 34

how does the pupil dilate?

Back 34

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

Front 35

how to distinguish physiologic anisocoria from pathologic?

Back 35

if it is physiologic, then the degree of anisocoria will not change with different illumination

Front 36

how to determine if anasocoria is caused by horner's syndrome

Back 36

cocaine drops will fail to dilate the affected pupil

Front 37

if cocaine test for anasocoria is negative, what can be used to distinguish a preganglionic from a post-ganglionic horner's syndrome

Back 37

hydroxyamphetamine - if post-ganglionic, then horner's syndrome is post-ganglionic

Front 38

sx of CN III palsy

Back 38

"down and out with a 3rd nerve palsy"
ptosis
dilated pupil
ophthalmoplegia

Front 39

transverse myelitis

Back 39

inflammatory demylenation in spinal cord with certain spinal tracts affected
--> b/l or u/l weakness below lesion -> bowel/bladder loss, hyperreflexia, + babinski

Front 40

uhthoff's phenomenon

Back 40

worsening of ms sx in heat

Front 41

prognosis for ms

Back 41

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

Front 42

what do new ms lesions look like on mri

what do old lesions look like?

Back 42

T2 shows hyperintense areas in white matter

T1 shows hypodense (looks like black hole)

Front 43

most common locations for ms lesions

Back 43

periventricular white matter
juxtacortical regions
corpus callosum
cbl peduncles

Front 44

dawson's fingers

Back 44

in ms, there is demyelination spreading from corpus callossum

Front 45

what are oligoclonal bnads

Back 45

IgG AB from plasma cells, seen in ms

Front 46

how to evaluate old optic neuritis in ms

Back 46

visual evoked potential... can be used to show how fast signals travel down optic nerve

Front 47

chronic tx of ms

Back 47

interferons B-1a/1b, glatiramer, metoxantrone--> decreased rate of relapses

Front 48

tx for acute relapses of ms

Back 48

corticosteroids (shortens duration of relapse)

Front 49

what can be used if ms doesn't respond to traditional tx

Back 49

azathioprine
cyclophosphamide
mtx

Front 50

AIDP

Back 50

aka Guillan Barre
rapid ascending areflexic motor paralysis; no sensory problems
starts with pins/needles in feet

Front 51

ADEM and how can it be distinguished from ms

Back 51

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)

Front 52

csf of adem

Back 52

lymphocytic pleiocytosis with increased protein
oligoclonal bands rarely occcur

Front 53

prognosis of adem
tx

Back 53

neuro recovery is usually complete
steroids decrease duration of episode

Front 54

where does corticospinal tract cross
clinical manifestations if there is a lesion here

Back 54

crosses in medulla

umn signs and weakness

Front 55

where does spinothalamic tract cross

Back 55

1-2 levels above the lesion, anterior commissure

Front 56

where do dorsal columns cross

Back 56

medulla

Front 57

sx of brown-sequard syndrome

Back 57

ipsilateral weakness, umn signs (from corticospinal tract)
ipsilateral decrease in vibration/position sense
contralateral decrease in pain/temp

Front 58

where is the lesion in polio
clinical features

Back 58

anterior horns
flaccid paralysis, lmn sx

Front 59

where is the lesion in als
clinical features

Back 59

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

Front 60

clinical features if there is an occlusion of anterior spinal artery

Back 60

corticospinal tract, anterior horns, and spinothalamic tract are all affected

dorsal columns are spared

Front 61

where is the lesion in tabes dorsalis
clinical features

Back 61

dorsal columns and dorsal roots
impaired proprioception and sensory ataxia

Front 62

where is the lesion in syringomyelia
clinical features

Back 62

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)

Front 63

how do fibers of corticospinal tract travel

Back 63

start in motor cortex, pass through basal ganglia, cross in medulla, travel down spinal cord via corticospinal tract, synapse in anterior horn, to muscle

Front 64

what other condition is associated with syringomyelia

Back 64

chiari syndrome

Front 65

chiari syndrome I

chiary syndrome ii

Back 65

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

Front 66

what bv supplies the dorsal columns

Back 66

posterior spinal artery

Front 67

where is the spinal cord lesion in b12 deficiency

Back 67

dorsal columns and corticospinal tracts

Front 68

csf in pt with adem

Back 68

lymphocytic pleiocytosis and increased protein
oligoclonal bands are RARE

Front 69

prognosis for adem

Back 69

recovery is common and is usually complete

Front 70

tx fo adem

Back 70

steroids to decrease duration of episode

Front 71

pml

Back 71

jc virus gets reactivated --> demylenation by infected oligodenrocytes, seen in immunocompromised

Front 72

htn leukoencephalopathy

Back 72

sudden increase in bp, p/w acute confusional states, sz, ha, vomiting,
papilladema, retinal hemorrhages
reversible but can lead to coma/death

Front 73

what is required for the dx of narcolepsy

Back 73

sleep latency <5 min in 2/5 naps measured in sleep study, and must have rapid rem onset

Front 74

possible causes of restless leg syndrome

Back 74

fe deficiency,
etoh, uremia

Front 75

tx of restless leg syndrome

Back 75

da agonists, BZ, fe (if deficient)

Front 76

pathogenesis of ha

Back 76

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

Front 77

what, if physically disturbed would not cause ha

Back 77

brain parenchyma and bones

Front 78

pathophysiology of ha pain

Back 78

cn v adn uppercervical roots carry pain info to brain when pain sensitive structures are irritated

Front 79

clinical finding of trigeminal neuralgia

Back 79

pain in V2, V3

Front 80

what body position can alleviate migraines? what can this be used to help differentiate?

Back 80

laying down
if from increased icp, then it would be relieved by sitting up

Front 81

what structure is involved in a cluster ha

Back 81

superior pericarotid cavernous sinus plexus

Front 82

"worst headache of my life"

Back 82

subarachnoid hemorrhage

Front 83

clinical features of subarachnoid hemorrhage

Back 83

sudden, severe ha, with vomiting, neck stiffness, cessation of activity, and loc

Front 84

dx of subarachnoid hemorrhage via lp

Back 84

heme breakdown in csf

Front 85

tx of trigeminal neuralgia

Back 85

carbamazepine
if that doesn't work, rf ablation

Front 86

risk factors for pseudotumor cerebri

Back 86

obesity, women,

Front 87

neuro findings in pseudotumor cerebri

Back 87

b/l visual sx + ha
scotomas, dbl vision, papilledema, otherwise nml neuro exam
ct/mri nml

Front 88

tx for pseudotumor cerebri

Back 88

acetazolamide, furosemide, steroids, **weight loss**

Front 89

most common cause for low pressure ha
TX

Back 89

lp
caffeine or a blood patch (periph blood injected into lp site, and causes clots (on purpose), to seal of puncture site adn

Front 90

cidp

Back 90

slowly evolving weakness starting in legs
widespread areflexia
loss of vibration sense
weakness in neck flexors

Front 91

tx fo cidp

Back 91

steroids (aidp has no response to steroids)
plasmapheresis and ivig are also useful

Front 92

mechanism behind etoh intoxication - which receptors are involved?

Back 92

inhibits glutamate nmda (excitatory) receptors
agonizes gaba
inhibits reticular activating system (--> sedation) and impaired hand-eye coordination (parietal association cortex)

Front 93

long term effects of etoh on receptors

Back 93

down reg of gaba neurotransmission and upregulation of glutamate neurotransmission --> tolerance

Front 94

which cranial nerves have autonomic function

Back 94

III, VII, IX, X

Front 95

what cranial foramen does CN I travel through

Back 95

cribriform plate

Front 96

what cranial foramen does CN II travel through

Back 96

optic foramen

Front 97

what cranial foramen does CN III travel through

Back 97

superior orbital fissure

Front 98

what cranial foramen does CN IV travel through

Back 98

superior orbital fissure

Front 99

what cranial foramen does CN V1 travel through

Back 99

superior orbital fissure

Front 100

what cranial foramen does CN V2 travel through

Back 100

foramen rotundum

Front 101

what cranial foramen does CN V3 travel through

Back 101

foramen ovale

Front 102

what cranial foramen does CN VI travel through

Back 102

superior orbital fissure

Front 103

what cranial foramen does CN VII travel through

Back 103

internal auditory meatus

Front 104

what cranial foramen does CN VIII travel through

Back 104

internal auditory meatus

Front 105

what cranial foramen does CN IX travel through

Back 105

jugular foramen

Front 106

what cranial foramen does CN X travel through

Back 106

jugular foramen

Front 107

what cranial foramen does CN XI travel through

Back 107

jugular foramen

Front 108

what cranial foramen does CN XII travel through

Back 108

hypoglossal foramen

Front 109

which CNs travel through superior orbital fissure

Back 109

III, IV, V1, VI

Front 110

which CNs travel through jugular foramen

Back 110

IX, X, XI

Front 111

which CNs travel through the internal auditory meatus

Back 111

VII, VIII

Front 112

olfactory pathway

Back 112

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)

Front 113

what can meningiomas compress if they primarily affect olfactory bulb

Back 113

visual impaiarment -> blindness
frontal lobes and anterior cerebral arteries

Front 114

where do meningiomas affecting smell most commonly occur

Back 114

olfactory bulbs adn primary olfactory fibers that project to them from olfactory epithelium

Front 115

mechanism behind anosmia following trauam

Back 115

sheering of olfactory bulbs passing through cribriform plate
or bilateral contusion of orbitofrontal cortex

Front 116

if pituitary tumor compresses optic chiasm from the side or posteriorly, what visual defect in visual fields would there be

Back 116

homonymous hemianopia

Front 117

pathophysiology of ha 2/2 pituitary tumor

Back 117

stretching of diaphrama sella and other pain sensitive structures
they are frontal b/c these structures are innervated by V1

Front 118

why do non-secretory pituitary tumors sometimes cause amenorrhea, elevated gh, fsh, lh, and prl

Back 118

pituitary stalk compression and interruption of da fibers that normally inhibit prl release

Front 119

explain macular sparing as is seen when there is occipital pole damage

Back 119

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

Front 120

is visual acuity affected in occipital pole damage

Back 120

should be spared as long as the postchiasmal lesion is unilateral

Front 121

when is optic atrophy seen?
what does it look like?

Back 121

glaucoma, neurotoxins, optic nerve compression from neoplasms, infarction, trauma, ms, degen dz, long-standing papilledema

pale optic disk

Front 122

optic neuritis findings on mri

Back 122

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)

Front 123

what type of visual defect is normally seen in optic neuritis and why

Back 123

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

Front 124

prognosis of optic neuritis

Back 124

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

Front 125

tx of optic neuritis

Back 125

corticosteroids

Front 126

residua following recovery from optic neuritis

Back 126

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

Front 127

what is seen in papilledema on eye exam

Back 127

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

Front 128

what drug will decrease frequency of tias and likelihood of cerebral infarction

Back 128

asa

Front 129

define myoclonus
when is it physiologic
when is it pathologic

Back 129

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

Front 130

defining features of a tremor

Back 130

involuntary and it oscillates, can be regular/irregular, distal or proximal and intermittent/continuous

Front 131

physiologic tremor

Back 131

tremor in fingers of outstretched arms
irregular rhythm, accentuated by nervousness

Front 132

what dzs accentuate phsyiologic tremor

Back 132

thyrotoxicosis
etoh w/d
renal/liver failure

Front 133

features of essential tremor
tx

Back 133

induced by intentional activity
tremor improves with etoh
distorted handwriting is present
propanolol

Front 134

intention tremor
structure involved

Back 134

tremor that increases as target is approached
cbl and cbl outflow tracts (cbl peduncle), red nucleus may be damaged as well

Front 135

what types of dzs --> intention tremor

Back 135

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)
infarction
tumor
drugs

Front 136

describe tremor seen in parkinson's dz

Back 136

RESTING TREMOR!
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)

Front 137

difference between asterixis and myoclonus

Back 137

myoclonus is an active muscle contraction (seen in renal failure only)
asterixis is a relaxation of contracted muscle (seen in hepatic and renal failure)

Front 138

how to evoke chorea during exam

Back 138

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

Front 139

describe athetosis
when is it seen?

Back 139

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

Front 140

describe dystonia

Back 140

similar to athetosis, and positions tend to be held for a long time (torticollis and tortipelvis are examples)
often dependent on posture

Front 141

describe ballism
which area of the brain is involved

Back 141

proximal continuous flinging movt of arm
acute lesions of subthalamic nucleus (usually from occlusive ro hemorrhagic stroke)

Front 142

myerson's sign

Back 142

tapping of glabelllar area on forehead --> uncontrollable blinking

Front 143

common physical findings in parkinsons' pt

Back 143

spontaneous movt
masked facies
infrequent blinking
soft voice, syllables run together

Front 144

how would a lesion in occipital lobe present

Back 144

loss of ability to perceive motion, or selective loss of depth or color vision

Front 145

term given to lack of any color vision, from absence of 2 or 3 cone types

Back 145

achromatopsia

Front 146

where in the retina would be damaged if there was a loss of blue color discrimination?
loss of red discrimination?

Back 146

outer retinal dz
inner retinal dz

Front 147

teichopsia

Back 147

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

Front 148

pathophys of migraine ha

Back 148

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

Front 149

moa of ergotamine

Back 149

increase threshold for cortical spreading depression and abort migraine attacks

Front 150

moa triptans

Back 150

5-ht agonists; don't affect cortical spreading depression but may decrease cortical input to spinal trigeminal nucleus

Front 151

what role does NO play in migraines

Back 151

activation of NO-cGMP pathway precipitates migraine attacks

Front 152

most common cause of unilateral miosis

Back 152

lung ca that affects sypathetic cervical ganglia

Front 153

what causes the ptosis in horner's syndrome

Back 153

denervation of smooth tarsal muscles w/i eyelid

Front 154

explain why cocaine has the result it does in horner's syndrome

Back 154

cocaine blocks the presynaptic reuptake of norE, if neuron hasn't fired, there is no synaptic NT to block

Front 155

describe why hydroxyamphetamine has the results it does in horner's syndrome

Back 155

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

Front 156

if a pt can't elevate the eye when it is abducted where is the problem

Back 156

either superior rectus or CN III

Front 157

if a pt can't lower the eye when it is adducted where is the lesion

Back 157

superior oblique or CN IV

Front 158

if a pt can't lower the eye when it is abducted, where is the lesion

Back 158

inf rectus or CN III

Front 159

if a pt can't elevate eye when it is adducted, where is the problem

Back 159

inf oblique or CN III

Front 160

what is seen in 4th nerve palsy

Back 160

head tilt away from the side of the lesion

Front 161

gaze palsy

Back 161

from certain cns lesions
eyes remain conjugate adn there is no diplopia but neither eye moves fully in a particular direction

Front 162

what triggers saccadic movements

Back 162

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

Front 163

physical findings that would suggest that a horizontal gaze palsy is from cerebral vs brain stem lesion

Back 163

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)

Front 164

what happens if there is destruction of the pprf

Back 164

contralateral deviation and inability to move eyes conjugately in the direction of the lesion

Front 165

what is pprf

Back 165

area adjacent to CN VI nucleus, involved in horizontal gaze

Front 166

what does the mlf do

Back 166

connects CN VI with contraolateral CN III nucleus

Front 167

what causes one and a half syndrome

Back 167

damage to pprf and ipsilateral mlf --> ipsilateral gaze palsy and ino on contralateral side

Front 168

clinical features of right sided ino (internuclear ophthalmoplegia)

Back 168

inability to adduct right eye in left lateral gaze, convergence is preserved

Front 169

where (brainstem or cortex) would you expect a lesion if a pt can't gaze leftward and also has a left hemiparesis

Back 169

cortex

Front 170

where (brainstem or cortex) would you expect a lesion if a pt can't gaze leftward and also has a right hemiparesis

Back 170

brainstem

Front 171

what disturbance in eye movement would you expect if there was an injury to the left frontal cortex

Back 171

impaired gaze to the right

Front 172

what disturbance in eye movement would you expect if there was an injury to the left mlf

Back 172

impaired adduction of left eye during rightward gaze
adduction during convergence is intact

Front 173

what disturbance in eye movement would you expect if there was an injury to left CN III

Back 173

left eye goes down and out

Front 174

what disturbance in eye movement would you expect if there was an injury to right abducens nerve

Back 174

inability to fully abduct right eye

Front 175

what disturbance in eye movement would you expect if there was an injury to left CN VIII

Back 175

horizontal rightward jerking nystagmus

Front 176

how would a pineal tumor affect vision

Back 176

can --> impaired upward gaze, with intact downward gaze

Front 177

features of pendular nystagmus
what causes it

Back 177

nystagmus with equal velocity b/l
result of severe visual impairment during childhood

Front 178

features of jerk nystagmus
WHAT causes it

Back 178

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

Front 179

most common causes of horizontal and rotary nystgmus

Back 179

vestibular lesions (either periph or central)
mlf lesion

Front 180

causes of vertical nystagmus

Back 180

brain stem lesion (ms/syringobulbia if intrinsic) or (cbl tumor/chiari malformation if extrinsic)

Front 181

type of nystagmus seen in barbiturates and phenytoin

Back 181

horizontal

Front 182

how to test for nystagmus

Back 182

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)

Front 183

when does opticokinetic testing fail to produce nystagmus

Back 183

anterior cerebral lesions b/c there are no corrective saccades
posterior cerebral lesions b/c there is no initial pursuit

Front 184

what type of sz does phenytoin treat

Back 184

simple/complex partial
gtc

Front 185

what type of sz does carbamazepine treat

Back 185

simple/complex partial
gtc

Front 186

what type of sz does lamotrigine treat

Back 186

simple/complex partial
gtc

Front 187

what type of sz does gabapentin treat

Back 187

simple/complex partial
gtc

Front 188

what type of sz does topirimate treat

Back 188

simpile/complex partial
gtc

Front 189

what type of sz does topiramate treat

Back 189

simple/complex partial
gtc

Front 190

what type of sz does phenobarbital treat

Back 190

simple/complex partial
gtc

Front 191

what type of sz does valproic acid treat

Back 191

simple/complex partial
gtc
absence

Front 192

what type of sz does ethosuximide treat

Back 192

absence

Front 193

what role do bz play in sz

Back 193

1st line for acute status epilepticus

Front 194

what is used for status epilepticus proph

Back 194

phenytoin

Front 195

MOA phenytoin

Back 195

increased na channel inactivation

Front 196

MOA carbamazepine

Back 196

increased na channel inactivation

Front 197

MOA lamotrigine

Back 197

blocks voltage gated na channels

Front 198

MOA gabapentin

Back 198

increased GABA release

Front 199

MOA topirimate

Back 199

blocks na channels
increased GABA action

Front 200

MOA phenobarbital

Back 200

increased GABA-A action

Front 201

MOA valproic acid

Back 201

increased na channel inactivation and increased GABA concentration

Front 202

MOA ethosuximide

Back 202

blocks thalamic t-type Ca channels

Front 203

MOA BZ

Back 203

increased GABA action

Front 204

adverse effects of phenytoin

Back 204

gingival hyperplasia
hirsutism
megaloblastic anemia (prob with folate metabolism)
teratogenic in pregnancy
hepatotoxic diplopia
ataxia
sle like syndrome

Front 205

tx for trigeminal neuralgia

Back 205

carbamazepine

Front 206

toxicity of carbamazepine

Back 206

diplopia
ataxia
agranulocytosis
aplastic anemia
hepatotoxicity

Front 207

toxicity of ethosuximide

Back 207

gi distress
lethargy
ha
urticaria
steven's-johnson syndrome

Front 208

toxicity of valproic acid

Back 208

rare, but fatal hepatotoxicity
NTDs in pregnancy
gi distress

Front 209

toxicity of lamotrigine

Back 209

stevens-johnson syndrome

Front 210

toxicity of gabapentin

Back 210

sedation, ataxia

Front 211

toxicity of topiramate

Back 211

sedation
mental dulling
kidney stones
weight loss

Front 212

which epilepsy med should be used in pregancy and children

Back 212

lamotrigine

Front 213

which epilepsy drug should be used in sz during eclampsia

Back 213

bzs

Front 214

what can be used to prevent sz of eclampsia

Back 214

MgSO4

Front 215

difference between umn lesion of facial nerve and lmn lesion

Back 215

umn lesion: contralateral lower face weakness
lmn lesion: ipsilateral upper and lower facial weakness

Front 216

things that could cause a lmn cn vii lesion

Back 216

cerebellopontine angle neoplasm
bell's palsy

Front 217

what type of dz can cause an umn cn vii lesion

Back 217

suprasegmental stroke or brain tumor

Front 218

what type of facial weakness is seen if there is a lesion of the motor cortex

Back 218

facial movements associated with emotion are preserved but not preserved when asked to do a facial movement on command, there will be weakness

Front 219

what type of facial weakness is seen if there is a lesion in the amygdala

Back 219

facial muscle strenght is normal but an emotionally produced smile is crooked

Front 220

what can occur following peripheral nerve injury (bell palsy/trauma) upon reinnervation

why does this occur

Back 220

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

Front 221

what causes hyperacusis

Back 221

denervation of the stapedius muscle of middle ear, so can't dampen the ossicles during loud noise

Front 222

pathophysiology behind crocodile tears

Back 222

lacrimal-salivatory synkinesis with ipsilateral lacrimation stimulated by eating following a bell palsy

(lacrimation and salivation are both mediated by cn vii)

Front 223

what autonomic functions are mediated by cn vii

Back 223

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)

Front 224

where is the lesion if there is unilateral facial weakness that spares the forehead (esp if ipsilateral limb weakness)

Back 224

contralateral motor cortex

Front 225

where is the lesion if there is unilateral facial weakness of forehead, as well as ipsilateral abducens weakness

Back 225

pons
(and if there is hemiparesis, it will be contralateral)

Front 226

where is the lesion if there is unilateral facial weakness in forehead, and if taste, salivation, and lacrimation are affectd

Back 226

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

Front 227

where is the lesion if there is unilateral facial weakness in the forehead, that is unaccompanied by other abnormalities

Back 227

lesion is either of the facial nucleus in th epons or the nerve distal to the chorda tympani

Front 228

if a person can unilaterally raise one eyebrow voluntarily, what does that mean about their innervation

Back 228

there is mostly contralateral facial representation in teh motor cortex

Front 229

describe the innervation of the tongue

Back 229

the motor cortex sends fibers bilaterally to the hypoglossal nucleus in the medial medulla

Front 230

what type of lesion does atrophy of the tongue indicate

Back 230

lmn lesion (either centrally or peripherally)

Front 231

bulbar palsy

Back 231

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

Front 232

pseudobulbar palsy

Back 232

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

Front 233

progressive supranuclear palsy

Back 233

degen d/o --> d/o eye mov't, pseudobulbar palsy, dystonia, dementia, pyramidal and cbl dysfxn

Front 234

what nerve carries info from the barorecpetors in carotid body and aortic arch

Back 234

cn x

Front 235

which nerves comprise the nucleus solitarius
what kind of info does this carry

Back 235

vii, ix, x
visceral sensory info taste, baroreeptors, gut distention)

Front 236

which nerves are through the nucleus ambiguous
what info does this carry

Back 236

ix, x, xi

motor innervation of pharynx, larynx, and upper esophagus

Front 237

what info is carried in the dorsal motor nucleus

Back 237

cn x, that sense parasymp fibers to the heart, lungs, adn upper gi

Front 238

what type of lesion is suggested if a pt has a nasal voice

Back 238

palatal weakness

Front 239

what type of lesion is suggested if a pt has h/o nasal regurg of fluids

Back 239

palatal weakness

Front 240

what type of lesion is suggested if a pt has hoarseness or reduced cough

Back 240

laryngeal weakness

Front 241

what type of lesion is suggested if a pt chokes on saliva while talking

Back 241

pharyngeal weakness

Front 242

what type of lesion is suggested if a pt has dysphagia to solid foods only

Back 242

mechanical obstruction (carcinoma)

Front 243

what type of lesion is suggested if a pt has dysphagia to solids and liquids

Back 243

neurological dysfxn

Front 244

to what side dose the uvula deviate if it does not rise symmetrically

Back 244

towards the normal side (away from the side of the lesion)

Front 245

when testing the gag reflex, what is suggested by b/l weakness with preserved sensation

Back 245

motor neuron dz (als, polio), neuromuscular junction dz (ex - mg) or myopathy

Front 246

when testing the gag reflex, what is suggested by u/l motor and sensory loss

Back 246

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)

Front 247

when testing the gag reflex, what is suggested by b/l motor and sensory loss in posterior pharynx

Back 247

intraparenchymal medullary lesion where other cn and long tracts are probably present

Front 248

when testing the gag reflex, what is suggested by b/l sensory loss with nml movement on phoation

Back 248

psychiatric dz... very rare

Front 249

if there is weakness in the right scm, where is the lesion

Back 249

RIGHT cortex (the only muscle with ipsilateral muscle innervation from cortex)

Front 250

if there is weakness in the right trapezius, where is the lesion

Back 250

LEFT cortex

Front 251

jugular foramen syndrome

Back 251

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

Front 252

causes of central spinal cord compression

Back 252

syringomyelia
neck flexion-extension injury
intrinsic tumor

Front 253

si and sx of foramen magnum lesion

Back 253

spastic quadriparesis
neck pain and stiffness
c2-c4 and upper facial numbness
ipsilateral horner's ysndroem
ipsilateral tongue and trapezius muscle weakness

Front 254

si and sx of conus medullaris lesion

Back 254

lower sacral saddle sensory loss (s2-s5)
sphincter dysfxn
inpotence
aching back
rectal pain
l5 and s1 motor probs (ankle and foot weakness)

Front 255

si and sx of cauda equina syndrome

Back 255

sphincter dysfxn
paraparesis with weakness in multiple nerve roots
sensory loss in multiple bilateral dermatomes

Front 256

what does contrast enhancement mean in a ct

Back 256

presence of a disrupted bbb

Front 257

when should contrast be used in ct

Back 257

suspected neoplasm, abscess, vascular malformation, new onset sz

Front 258

what things appear black in a ct

Back 258

air
fat
water

Front 259

what things appear white in a ct

Back 259

acute hemorrhage
iv contrast
bone/metal

Front 260

what are t1 mris used for

Back 260

to detect anatomy
most pathologic processes are associated w increased water content and appear darker than normal brain

Front 261

what are t2 mris used for

Back 261

to detect pathology (they will look white to reflect increased water content)

Front 262

what color are fat and subacute blood in t1 mri

Back 262

white

Front 263

what things are white in t2 mri

Back 263

water

Front 264

when is diffusion weighted imaging used

Back 264

to detect hyperacute ischemia in pts with acute stroke

changes are seen w/i minutes

Front 265

when is mr angiography used (mra)

Back 265

used to detect large scale lesions (carotids or large aneurysms) not good for smaller lesions, must use conventional angiography

Front 266

what can standard angiography detect

Back 266

stenosis/occlusion
arterial dissection
aneurysms
avm
vasculitic narrowing
dural venous sinus thrombosis

Front 267

most impt complication of angiography test

Back 267

1-2% --> stroke secondary to emboli generated by the catheter (seen mostly in elderly with atherosclerotic dz)

Front 268

how do simple szs affect consciousness

Back 268

simple partial sz have no impairment in consciousness

complex partial sz has alteration in consciousness

Front 269

how do complex szs affect consciousness

Back 269

complete loss of consciousness

Front 270

definition of status epilepticus

Back 270

10+ minutes of continuous szs where pt fails to fully awaken

Front 271

differential dx of sz

Back 271

Vascular
Infectious
Trauma
Autoimmune (seen in sle, vasculitis, ms)
Metabolic
Idiopathic
Neoplasm (most common way for neoplasm to present if it is in brain)
Structural

Front 272

what are things to be concerned for in pt actively seizing, or prolonged szs

Back 272

aspiration of gastric contents if airway is not protected
head injury
lactic acidosis
hypoxia
hyperthermia
rhabdo
cerebral edema
hypotension

Front 273

tx for status epilepticus

Back 273

full dose of bz, followed by fosphenytoin, but risk of recurrence is very high

Front 274

what is the best way to secure the airway in coma

Back 274

endotracheal intubation

Front 275

why should you give thiamine before dextrose

Back 275

hyperglycemia promotes the consumption of thiamine and will acutely worsen wernicke's

Front 276

what does naloxone do

Back 276

reverses opiate intoxication

Front 277

what does flumazenil do

Back 277

reverse come from bz intox

Front 278

top 3 causes (in order) for coma/stupor

Back 278

toxic/metabolic d/o (66%)
structural intracranal d/o (33%)
psychiatric d/o (1%)

Front 279

role of unilateral hemispheric lesion in producing stupor or coma

Back 279

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

Front 280

how do focal brainstem lesons --> coma

Back 280

disrupting the reticular activating system

Front 281

3 common, treatable causes that can rapidly --> coma/death

Back 281

increased icp
herniation and brainstem compression
meningitis/encephalitis

Front 282

tx of herniation and brainstem compression

Back 282

neurosurgery (it's an emergency1)

Front 283

tx of increased icp

Back 283

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

Front 284

why is increased icp so dangerous

Back 284

--> impaired cerebral perfusion and global hypoxic-ischemic injury

Front 285

bladder fxn in als

Back 285

spared until final stages of illness

Front 286

why does muscle cramping occur in als

Back 286

irritability of denervate muscles

Front 287

mode of inheritance of als

Back 287

5-10% are familial, autosomal inheritance
SOD1 deficiency is involved, coded for in q21 arm of chromosome 21

Front 288

relationship between SOD1 and als

Back 288

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

Front 289

what is the difference between dominantly inherited als compared w sporadic als

Back 289

clinical features are identical, but familial develops 10 yrs earlier

Front 290

hypothesis of pathogenesis in sporadic als

Back 290

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

Front 291

tx for als

Back 291

riluzole (a glutamate antagonist) may slow progression of dz

ivig may also be helpful

Front 292

what causes waddling gait
describe waddling gait

Back 292

weakness of gluteus medius muscle
pts pelvis drops with each step

Front 293

describe gower's sign

Back 293

to rise from sitting position, pt puts his hands on his knees, pushes his trunk back and works his hands up thighs

Front 294

what is seen on muscle biopsy in muscular dystrophy

Back 294

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

Front 295

which gene is involved in duchenne's muscular dystrophy

Back 295

X chromosome, 21p --> dystrophin

Front 296

what does dystrophin do

Back 296

links actin within the muscle fiber and laminin on muscle fiber's external surface

in DMD, no dystrophin is produced

Front 297

types of hypertonicity

Back 297

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

Front 298

describe cogwheel rigidity

Back 298

rapidly alternating contractions of agonist and antagonist muscles (seen in parkinson's)

Front 299

what happens to tone following severe spinal cord injury

Back 299

flaccid areflexia (aka spinal shock), followed by spastic hyperreflexia (cause of this change is unknown)

Front 300

describe spinal shock

Back 300

results from the removal of suprasegmental descending systems that facilitate spinal motor neurons
there is flaccid areflexia

Front 301

what effect does noxious stimuli cause below level of complete spinal transection

Back 301

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

Front 302

describe dichotomous findings with sweating seen in complete spinal cord transection

Back 302

noxious stimuli --> sweating, but warm environment does not

Front 303

moa baclofen

Back 303

gaba agonist that likely acts at substance p synapses in dorsal horn

Front 304

describe pain seen in spinal cord transection that is present below the lesion

Back 304

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

Front 305

what is cushing's response

Back 305

bradycardia
hypertension
respiratory depression

they all occur as a consequence of increased icp

Front 306

cerebral perfusion pressure

Back 306

cpp = mabp - icp
the goal is to keep cpp constant, so if icp increases, then mabp will increase

Front 307

what is the acceptable range of cpp

Back 307

70-120 mm hg
if it is above that --> cerebral edema
if it is below that --> hypoxic injury

Front 308

how does jvp relate to icp

Back 308

csf is reabsorbed across meninges into venous circulation, so if jvp is elevated, then csf can't get out --> increased icp

Front 309

what are the 3 components w/i the cranium that contribute to volume

Back 309

brain
csf
blood

Front 310

what are the clinical signs of herniation

Back 310

(all occurring from brainstem compression)
1. loss of pupillary reactivity
2. impairment of eye movements
3. hyperventilation
4. motor posturing (flexion/extension)

Front 311

when should increased icp be suspected

Back 311

in pts with known or suspected intracranial pathology (stroke, trauma, neoplasm) and have depressed level of consciousness, htn w/ or w/o bradycardia

Front 312

most common causes of increased intracranial volume

Back 312

extrinsic mass lesions
hydrocephalus
cerebral edema

Front 313

describe the cerebral autoregulation curve

Back 313

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

Front 314

what fibers are carried in the internal capsule

Back 314

posterior limb carries corticospinal fibers and sensory fibers

genu carries corticobulbar fibers

anterior limb carries frontopointine and spinothalamic fibers

Front 315

blood supply of the internal capsule

Back 315

striate arteries that come off of the mca

Front 316

csf in guillain-barre

Back 316

high protein count mild wbc (pleocytosis usually <10 lymphos/dL)

albumin/cytologic protein dissociation

Front 317

charcot-marie-tooth dz

Back 317

progressive muscular atrophy that starts in feet and then spreads to hands; sensation affected less or not at all
aka peroneal muscular atrophy

Front 318

mode of inheritance of charcot-marie-tooth

Back 318

x linked

Front 319

which dz that causes elevated gamma-globulins (M-proteins) will also --> senosorimotor periopheral neuropathy

Back 319

MGUS
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

Front 320

explain why long nerves tend to be more affected in demyelinating processes, compared to short nerves

Back 320

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

Front 321

what is an easy way to distinguish between a myopathic motor problem and a neuropathic motor problem

Back 321

myopathic problems will usually affect proximal muscles (with a few exceptions)
neuropathic problems will usually affect distal muscles

Front 322

signs of denervation on emg

Back 322

fibrillations, positive waves, polyphasic potentials of increased duration and amplitude

Front 323

spinal muscular atrophy

Back 323

hereditary progressive degeneration of motor neurons in anterior horn of spinal cord

Front 324

type of gait seen with cbl dz

Back 324

broad based gait
fall towards side of lesion

Front 325

if a pt is standing with their feet together, what is seen in cbl vermal lesions or b/l vestibular lesions

Back 325

they will fall backward or fall inconsistently in any direction

Front 326

what is circumduction and when is it seen

Back 326

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

Front 327

what causes a stiff spastic gait
describe the gait

Back 327

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

Front 328

what findings of gait are there in a pt with impaired proprioception

Back 328

they watch their feet as they walk
leg(s) may move randomly in different directions

Front 329

what are the main differences between bulbar and pseudobulbar palsy

Back 329

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

Front 330

what happens when a parkinsons pt tries to rise from sitting

Back 330

they can't, unless they use their arms

Front 331

what is magnetic gait and when is it seen

Back 331

legs are broad based adn feet never leave the ground, takes tiny steps,
cause by b/l frontal lobe dz, seen in chronic nph

Front 332

what is titubation and when is it seen

Back 332

coarse tremor of head and neck
seen in cbl dz

Front 333

describe jacksonian march

Back 333

focal motor sz that has a clonic jerking that rapidly spreads proximally from one or more digits, up a limb

Front 334

what way do eyes deviate during a sz

Back 334

deviated away from the lesion

Front 335

what is todd paresis

Back 335

transient postictal focal weakness, signifying functional unresponsiveness of neurons in the area of maximal discharge, could be from excessive glutamate neurotransmission

Front 336

what is the difference seen in electrical activity in a pt with partial szs who generalizes, compared to a pt with primary generalized szs

Back 336

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

Front 337

most common cause of a tia

Back 337

usually they are embolic

Front 338

less common cause for a tia

Back 338

transient hypotension in the presence of severe carotid stenosis (>75%)

Front 339

most common etiology of cva

Back 339

infarction from embolic strokes - most common origin of embolus is secondary to embolization of mural thrombus in pts with a-fib

Front 340

what are the 3 most common causes of stroke

Back 340

infarction (embolus, atherothrombotic, lacunar)
intracerebral hemorrhage
subarachnoid hemorrhage
misc causes

Front 341

when should htn be treated immediately following a stroke

Back 341

if there is a htn emergency
if bp >220/120
bp can be lowered if there is evidence of a hemorrhagic stroke on ct

Front 342

major threats to life following stroke

Back 342

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)

Front 343

presentation of SAH

Back 343

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

Front 344

why is sah so dangerous

Back 344

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!

Front 345

what will a ct scan of sah show

Back 345

hyperdensity in sulci, major fissures, and around brainstem

Front 346

if the ct is negative for sah, but clinical suspicion is still high, what is the next step in dx

Back 346

lp - csf will show xanthochromia; can also r/o meningitis

Front 347

after sah is dx, what is the next diagnostic step

Back 347

catheter angiography to r/o additional unruptured aneurysms

Front 348

difference in presentation of sah vs other stroke types

Back 348

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

Front 349

stroke sx that are suggestive of cardioembolic strokes

Back 349

sudden deficit, maximal at onset
hemianopia w/o hemiparesis, pure wernicke's aaphasia, and top of the basilar syndrome

Front 350

most common location for aneurysms

Back 350

pca, aca, mca

Front 351

what presentation is likely to suggest large-vessel stenosis as basis for stroke

Back 351

fractional weakness (shoulder weaker than the hand, hip weaker than the ankle)

Front 352

risk factors commonly associated with large vessel stenosis

Back 352

male
htn
dm

Front 353

presentation of lacunar stroke

Back 353

no cortical signs/sx
clumsy hand dysarthria, pure motor hemiparesis, ataxic hemiparesis, sensorimotor syndrome

Front 354

management of ischemic stroke

Back 354

ct/mri
if stroke sx <3 hrs and ct shows no hemorrhage, give tpa

Front 355

presentation of intracerebral hemorrhage

Back 355

higher incdidence of ha and severe htn c/w ischemic stroke
otherwise caan be identical

Front 356

pathogenesis of intercerebral hemorrhage

Back 356

chronic htn
results from rupture of smallest penetrating arteries

Front 357

most common sites for intercerebral hemorrhage

Back 357

most commonly in basal ganglia and thalamus (70%)
brainstem
cbl

Front 358

management of hemorrhagic stroke

Back 358

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

Front 359

when should CEA be considered to prevent stroke

Back 359

sx pts: carotid stenosis >70%
asx pts: no surgery; just lower atherosclerotic rsk factors and give asa

Front 360

ha that can can cause major threat to life

Back 360

meningitis
sah
herniation from intracranial mass lesion

Front 361

preventive measures for cluster ha

Back 361

prednisone + verapamil and lithium (prednisone use is not long term, should be tapered over a couple of weekS)

Front 362

triad of sx in pseudotumor cerebri

Back 362

ha, increased icp, papilledema in absence of mass or hydrocephalus

Front 363

what type of intracranial pathology is likely to be seen in trigeminal neuralgia

Back 363

vascular compression of the pons , although it might not be seen on imaging

Front 364

what are the 2 most common causes for acute paralysis + ventilator failure

others?

Back 364

myasthenia gravis
guillan barre

c-spine correction
transverse myelitis
als
polio
cidp
aids
diphtheritic polyneuropathy
organophosphate intox
polymyositis
myopathy

Front 365

poor prognostic factors in guillan barre

Back 365

advanced age
low distal motor amplitudes
rapidly progressive weakness over the first week
resp failure --> intubation

Front 366

in aidp, which is more affected, proximal or distal muscles

Back 366

proximal

Front 367

csf in guillan barre

Back 367

cytologic-albumin dissociation
eleated protein
mild pleocytosis

Front 368

what is seen on emg of a pt with aidp

Back 368

reduced conduction velocities
occ reduced amplitude

Front 369

aside from ascending paralysis and areflexia, what other clinical signs/symptoms are seen in aidp

Back 369

pain (from meningeal inflammation or neuropathic mechanisms)
dysautonomia (htn or tachycardia)

Front 370

pathophysiology behind myasthenia gravis

Back 370

auto-ab directed against nicotinic ach receptors --> defect in nm transmission

Front 371

most common muscles affectd by myasthenia gravis

Back 371

eyes
face
neck
oropharynx
limbs

Front 372

remission of myasthenia gravis

Back 372

can occur within 2 years of onset
30% remit

Front 373

what tumor is associated with myasthenia gravis

Back 373

malignant thymoma (assoc with more severe dz)

Front 374

myasthenic crisis

Back 374

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

Front 375

dx of myasthenia gravis

Back 375

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)

Front 376

what is anti-musk

Back 376

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

Front 377

tx for myasthenia gravis

Back 377

symptomatic tx: acetylcolinesterase inhibitors (pyridostigmine)
s-t dz suppression: plasmapheresis and ivig
long-term immunosuppresion: thymectomy, steroids, azathioprine, chemotherapy

Front 378

tx for botulism

Back 378

botulism trivalent antitoxin
guanidine hydrochloride (ACh agonist that counteracts the presynaptic blockade caused by the toxin)

Front 379

why does botulism toxin --> weakness

Back 379

inhibits presynaptic ACh release

Front 380

sx of botulism

Back 380

gi complaints
dilated and nonreactive pupils
blurred vision
weakness (beginning in extraocular and oropharyngeal muscles, then --> generalized)
urinary retention
anhidrosis
dry mouth

(impaired parasympathetics)

Front 381

what differentiates guillan barre from polio

Back 381

polio has fever, headache, mental status change, asymmetric weakness
neutrophils on csf

otherwise, both are flaccid areflexic paralysis

Front 382

medical tx of tetanus

Back 382

assist ventilation
immune globulin
procaine penicillin to eradicate the soft-tissue infection

Front 383

what triad of sx should always be treated as a cns infection

Back 383

fever
ha
neurologic signs/sx
(any 2/3 require lp, with ct prior)

Front 384

pathogenesis of acute bacterial meningitis

Back 384

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

Front 385

common tx for community acquired meningitis for adults, children

Back 385

ceftriaxone and vanco until cx return
+ dexamethasone

Front 386

common tx for community acquired meningitis in infants, immunosuppressed, and older

Back 386

ampicillin should be added to cover listeria

Front 387

presentation of viral meningitis

Back 387

neurologic dysfxn is not seen, otherwise similar to bacterial meningitis

Front 388

how to treat viral meningitis

Back 388

it is self-limited

Front 389

most common viruses --> viral meningitis

Back 389

enterovirus
arthropod born (WNV)
HSV-2
HIV
(meds can do it too)

Front 390

definition of chronic meningitis

Back 390

develops over 2 wks

Front 391

physical sx of tuberculosis meningitis

Back 391

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

Front 392

late complications of tb meningitis

Back 392

hydrocephalus
sz
cognitive impairment

Front 393

dx of tb meningitis

Back 393

csf shows lymphocytic pleocytosis, increased protein level, moderately reduced glucose level
acid-fast mycobacteria in csf

ppd not reliable in th meningitis wu

Front 394

tx of tb meningitis

Back 394

inh
rif
ethambutol
pyrazinamide

dexamethasone can be given in severe cases to limit inflammation and damage

Front 395

manifestations of tertiary neurosyphilis

Back 395

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)

Front 396

what is the difference in presentation btwn hiv + pts and nonimmunosuppressed pts with neurosyphilis

Back 396

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

Front 397

tx of neurosyphilis

Back 397

penicillin G

Front 398

dx fo cns lyme dz

Back 398

evidence of intrathecal production of igg ab to borrelia
in csf, see lymphocytic pleocytosis with mildly elevated protein

Front 399

sx of cns lyme

Back 399

early: mild meningitis/meningoencephalitis
cranial neuropathy
myelitis
radicloneuritis

chronic:
lyme encephalopathy (immune mediated)
recurrent/chronic meningoencephalitis
chronic myelitis

Front 400

causes of chronic fungal meningitis

Back 400

cryptococcus
coccidiodes
candida
histoplasma
blastomyces

Front 401

dx of fungal meningitis

Back 401

demonstrates the organism by wet smear

Front 402

stain used to dx cryptococcus

Back 402

india ink

Front 403

tx of fungal meningitis

Back 403

fluconazole for mild cases
amphotericin b for severe cases

Front 404

presentation of bacterial abscess

Back 404

subacute progression of ha, altered ms, focal neurologic signs and fever

Front 405

how are most brain abscesses formed

Back 405

contiguous spread from a parameningeal infection (aom, osteomyelitis, sinusitis) or hematogenous spread in pts with endocarditis, bronchiectasis, congenital cyanotic heart dz

Front 406

what are the most common orgs seen in brain abscesses

Back 406

staph
enterobacteriacae
b fragilis

Front 407

dx fo brain abscess

Back 407

ring enhancing lesion on ct/mri
perform blood cultures and lp if etiology is not known

Front 408

tx of brain abscess

Back 408

broad spectrum tx:
penicillin
metronidazole
vanco (if pt is post-surgical or post-traumatic and staph is a concern)

Front 409

tx of subdural empyema

Back 409

surgical drainage

Front 410

what setting are cranial/spinal abscesses normally seen

Back 410

often seen with osteomyelitis

Front 411

presentation of cranial epidural abscess

Back 411

localized pain and tenderness --> cn defects

Front 412

sx of spinal epidural abscess `

Back 412

intense local pain and tenderness
local root pain irritation with referred pain
cord compression

Front 413

what are the most common organisms sen in spinal epidural abscess

Back 413

staph
gram -
tb (pott's dz)

Front 414

tx of spinal epidural abscess

Back 414

surgical drainage to prevent cord compression
vanco + ceftriaxone

Front 415

most common cause of sporadic viral encephalitis

Back 415

hsv-1

Front 416

presentation of hsv-1 encephalitis

Back 416

fever
altered ms
ha
sz

Front 417

pathogenesis of hsv-1 encephalitis

Back 417

reactivation of dormant hsv-1 within trigeminal ganglion with viral spread via sensory pathways to brain

Front 418

dx of hsv-1 encephalitis

Back 418

intrathecal hsv ab
+ hsv pcr from csf

Front 419

what is seen on hsv-1 encephalitis imaging

Back 419

focal necrotizing lesions of inferior frontal and temporal lobes

Front 420

tx of hsv-1 encephalitis

Back 420

acyclovir
anticonvulsants

Front 421

wnv encephalitis - how common is it?
clinical sx

Back 421

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

Front 422

dx of neuroinvasive wnv

Back 422

based on clinical suspicion + wnv igm in blood/csf

Front 423

tx of neuroinvasive wnv

Back 423

supportive

Front 424

difference between bacterial and viral meningitis

Back 424

in viral meningitis the neurologic dysfxn doesn't occur, it's only ha and fever

Front 425

features of tb meningitis

Back 425

severe granulomatous inflammation of basal meninges
vasculitic small vessel infarction
obstructive hydrocephalus
spinal arachnoiditis

Front 426

tx of tb meningitis

Back 426

inh
rif
pyrazinamide
ethambutol

Front 427

features of neurosyphilis

Back 427

general paresis- dementia with psych features and b/l umn signs
tabes dorsalis
argyll-robertson pupils

Front 428

dx of neurosyphilis

Back 428

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

Front 429

which hsv virus --> encephalitis
pathogenesis

Back 429

hsv-1
hsv is w/i trigeminal ganglion, gets reactivated and then there is viral spread via sensory pathways into the brain

Front 430

tx of hsv encephalitis

Back 430

acyclovir
phenytoin to prevent sz

Front 431

tx of wnv encephalitis

Back 431

supportive

Front 432

opportunistic complication of AIDS

Back 432

cns toxo
cryptococcus
pml
cmv
primary cns lymphoma
shingles
syphilis
hiv meningitis

Front 433

proph of toxo in hiv +
tx of toxo

Back 433

bactrim
sulfadiazine and pyrimethamine

Front 434

proph of mac
tx of mac

Back 434

rifabutin
clarithromycin and ethambutol

Front 435

proph of cryptococcus
tx of cryptococcus

Back 435

fluconazole
flucytosine/fluconazole/amphotericin

Front 436

presentation of toxo

Back 436

fever
subatue encephalopathy
focal neurologic deficits
sz

Front 437

presentation of cryptococcus

Back 437

suspect in any hiv + pt with a ha
fever is usually present

Front 438

presentation of pml

Back 438

subacute onset of focal neurologic deficits and dementia
peripheral ns is spared

Front 439

mri of pml

Back 439

striking white matter hyperintensities

Front 440

tx of pml

Back 440

haart

Front 441

presentation of cmv retinitis

Back 441

slowly progressive, painless loss of vision

Front 442

dx of cmv

Back 442

pcr is highly sensitive

Front 443

what does mri show in cmv

Back 443

ependymal enchancement (area around ventricles and spinal cord)

Front 444

tx of cmv

Back 444

gancyclovir

Front 445

neuro complications of shingles

Back 445

cns vasculopathy, presenting with stroke-like sx or myelopathy

Front 446

sx of hiv myelopathy

Back 446

insidious onset of spastic paraparesis, sensory ataxia, and bowel/bladder/erectile dysfxn (looks similar to b12 deficiency)

Front 447

nonopportunistic infections associated with hiv

Back 447

distal sensory polyneuropathy
dementia
myelopathy
myopathy
neuromuscular weakness syndrome
aidp

Front 448

features of distal sensory polyneuropathy

Back 448

most common hiv related neuro complication
caused by immune mediated pathway or antiretroviral toxicity

Front 449

presentation of distal sensory polyneuropathy

Back 449

symmetric, painful paresthesias
sensory loss
allodynnia in a stocking/glove distribution
loss of ankel jersks

Front 450

tx of distal sensory polyneuropathy

Back 450

better control with haart

Front 451

pathogenesis of hiv asssociated dimentia

Back 451

hiv infects non-neuronal cells shortly after primary viremia
wiht immune failure, chronic encephalitis ensues

Front 452

presentation of hiv associated dementia

Back 452

motor slowing
behavioral change

Front 453

tx of hiv associated dementia

Back 453

haart can arrest and sometimes reverse dementing process

Front 454

major causes of syncope

Back 454

reflex vasodilation
cardiac
orthostatics
neurologic causes
psych causes

Front 455

different reflex vasodilation disturbances --> syncope

Back 455

vasovagal
hypersensitive carotid body
situational syncope

Front 456

cardiac causes of syncope

Back 456

arrythmias
flow/pump failure (outflow obstructions - stenosis, hocm, dissection, myxoma, mi, cardiac tamponade)

Front 457

orthostatic causes of syncope

Back 457

volume depletion
dru induced
autonomic dysfunction (shy-drager is a central dysfxn, autonomic neuropathy is a peripheral cause)

Front 458

neuro causes for syncope

Back 458

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)

Front 459

how long is a pt unconscious before it is considered a coma

Back 459

15 mins

Front 460

syncope:
what sx would suggest it's from cardiac arrhythmia

Back 460

palpitations
no prodromal sx

Front 461

syncope:
what sx would suggest it's from vasovagal causes

Back 461

dizziness, lightheadedness, pallor, diaphoresis, dimming vision

Front 462

syncope:
what sx would suggest it's from carotid sinus

Back 462

during turning head to one side

Front 463

syncope:
what sx would suggest it's from
vertebrobasilar insuff

Back 463

1+ episodes of vertigo, diplopia, dysarthria, numbness, weakness, ataxia

Front 464

what normally happens to bp in syncope? what is the exception

Back 464

usually it drops, unless it's from sah, then pt is htn

Front 465

tx for vasovagal syncope

Back 465

if table tilt test is +, beta blocker or paroxetine

Front 466

subclavian steal syndrome

Back 466

--> 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

Front 467

tx of autonomic dysfxn --> orthostatics

Back 467

fludrocortisone, support stockings

Front 468

how does hypervent --> syncope

Back 468

hypocapnia decreases cbf 2ndary to cerebral vasoconstriction

Front 469

what part of the spine normally is affected by mets
why

Back 469

thoracic spine
there is the most drainage from visceral organs through the spinal extardural venous plexuses

Front 470

empedymomas

Back 470

intrinsic cord tumors that mimc extra axial compressive lesions

Front 471

what is the difference between how cervical disks herniate and lumbar disks herniate

Back 471

cervical disks herniate centrally

lumbar herniates laterally and --> radicular sx

Front 472

where is the herniation in an acute cauda equina syndrome

Back 472

l1-l2

Front 473

what types of sx can be associated with arnold-chiari malformation

Back 473

spastic diplegia of legs
cervical myelopathy
(pts are predisposed to subluxation or dislocation)

Front 474

how should an acute traumatic sci be treated

Back 474

1. methylprednisolone
2. blood tests in case surgery is needed
3. imaging, if stable

Front 475

anti-inflamm tx for spinal neoplasm

Back 475

dexamethasone

Front 476

what does an anterior cord compression of c-spine suggest

Back 476

cervical disk herniation

Front 477

what does a posterior cord syndrome in t-spine suggest

Back 477

bony mets

Front 478

can tendderness in lumbar/sacral spine --> cord compression

Back 478

no, the spinal cord stops at l1

Front 479

features of anterior cod syndrome

Back 479

b/l spinothalamic tract
umn paralysis below lesion
lmn paralysis at lesion
sphincter dysfxn
preserved dorsal column sensation

Front 480

mononeuritis multiplex

Back 480

multiple, asymmetric regions of sensory loss, corresponding to multiple peripheral nerves

Front 481

sx of spinal muscular atrophy

Back 481

lmn degen
infantile or chiildhood onset; adult forms are rarer

Front 482

pathophys of multifocal motor neuropathy

Back 482

immune mediated motor neuropathy; conduction block present on nerve conduction studies

Front 483

tx multifocal motor neuropathy

Back 483

ivig

Front 484

parsonage-turner syndrome

Back 484

idiopathic brachial neuritis (sudden onset of pain in shoulder and arm; weakness and muscle wasting become evident after 2-4 wks)

Front 485

ramsay hunt syndrome

Back 485

herpes zoster infection of ipsilateral geniculate ganglion

Front 486

when to suspect neurosarcoidosis

Back 486

interstitial lung dz with hilar adenopathy, uveitis, or parotitis

Front 487

what is suggested by decreased hearing or a decreased afferent corneal reflex

Back 487

cerebellopontine angle tumor

Front 488

tx of idiopathic bell's palsy

Back 488

prednisone

Front 489

tx of ramsay hunt syndrome

Back 489

acyclovir

Front 490

differential for mononeuropathy multiplex

Back 490

vasculitis (esp PAN)
DM
leprosy
sarcoidosis
hiv
lymphoma
lyme
cidp

Front 491

different types of neuropathy caused by dm

Back 491

distal axonal sensorimotor neuropathy
autonomic neuropathy
mononeuropathy
mononeuropathy multiplex
diabetic amytrophy

Front 492

what is diabetic amytrophy

Back 492

asymmetric proximal leg wekaness and wasting, not limited to a root, plexus or nerve territory

Front 493

paraprotein associated neuropathy

Back 493

demyelinating or axonal sensorimotor neuropathy

can be seen in plasma cell dyscrasia, mm, amyloidosis, lymphoma, leukemia, waldenstroms'

Front 494

tx of paraprotein associated neuropathy

Back 494

prednisone
plasmapheresis, ivig, azathioprine

Front 495

lambert-eaton myasthenic syndrome

Back 495

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

Front 496

dx of lambert-eaton

Back 496

incremental response on repeated nerve stimulation

Front 497

tx of lambert-eaton

Back 497

guanidine
diaminopyridine

Front 498

dx of polymyositis

Back 498

ck levels elevated
emg shhhows myopathic findings with denervation
bx shows endomesial lyphocytic infiltrates, necrotic and atrophic muscles fibers and ct deposition

Front 499

tx of polymyositis

Back 499

prednisone

Front 500

sx of dermatomyositis

Back 500

same as polymyositis, but with heliotropic rash on eyelids, erythematous rash on face and trunk
violaceous scaly eruptions on knuckles
subcutaneous calcifications

Front 501

gottron's papules

Back 501

violaceous scaly eruptions on knuckles
assoc with dermatomyositis

Front 502

dx of dermatomyositis

Back 502

different findings on bx (c/w polymyositis)
shows perivascular inflammation adn perifascicular atrophy

Front 503

tx of dermatomyositis

Back 503

prednisone

Front 504

sx of inclusion body myositis

Back 504

different from polymyositis b/c it prodcues distal and asymmetric weakness
poor response to steroids

Front 505

endocrine dz that can --> myopathy

Back 505

cushings
thyroid dz
parathyroid

Front 506

sx of myotonic dystrophy

Back 506

distal myopathy
ptosis, frontal balding, cataracts, cardiac conduction defects, gonadal atrophy and mental impairment

Front 507

periodic paralysis

Back 507

genetic abnormalities in ion channels , pts are nml between attacks of severe weakness

Front 508

sx of mitochondrial myopathy

Back 508

ptosis
ophthalmoparesis
high serum lactate levels

Front 509

most common type of primary brain tumor

Back 509

glioma

Front 510

most common type of glioma

Back 510

astrocytoma

Front 511

most common type of astrocytoma

Back 511

gbm

Front 512

dx of gbm

Back 512

mri with gad
shows ring enhancing lesions
can show butterfly glioma if it grows along white matter tracts like corpus callosum

Front 513

presentation of gbm

Back 513

ha
ms changes
focal motor deficits
sz are less common

Front 514

presentation of anaplastic astrocytoma

Back 514

sz
ha
focal deficit

Front 515

dx of anaplastic astrocytoma

Back 515

gad-enhanced mri
bx is needed to make definitive dx

Front 516

most common presentation of low-grade astrocytoma

Back 516

sz

Front 517

imaging of low grade astrocytoma

Back 517

mri (no gad)
see very little mass effect
bx for confirmation of dx

Front 518

pathologic appearance (under microscope) of oligodendroglioma

Back 518

fried egg appearance

Front 519

presentation of oligodendroglioma

Back 519

sz
ha
behavioral changes
cognitive changes

Front 520

mri of oligodendroglioma

Back 520

mri shows tumor with indistinct margins and variable amounts of contrast enhancement

Front 521

what age group is ependymoma most coommon in

Back 521

children and young adults

Front 522

where do ependymomas usually occur

Back 522

in children, on the floor of the 4th ventricle

Front 523

presentation of ependymoma

Back 523

noncommunicating hydrocephalus --> increased icp with ha, vomiting, ataxia

Front 524

dx of ependymoma

Back 524

mri with gad
will fill subarachnoid space through foramina of luschka and magendie
MUST GET SPINAL MRI AND LP TO DETECT DROP METS

Front 525

drop metastases

Back 525

results from seeding via csf

Front 526

pnet

Back 526

primitive neuroectodermal tumor
highly malignant
seen exclusively in children and adolescents

Front 527

presentation of pnet

Back 527

depends on location
extraneural mets occur more often with pnet c/w any other cns neoplasm

Front 528

dx of primary cns lymphoma (pcnsl)

Back 528

mri (will appear isointense on ct)
seen periventricularly and enhances uniformly with gad

Front 529

what type of lymphoma is a pcnsl

Back 529

non-hodgkin's

Front 530

presentation if there is a meningioma in the hemisphere

Back 530

ha
focal sx
sz

Front 531

presentation if there is a meningioma in the sphenoid wing

Back 531

ha
diplopia
visual loss

Front 532

presentation if there is a meningioma in the olfactory groove

Back 532

dementi
ipsilateral optic atrophy and c/l papilledema

Front 533

presentation if there is a meningioma in the suprasella

Back 533

ha
bitemporal hemianopia
sometimes hypothalamic dysfxn

Front 534

presentation if there is a meningioma in the posterior fossa

Back 534

cn efects
sx of brainstem compression

Front 535

dx of meningioma

Back 535

dural tail on mri
see braod based dural attachment

Front 536

what dz is associated with acoustic neuroma

Back 536

neurofibromatosis type 2

Front 537

pathophys of acoustic neuroma

Back 537

arises within internal acoustic canal, follows path of least resistance, growing into cerebellopontine angle

Front 538

presentation of acoustic neuroma

Back 538

tinnitus or hearing loss u/l

Front 539

dx of acoustic neuroma

Back 539

gad enchanced mri shows small intracanalicular tumors

Front 540

tx of prolactinoma

Back 540

da agonist (bromocriptine) first, otherwise if it doesn't work, then operate

Front 541

most common malignant tumor of childhood/adolescence

Back 541

medulloblastoma

Front 542

where does medulloblastoma arise

Back 542

cbl, and can present with signs of increased icp when mass effect causes obstruction

Front 543

dx fo medulloblastoma

Back 543

mri/ct shows contrast enhancing tumor, usually midline and distorts or obliterates 4th ventricle

Front 544

sx of thalamic pain syndrome

Back 544

spontaneous contralateral pain and dysesthesia is areas of impaired sensation

Front 545

pathophys of thalamic pain syndrome

Back 545

hemisensory loss from interruption of spinothalamic and dorsal column system at level of ventral posterior nucelus of thalamus

dorsal column --> severe contraolateral ataxia

Front 546

path of dorsal columns from spinal cord

Back 546

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

Front 547

what would happen if there is a lesion in the primary sensory cortex

Back 547

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)

Front 548

cause of wallenberg's syndrome

Back 548

occlusion of lateral medullary branches of vertebral artery and pica
(posteriolateral region of brainstem)

Front 549

what neurologic injury (in brain) can hiccups be attributed to

Back 549

lateral medullary infarction

Front 550

what does pica supply

Back 550

dorsolateral medulla
posterior inferior cbl

Front 551

what is preserved in wallenberg's syndrome and why?

Back 551

tongue fxn
weakness
pyramidal signs
contralateral loss of proprioception and discriminative touch

Front 552

path of anterolateral system starting at spinal cord

Back 552

dorsal horn --> x midline --> brainstem and intralaminar nuclei of thalamus --> praimary seonsry and association cortex

Front 553

sx of vertebral artery dissection

Back 553

neck or posterior head pain
horner's syndrome
dysarthria
dysphagia
decreased pain and temp of face, contralateral body
dysmetria
ataxia
vertigo

Front 554

how to dx a vertebral artery dissection

Back 554

mri and mra of neck

Front 555

juvenile myoclonic epilepsy

Back 555

myoclonic jerks that lead to generalized tonic clonic sz (suspect when all things on exam and imaging are nml)

Front 556

what sized symptomatic meningioma should not be operated on

Back 556

<3 cm, should give radiation

Front 557

presenilin-1

Back 557

causes familial alzheimer's dz

Front 558

clinical features of frontotemporal dementia

Back 558

personality change
lost initiaitve
slowing though
recent memory is preserved

Front 559

imaging for frontotemporal dementia

Back 559

mri
see disproportionate atrophy of anterior frontal and temporal lobes

Front 560

difference between activity levels of pts with migraines vs cluster ha

Back 560

migraines: lay down
cluster: mobile b/c laying down makes their ha worse

Front 561

transverse myelitis

Back 561

bilateral sensory and motor dysfunction
autonomic dysfxn
umn signs
sx present acutely or subacutely

Front 562

tx of transverse myelitis

Back 562

high dose corticosteroids

Front 563

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?

Back 563

warfarin
HEPARIN HAS NO ROLE IN ACUTE TX OF STROKE

Front 564

post-ictal confusion in simple partial sz

Back 564

not present

Front 565

spinal muscular atrophy

Back 565

motor neuron dz NOT associated with any sensory abnormalities
generally presents with symetric proximal muscle weakness and atrophy

Front 566

limb-girdle muscular dystrophy

Back 566

symmetric proximal muscle weakness
nml sensation

Front 567

what is commonly associated with cervical dystonia

Back 567

cervical spondylosis

Front 568

common tx for cervical dystonia

Back 568

trihexiphenidyl
clonazepam
baclofen

Front 569

course of tias over time

Back 569

they would worsen in severity over time

Front 570

what does lermitte's sign mean

Back 570

indicates the presence of cervical spinal cord problem

Front 571

features of cervical spondylosis

Back 571

chronic degenerative and hypertrophic changes of vertebrae, ligaments, and disks --> narrowing of spinal cord

Front 572

in a pt with stroke >3 hrs ago, how to tx

Back 572

early admin of asa --> modest reduction of risk of recurrent stroke in short term and less death and disability in the long term

Front 573

dz associated with mononeuritis multiplex

Back 573

vasculitides
dm

Front 574

sx of mononeuritis multiplex

Back 574

asymmetric weakness
sensory loss
severe pain

Front 575

sx of lewy body dementia

Back 575

fluctuating encephalopathy
parkinsonism
visual hallucinations

Front 576

what is deficient in pts with lewy body dementia

Back 576

central cholinergic activity

Front 577

tx of lewy body dementia

Back 577

centrally actiing anticholinesterase agent (donezepil, galantamine, rivastigmine)

Front 578

what would happen to a pt w lewy body dementia who took a da agonist

Back 578

exacerbation of encephalopathy

Front 579

what would happen to a pt w lewy body dementia who took a nueroleptic agent

Back 579

increased risk for neuroleptic malignant syndrome and increased mortality

Front 580

risk to fetus if mother is on interferon or glatiramer acetate for ms

Back 580

increased risk of spontaneous abortion and lbw

Front 581

how to handle pregnancy in a woman with ms who is on disease modifying meds for ms

Back 581

discontinue interferon or glatiramer several months before wishing to conceive

Front 582

what effect does pregnancy have on a woman with ms

Back 582

decreased frequency of relapse in the 3rd trimester
rebound increase in relapse during the first 6 months post-partum

Front 583

hereditary component of ms

Back 583

1st degree relatives have a 20-50x increase of having ms compared w general population

Front 584

how does wilson's dz differ from huntington's dz

Back 584

in huntington's dz, there are cognitive deficits
in wilson's dz ,the deficits are more psychiatric

Front 585

mov't d/o associated with frontotemporal dementia

Back 585

parkinsonism

Front 586

paroxysmal hemicrania

Back 586

u/l ha of seconds-minutes that can be very disabling despite its brevity

Front 587

in a pt with suspected vascular dementia, with nml head ct, what should be done

Back 587

f/u imaging

Front 588

sx of optic neuritis

Back 588

smudging of central vision, graudually worsening so pt can read with affected eye
central scotoma present
rapd preseent
fundoscopic exam nml

Front 589

deficiency sometimes associated w restless leg syndrome

Back 589

iron
if low ferritin levels, iron supplementation can improve sx

Front 590

meds associated with development of pseudotumor cerebri

Back 590

oral contraceptives
tetracyclines

Front 591

how sensitive is ct scan in picking up sah

Back 591

90%, but it is most likely to be missed if there is a delay in pt presentation, so lp must be done instead

Front 592

how long is lp able to detect xanthochromia following a hemorrhagic event

Back 592

14 days

Front 593

who is most likely to remain sz free after being taken off epilepsy meds

Back 593

those with no structural brain lesion
no epileptiform or focal abnormalities on eeg
sustained sz free pd
no abnormalities on neuro exam

Front 594

csf in critical illness polyneuropathy

Back 594

nml

Front 595

sx of critical illness polyneuropathy

Back 595

same as guillan barre but follos admission to icu (predisposed by sepsis and/or multi-organ failure)

Front 596

which structures are implicated in short term memory fxn

Back 596

dorsomedial thalamus
dorsolateral prerontal cortex
hippocampi
parahippocampus

Front 597

how do pts with alzheimers react to their memory loss

Back 597

they lack insight into their condition

Front 598

abnml physical findings in alzheimers pts

Back 598

paratoni a
extrapyramidal rigidity

Front 599

are scans necessary in dx alzheimers

Back 599

they are required in order to r/o any other etiology causing memory problems

Front 600

meds for alzheimers

Back 600

anti-cholinergics:
donepezil
rivastigmine
galantamine
in late stages: memantine

Front 601

use of antipsychotic meds in pts with alzheimers

Back 601

can be used to treat behavioral probs in ad but should bge used with caution b/c of risk of sedation and extrapyramidal sx

Front 602

another name for frontotemporal dementia

Back 602

pick's dz

Front 603

sx of frontotemporal dementia

Back 603

behavior dominant or language dominant sx
memory and spatial ability are spared early on

Front 604

sx of behavioral frontotemporal dementia

Back 604

early progressive personality changes and early decline in social interpersonal contact
lack of insight into these features
decreased spontaneous speech = and language

Front 605

primary progressive aphasia

Back 605

form of frontotemporal dementia
loss of speech fluency
anomia
inappropriate word order and simplified sentence structure
stuttering
oral apraxia
impaired repetition
alexia
agraphia
eventually become mute and behavioral changes can occur

Front 606

semantic dementia

Back 606

form of frontotemporal dementia
fluent but empty spontaneous speech with loss of word meaning

Front 607

What region of the brain is affected in semantic dementia

Back 607

left anterior temporal lobe is usually affected

Front 608

what region of the brain is affected in primary progressive aphasia

Back 608

left perisylvian atrophy, usually more anterior than posterior

Front 609

sx of cortical basal ganglionic degeneration

Back 609

form of frontotemporal dementia
progressive cognitive impairment with associated asymmetric rigidity, apraxia, cortical sensory loss, and pyramidal dysfxn
myoclonus
limb dystonia

Front 610

tx of frontotemporal dementia

Back 610

symptomatic

Front 611

sx of lewy body dementia

Back 611

early dementia
fluctuations in cognition and consciousness
visual hallucinations
subsequent development of parkinsonism
action tremor
autonomic dysfxn

Front 612

form of dementia where pts won't recognize their own reflection

Back 612

lewy body dementia

Front 613

form of dementia where capgras syndrome can occur

Back 613

lewy body dementia

Front 614

tx for lewy body dementia

Back 614

cholinesterase inhibitors can be helpful but don't modify dz

Front 615

what drugs are contraindicated in lewy body dementia

Back 615

typical neuroloeptics b/c it can --> irreversible parkinsonism
atypicals can be used cautiously

Front 616

which form of dementia is associated with rem-behavioral d/o

Back 616

lewy body

Front 617

tx of rem behavioral d/o

Back 617

clonazepam qhs

Front 618

parkinson's dementia

Back 618

similar to lewy body dementia

Front 619

how is lewy body dementia different from parkinsons dementia

Back 619

the time course is different (early in lewy body and late or not at all in parkinsons)

Front 620

dementia seen in huntington's dz

Back 620

forgetfulness and concentration difficulty early on
later there is more severe memory decline, difficulty learning, language decline, adn apraxia

Front 621

meds used in huntington's dementia

Back 621

antipsychotics to help with the psychosis
ssris for any ocd or depression that may develop

Front 622

pathyophysiology of nph

Back 622

communicating hydrocephalus develops in elderly pts w/o clear obstruction to csf outflow

Front 623

what does imaging show in nph

Back 623

enlarged ventricles out of proportion to brain atrophy

Front 624

dx of nph

Back 624

imaging
lp which should improve gait substantially and should be reproducible; they should then be referred for a shunt

Front 625

sx transient global amnesia

Back 625

during a stressful situation, there is profound anterograde and retrograde amnesia
self limiting condition

Front 626

in pt with pcnsl what is the first step in dx

Back 626

do an eye exam; some pts have vitreal/uveal involvement and dx can be made w vitrectomy, so no need for brain bx

Front 627

is resection recommended in pcnsl

Back 627

no, it is prone to hemorrhage and doesn't improve survival

Front 628

tx of pcnsl

Back 628

once dx is made, mtx is tx of choice

Front 629

adverse effects of donezepil

Back 629

increased vagal tone
bradycardia
av block

Front 630

adverse effects of memantine

Back 630

hallucinations
confusion
restlessness
anxiety
dizziness
fatigue
constipation

Front 631

secondary progressive ms

Back 631

begins as relapsing/remitting ms, 85% become 2dary progressive
recurrent progression of neuro sx

Front 632

primary progressive ms

Back 632

starts with spinal cord dysfxn or ataxia
no acute exacerbations
fewer cerebral lesions
more common in men

Front 633

why does metoclopramide --> parkinsonism

Back 633

it is a da antagonist

Front 634

when to refer an epileptic for surgery

Back 634

after pt has failed on 3 aeds

Front 635

correct sequence of dx and treating pseudotumor cerebri

Back 635

do imaging to r/o organic brain dz
perform lp
confirm dx and tx w acetazolamide

Front 636

pvs

Back 636

sleep-wake cycles are maintained
brainstem and hypothalamic fxn is preserved

Front 637

pathology of ms lesions

Back 637

demyelinated areas surrounded by macrophages and lymphocytes

Front 638

how does ms differ from leukodystrophies

Back 638

ms has focal demyelination

Front 639

sx of optic neuritis

Back 639

periorbital pain with eye movements
subtle loss of vision
red desaturation

Front 640

if there is tremor in ms, where would you expect the lesion

Back 640

plaques affecting cbl afferent/efferent pathways

Front 641

adverse effects of glatirimer acetate

Back 641

chest tightness
flushing
anxiety
dyspnea
palpitations

Front 642

moa mitoxantrone

Back 642

topo II inhibitor

Front 643

moa natalizumab

Back 643

blocks interaction between vla4 and vcan 1 which is needed for adherence to vascular endothelium

Front 644

sx of acute transverse myelitis

Back 644

b/l le weakness
loss of sphincter tone
sensory loss at a spinal cord level

Front 645

tx of acute transverse myelitis

Back 645

steroids + acyclovir
plasma exchange if above not successful

Front 646

sx of acute ms

Back 646

rare, fulminant demylenation dz
large edematous contrast enhancing lesions with mass effect

entire brainstem demyelination --> death

Front 647

tx of acute ms

Back 647

plasma exchange + steroids
if pt survives acute attack, put pt on immunosuppressents

Front 648

sx of ADEM

Back 648

seen in children commonly after vaccination or infection
monophasic, multifocal inflammation and demylenation
can be associated with sz and loc

Front 649

tx of adem

Back 649

plasma exchange and ivig
add steroids if necessary

Front 650

sx of neurosarcoidosis

Back 650

chronic meningitis
sx depend on location of granulomata

Front 651

blood test findings in neurosarcoidosis

Back 651

hypercalcemia
hyperuricemia
increased ACE increased serum globulin

Front 652

tx of neurosarcoidosis

Back 652

steroids + azathioprine

Front 653

behcet's dz

Back 653

relapsing iritis/uveitis + oral/genital aphthous ulcers
can have abrupt onset of meningoencephalitis + cn palsies

Front 654

central pontine myelinolysis

Back 654

symmetric destruction of the white matter in the pons

Front 655

who is more prone to developing central pontine myelinolysis

Back 655

EtOH abusers
malnourished
ppl with multiorgan failrue

Front 656

presentation of central pontine myelinolysis

Back 656

rapidly progressive spastic quadriplegia
facial, glottal, pharyngeal paralysis
--> locked in syndrome

Front 657

where is cmV localized to in brain?
toXo?

Back 657

periVentricular

corteX

Front 658

myotonic dystrophy

Back 658

can't release grip
cardiac problems

Front 659

mptp

Back 659

--> parkinsonism in drug users
can be treated with amantadine

Front 660

eye deviation in stroke of
cortex
pons
putamen
cbl

Back 660

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

Front 661

describe CN III neuropathy in dm

Back 661

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

Front 662

side effects of riluzole

Back 662

dizziness
n/v
weight loss
increased lfts
weakness

Front 663

moa riluzole

Back 663

glutamate inhibitor

Front 664

when is hemineglect seen

Back 664

lesion in non-dominant parietal lobe

Front 665

describe tremor seen in wilson's dz

Back 665

wing beating tremor

Front 666

eeg findings in cjd

Back 666

triphasic synchronous waves

Front 667

neurologic uses of amantadine

Back 667

parkinsons dz
tx of ms related fatigue

Front 668

where is the lesion that causes locked-in syndrome

Back 668

lesion at base of the pons
vertebro-basilar artery

Front 669

spinal muscular atrophy

Back 669

affects anterior horn cells (sim to polio)

Front 670

persistent vegitative state

Back 670

awake but not aware
caused by cortical anoxia
brainstem still fxns and there are brainstem reflexes present
cortex doesn't work

Front 671

when should berry aneurysms be repaired

Back 671

>7mm

Front 672

what is the main cause of morbidity and mortality in huntington's pts

Back 672

dysphagia

Front 673

what does mri of hd show

Back 673

bilateral atrophy in cerebral hemispheres, corpus callosum, brainstem

Front 674

sx of cerebral venous thrombosis

Back 674

ha --> change in ms, somnolence, death