olfactory sensory neurons are w/i epithelium of dosrsal posterior nasal cavity they project into neurons of olfactory bulb , which rest on cribriform plate (on ethmoid bone)

what can meningiomas compress if they primarily affect olfactory bulb

visual impaiarment -> blindness frontal lobes and anterior cerebral arteries

where do meningiomas affecting smell most commonly occur

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

mechanism behind anosmia following trauam

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

pathophysiology of ha 2/2 pituitary tumor

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

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

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

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

there is anastomotic blood supply to occipital pole, where foveal vision is represented; when posterior cerebral artery is occluded, collaterals from mca take over blood supply also, more than 1/2 of visual cortex is devoted to representing foveal vision

is visual acuity affected in occipital pole damage

should be spared as long as the postchiasmal lesion is unilateral

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

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

optic neuritis findings on mri

t2 shows abnormally increased signal w/i optic nerve (= demyelination) t1 shows nml scan, unless there is gadolinium, then it shows the lesion (= breakdown of bbb)

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

central scotoma demyelinating lesions from optic neuritis are deep within the nerve, so affect fibers traveling from macular area of retina, representing central vision also there may be impaired color vision b/c teh fovea contains many cones

prognosis of optic neuritis

depends on severity of attack, and if pt has ms if lesion is mild, axons are mostly undamaged, and when axons get remyelinated, axonal fxn returns

residua following recovery from optic neuritis

decreased visual acuity, afferent pupillary defect nodes of ranvier are closer together than before so saltatory conduction is slower slower velocity seen in evoked potential

what is seen in papilledema on eye exam

disk margins become blurred optic disk becomes less evident disk color darkens and is almost the same color as the retina in icp, ratio of diamter of retinal veins:arteries increaes retinal hemorrhages and whitish exudates

define myoclonus when is it physiologic when is it pathologic

sudden involuntary jerk of muscle/muscle group sleep myoclonus and hiccups are not pathological early sx in subacute sclerosing panencephalitis and a late sx in cjd, early sign in renal failure, gaucher's dz, segmental myoclonus can occur if there is a spinal cord lesion

defining features of a tremor

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

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

what dzs accentuate phsyiologic tremor

thyrotoxicosis etoh w/d renal/liver failure

features of essential tremor tx

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

intention tremor structure involved

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

what types of dzs --> intention tremor

ms (may be seen esp when walking) wilson's dz (large amplitue flapping as finger approaches nose, then arm may flail in a way similar to chorea - cbl and basal ganglia may both be involved) infarction tumor drugs

describe tremor seen in parkinson's dz

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)

difference between asterixis and myoclonus

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

how to evoke chorea during exam

continuous, but increase w intention or anxiety, dampened with relaxation pt should hold arms above head with palms facing forward, or they should protrude tongue (neither position can be maintained for very long) can also look for resp irregularities and hyperextension of fingers when arms are prone

describe athetosis when is it seen?

similar to chorea, but is slower and leads to writhing movt's of fingers, hands, feet, or face often seen in fetal/perinatal birth injury - one form of cp

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

describe ballism which area of the brain is involved

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

tapping of glabelllar area on forehead --> uncontrollable blinking

common physical findings in parkinsons' pt

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

how would a lesion in occipital lobe present

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

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

outer retinal dz inner retinal dz

fortification scotoma (scotoma in a string of connected z's) pathognomonic for migraines comes from spontaneous firing of complex ro hypercomplex cells w/i visual cortex

pathophys of migraine ha

2 phases: 1. central transmission to spinal trigeminal nucleus from cortex --> pain 2. stimulated spinal trigeminal neurons fire antidromically DOWN axons to nerve endings on BV of brain and meninges; this wrong way firing --> vasoactive peptide release --> vasodilation, plasma protein extravastation and release of other substances that sensitize nerve endings sustain pain

increase threshold for cortical spreading depression and abort migraine attacks

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

what role does NO play in migraines

activation of NO-cGMP pathway precipitates migraine attacks

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Neurology Shelf 101-200

Neurology Shelf 101-200

by arrozito, Jan. 2014

Subjects: 14 2 clinical exam mksap nbme neurology shelf step usmle

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	what cranial foramen does CN V3 travel through	foramen ovale
	what cranial foramen does CN VI travel through	superior orbital fissure
	what cranial foramen does CN VII travel through	internal auditory meatus
	what cranial foramen does CN VIII travel through	internal auditory meatus
	what cranial foramen does CN IX travel through	jugular foramen
	what cranial foramen does CN X travel through	jugular foramen
	what cranial foramen does CN XI travel through	jugular foramen
	what cranial foramen does CN XII travel through	hypoglossal foramen
	which CNs travel through superior orbital fissure	III, IV, V1, VI
	which CNs travel through jugular foramen	IX, X, XI
	which CNs travel through the internal auditory meatus	VII, VIII
	olfactory pathway	olfactory sensory neurons are w/i epithelium of dosrsal posterior nasal cavity they project into neurons of olfactory bulb , which rest on cribriform plate (on ethmoid bone)
	what can meningiomas compress if they primarily affect olfactory bulb	visual impaiarment -> blindness frontal lobes and anterior cerebral arteries
	where do meningiomas affecting smell most commonly occur	olfactory bulbs adn primary olfactory fibers that project to them from olfactory epithelium
	mechanism behind anosmia following trauam	sheering of olfactory bulbs passing through cribriform plate or bilateral contusion of orbitofrontal cortex
	if pituitary tumor compresses optic chiasm from the side or posteriorly, what visual defect in visual fields would there be	homonymous hemianopia
	pathophysiology of ha 2/2 pituitary tumor	stretching of diaphrama sella and other pain sensitive structures they are frontal b/c these structures are innervated by V1
	why do non-secretory pituitary tumors sometimes cause amenorrhea, elevated gh, fsh, lh, and prl	pituitary stalk compression and interruption of da fibers that normally inhibit prl release
	explain macular sparing as is seen when there is occipital pole damage	there is anastomotic blood supply to occipital pole, where foveal vision is represented; when posterior cerebral artery is occluded, collaterals from mca take over blood supply also, more than 1/2 of visual cortex is devoted to representing foveal vision
	is visual acuity affected in occipital pole damage	should be spared as long as the postchiasmal lesion is unilateral
	when is optic atrophy seen? what does it look like?	glaucoma, neurotoxins, optic nerve compression from neoplasms, infarction, trauma, ms, degen dz, long-standing papilledema pale optic disk
	optic neuritis findings on mri	t2 shows abnormally increased signal w/i optic nerve (= demyelination) t1 shows nml scan, unless there is gadolinium, then it shows the lesion (= breakdown of bbb)
	what type of visual defect is normally seen in optic neuritis and why	central scotoma demyelinating lesions from optic neuritis are deep within the nerve, so affect fibers traveling from macular area of retina, representing central vision also there may be impaired color vision b/c teh fovea contains many cones
	prognosis of optic neuritis	depends on severity of attack, and if pt has ms if lesion is mild, axons are mostly undamaged, and when axons get remyelinated, axonal fxn returns
	tx of optic neuritis	corticosteroids
	residua following recovery from optic neuritis	decreased visual acuity, afferent pupillary defect nodes of ranvier are closer together than before so saltatory conduction is slower slower velocity seen in evoked potential
	what is seen in papilledema on eye exam	disk margins become blurred optic disk becomes less evident disk color darkens and is almost the same color as the retina in icp, ratio of diamter of retinal veins:arteries increaes retinal hemorrhages and whitish exudates
	what drug will decrease frequency of tias and likelihood of cerebral infarction	asa
	define myoclonus when is it physiologic when is it pathologic	sudden involuntary jerk of muscle/muscle group sleep myoclonus and hiccups are not pathological early sx in subacute sclerosing panencephalitis and a late sx in cjd, early sign in renal failure, gaucher's dz, segmental myoclonus can occur if there is a spinal cord lesion
	defining features of a tremor	involuntary and it oscillates, can be regular/irregular, distal or proximal and intermittent/continuous
	physiologic tremor	tremor in fingers of outstretched arms irregular rhythm, accentuated by nervousness
	what dzs accentuate phsyiologic tremor	thyrotoxicosis etoh w/d renal/liver failure
	features of essential tremor tx	induced by intentional activity tremor improves with etoh distorted handwriting is present propanolol
	intention tremor structure involved	tremor that increases as target is approached cbl and cbl outflow tracts (cbl peduncle), red nucleus may be damaged as well
	what types of dzs --> intention tremor	ms (may be seen esp when walking) wilson's dz (large amplitue flapping as finger approaches nose, then arm may flail in a way similar to chorea - cbl and basal ganglia may both be involved) infarction tumor drugs
	describe tremor seen in parkinson's dz	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)
	difference between asterixis and myoclonus	myoclonus is an active muscle contraction (seen in renal failure only) asterixis is a relaxation of contracted muscle (seen in hepatic and renal failure)
	how to evoke chorea during exam	continuous, but increase w intention or anxiety, dampened with relaxation pt should hold arms above head with palms facing forward, or they should protrude tongue (neither position can be maintained for very long) can also look for resp irregularities and hyperextension of fingers when arms are prone
	describe athetosis when is it seen?	similar to chorea, but is slower and leads to writhing movt's of fingers, hands, feet, or face often seen in fetal/perinatal birth injury - one form of cp
	describe dystonia	similar to athetosis, and positions tend to be held for a long time (torticollis and tortipelvis are examples) often dependent on posture
	describe ballism which area of the brain is involved	proximal continuous flinging movt of arm acute lesions of subthalamic nucleus (usually from occlusive ro hemorrhagic stroke)
	myerson's sign	tapping of glabelllar area on forehead --> uncontrollable blinking
	common physical findings in parkinsons' pt	spontaneous movt masked facies infrequent blinking soft voice, syllables run together
	how would a lesion in occipital lobe present	loss of ability to perceive motion, or selective loss of depth or color vision
	term given to lack of any color vision, from absence of 2 or 3 cone types	achromatopsia
	where in the retina would be damaged if there was a loss of blue color discrimination? loss of red discrimination?	outer retinal dz inner retinal dz
	teichopsia	fortification scotoma (scotoma in a string of connected z's) pathognomonic for migraines comes from spontaneous firing of complex ro hypercomplex cells w/i visual cortex
	pathophys of migraine ha	2 phases: 1. central transmission to spinal trigeminal nucleus from cortex --> pain 2. stimulated spinal trigeminal neurons fire antidromically DOWN axons to nerve endings on BV of brain and meninges; this wrong way firing --> vasoactive peptide release --> vasodilation, plasma protein extravastation and release of other substances that sensitize nerve endings sustain pain
	moa of ergotamine	increase threshold for cortical spreading depression and abort migraine attacks
	moa triptans	5-ht agonists; don't affect cortical spreading depression but may decrease cortical input to spinal trigeminal nucleus
	what role does NO play in migraines	activation of NO-cGMP pathway precipitates migraine attacks
	most common cause of unilateral miosis	lung ca that affects sypathetic cervical ganglia
	what causes the ptosis in horner's syndrome	denervation of smooth tarsal muscles w/i eyelid
	explain why cocaine has the result it does in horner's syndrome	cocaine blocks the presynaptic reuptake of norE, if neuron hasn't fired, there is no synaptic NT to block
	describe why hydroxyamphetamine has the results it does in horner's syndrome	hydroxyampthetamine acts as an adrenergic agonist by releasing norE from nerve endings; if the nerve in contact with the iris is damaged, it doesn't matter if the norE is there or not, it won't work --> no dilation if the preganglionic nerve is affected, there will be a dilation of the pupil
	if a pt can't elevate the eye when it is abducted where is the problem	either superior rectus or CN III
	if a pt can't lower the eye when it is adducted where is the lesion	superior oblique or CN IV
	if a pt can't lower the eye when it is abducted, where is the lesion	inf rectus or CN III
	if a pt can't elevate eye when it is adducted, where is the problem	inf oblique or CN III
	what is seen in 4th nerve palsy	head tilt away from the side of the lesion
	gaze palsy	from certain cns lesions eyes remain conjugate adn there is no diplopia but neither eye moves fully in a particular direction
	what triggers saccadic movements	frontal eye fields, ant to motor cortex on cerebral convexity stimulation of this area (as is seen in szs) --> conjugate horizontal eye movts in direction CONTRALATERAL to the side of the stimulus if the area is destroyed, there is a conjugate deviation of the eyes towards the side f the lesion and an inability to move them voluntarily to the opposite side
	physical findings that would suggest that a horizontal gaze palsy is from cerebral vs brain stem lesion	frontal lesions spare reflexive pursuit (pt fixates n a target and then doesn't lose fixation when head is passively moved) smooth pursuit is controlled by posterior temproal lobes (projections go from posterior limb of internal capsule to cbl/vestiblar structures - no pprf involvment)
	what happens if there is destruction of the pprf	contralateral deviation and inability to move eyes conjugately in the direction of the lesion
	what is pprf	area adjacent to CN VI nucleus, involved in horizontal gaze
	what does the mlf do	connects CN VI with contraolateral CN III nucleus
	what causes one and a half syndrome	damage to pprf and ipsilateral mlf --> ipsilateral gaze palsy and ino on contralateral side
	clinical features of right sided ino (internuclear ophthalmoplegia)	inability to adduct right eye in left lateral gaze, convergence is preserved
	where (brainstem or cortex) would you expect a lesion if a pt can't gaze leftward and also has a left hemiparesis	cortex
	where (brainstem or cortex) would you expect a lesion if a pt can't gaze leftward and also has a right hemiparesis	brainstem
	what disturbance in eye movement would you expect if there was an injury to the left frontal cortex	impaired gaze to the right
	what disturbance in eye movement would you expect if there was an injury to the left mlf	impaired adduction of left eye during rightward gaze adduction during convergence is intact
	what disturbance in eye movement would you expect if there was an injury to left CN III	left eye goes down and out
	what disturbance in eye movement would you expect if there was an injury to right abducens nerve	inability to fully abduct right eye
	what disturbance in eye movement would you expect if there was an injury to left CN VIII	horizontal rightward jerking nystagmus
	how would a pineal tumor affect vision	can --> impaired upward gaze, with intact downward gaze
	features of pendular nystagmus what causes it	nystagmus with equal velocity b/l result of severe visual impairment during childhood
	features of jerk nystagmus WHAT causes it	slow drift in one direction and a rapid corrective mov't in the other, accentuated by ocular deviation; fast component is in the direction of the gaze
	most common causes of horizontal and rotary nystgmus	vestibular lesions (either periph or central) mlf lesion
	causes of vertical nystagmus	brain stem lesion (ms/syringobulbia if intrinsic) or (cbl tumor/chiari malformation if extrinsic)
	type of nystagmus seen in barbiturates and phenytoin	horizontal
	how to test for nystagmus	use tape with vertical stripes (tape measurer, ex) and pass it horizontally in front of eyes fast component is in direction opposite to the direction the tape is moving; this happens b/c visual stimulus of tape --> reflexic pursuit eye mov't in the same diection, which is corrected by the saccades in opposite direction (this is called opticokinetic testing)
	when does opticokinetic testing fail to produce nystagmus	anterior cerebral lesions b/c there are no corrective saccades posterior cerebral lesions b/c there is no initial pursuit
	what type of sz does phenytoin treat	simple/complex partial gtc
	what type of sz does carbamazepine treat	simple/complex partial gtc
	what type of sz does lamotrigine treat	simple/complex partial gtc
	what type of sz does gabapentin treat	simple/complex partial gtc
	what type of sz does topirimate treat	simpile/complex partial gtc
	what type of sz does topiramate treat	simple/complex partial gtc
	what type of sz does phenobarbital treat	simple/complex partial gtc
	what type of sz does valproic acid treat	simple/complex partial gtc absence
	what type of sz does ethosuximide treat	absence
	what role do bz play in sz	1st line for acute status epilepticus
	what is used for status epilepticus proph	phenytoin
	MOA phenytoin	increased na channel inactivation
	MOA carbamazepine	increased na channel inactivation
	MOA lamotrigine	blocks voltage gated na channels
	MOA gabapentin	increased GABA release
	MOA topirimate	blocks na channels increased GABA action
	MOA phenobarbital	increased GABA-A action
	MOA valproic acid	increased na channel inactivation and increased GABA concentration
	MOA ethosuximide	blocks thalamic t-type Ca channels
	MOA BZ	increased GABA action
	adverse effects of phenytoin	gingival hyperplasia hirsutism megaloblastic anemia (prob with folate metabolism) teratogenic in pregnancy hepatotoxic diplopia ataxia sle like syndrome
	tx for trigeminal neuralgia	carbamazepine
	toxicity of carbamazepine	diplopia ataxia agranulocytosis aplastic anemia hepatotoxicity
	toxicity of ethosuximide	gi distress lethargy ha urticaria steven's-johnson syndrome
	toxicity of valproic acid	rare, but fatal hepatotoxicity NTDs in pregnancy gi distress
	toxicity of lamotrigine	stevens-johnson syndrome
	toxicity of gabapentin	sedation, ataxia
	toxicity of topiramate	sedation mental dulling kidney stones weight loss
	which epilepsy med should be used in pregancy and children	lamotrigine
	which epilepsy drug should be used in sz during eclampsia	bzs
	what can be used to prevent sz of eclampsia	MgSO4
	difference between umn lesion of facial nerve and lmn lesion	umn lesion: contralateral lower face weakness lmn lesion: ipsilateral upper and lower facial weakness
	things that could cause a lmn cn vii lesion	cerebellopontine angle neoplasm bell's palsy
	what type of dz can cause an umn cn vii lesion	suprasegmental stroke or brain tumor
	what type of facial weakness is seen if there is a lesion of the motor cortex	facial movements associated with emotion are preserved but not preserved when asked to do a facial movement on command, there will be weakness
	what type of facial weakness is seen if there is a lesion in the amygdala	facial muscle strenght is normal but an emotionally produced smile is crooked
	what can occur following peripheral nerve injury (bell palsy/trauma) upon reinnervation why does this occur	synkinesis - eye closure --> involuntary elevation of the angle of the mouth on affected side baring teeth --> ipsilateral eye closure this can be caused by aberrant regeneration (damaged axons regrow distally, but make wrong turns) and there is also cross talk so that damaged axons make nonsynaptic electrical contact with each other
	what causes hyperacusis	denervation of the stapedius muscle of middle ear, so can't dampen the ossicles during loud noise
	pathophysiology behind crocodile tears	lacrimal-salivatory synkinesis with ipsilateral lacrimation stimulated by eating following a bell palsy (lacrimation and salivation are both mediated by cn vii)
	what autonomic functions are mediated by cn vii	intermedius portion of cn vii --> innervation of lacrimal gland (via pterygopalatine ganglion) and the chorda tympani (via submandibular ganglion) innervates the submandibular ganglion and submaxillary salivary glands (chorda tympani also innervates the ant 2/3 of tongue)
	where is the lesion if there is unilateral facial weakness that spares the forehead (esp if ipsilateral limb weakness)	contralateral motor cortex
	where is the lesion if there is unilateral facial weakness of forehead, as well as ipsilateral abducens weakness	pons (and if there is hemiparesis, it will be contralateral)
	where is the lesion if there is unilateral facial weakness in forehead, and if taste, salivation, and lacrimation are affectd	facial nerve before the take off of the greater superficial petrosal and chorda tympani branches (i.e.: geniculate ganglion) if v, vii, viii are all affected, then it is at the cerebellopontine angle
	where is the lesion if there is unilateral facial weakness in the forehead, that is unaccompanied by other abnormalities	lesion is either of the facial nucleus in th epons or the nerve distal to the chorda tympani
	if a person can unilaterally raise one eyebrow voluntarily, what does that mean about their innervation	there is mostly contralateral facial representation in teh motor cortex
	describe the innervation of the tongue	the motor cortex sends fibers bilaterally to the hypoglossal nucleus in the medial medulla
	what type of lesion does atrophy of the tongue indicate	lmn lesion (either centrally or peripherally)
	bulbar palsy	b/l weakness of muscles innervated by cn in the lower brainstem,(to less of an extent if the cerebrum or upper brainstem lesions are unilateral) no movt of palate or pharynx with phonation gag reflex is absent
	pseudobulbar palsy	b/l lesions of cerebrum or upper brainstem --> severe dysarthria and dysphagia tongue is paralyzed, but is not atrophic and doesn't fasciculate gag reflex is hyperactive extremely labile emotional response
	progressive supranuclear palsy	degen d/o --> d/o eye mov't, pseudobulbar palsy, dystonia, dementia, pyramidal and cbl dysfxn
	what nerve carries info from the barorecpetors in carotid body and aortic arch	cn x
	which nerves comprise the nucleus solitarius what kind of info does this carry	vii, ix, x visceral sensory info taste, baroreeptors, gut distention)
	which nerves are through the nucleus ambiguous what info does this carry	ix, x, xi motor innervation of pharynx, larynx, and upper esophagus
	what info is carried in the dorsal motor nucleus	cn x, that sense parasymp fibers to the heart, lungs, adn upper gi
	what type of lesion is suggested if a pt has a nasal voice	palatal weakness
	what type of lesion is suggested if a pt has h/o nasal regurg of fluids	palatal weakness
	what type of lesion is suggested if a pt has hoarseness or reduced cough	laryngeal weakness
	what type of lesion is suggested if a pt chokes on saliva while talking	pharyngeal weakness
	what type of lesion is suggested if a pt has dysphagia to solid foods only	mechanical obstruction (carcinoma)
	what type of lesion is suggested if a pt has dysphagia to solids and liquids	neurological dysfxn
	to what side dose the uvula deviate if it does not rise symmetrically	towards the normal side (away from the side of the lesion)
	when testing the gag reflex, what is suggested by b/l weakness with preserved sensation	motor neuron dz (als, polio), neuromuscular junction dz (ex - mg) or myopathy
	when testing the gag reflex, what is suggested by u/l motor and sensory loss	ipsilateral lesion of lower brainstem (eg- lat medullary infarction or combined lesions of cn xii and x either in posterior fossa or as they exit through jugular foramen)
	when testing the gag reflex, what is suggested by b/l motor and sensory loss in posterior pharynx	intraparenchymal medullary lesion where other cn and long tracts are probably present
	when testing the gag reflex, what is suggested by b/l sensory loss with nml movement on phoation	psychiatric dz... very rare
	if there is weakness in the right scm, where is the lesion	RIGHT cortex (the only muscle with ipsilateral muscle innervation from cortex)
	if there is weakness in the right trapezius, where is the lesion	LEFT cortex
	jugular foramen syndrome	affects cn ix, x, xi loss of sensation over palate and pharynx loss of general sensation over palate and pharynx loss of general sensaton and tasste over posterior third of tongue paralysis of palate, pharynx, and larynx weakness of scm and trapezius the hypglossal foramen is adjacent to jugular foramen --> weakness of tongue with atrophy and fasciculations
	causes of central spinal cord compression	syringomyelia neck flexion-extension injury intrinsic tumor
	si and sx of foramen magnum lesion	spastic quadriparesis neck pain and stiffness c2-c4 and upper facial numbness ipsilateral horner's ysndroem ipsilateral tongue and trapezius muscle weakness
	si and sx of conus medullaris lesion	lower sacral saddle sensory loss (s2-s5) sphincter dysfxn inpotence aching back rectal pain l5 and s1 motor probs (ankle and foot weakness)
	si and sx of cauda equina syndrome	sphincter dysfxn paraparesis with weakness in multiple nerve roots sensory loss in multiple bilateral dermatomes
	what does contrast enhancement mean in a ct	presence of a disrupted bbb
	when should contrast be used in ct	suspected neoplasm, abscess, vascular malformation, new onset sz
	what things appear black in a ct	air fat water
	what things appear white in a ct	acute hemorrhage iv contrast bone/metal
	what are t1 mris used for	to detect anatomy most pathologic processes are associated w increased water content and appear darker than normal brain
	what are t2 mris used for	to detect pathology (they will look white to reflect increased water content)
	what color are fat and subacute blood in t1 mri	white
	what things are white in t2 mri	water
	when is diffusion weighted imaging used	to detect hyperacute ischemia in pts with acute stroke changes are seen w/i minutes
	when is mr angiography used (mra)	used to detect large scale lesions (carotids or large aneurysms) not good for smaller lesions, must use conventional angiography
	what can standard angiography detect	stenosis/occlusion arterial dissection aneurysms avm vasculitic narrowing dural venous sinus thrombosis
	most impt complication of angiography test	1-2% --> stroke secondary to emboli generated by the catheter (seen mostly in elderly with atherosclerotic dz)
	how do simple szs affect consciousness	simple partial sz have no impairment in consciousness complex partial sz has alteration in consciousness
	how do complex szs affect consciousness	complete loss of consciousness
	definition of status epilepticus	10+ minutes of continuous szs where pt fails to fully awaken
	differential dx of sz	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
	what are things to be concerned for in pt actively seizing, or prolonged szs	aspiration of gastric contents if airway is not protected head injury lactic acidosis hypoxia hyperthermia rhabdo cerebral edema hypotension
	tx for status epilepticus	full dose of bz, followed by fosphenytoin, but risk of recurrence is very high
	what is the best way to secure the airway in coma	endotracheal intubation
	why should you give thiamine before dextrose	hyperglycemia promotes the consumption of thiamine and will acutely worsen wernicke's
	what does naloxone do	reverses opiate intoxication
	what does flumazenil do	reverse come from bz intox
	top 3 causes (in order) for coma/stupor	toxic/metabolic d/o (66%) structural intracranal d/o (33%) psychiatric d/o (1%)
	role of unilateral hemispheric lesion in producing stupor or coma	doesn't usually cause it, unless there is a mass effect sufficient to raise icp or compress either the contralateral hemisphere or brainstem, or compresses the contralateral hemisphere/brainstem
	how do focal brainstem lesons --> coma	disrupting the reticular activating system
	3 common, treatable causes that can rapidly --> coma/death	increased icp herniation and brainstem compression meningitis/encephalitis
	tx of herniation and brainstem compression	neurosurgery (it's an emergency1)
	tx of increased icp	1. elevate head of bed 2. intubation and hyperventilation (this will cause cerebral vasoconstriction and lowering of intracranial volume) 3. sedation if pt is agitated 4. osmotic diuresis with mannitol all of these things will be used to buy time before neurosurg urgent ct of the head should also be obtained
	why is increased icp so dangerous	--> impaired cerebral perfusion and global hypoxic-ischemic injury
	bladder fxn in als	spared until final stages of illness
	why does muscle cramping occur in als	irritability of denervate muscles
	mode of inheritance of als	5-10% are familial, autosomal inheritance SOD1 deficiency is involved, coded for in q21 arm of chromosome 21
	relationship between SOD1 and als	there is a mutant variation of SOD1 in als; it is not the loss of fxn of SOD1 that leads to sx, but the toxicity of the altered SOD1 (gain of fxn d/O) SOD1 is not affected in sporadic (non-familial) cases of als
	what is the difference between dominantly inherited als compared w sporadic als	clinical features are identical, but familial develops 10 yrs earlier
	hypothesis of pathogenesis in sporadic als	glutamate excitotoxicity (acts on nmda, ampa, and kainate receptors) --> selective neuronal damage in other pts there are abs to voltage gated ca channels other pts have monoclonal and polyclonal abs to gm1
	tx for als	riluzole (a glutamate antagonist) may slow progression of dz ivig may also be helpful
	what causes waddling gait describe waddling gait	weakness of gluteus medius muscle pts pelvis drops with each step
	describe gower's sign	to rise from sitting position, pt puts his hands on his knees, pushes his trunk back and works his hands up thighs
	what is seen on muscle biopsy in muscular dystrophy	degeneration and regeneration of muscle fibers of varying sizes there is no inflammation or storage of a metabolic product replacement of muscle by fat and ct --> pseudohypertrophy of gastroc
	which gene is involved in duchenne's muscular dystrophy	X chromosome, 21p --> dystrophin
	what does dystrophin do	links actin within the muscle fiber and laminin on muscle fiber's external surface in DMD, no dystrophin is produced
	types of hypertonicity	spasticity: from lesions in frontal lobe, or descending corticospinal projections --> resistance to passive movements that increases with speed of movement; tends to affect flexor muscles in arms and extensor muscles in legs rigidity: associated with parkinsons and other basal ganglion d/o --> plastic resistnace (lead pipe rigidity) that is not dependent on velocity and is constant throughout the rom
	describe cogwheel rigidity	rapidly alternating contractions of agonist and antagonist muscles (seen in parkinson's)
	what happens to tone following severe spinal cord injury	flaccid areflexia (aka spinal shock), followed by spastic hyperreflexia (cause of this change is unknown)
	describe spinal shock	results from the removal of suprasegmental descending systems that facilitate spinal motor neurons there is flaccid areflexia
	what effect does noxious stimuli cause below level of complete spinal transection	called "mass reflex" full flexion + urination + sweating and piloerection below the level of injury this occurs secondary to disinhibition of sympathetic response that relesase norE and epi released from adrenal glands
	describe dichotomous findings with sweating seen in complete spinal cord transection	noxious stimuli --> sweating, but warm environment does not
	moa baclofen	gaba agonist that likely acts at substance p synapses in dorsal horn
	describe pain seen in spinal cord transection that is present below the lesion	not well understood, usually clears spontaneously over several months may be from sympathetic splanchnic nerves that enter the spinal cord above the level of the injury
	what is cushing's response	bradycardia hypertension respiratory depression they all occur as a consequence of increased icp
	cerebral perfusion pressure	cpp = mabp - icp the goal is to keep cpp constant, so if icp increases, then mabp will increase
	what is the acceptable range of cpp	70-120 mm hg if it is above that --> cerebral edema if it is below that --> hypoxic injury
	how does jvp relate to icp	csf is reabsorbed across meninges into venous circulation, so if jvp is elevated, then csf can't get out --> increased icp
	what are the 3 components w/i the cranium that contribute to volume	brain csf blood
	what are the clinical signs of herniation	(all occurring from brainstem compression) 1. loss of pupillary reactivity 2. impairment of eye movements 3. hyperventilation 4. motor posturing (flexion/extension)
	when should increased icp be suspected	in pts with known or suspected intracranial pathology (stroke, trauma, neoplasm) and have depressed level of consciousness, htn w/ or w/o bradycardia
	most common causes of increased intracranial volume	extrinsic mass lesions hydrocephalus cerebral edema
	describe the cerebral autoregulation curve	in nml pts, cbf can remain constant with bp between ~60-160 mmHg in htn pts, cbf will remain constant between ~75-180 in pts with vasospasm and/or ischemia, autoregulation is not possible, so there is an upward linear line that increases as the arterial bp increases
	what fibers are carried in the internal capsule	posterior limb carries corticospinal fibers and sensory fibers genu carries corticobulbar fibers anterior limb carries frontopointine and spinothalamic fibers
	blood supply of the internal capsule	striate arteries that come off of the mca
	csf in guillain-barre	high protein count mild wbc (pleocytosis usually <10 lymphos/dL) albumin/cytologic protein dissociation
	charcot-marie-tooth dz	progressive muscular atrophy that starts in feet and then spreads to hands; sensation affected less or not at all aka peroneal muscular atrophy
	mode of inheritance of charcot-marie-tooth	x linked
	which dz that causes elevated gamma-globulins (M-proteins) will also --> senosorimotor periopheral neuropathy	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
	explain why long nerves tend to be more affected in demyelinating processes, compared to short nerves	stocking and glove distribution is common; statistically, anything that is going to affect a long nerve has more of a chance to do it than a short nerve also, when compensatory sprouting of fibers from short nerves occurs, they are more likely to reach their end-targets, compared to the sprouts from long nerves
	what is an easy way to distinguish between a myopathic motor problem and a neuropathic motor problem	myopathic problems will usually affect proximal muscles (with a few exceptions) neuropathic problems will usually affect distal muscles
	signs of denervation on emg	fibrillations, positive waves, polyphasic potentials of increased duration and amplitude
	spinal muscular atrophy	hereditary progressive degeneration of motor neurons in anterior horn of spinal cord
	type of gait seen with cbl dz	broad based gait fall towards side of lesion
	if a pt is standing with their feet together, what is seen in cbl vermal lesions or b/l vestibular lesions	they will fall backward or fall inconsistently in any direction
	what is circumduction and when is it seen	dragging of contralateral foot, leg may swing outward from the hip \; if lesion is above c-spine, the ipsilateral arm swing may be reduced u/l umn lesions
	what causes a stiff spastic gait describe the gait	b/l umn lesions dragging o fboth feet, and scissoring (both feet will cross over each other) if there is preserved gastroc power, --> toe walking and eventual contracture in plantar flexion
	what findings of gait are there in a pt with impaired proprioception	they watch their feet as they walk leg(s) may move randomly in different directions
	what are the main differences between bulbar and pseudobulbar palsy	bulbar: b/l lmn dz --> fasciculations in tongue (not seen in pseudobulbar), no mov't of pharynx or palate with phonation, absent gag reflex (hyper-reflexive in pseudobulbar) pseudobulbar: b/l umn lesions --> hyper-reflexive gag, NO tongue fasiculations, and absence of mov't of pharynx and palate with phonation
	what happens when a parkinsons pt tries to rise from sitting	they can't, unless they use their arms
	what is magnetic gait and when is it seen	legs are broad based adn feet never leave the ground, takes tiny steps, cause by b/l frontal lobe dz, seen in chronic nph
	what is titubation and when is it seen	coarse tremor of head and neck seen in cbl dz
	describe jacksonian march	focal motor sz that has a clonic jerking that rapidly spreads proximally from one or more digits, up a limb
	what way do eyes deviate during a sz	deviated away from the lesion
	what is todd paresis	transient postictal focal weakness, signifying functional unresponsiveness of neurons in the area of maximal discharge, could be from excessive glutamate neurotransmission
	what is the difference seen in electrical activity in a pt with partial szs who generalizes, compared to a pt with primary generalized szs	secondary generalization: cortical focus that spreads via corpus callosum to contralateral hemisphere; then projects to thalamus; widespread thalamocortical projections activate both cerebral hemispherse --> generalization in primary generalized szs, activity begins in the thalamocortical discharge and spreads to b/l cerebral hemispheres
	most common cause of a tia	usually they are embolic
	less common cause for a tia	transient hypotension in the presence of severe carotid stenosis (>75%)
	most common etiology of cva	infarction from embolic strokes - most common origin of embolus is secondary to embolization of mural thrombus in pts with a-fib
	what are the 3 most common causes of stroke	infarction (embolus, atherothrombotic, lacunar) intracerebral hemorrhage subarachnoid hemorrhage misc causes
	when should htn be treated immediately following a stroke	if there is a htn emergency if bp >220/120 bp can be lowered if there is evidence of a hemorrhagic stroke on ct
	major threats to life following stroke	transtentorial herniation cbl infarction or hemorrhage (need neurosurg evaluation) aspiration pna (v common cause of death; consider pt to have impaired swallowing until proven otherwise)
	presentation of SAH	sudden, severe ha (drom ruptured cerebral aneurysm) stiff neck and photophobia reported (must r/o meningitis) chaged in ms focal signs are not as common as in other stroke types
	why is sah so dangerous	50% fatality if not treated, the majority of which are from hemorrhage, but there is significant risk for re-rupture as well aneurysm must be surgically clipped!
	what will a ct scan of sah show	hyperdensity in sulci, major fissures, and around brainstem
	if the ct is negative for sah, but clinical suspicion is still high, what is the next step in dx	lp - csf will show xanthochromia; can also r/o meningitis
	after sah is dx, what is the next diagnostic step	catheter angiography to r/o additional unruptured aneurysms
	difference in presentation of sah vs other stroke types	other stroke types don't prsent wiht any pain, and they have focal neurologic findings sah has ha with focal findings rare sah presents with meningeal signs
	stroke sx that are suggestive of cardioembolic strokes	sudden deficit, maximal at onset hemianopia w/o hemiparesis, pure wernicke's aaphasia, and top of the basilar syndrome
	most common location for aneurysms	pca, aca, mca
	what presentation is likely to suggest large-vessel stenosis as basis for stroke	fractional weakness (shoulder weaker than the hand, hip weaker than the ankle)
	risk factors commonly associated with large vessel stenosis	male htn dm
	presentation of lacunar stroke	no cortical signs/sx clumsy hand dysarthria, pure motor hemiparesis, ataxic hemiparesis, sensorimotor syndrome
	management of ischemic stroke	ct/mri if stroke sx <3 hrs and ct shows no hemorrhage, give tpa
	presentation of intracerebral hemorrhage	higher incdidence of ha and severe htn c/w ischemic stroke otherwise caan be identical
	pathogenesis of intercerebral hemorrhage	chronic htn results from rupture of smallest penetrating arteries
	most common sites for intercerebral hemorrhage	most commonly in basal ganglia and thalamus (70%) brainstem cbl
	management of hemorrhagic stroke	correction of coagulopathy - give ffp if there is coag d/o control bp: systolic between 160-180 to help prevent recurrent bleeding hyperventilation to control increased icp
	when should CEA be considered to prevent stroke	sx pts: carotid stenosis >70% asx pts: no surgery; just lower atherosclerotic rsk factors and give asa
	ha that can can cause major threat to life	meningitis sah herniation from intracranial mass lesion
	preventive measures for cluster ha	prednisone + verapamil and lithium (prednisone use is not long term, should be tapered over a couple of weekS)
	triad of sx in pseudotumor cerebri	ha, increased icp, papilledema in absence of mass or hydrocephalus
	what type of intracranial pathology is likely to be seen in trigeminal neuralgia	vascular compression of the pons , although it might not be seen on imaging
	what are the 2 most common causes for acute paralysis + ventilator failure others?	myasthenia gravis guillan barre c-spine correction transverse myelitis als polio cidp aids diphtheritic polyneuropathy organophosphate intox polymyositis myopathy
	poor prognostic factors in guillan barre	advanced age low distal motor amplitudes rapidly progressive weakness over the first week resp failure --> intubation
	in aidp, which is more affected, proximal or distal muscles	proximal
	csf in guillan barre	cytologic-albumin dissociation eleated protein mild pleocytosis
	what is seen on emg of a pt with aidp	reduced conduction velocities occ reduced amplitude
	aside from ascending paralysis and areflexia, what other clinical signs/symptoms are seen in aidp	pain (from meningeal inflammation or neuropathic mechanisms) dysautonomia (htn or tachycardia)
	pathophysiology behind myasthenia gravis	auto-ab directed against nicotinic ach receptors --> defect in nm transmission
	most common muscles affectd by myasthenia gravis	eyes face neck oropharynx limbs
	remission of myasthenia gravis	can occur within 2 years of onset 30% remit
	what tumor is associated with myasthenia gravis	malignant thymoma (assoc with more severe dz)
	myasthenic crisis	resp failure requiring intubation and mechanical ventilation provoked by infection, but can also occur spontaneously 70% recover by 1 month 30% likely to experience it again
	dx of myasthenia gravis	edrophonium testing (shows transient improvment of sx) repetitive nerve stimulation --> >10% decrement in amplitude between the first and fifth stimulation ACh antibodies single fiber emg: see jitter variation (95% sensitive) anti-muSK abx (seen in those who are lacking the ACh abx)
	what is anti-musk	associated with myasthenia gravis, seen in pts w/o the ach ab anti-muscle specific tyrosine kinase usualy seen in females with predominant neck and oropharyngeal weakness
	tx for myasthenia gravis	symptomatic tx: acetylcolinesterase inhibitors (pyridostigmine) s-t dz suppression: plasmapheresis and ivig long-term immunosuppresion: thymectomy, steroids, azathioprine, chemotherapy
	tx for botulism	botulism trivalent antitoxin guanidine hydrochloride (ACh agonist that counteracts the presynaptic blockade caused by the toxin)
	why does botulism toxin --> weakness	inhibits presynaptic ACh release
	sx of botulism	gi complaints dilated and nonreactive pupils blurred vision weakness (beginning in extraocular and oropharyngeal muscles, then --> generalized) urinary retention anhidrosis dry mouth (impaired parasympathetics)
	what differentiates guillan barre from polio	polio has fever, headache, mental status change, asymmetric weakness neutrophils on csf otherwise, both are flaccid areflexic paralysis
	medical tx of tetanus	assist ventilation immune globulin procaine penicillin to eradicate the soft-tissue infection
	what triad of sx should always be treated as a cns infection	fever ha neurologic signs/sx (any 2/3 require lp, with ct prior)
	pathogenesis of acute bacterial meningitis	seeding of leptomeninges occurs from hematogenous spread of infecting organisms can also spread form parameningeal infection (otitis media) or following trauma, cochlear implants, o neurosurgery
	common tx for community acquired meningitis for adults, children	ceftriaxone and vanco until cx return + dexamethasone
	common tx for community acquired meningitis in infants, immunosuppressed, and older	ampicillin should be added to cover listeria
	presentation of viral meningitis	neurologic dysfxn is not seen, otherwise similar to bacterial meningitis
	how to treat viral meningitis	it is self-limited
	most common viruses --> viral meningitis	enterovirus arthropod born (WNV) HSV-2 HIV (meds can do it too)
	definition of chronic meningitis	develops over 2 wks
	physical sx of tuberculosis meningitis	cn palsies vasculitic small vessel infarction obstructive hydrocephalus all result from severe granulomatous inflammation of the basal meninges all occur from severe granulomatous inflammation fo basal meninges --> tuberculoma evidence of active pulm dz present in 30% of pts
	late complications of tb meningitis	hydrocephalus sz cognitive impairment
	dx of tb meningitis	csf shows lymphocytic pleocytosis, increased protein level, moderately reduced glucose level acid-fast mycobacteria in csf ppd not reliable in th meningitis wu
	tx of tb meningitis	inh rif ethambutol pyrazinamide dexamethasone can be given in severe cases to limit inflammation and damage
	manifestations of tertiary neurosyphilis	general paresis (from chronic, diffuse encephalitis --> dementia w psychiatric features and b/l umn signs) tabes dorsalis (from chronic spinal polyradiculitis with secondary dorsal root and column degeneration) argyll-robertson pupils (react to accomodation but not to light --> blindness from optic atrophy)
	what is the difference in presentation btwn hiv + pts and nonimmunosuppressed pts with neurosyphilis	in most ppl, it takes 10-15 yrs of asx syphilis before tertiary neurosyphilis develops; in hiv + it is accelerated and meningitis and meningovasculitis predominate
	tx of neurosyphilis	penicillin G
	dx fo cns lyme dz	evidence of intrathecal production of igg ab to borrelia in csf, see lymphocytic pleocytosis with mildly elevated protein
	sx of cns lyme	early: mild meningitis/meningoencephalitis cranial neuropathy myelitis radicloneuritis chronic: lyme encephalopathy (immune mediated) recurrent/chronic meningoencephalitis chronic myelitis
	causes of chronic fungal meningitis	cryptococcus coccidiodes candida histoplasma blastomyces
	dx of fungal meningitis	demonstrates the organism by wet smear
	stain used to dx cryptococcus	india ink
	tx of fungal meningitis	fluconazole for mild cases amphotericin b for severe cases
	presentation of bacterial abscess	subacute progression of ha, altered ms, focal neurologic signs and fever
	how are most brain abscesses formed	contiguous spread from a parameningeal infection (aom, osteomyelitis, sinusitis) or hematogenous spread in pts with endocarditis, bronchiectasis, congenital cyanotic heart dz
	what are the most common orgs seen in brain abscesses	staph enterobacteriacae b fragilis
	dx fo brain abscess	ring enhancing lesion on ct/mri perform blood cultures and lp if etiology is not known
	tx of brain abscess	broad spectrum tx: penicillin metronidazole vanco (if pt is post-surgical or post-traumatic and staph is a concern)
	tx of subdural empyema	surgical drainage
	what setting are cranial/spinal abscesses normally seen	often seen with osteomyelitis
	presentation of cranial epidural abscess	localized pain and tenderness --> cn defects
	sx of spinal epidural abscess `	intense local pain and tenderness local root pain irritation with referred pain cord compression
	what are the most common organisms sen in spinal epidural abscess	staph gram - tb (pott's dz)
	tx of spinal epidural abscess	surgical drainage to prevent cord compression vanco + ceftriaxone
	most common cause of sporadic viral encephalitis	hsv-1
	presentation of hsv-1 encephalitis	fever altered ms ha sz
	pathogenesis of hsv-1 encephalitis	reactivation of dormant hsv-1 within trigeminal ganglion with viral spread via sensory pathways to brain
	dx of hsv-1 encephalitis	intrathecal hsv ab + hsv pcr from csf
	what is seen on hsv-1 encephalitis imaging	focal necrotizing lesions of inferior frontal and temporal lobes
	tx of hsv-1 encephalitis	acyclovir anticonvulsants
	wnv encephalitis - how common is it? clinical sx	20% with wnv are sx, and 1% of those --> neuroinvasive wnv usually presents as meningoencephalitis characterized by altered ms, focal neuro deficitis, tremor, can also present as meningitis
	dx of neuroinvasive wnv	based on clinical suspicion + wnv igm in blood/csf
	tx of neuroinvasive wnv	supportive
	difference between bacterial and viral meningitis	in viral meningitis the neurologic dysfxn doesn't occur, it's only ha and fever
	features of tb meningitis	severe granulomatous inflammation of basal meninges vasculitic small vessel infarction obstructive hydrocephalus spinal arachnoiditis
	tx of tb meningitis	inh rif pyrazinamide ethambutol
	features of neurosyphilis	general paresis- dementia with psych features and b/l umn signs tabes dorsalis argyll-robertson pupils
	dx of neurosyphilis	vdrl is specific but not very sensitive, so use: csf fta-abs (very sensitive, but not as specific) if both are - then can definitely r/o syphilis
	which hsv virus --> encephalitis pathogenesis	hsv-1 hsv is w/i trigeminal ganglion, gets reactivated and then there is viral spread via sensory pathways into the brain
	tx of hsv encephalitis	acyclovir phenytoin to prevent sz
	tx of wnv encephalitis	supportive
	opportunistic complication of AIDS	cns toxo cryptococcus pml cmv primary cns lymphoma shingles syphilis hiv meningitis
	proph of toxo in hiv + tx of toxo	bactrim sulfadiazine and pyrimethamine
	proph of mac tx of mac	rifabutin clarithromycin and ethambutol
	proph of cryptococcus tx of cryptococcus	fluconazole flucytosine/fluconazole/amphotericin
	presentation of toxo	fever subatue encephalopathy focal neurologic deficits sz
	presentation of cryptococcus	suspect in any hiv + pt with a ha fever is usually present
	presentation of pml	subacute onset of focal neurologic deficits and dementia peripheral ns is spared
	mri of pml	striking white matter hyperintensities
	tx of pml	haart
	presentation of cmv retinitis	slowly progressive, painless loss of vision
	dx of cmv	pcr is highly sensitive
	what does mri show in cmv	ependymal enchancement (area around ventricles and spinal cord)
	tx of cmv	gancyclovir
	neuro complications of shingles	cns vasculopathy, presenting with stroke-like sx or myelopathy
	sx of hiv myelopathy	insidious onset of spastic paraparesis, sensory ataxia, and bowel/bladder/erectile dysfxn (looks similar to b12 deficiency)
	nonopportunistic infections associated with hiv	distal sensory polyneuropathy dementia myelopathy myopathy neuromuscular weakness syndrome aidp
	features of distal sensory polyneuropathy	most common hiv related neuro complication caused by immune mediated pathway or antiretroviral toxicity
	presentation of distal sensory polyneuropathy	symmetric, painful paresthesias sensory loss allodynnia in a stocking/glove distribution loss of ankel jersks
	tx of distal sensory polyneuropathy	better control with haart
	pathogenesis of hiv asssociated dimentia	hiv infects non-neuronal cells shortly after primary viremia wiht immune failure, chronic encephalitis ensues
	presentation of hiv associated dementia	motor slowing behavioral change
	tx of hiv associated dementia	haart can arrest and sometimes reverse dementing process
	major causes of syncope	reflex vasodilation cardiac orthostatics neurologic causes psych causes
	different reflex vasodilation disturbances --> syncope	vasovagal hypersensitive carotid body situational syncope
	cardiac causes of syncope	arrythmias flow/pump failure (outflow obstructions - stenosis, hocm, dissection, myxoma, mi, cardiac tamponade)
	orthostatic causes of syncope	volume depletion dru induced autonomic dysfunction (shy-drager is a central dysfxn, autonomic neuropathy is a peripheral cause)
	neuro causes for syncope	brainstem ischemia (vertebrobasilar stenosis/occlusion) or subclavian steal syndrome vilateral hemispheric ischemia from carotic artery stenosis/occlusion sah, space occupying lesion (both secondary to icp)
	how long is a pt unconscious before it is considered a coma	15 mins
	syncope: what sx would suggest it's from cardiac arrhythmia	palpitations no prodromal sx
	syncope: what sx would suggest it's from vasovagal causes	dizziness, lightheadedness, pallor, diaphoresis, dimming vision
	syncope: what sx would suggest it's from carotid sinus	during turning head to one side
	syncope: what sx would suggest it's from vertebrobasilar insuff	1+ episodes of vertigo, diplopia, dysarthria, numbness, weakness, ataxia
	what normally happens to bp in syncope? what is the exception	usually it drops, unless it's from sah, then pt is htn
	tx for vasovagal syncope	if table tilt test is +, beta blocker or paroxetine
	subclavian steal syndrome	--> vertebrobasliar insuff 1 subclavian artery is occluded proximal to the vertebral art distal subclavian art is supplied by retrograde flow from ipsilateral vert art that "steals" from basilar and contralateral vertebral arteries
	tx of autonomic dysfxn --> orthostatics	fludrocortisone, support stockings
	how does hypervent --> syncope	hypocapnia decreases cbf 2ndary to cerebral vasoconstriction
	what part of the spine normally is affected by mets why	thoracic spine there is the most drainage from visceral organs through the spinal extardural venous plexuses
	empedymomas	intrinsic cord tumors that mimc extra axial compressive lesions
	what is the difference between how cervical disks herniate and lumbar disks herniate	cervical disks herniate centrally lumbar herniates laterally and --> radicular sx
	where is the herniation in an acute cauda equina syndrome	l1-l2
	what types of sx can be associated with arnold-chiari malformation	spastic diplegia of legs cervical myelopathy (pts are predisposed to subluxation or dislocation)
	how should an acute traumatic sci be treated	1. methylprednisolone 2. blood tests in case surgery is needed 3. imaging, if stable
	anti-inflamm tx for spinal neoplasm	dexamethasone
	what does an anterior cord compression of c-spine suggest	cervical disk herniation
	what does a posterior cord syndrome in t-spine suggest	bony mets
	can tendderness in lumbar/sacral spine --> cord compression	no, the spinal cord stops at l1
	features of anterior cod syndrome	b/l spinothalamic tract umn paralysis below lesion lmn paralysis at lesion sphincter dysfxn preserved dorsal column sensation
	mononeuritis multiplex	multiple, asymmetric regions of sensory loss, corresponding to multiple peripheral nerves
	sx of spinal muscular atrophy	lmn degen infantile or chiildhood onset; adult forms are rarer
	pathophys of multifocal motor neuropathy	immune mediated motor neuropathy; conduction block present on nerve conduction studies
	tx multifocal motor neuropathy	ivig
	parsonage-turner syndrome	idiopathic brachial neuritis (sudden onset of pain in shoulder and arm; weakness and muscle wasting become evident after 2-4 wks)
	ramsay hunt syndrome	herpes zoster infection of ipsilateral geniculate ganglion
	when to suspect neurosarcoidosis	interstitial lung dz with hilar adenopathy, uveitis, or parotitis
	what is suggested by decreased hearing or a decreased afferent corneal reflex	cerebellopontine angle tumor
	tx of idiopathic bell's palsy	prednisone
	tx of ramsay hunt syndrome	acyclovir
	differential for mononeuropathy multiplex	vasculitis (esp PAN) DM leprosy sarcoidosis hiv lymphoma lyme cidp
	different types of neuropathy caused by dm	distal axonal sensorimotor neuropathy autonomic neuropathy mononeuropathy mononeuropathy multiplex diabetic amytrophy
	what is diabetic amytrophy	asymmetric proximal leg wekaness and wasting, not limited to a root, plexus or nerve territory
	paraprotein associated neuropathy	demyelinating or axonal sensorimotor neuropathy can be seen in plasma cell dyscrasia, mm, amyloidosis, lymphoma, leukemia, waldenstroms'
	tx of paraprotein associated neuropathy	prednisone plasmapheresis, ivig, azathioprine
	lambert-eaton myasthenic syndrome	ab vs ca channels of presynaptic nerve terminals --> impaired neuromuscular transmission (usually neoplastic cause) see proximal limb weakness, lower extremity areflexia, dry mouth, myalgias, and impotence
	dx of lambert-eaton	incremental response on repeated nerve stimulation
	tx of lambert-eaton	guanidine diaminopyridine
	dx of polymyositis	ck levels elevated emg shhhows myopathic findings with denervation bx shows endomesial lyphocytic infiltrates, necrotic and atrophic muscles fibers and ct deposition
	tx of polymyositis	prednisone
	sx of dermatomyositis	same as polymyositis, but with heliotropic rash on eyelids, erythematous rash on face and trunk violaceous scaly eruptions on knuckles subcutaneous calcifications
	gottron's papules	violaceous scaly eruptions on knuckles assoc with dermatomyositis
	dx of dermatomyositis	different findings on bx (c/w polymyositis) shows perivascular inflammation adn perifascicular atrophy
	tx of dermatomyositis	prednisone
	sx of inclusion body myositis	different from polymyositis b/c it prodcues distal and asymmetric weakness poor response to steroids
	endocrine dz that can --> myopathy	cushings thyroid dz parathyroid
	sx of myotonic dystrophy	distal myopathy ptosis, frontal balding, cataracts, cardiac conduction defects, gonadal atrophy and mental impairment
	periodic paralysis	genetic abnormalities in ion channels , pts are nml between attacks of severe weakness
	sx of mitochondrial myopathy	ptosis ophthalmoparesis high serum lactate levels
	most common type of primary brain tumor	glioma
	most common type of glioma	astrocytoma
	most common type of astrocytoma	gbm
	dx of gbm	mri with gad shows ring enhancing lesions can show butterfly glioma if it grows along white matter tracts like corpus callosum
	presentation of gbm	ha ms changes focal motor deficits sz are less common
	presentation of anaplastic astrocytoma	sz ha focal deficit
	dx of anaplastic astrocytoma	gad-enhanced mri bx is needed to make definitive dx
	most common presentation of low-grade astrocytoma	sz
	imaging of low grade astrocytoma	mri (no gad) see very little mass effect bx for confirmation of dx
	pathologic appearance (under microscope) of oligodendroglioma	fried egg appearance
	presentation of oligodendroglioma	sz ha behavioral changes cognitive changes
	mri of oligodendroglioma	mri shows tumor with indistinct margins and variable amounts of contrast enhancement
	what age group is ependymoma most coommon in	children and young adults
	where do ependymomas usually occur	in children, on the floor of the 4th ventricle
	presentation of ependymoma	noncommunicating hydrocephalus --> increased icp with ha, vomiting, ataxia
	dx of ependymoma	mri with gad will fill subarachnoid space through foramina of luschka and magendie MUST GET SPINAL MRI AND LP TO DETECT DROP METS
	drop metastases	results from seeding via csf
	pnet	primitive neuroectodermal tumor highly malignant seen exclusively in children and adolescents
	presentation of pnet	depends on location extraneural mets occur more often with pnet c/w any other cns neoplasm
	dx of primary cns lymphoma (pcnsl)	mri (will appear isointense on ct) seen periventricularly and enhances uniformly with gad
	what type of lymphoma is a pcnsl	non-hodgkin's
	presentation if there is a meningioma in the hemisphere	ha focal sx sz
	presentation if there is a meningioma in the sphenoid wing	ha diplopia visual loss
	presentation if there is a meningioma in the olfactory groove	dementi ipsilateral optic atrophy and c/l papilledema
	presentation if there is a meningioma in the suprasella	ha bitemporal hemianopia sometimes hypothalamic dysfxn
	presentation if there is a meningioma in the posterior fossa	cn efects sx of brainstem compression
	dx of meningioma	dural tail on mri see braod based dural attachment
	what dz is associated with acoustic neuroma	neurofibromatosis type 2
	pathophys of acoustic neuroma	arises within internal acoustic canal, follows path of least resistance, growing into cerebellopontine angle
	presentation of acoustic neuroma	tinnitus or hearing loss u/l
	dx of acoustic neuroma	gad enchanced mri shows small intracanalicular tumors
	tx of prolactinoma	da agonist (bromocriptine) first, otherwise if it doesn't work, then operate
	most common malignant tumor of childhood/adolescence	medulloblastoma
	where does medulloblastoma arise	cbl, and can present with signs of increased icp when mass effect causes obstruction
	dx fo medulloblastoma	mri/ct shows contrast enhancing tumor, usually midline and distorts or obliterates 4th ventricle
	sx of thalamic pain syndrome	spontaneous contralateral pain and dysesthesia is areas of impaired sensation
	pathophys of thalamic pain syndrome	hemisensory loss from interruption of spinothalamic and dorsal column system at level of ventral posterior nucelus of thalamus dorsal column --> severe contraolateral ataxia
	path of dorsal columns from spinal cord	dorsal colums go to dorsal column nuclei, x midline at medial lemniscus --> ventral posterior lateral nucelus of thalamu and posterior nuclei of thalamus vpln -->primary sensory crtex --> posterior parietal cortex and secondary sensory cortex
	what would happen if there is a lesion in the primary sensory cortex	severe impairment of discriminative sensations, but only modest impairment of affective sensations such as pain (b/c of the dual projection of the spinothalamic tract)
	cause of wallenberg's syndrome	occlusion of lateral medullary branches of vertebral artery and pica (posteriolateral region of brainstem)
	what neurologic injury (in brain) can hiccups be attributed to	lateral medullary infarction
	what does pica supply	dorsolateral medulla posterior inferior cbl
	what is preserved in wallenberg's syndrome and why?	tongue fxn weakness pyramidal signs contralateral loss of proprioception and discriminative touch
	path of anterolateral system starting at spinal cord	dorsal horn --> x midline --> brainstem and intralaminar nuclei of thalamus --> praimary seonsry and association cortex
	sx of vertebral artery dissection	neck or posterior head pain horner's syndrome dysarthria dysphagia decreased pain and temp of face, contralateral body dysmetria ataxia vertigo
	how to dx a vertebral artery dissection	mri and mra of neck
	juvenile myoclonic epilepsy	myoclonic jerks that lead to generalized tonic clonic sz (suspect when all things on exam and imaging are nml)
	what sized symptomatic meningioma should not be operated on	<3 cm, should give radiation
	presenilin-1	causes familial alzheimer's dz
	clinical features of frontotemporal dementia	personality change lost initiaitve slowing though recent memory is preserved
	imaging for frontotemporal dementia	mri see disproportionate atrophy of anterior frontal and temporal lobes
	difference between activity levels of pts with migraines vs cluster ha	migraines: lay down cluster: mobile b/c laying down makes their ha worse
	transverse myelitis	bilateral sensory and motor dysfunction autonomic dysfxn umn signs sx present acutely or subacutely
	tx of transverse myelitis	high dose corticosteroids
	if a pt has afib and is s/p stroke, but it is after the 3 hr window for tx with tpa, how to tx the pt?	warfarin HEPARIN HAS NO ROLE IN ACUTE TX OF STROKE
	post-ictal confusion in simple partial sz	not present
	spinal muscular atrophy	motor neuron dz NOT associated with any sensory abnormalities generally presents with symetric proximal muscle weakness and atrophy
	limb-girdle muscular dystrophy	symmetric proximal muscle weakness nml sensation
	what is commonly associated with cervical dystonia	cervical spondylosis
	common tx for cervical dystonia	trihexiphenidyl clonazepam baclofen
	course of tias over time	they would worsen in severity over time
	what does lermitte's sign mean	indicates the presence of cervical spinal cord problem
	features of cervical spondylosis	chronic degenerative and hypertrophic changes of vertebrae, ligaments, and disks --> narrowing of spinal cord
	in a pt with stroke >3 hrs ago, how to tx	early admin of asa --> modest reduction of risk of recurrent stroke in short term and less death and disability in the long term
	dz associated with mononeuritis multiplex	vasculitides dm
	sx of mononeuritis multiplex	asymmetric weakness sensory loss severe pain
	sx of lewy body dementia	fluctuating encephalopathy parkinsonism visual hallucinations
	what is deficient in pts with lewy body dementia	central cholinergic activity
	tx of lewy body dementia	centrally actiing anticholinesterase agent (donezepil, galantamine, rivastigmine)
	what would happen to a pt w lewy body dementia who took a da agonist	exacerbation of encephalopathy
	what would happen to a pt w lewy body dementia who took a nueroleptic agent	increased risk for neuroleptic malignant syndrome and increased mortality
	risk to fetus if mother is on interferon or glatiramer acetate for ms	increased risk of spontaneous abortion and lbw
	how to handle pregnancy in a woman with ms who is on disease modifying meds for ms	discontinue interferon or glatiramer several months before wishing to conceive
	what effect does pregnancy have on a woman with ms	decreased frequency of relapse in the 3rd trimester rebound increase in relapse during the first 6 months post-partum
	hereditary component of ms	1st degree relatives have a 20-50x increase of having ms compared w general population
	how does wilson's dz differ from huntington's dz	in huntington's dz, there are cognitive deficits in wilson's dz ,the deficits are more psychiatric
	mov't d/o associated with frontotemporal dementia	parkinsonism
	paroxysmal hemicrania	u/l ha of seconds-minutes that can be very disabling despite its brevity
	in a pt with suspected vascular dementia, with nml head ct, what should be done	f/u imaging
	sx of optic neuritis	smudging of central vision, graudually worsening so pt can read with affected eye central scotoma present rapd preseent fundoscopic exam nml
	deficiency sometimes associated w restless leg syndrome	iron if low ferritin levels, iron supplementation can improve sx
	meds associated with development of pseudotumor cerebri	oral contraceptives tetracyclines
	how sensitive is ct scan in picking up sah	90%, but it is most likely to be missed if there is a delay in pt presentation, so lp must be done instead
	how long is lp able to detect xanthochromia following a hemorrhagic event	14 days
	who is most likely to remain sz free after being taken off epilepsy meds	those with no structural brain lesion no epileptiform or focal abnormalities on eeg sustained sz free pd no abnormalities on neuro exam
	csf in critical illness polyneuropathy	nml
	sx of critical illness polyneuropathy	same as guillan barre but follos admission to icu (predisposed by sepsis and/or multi-organ failure)
	which structures are implicated in short term memory fxn	dorsomedial thalamus dorsolateral prerontal cortex hippocampi parahippocampus
	how do pts with alzheimers react to their memory loss	they lack insight into their condition
	abnml physical findings in alzheimers pts	paratoni a extrapyramidal rigidity
	are scans necessary in dx alzheimers	they are required in order to r/o any other etiology causing memory problems
	meds for alzheimers	anti-cholinergics: donepezil rivastigmine galantamine in late stages: memantine
	use of antipsychotic meds in pts with alzheimers	can be used to treat behavioral probs in ad but should bge used with caution b/c of risk of sedation and extrapyramidal sx
	another name for frontotemporal dementia	pick's dz
	sx of frontotemporal dementia	behavior dominant or language dominant sx memory and spatial ability are spared early on
	sx of behavioral frontotemporal dementia	early progressive personality changes and early decline in social interpersonal contact lack of insight into these features decreased spontaneous speech = and language
	primary progressive aphasia	form of frontotemporal dementia loss of speech fluency anomia inappropriate word order and simplified sentence structure stuttering oral apraxia impaired repetition alexia agraphia eventually become mute and behavioral changes can occur
	semantic dementia	form of frontotemporal dementia fluent but empty spontaneous speech with loss of word meaning
	What region of the brain is affected in semantic dementia	left anterior temporal lobe is usually affected
	what region of the brain is affected in primary progressive aphasia	left perisylvian atrophy, usually more anterior than posterior
	sx of cortical basal ganglionic degeneration	form of frontotemporal dementia progressive cognitive impairment with associated asymmetric rigidity, apraxia, cortical sensory loss, and pyramidal dysfxn myoclonus limb dystonia
	tx of frontotemporal dementia	symptomatic
	sx of lewy body dementia	early dementia fluctuations in cognition and consciousness visual hallucinations subsequent development of parkinsonism action tremor autonomic dysfxn
	form of dementia where pts won't recognize their own reflection	lewy body dementia
	form of dementia where capgras syndrome can occur	lewy body dementia
	tx for lewy body dementia	cholinesterase inhibitors can be helpful but don't modify dz
	what drugs are contraindicated in lewy body dementia	typical neuroloeptics b/c it can --> irreversible parkinsonism atypicals can be used cautiously
	which form of dementia is associated with rem-behavioral d/o	lewy body
	tx of rem behavioral d/o	clonazepam qhs
	parkinson's dementia	similar to lewy body dementia
	how is lewy body dementia different from parkinsons dementia	the time course is different (early in lewy body and late or not at all in parkinsons)
	dementia seen in huntington's dz	forgetfulness and concentration difficulty early on later there is more severe memory decline, difficulty learning, language decline, adn apraxia
	meds used in huntington's dementia	antipsychotics to help with the psychosis ssris for any ocd or depression that may develop
	pathyophysiology of nph	communicating hydrocephalus develops in elderly pts w/o clear obstruction to csf outflow
	what does imaging show in nph	enlarged ventricles out of proportion to brain atrophy
	dx of nph	imaging lp which should improve gait substantially and should be reproducible; they should then be referred for a shunt
	sx transient global amnesia	during a stressful situation, there is profound anterograde and retrograde amnesia self limiting condition
	in pt with pcnsl what is the first step in dx	do an eye exam; some pts have vitreal/uveal involvement and dx can be made w vitrectomy, so no need for brain bx
	is resection recommended in pcnsl	no, it is prone to hemorrhage and doesn't improve survival
	tx of pcnsl	once dx is made, mtx is tx of choice
	adverse effects of donezepil	increased vagal tone bradycardia av block
	adverse effects of memantine	hallucinations confusion restlessness anxiety dizziness fatigue constipation
	secondary progressive ms	begins as relapsing/remitting ms, 85% become 2dary progressive recurrent progression of neuro sx
	primary progressive ms	starts with spinal cord dysfxn or ataxia no acute exacerbations fewer cerebral lesions more common in men
	why does metoclopramide --> parkinsonism	it is a da antagonist
	when to refer an epileptic for surgery	after pt has failed on 3 aeds
	correct sequence of dx and treating pseudotumor cerebri	do imaging to r/o organic brain dz perform lp confirm dx and tx w acetazolamide
	pvs	sleep-wake cycles are maintained brainstem and hypothalamic fxn is preserved
	pathology of ms lesions	demyelinated areas surrounded by macrophages and lymphocytes
	how does ms differ from leukodystrophies	ms has focal demyelination
	sx of optic neuritis	periorbital pain with eye movements subtle loss of vision red desaturation
	if there is tremor in ms, where would you expect the lesion	plaques affecting cbl afferent/efferent pathways
	adverse effects of glatirimer acetate	chest tightness flushing anxiety dyspnea palpitations
	moa mitoxantrone	topo II inhibitor
	moa natalizumab	blocks interaction between vla4 and vcan 1 which is needed for adherence to vascular endothelium
	sx of acute transverse myelitis	b/l le weakness loss of sphincter tone sensory loss at a spinal cord level
	tx of acute transverse myelitis	steroids + acyclovir plasma exchange if above not successful
	sx of acute ms	rare, fulminant demylenation dz large edematous contrast enhancing lesions with mass effect entire brainstem demyelination --> death
	tx of acute ms	plasma exchange + steroids if pt survives acute attack, put pt on immunosuppressents
	sx of ADEM	seen in children commonly after vaccination or infection monophasic, multifocal inflammation and demylenation can be associated with sz and loc
	tx of adem	plasma exchange and ivig add steroids if necessary
	sx of neurosarcoidosis	chronic meningitis sx depend on location of granulomata
	blood test findings in neurosarcoidosis	hypercalcemia hyperuricemia increased ACE increased serum globulin
	tx of neurosarcoidosis	steroids + azathioprine
	behcet's dz	relapsing iritis/uveitis + oral/genital aphthous ulcers can have abrupt onset of meningoencephalitis + cn palsies
	central pontine myelinolysis	symmetric destruction of the white matter in the pons
	who is more prone to developing central pontine myelinolysis	EtOH abusers malnourished ppl with multiorgan failrue
	presentation of central pontine myelinolysis	rapidly progressive spastic quadriplegia facial, glottal, pharyngeal paralysis --> locked in syndrome
	where is cmV localized to in brain? toXo?	periVentricular corteX
	myotonic dystrophy	can't release grip cardiac problems
	mptp	--> parkinsonism in drug users can be treated with amantadine
	eye deviation in stroke of cortex pons putamen cbl	if in cortex, eyes will deviate towards lesion if in pons, eyes will deviate away from lesion and look at affected limbs in putamen, eyes deviate towards lesion in cbl, eyes deviate away from lesion
	describe CN III neuropathy in dm	it is ischemic in dm there are 2 blood sources to the nerve fibers in cn iii, and in dm only the somatic fibers are affected, so accomadation and light response is ok
	side effects of riluzole	dizziness n/v weight loss increased lfts weakness
	moa riluzole	glutamate inhibitor
	when is hemineglect seen	lesion in non-dominant parietal lobe
	describe tremor seen in wilson's dz	wing beating tremor
	eeg findings in cjd	triphasic synchronous waves
	neurologic uses of amantadine	parkinsons dz tx of ms related fatigue
	where is the lesion that causes locked-in syndrome	lesion at base of the pons vertebro-basilar artery
	spinal muscular atrophy	affects anterior horn cells (sim to polio)
	persistent vegitative state	awake but not aware caused by cortical anoxia brainstem still fxns and there are brainstem reflexes present cortex doesn't work
	when should berry aneurysms be repaired	>7mm
	what is the main cause of morbidity and mortality in huntington's pts	dysphagia
	what does mri of hd show	bilateral atrophy in cerebral hemispheres, corpus callosum, brainstem
	sx of cerebral venous thrombosis	ha --> change in ms, somnolence, death

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