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98 Cards in this Set
- Front
- Back
Facial (VII) nerve LMN lesion
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Bell's palsy: paralysis of ipsilateral upper and lower face
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DDx of Bell's palsy
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ALexander Bell with STD:
1. AIDS 2. Lyme 3. Sarcoid 4. Tumors 5. Diabetes |
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Facial (VII) nerve UMN lesion
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Paralysis of contralateral lower face only
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MCA territory stroke symptoms
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Aphasia if dominent hemisphere
Neglect if nondominant Contralateral paresis and sensory loss in face and arm Gaze preference toward side of lesion Homonymous hemianopia |
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ACA territory stroke symptoms
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Contralateral paresis and sensory loss in leg
Cognitive or personality changes |
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PCA territory stroke symptoms
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Homonymous hemianopia
Memory deficits Dyslexia/alexia |
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Basilar artery territory stroke symptoms
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Coma, "locked in syndrome"
CN palsies (vision, dysphagia, dysarthria, vertigo) Ipsilateral face/contralateral body sensory loss, weakness Apnea |
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Lacunar infarct symptoms
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Pure motor or sensory
Dysarthria Ataxic Hemiparesis |
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Contraindications to tPA therapy
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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 |
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Antihypertensives in setting of hemorrhagic stroke, extreme HTN in ischemic stroke
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labetalol
nicardipine |
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BP necessary to administer tPA
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SBP <185, DBP <110
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% occlusion for endarterectomy
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>60% in symptomatic
>70% in asymptomatic |
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Etiologies of stroke (5+)
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atherosclerosis
craniocervical dissection emboli (cardiac or aortic) hypercoaguability lacunar infarcts + "other," including venous sinus thrombosis, sickle cell anemia, vasculitis |
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Function, decussation, and origin of lateral corticospinal tract
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mvmt of contralateral limbs
pyramidal, at cervicomedullary junction primary motor cortex |
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Function, decussation, and origin of dorsal column medial lemniscus tract
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fine touch, vibration, conscious proprioception
arcuate fibers at the medulla Pacini's and Meissner's tactile disks, muscle spindles, and Golgi tendon organs |
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Function, decussation, and origin of spinothalamic tract
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pain, temperature
ventral white commissure at spinal cord level free nerve endings, pain fibers |
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UMN v. LMN: pattern of weakness
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UMN: pyramidal (arm extensors, leg flexors)
LMN: variable |
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UMN v. LMN: tone
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UMN: spastic (increased); initially flaccid (decreased)
LMN: flaccid (decreased) |
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UMN v. LMN: deep tendon reflexes
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UMN: increased (initially decreased or normal)
LMN: decreased |
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UMN v. LMN: miscellaneous signs
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UMN: Babinski, other CNS signs
LMN: atrophy, fasciculations |
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Hx/PEx of MCA stroke (5)
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aphasia if dominant hemisphere
neglect if non-dominant hemisphere contralateral paresis, sensory loss in face, arm gaze preference toward lesion homonymous hemianopia |
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Hx/PEx of ACA stroke (2)
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contralateral paresis, sensory loss in leg
cognitive/personality changes |
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"Deadly D's" of posterior stroke (4)
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1. diplopia
2. dizziness 3. dysphagia 4. dysarthria |
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Hx/PEx of PCA stroke (3)
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homonymous hemianopia
memory deficits dyslexia/alexia |
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Hx/PEx of basilar artery stroke (4)
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coma, "locked in" syndrome
CN palsies (visual Sx, dysphagia, dysarthria, vertigo) apnea "crossed" weakness affecting ipsilateral face and contralateral body |
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Hx/PEx of lacunar stroke (3)
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pure motor or sensory stroke
dysarthria-clumsy hand syndrome ataxic hemiparesis |
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Hx/PEx of TIA (2)
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neurologic deficit lasting <24h (most last <1h)
determined to be of ischemic etiology |
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Dx of stroke (5)
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emergent head CT w/o contrast
MRI ECG and echo if embolism is suspected vascular studies screening for hypercoagulable states |
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Tx of acute ischemic stroke (5)
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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) |
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Etiologies of subarachnoid hemorrhage (3)
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trauma
berry aneurysms AVM |
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Dx of SAH (4)
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CT w/o contrast
LP (RBCs, xanthochromia?) if CT negative 4-vessel angiography neurosurgery consult |
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Tx of SAH (5)
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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 |
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Conditions associated with berry aneurysms that can MAKE SAH more likely (7)
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"MAKE SAH"
Marfan syndrome Aortic coarctation Kidney disease (e.g. ADPKD) Ehlers-Danlos syndrome Sickle cell anemia Atherosclerosis History (familial) |
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Prevention of stroke (4)
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ASA, clopidogrel
carotid endarterectomy anticoagulation management of medical issues (*HTN*, lipids, DM) |
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Hx (4)/PEx (2) of intracerebral hemorrhage
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sudden onset severe headache
nausea/vomiting lethargy/obtundation seizures presents with focal motor and sensory deficits deficits worsen as hematoma expands |
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Subdural hematoma features (2)
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typically after head trauma (falls/assaults in elderly/alcoholics)
rupture of bridging veins |
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Hx/PEx of subdural hematoma (3)
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headache
altered mental status contralateral hemiparesis |
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subdural hematoma
does it cross the midline? when to operate? |
no
if symptomatic; subdural blood may regress spontaneously if chronic |
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sites of herniation syndromes (4)
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cingulate (under falx)
downward transtentorial uncal cerebellar tonsillar |
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presentation of cingulate (subfalcine) herniation
[secondary to mass lesions of frontal lobes] |
no specific S/S, frequently seen on CT
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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 |
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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) |
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presentation of cerebellar tonsillar herniation (3)
[secondary to posterior fossa mass lesions] |
tonsillar herniation
medullary compression respiratory arrest usually rapidly fatal |
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Etiology of epidural hematoma
*emergent neurosurgical evacuation* |
usually lateral skull fracture leading to middle meningeal artery tear
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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 |
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red glass test
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the eye is not moving where the red image appears to be
the outside image is always the false image |
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Sturge-Weber associated with:
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glaucoma
contralateral hemiparesis (to port wine stain) seizures |
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ocular bobbing
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seen with pontine damage
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most common form of retinal degeneration?
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retinitis pigmentosa
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MCC acute monocular blindness?
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anterior ischemic optic neuropathy
a sudden, painless loss of vision in one eye; permanent |
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what is "nicking?"
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compression of retinal venules by retinal arterioles at the point where they cross
seen in HTN |
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significance of optic nerve pallor
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indicates previous damage, e.g. infarction (in AION) and inflammation of CNII (MS, optic neuritis)
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causes of nyctalopia (3)
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retinal degeneration, vit A deficiency, color blindness
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asymmetric optokinetic nystagmus indicates:
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a parietal lesion
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What is PRES?
What drugs may cause it? |
posterior reversible encephalopathic syndrome; usually with HTN, cortical blindness or scotomas
cyclosporine, tacrolimus |
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swinging flashlight test?
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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
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lateral medullary syndrome (5)
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progressive vertigo
ataxia sensory loss dysphagia hiccups |
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MCC of lateral medullary syndrome?
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distal vertebral artery occlusion
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ASA: makes tinnitus better or worse?
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worse
may also lead to toxic labyrinthitis (with EtOH, quinine, and aminoglycosides) |
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olfaction: fibers through thalamus?
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no
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initial hearing loss in Meniere's?
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low frequency
high frequency loss later in disease, along with fewer episodes of vertigo |
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etiologies of transverse myelitis (4)
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MS
sarcoid viral infxn parasitic infxn |
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vessels that supply the spinal cord arise from which arteries?
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vertebral
hypogastric also branches directly from aorta |
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anterior medullary artery eponym, significance
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of Adamkiewicz
supplies anterior median spinal artery |
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spinal cord ischemia: what usual territory?
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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 |
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What headaches typically have diurnal variation?
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cluster headaches and those from elevated ICP
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Migraines:
males or females more commonly? onset typically by what age? |
females
early 20s |
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What are common migraine triggers?
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certain foods (e.g. red wine)
fasting stress menses OCPs bright light disruptions in normal sleep patterns |
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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 |
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Distinguish between classic and common migraines.
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classic: unilateral, with auras (scintillating scotomas or visual field cuts)
common: bilateral, periorbital, no auras |
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What are sequential abortive therapies for migraine?
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OTC NSAIDs
triptans metoclopramide (consider symptomatic treatment for nausea) |
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What agents may be used for migraine prophylaxis?
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anticonvulsants (gabapentin, topiramate)
TCAs beta-blockers (propranolol) CCBs |
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Cluster headache:
males or females more commonly? average age of onset? |
males
~25 |
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How does a cluster headache present?
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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 |
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What are options for acute therapy of cluster headaches?
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100% O2
dihydroergotamine octreotide -triptan |
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What are options for prophylaxis therapy of cluster headaches?
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prednisone
ergotamine verapamil methysergide lithium valproic acid topiramate |
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Tension-type headache:
more commonly males or females? specific diagnostic clues? |
females
there are none; it is a Dx of exclusion |
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How do tension-type headaches commonly present?
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tight, bandlike pain NOT associated with sensory phobia, n/v, or auras
typically triggered by fatigue or stress frontal, occipital, or next regions |
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What important Dx should be ruled out when considering tension-type headache in a patient >50 years old?
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giant cell arteritis (get ESR)
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What are treatment options for tension-type headaches?
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relaxation
massage hot baths avoidance of exacerbating factors NSAIDs acetaminophen (may consider triptans) |
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What is the usual etiology of cavernous sinus thrombosis?
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suppurative process of the orbit, nasal sinuses, or central face that leads to septic thrombosis of the cavernous sinus
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What is the most common causative agent in cavernous sinus thrombosis?
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S. aureus
(may also be seen with Mucor or Aspergillus) |
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What symptoms are associated with cavernous sinus thrombosis?
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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 |
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How is cavernous sinus thrombosis diagnosed?
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elevated WBC counts
blood cultures 50% sensitive MRI w/ gadolinium Bx may be necessary to ID organism |
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How is cavernous sinus thrombosis treated?
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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 |
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What substance is elevated in serum immediately following an epileptic seizure?
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prolactin
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Define partial seizure.
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Arise from a discrete region in one cerebral hemisphere and do not lead to loss of consciousness UNLESS they secondarily generalize
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Distinguish between simple partial and complex partial seizures
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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 |
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What is the treatment for recurrent partial seizures?
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children: phenobarbital
adults: phenytoin, oxcarbazepine, carbamazepine, phenobarbital, valproic acid consider anterior temporal lobectomy for intractable temporal lobe seizures |
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What are the hallmarks of tonic-clonic/grand mal seizures?
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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 |
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What is first-line therapy for tonic-clonic/grand mal seizures?
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phenytoin
or fosphenytoin, valproate lamotrigine or topiramate as adjuncts |
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What is first-line therapy for secondarily generalized tonic-clonic/grand mal seizures?
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same as for PARTIAL seizures
(children: phenobarbital adults: phenytoin, oxcarbazepine, carbamazepine, phenobarbital, valproic acid) |
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What is the classic EEG finding in absence seizure?
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3 per second spike-and-wave discharges
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What is first-line treatment for absence seizures?
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ethosuximide
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What is the management of status epilepticus?
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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 |
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Define West syndrome.
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form of generalized epilepsy that typically begins within 6 months of birth; idiopathic or secondary to PKU, perinatal infxn, hypoxic-ischemic injury, tuberous sclerosis
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What is the treatment for West syndrome?
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ACTH
prednisone clonazepam or valproic acid |
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What is the treatment for BPPV?
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modified Epley maneuver
antivertigo medications contraindicated as they inhibit central compensation and may lead to unsteadiness and falls |