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98 Cards in this Set

  • Front
  • Back
Facial (VII) nerve LMN lesion
Bell's palsy: paralysis of ipsilateral upper and lower face
DDx of Bell's palsy
ALexander Bell with STD:

1. AIDS
2. Lyme
3. Sarcoid
4. Tumors
5. Diabetes
Facial (VII) nerve UMN lesion
Paralysis of contralateral lower face only
MCA territory stroke symptoms
Aphasia if dominent hemisphere
Neglect if nondominant
Contralateral paresis and sensory loss in face and arm
Gaze preference toward side of lesion
Homonymous hemianopia
ACA territory stroke symptoms
Contralateral paresis and sensory loss in leg
Cognitive or personality changes
PCA territory stroke symptoms
Homonymous hemianopia
Memory deficits
Dyslexia/alexia
Basilar artery territory stroke symptoms
Coma, "locked in syndrome"
CN palsies (vision, dysphagia, dysarthria, vertigo)
Ipsilateral face/contralateral body sensory loss, weakness
Apnea
Lacunar infarct symptoms
Pure motor or sensory
Dysarthria
Ataxic Hemiparesis
Contraindications to tPA therapy
SAMPLE STAGES

Stroke/head trauma within 3 mo
Anticoagulation (INR > 1.7 or high PTT)
MI (recent)
Prior intracranial hemorrhage
Low platelets (<100k)
Elevated BP (>185/110)
Surgery in past 14 days
TIA
Age <18
GI or urinary bleeding past 21d.
Elevated or low blood glucose <50, >400)
Seizures at stroke onset
Antihypertensives in setting of hemorrhagic stroke, extreme HTN in ischemic stroke
labetalol
nicardipine
BP necessary to administer tPA
SBP <185, DBP <110
% occlusion for endarterectomy
>60% in symptomatic
>70% in asymptomatic
Etiologies of stroke (5+)
atherosclerosis
craniocervical dissection
emboli (cardiac or aortic)
hypercoaguability
lacunar infarcts

+ "other," including venous sinus thrombosis, sickle cell anemia, vasculitis
Function, decussation, and origin of lateral corticospinal tract
mvmt of contralateral limbs

pyramidal, at cervicomedullary junction

primary motor cortex
Function, decussation, and origin of dorsal column medial lemniscus tract
fine touch, vibration, conscious proprioception

arcuate fibers at the medulla

Pacini's and Meissner's tactile disks, muscle spindles, and Golgi tendon organs
Function, decussation, and origin of spinothalamic tract
pain, temperature

ventral white commissure at spinal cord level

free nerve endings, pain fibers
UMN v. LMN: pattern of weakness
UMN: pyramidal (arm extensors, leg flexors)

LMN: variable
UMN v. LMN: tone
UMN: spastic (increased); initially flaccid (decreased)

LMN: flaccid (decreased)
UMN v. LMN: deep tendon reflexes
UMN: increased (initially decreased or normal)

LMN: decreased
UMN v. LMN: miscellaneous signs
UMN: Babinski, other CNS signs

LMN: atrophy, fasciculations
Hx/PEx of MCA stroke (5)
aphasia if dominant hemisphere
neglect if non-dominant hemisphere
contralateral paresis, sensory loss in face, arm
gaze preference toward lesion
homonymous hemianopia
Hx/PEx of ACA stroke (2)
contralateral paresis, sensory loss in leg
cognitive/personality changes
"Deadly D's" of posterior stroke (4)
1. diplopia
2. dizziness
3. dysphagia
4. dysarthria
Hx/PEx of PCA stroke (3)
homonymous hemianopia
memory deficits
dyslexia/alexia
Hx/PEx of basilar artery stroke (4)
coma, "locked in" syndrome
CN palsies (visual Sx, dysphagia, dysarthria, vertigo)
apnea
"crossed" weakness affecting ipsilateral face and contralateral body
Hx/PEx of lacunar stroke (3)
pure motor or sensory stroke
dysarthria-clumsy hand syndrome
ataxic hemiparesis
Hx/PEx of TIA (2)
neurologic deficit lasting <24h (most last <1h)
determined to be of ischemic etiology
Dx of stroke (5)
emergent head CT w/o contrast
MRI
ECG and echo if embolism is suspected
vascular studies
screening for hypercoagulable states
Tx of acute ischemic stroke (5)
tPA within 3h of Sx onset (r/o contraindications first)
ASA (within 48h)
allow permissive HTN and hypoxemia
treat fever, hyperglycemia
immediate labs (CBC, BMP, cardiac panel, coag panel, lipid panel)
Etiologies of subarachnoid hemorrhage (3)
trauma
berry aneurysms
AVM
Dx of SAH (4)
CT w/o contrast
LP (RBCs, xanthochromia?) if CT negative
4-vessel angiography
neurosurgery consult
Tx of SAH (5)
prevent rebleeding (SBP <150)
prevent vasospasm (5-7d later) with Ca2+ channel blockers)
phenytoin for seizure prophylaxis
decrease ICP (hyperventilate)
treat hydrocephalus through drain/LPs

surgical clipping is definitive for aneurysms
Conditions associated with berry aneurysms that can MAKE SAH more likely (7)
"MAKE SAH"

Marfan syndrome
Aortic coarctation
Kidney disease (e.g. ADPKD)
Ehlers-Danlos syndrome

Sickle cell anemia
Atherosclerosis
History (familial)
Prevention of stroke (4)
ASA, clopidogrel
carotid endarterectomy
anticoagulation
management of medical issues (*HTN*, lipids, DM)
Hx (4)/PEx (2) of intracerebral hemorrhage
sudden onset severe headache
nausea/vomiting
lethargy/obtundation
seizures

presents with focal motor and sensory deficits
deficits worsen as hematoma expands
Subdural hematoma features (2)
typically after head trauma (falls/assaults in elderly/alcoholics)
rupture of bridging veins
Hx/PEx of subdural hematoma (3)
headache
altered mental status
contralateral hemiparesis
subdural hematoma

does it cross the midline?

when to operate?
no

if symptomatic; subdural blood may regress spontaneously if chronic
sites of herniation syndromes (4)
cingulate (under falx)
downward transtentorial
uncal
cerebellar tonsillar
presentation of cingulate (subfalcine) herniation

[secondary to mass lesions of frontal lobes]
no specific S/S, frequently seen on CT
presentation of downward transtentorial herniation (4)

[large supratentorial mass pushes midbrain inferiorly]
rapid mental status change
small, reactive pupils b/l
Cheyne-Stokes respirations
flexor or extensor posturing
presentation of uncal herniation (3)

[secondary to mass lesions of the middle fossa]
fixed, dilated ipsilateral pupil
down/out deviation of eye
ipsilateral hemiparesis ("false localizing," from compression of cerebral peduncle opposite mass lesion against tentorial edge)
presentation of cerebellar tonsillar herniation (3)

[secondary to posterior fossa mass lesions]
tonsillar herniation
medullary compression
respiratory arrest

usually rapidly fatal
Etiology of epidural hematoma

*emergent neurosurgical evacuation*
usually lateral skull fracture leading to middle meningeal artery tear
Hx/PEx of epidural hematoma (4)

*emergent neurosurgical evacuation*
severe trauma leads to immediate loss of consciousness
followed by lucid interval of minutes to hours
uncal herniation, blown pupil
eventually, ipsilateral hemiparesis
red glass test
the eye is not moving where the red image appears to be

the outside image is always the false image
Sturge-Weber associated with:
glaucoma
contralateral hemiparesis (to port wine stain)
seizures
ocular bobbing
seen with pontine damage
most common form of retinal degeneration?
retinitis pigmentosa
MCC acute monocular blindness?
anterior ischemic optic neuropathy

a sudden, painless loss of vision in one eye; permanent
what is "nicking?"
compression of retinal venules by retinal arterioles at the point where they cross

seen in HTN
significance of optic nerve pallor
indicates previous damage, e.g. infarction (in AION) and inflammation of CNII (MS, optic neuritis)
causes of nyctalopia (3)
retinal degeneration, vit A deficiency, color blindness
asymmetric optokinetic nystagmus indicates:
a parietal lesion
What is PRES?

What drugs may cause it?
posterior reversible encephalopathic syndrome; usually with HTN, cortical blindness or scotomas

cyclosporine, tacrolimus
swinging flashlight test?
paradoxical dilation of a pupil when light is swung toward it; when swung back to other eye, original pupil constricts. This is a Marcus Gunn pupil
lateral medullary syndrome (5)
progressive vertigo
ataxia
sensory loss
dysphagia
hiccups
MCC of lateral medullary syndrome?
distal vertebral artery occlusion
ASA: makes tinnitus better or worse?
worse

may also lead to toxic labyrinthitis (with EtOH, quinine, and aminoglycosides)
olfaction: fibers through thalamus?
no
initial hearing loss in Meniere's?
low frequency

high frequency loss later in disease, along with fewer episodes of vertigo
etiologies of transverse myelitis (4)
MS
sarcoid
viral infxn
parasitic infxn
vessels that supply the spinal cord arise from which arteries?
vertebral
hypogastric

also branches directly from aorta
anterior medullary artery eponym, significance
of Adamkiewicz

supplies anterior median spinal artery
spinal cord ischemia: what usual territory?
anterior spinal artery

the posterior spinal artery is more of a plexus of anteries with many anastomoses; therefore posterior columns (vibration, position sense) typically spared in spinal cord ischemia
What headaches typically have diurnal variation?
cluster headaches and those from elevated ICP
Migraines:

males or females more commonly?

onset typically by what age?
females

early 20s
What are common migraine triggers?
certain foods (e.g. red wine)
fasting
stress
menses
OCPs
bright light
disruptions in normal sleep patterns
What is typical lifespan of a migraine headache?

What are associated symptoms?

What typically resolve(s) migraines?
>2 hours, usually <24 hours; almost never >72 hours

nausea, vomiting, photophobia, noise sensitivity

sleep and darkness
Distinguish between classic and common migraines.
classic: unilateral, with auras (scintillating scotomas or visual field cuts)

common: bilateral, periorbital, no auras
What are sequential abortive therapies for migraine?
OTC NSAIDs
triptans
metoclopramide

(consider symptomatic treatment for nausea)
What agents may be used for migraine prophylaxis?
anticonvulsants (gabapentin, topiramate)
TCAs
beta-blockers (propranolol)
CCBs
Cluster headache:

males or females more commonly?

average age of onset?
males

~25
How does a cluster headache present?
brief, unilateral, periorbital headache lasting 30-180 minutes; patient tends to be restless

PERIODICITY, with clusters of attacks at same time of day during certain season of the year

may be associated with ipsilateral lacrimation, conjunctival injection, Horner's syndrome, nasal congestion
What are options for acute therapy of cluster headaches?
100% O2
dihydroergotamine
octreotide
-triptan
What are options for prophylaxis therapy of cluster headaches?
prednisone
ergotamine

verapamil
methysergide
lithium
valproic acid
topiramate
Tension-type headache:

more commonly males or females?

specific diagnostic clues?
females

there are none; it is a Dx of exclusion
How do tension-type headaches commonly present?
tight, bandlike pain NOT associated with sensory phobia, n/v, or auras

typically triggered by fatigue or stress

frontal, occipital, or next regions
What important Dx should be ruled out when considering tension-type headache in a patient >50 years old?
giant cell arteritis (get ESR)
What are treatment options for tension-type headaches?
relaxation
massage
hot baths
avoidance of exacerbating factors
NSAIDs
acetaminophen

(may consider triptans)
What is the usual etiology of cavernous sinus thrombosis?
suppurative process of the orbit, nasal sinuses, or central face that leads to septic thrombosis of the cavernous sinus
What is the most common causative agent in cavernous sinus thrombosis?
S. aureus

(may also be seen with Mucor or Aspergillus)
What symptoms are associated with cavernous sinus thrombosis?
HEADACHE

also: orbital pain, edema, diplopia (secondary to CN III, IV, or VI involvement)

patient may describe a recent Hx of sinusitis or facial infection; ill-appearing and febrile
How is cavernous sinus thrombosis diagnosed?
elevated WBC counts
blood cultures 50% sensitive
MRI w/ gadolinium
Bx may be necessary to ID organism
How is cavernous sinus thrombosis treated?
penicillinase-resistant penicillin (nafcillin, oxacillin) + 3rd/4th gen cephalosporin (ceftriaxone, cefepime)

cover anaerobes (if sinus or dental source bug) with metronidazole

vanco if MRSA involved
What substance is elevated in serum immediately following an epileptic seizure?
prolactin
Define partial seizure.
Arise from a discrete region in one cerebral hemisphere and do not lead to loss of consciousness UNLESS they secondarily generalize
Distinguish between simple partial and complex partial seizures
simple partial: may include motor features, postictal focal deficit possible, but NO alteration of consciousness

complex partial: involves temporal lobe (~80%) with bilateral spread, automatisms, post-ictal confusion, WITH alteration of consciousness
What is the treatment for recurrent partial seizures?
children: phenobarbital

adults: phenytoin, oxcarbazepine, carbamazepine, phenobarbital, valproic acid

consider anterior temporal lobectomy for intractable temporal lobe seizures
What are the hallmarks of tonic-clonic/grand mal seizures?
sudden onset loss of consciousness
tonic extension of back and ext., continuing with 1-2 minutes of symmetric clonic movements
incontinence, tongue biting
+/- cyanosis during ictal period
What is first-line therapy for tonic-clonic/grand mal seizures?
phenytoin

or fosphenytoin, valproate

lamotrigine or topiramate as adjuncts
What is first-line therapy for secondarily generalized tonic-clonic/grand mal seizures?
same as for PARTIAL seizures

(children: phenobarbital

adults: phenytoin, oxcarbazepine, carbamazepine, phenobarbital, valproic acid)
What is the classic EEG finding in absence seizure?
3 per second spike-and-wave discharges
What is first-line treatment for absence seizures?
ethosuximide
What is the management of status epilepticus?
maintain ABCs
give thaimine, glucose, and naloxone (to treat potential etiologies)
IV benzodiazepine plus fosphenytoin

if continued seizure, intubate and load with phenobarbital; consider IV sedative

initiate continuous EEG monitoring
Define West syndrome.
form of generalized epilepsy that typically begins within 6 months of birth; idiopathic or secondary to PKU, perinatal infxn, hypoxic-ischemic injury, tuberous sclerosis
What is the treatment for West syndrome?
ACTH
prednisone
clonazepam or valproic acid
What is the treatment for BPPV?
modified Epley maneuver

antivertigo medications contraindicated as they inhibit central compensation and may lead to unsteadiness and falls