- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
![]()
PLAY BUTTON
![]()
PLAY BUTTON
![]()
61 Cards in this Set
- Front
- Back
|
How long does a benign febrile seizure last?
|
15 minutes or less
No focal features usually |
|
How likley is a person with a single benign febrile seizure likely to have a second benign febrile seizure?
|
two thirds have only a single seizure, fewer than 1/10 have more than 3
seizure in first hour of of fever in children less than 18 months or family history of febrile seizure 90% occur within 2 years of initial episode |
|
What are seizures in AIDS most commonly associated with. 2 other common diagnoses?
|
AIDS dementia complex
toxoplasmosis, cryptococcal meningitis |
|
What is toxicity associated with bromide compounds used in porphyria seizure treatment?
|
rash, GI symptoms, psychiatric disturbances, impaired consciousness
|
|
What are drug overdoses most commonly associated with seizure?
|
antidepressants, antipsychotics, cocaine, insulin, isoniazid, lidocaine, methylxanthines
|
|
Which chemotherapeutics are most commonly associated with seizures?
|
etoposide, ifosfamide, cisplatinum
|
|
Which neurons are especially vulnerable to hyperthermia? What sort of neurologic syndome are patients who have undergone significant hyperthermic injury prone to?
|
Cerebellar neurons
Ataxia |
|
How long do seizures have to continue for a person to be in status?
|
>30 minutes
Also if full consciousness is not restored between successive episodes |
|
What is the characteristic pattern on EEG for absence seizures?
|
3 Hertz spike and wave pattern
|
|
What are genetic syndromes in which myclonic seizures occur?
|
Unverricht, Lundborg disease
Lafora body disease neuronal ceroid lipofuscinosis sialidosis Mitochondrial encephalopmyopathy |
|
In what setting do atonic seizures typically occur?
|
developmental disroders especially Lennox Gastaut
|
|
What are myoclonic seizures typically treated with?
|
Valproic acid or clonazepam
|
|
Which AEDs should be avoided in genearlized seizures?
|
gabapentin, tiagabine
|
|
How should a person be changed from one AED to another
|
Discontinue first drug gradually once therapeutic levels of second drug are achieved
|
|
Who is eligable for a trial off of AEDs?
|
seizure free for 25 years on meds
|
|
At what neutrophil count should carbamazepine be discontinued?
|
1500 or lower
|
|
Treatment of status?
|
Ativan at .1mg/kg not greater than 2 mg/min or diazepam 10 mg IV over 2 min, diastat .2 mg/kg
fosphenytoin 1g-1.5 g IV at 150 mg/min or phenytoin 1g-1.5g at rate not greater than 50 mg/min Another 10 mg/kg of fospheny or pheny can be given Phenobarbital 1g - 1.5 g at 50mg/min General anesthesia |
|
What proportion of patients with TIA will go on to have stroke in 5 years?
|
1/3
|
|
What is ischemic brain injury which lasts longer than 24 hours but resolves completely or almost completely within a few days called?
|
RIND - reversible ischemci neurological deficit
|
|
What are the major branches from the posterior cerebral artery?
|
thalamoperforate, thalamogeniculate
|
|
Diagnosis of primary angiitis or granulomatous angiitis?
|
angiography showing focal or segmental narrowing of small arteries and veins
Meningeal biopsy is diagnostic |
|
How is primary angiitis treated?
|
corticosteroids alone or with cyclophosphamide
|
|
When after primary infection does syphilitic arteritis occur?
Which sized vessels are typically involved? |
within 5 years after primary infection
Medium sized penetrating vessels |
|
What vessels, areas are typically involved by fibromuscular dysplasia?
|
Extracranial more than intracranial, cervical portion of IC is more involved than vertebral artery
Bilateral lesions often |
|
Treatment of carotid or vertebral artery dissection?
|
Controversial
No treatment, removal of intramural hematoma, measures to prevent embolization from site of dissection (aspirin, anticoagulants, occlusion of vessel distal to dissection |
|
When does recurrant dissection occur relative to initial episode when it does occur?
|
Within 1 month of initial event
|
|
What are the distinguishing features of moya moya?
|
bilateral narrowing or occlusion of the distal internal carotid arteries and adjacent anterior and middle cerebral artery trunks
presence of fine network of collateral channels at base of brain |
|
Demographic amongst whom moya moya is most common?
|
Japanese girls
Sometimes inherited AR |
|
Disease associations for moya moya?
|
atherosclerosis
sickle cell disease history of basilar meningitis |
|
How to people with moya moya present?
|
children - ischemic strokes
adults - intracerebral, subdural, subarachnoid hemorrhage |
|
What is most common cause of stroke in cancer patients?
|
Marantic endocarditis
|
|
Which cancers are most commonly associated with marantic endocarditis?
|
Lung, GI
|
|
What platelet counts predispose to thrombosis?
|
> 1500
|
|
At what hematocrits can polycythemia cause stroke?
|
hematocrit over 46%
Further increases in risk with hematocrits over 50% and over 60% |
|
What is the most frequent neurologic complication of sickle cell disease?
|
stroke affecting intracranial IC, proximal middle or anterior cerebral artery
|
|
What intervention must be done in sickle cell disease requiring angiography?
|
Reduce hemoglobin S by exchange transfusion to less than 20% - contrast induces sickling
|
|
What levels of leukocytosis produce stroke?
|
>150
|
|
What is the most common cause of death in cerebral infarct within the first week?
|
Cerebral edema causing herniation of ipsilateral cingulate gyrus across dural falx and tehn downward displacement of brain along tentoria incisure
|
|
What areas are affected by superior middle cerebral artery stroke?
|
motor and sensory areas supplying face, arm, hand, Broca's area
|
|
What areas are affected by inferior middle cerebral artery stroke?
Clinical syndrome produced by stroke? |
loss of visual radiations, loss of visual cortex responsible for macular vision, receptive language area (Wernicke's area)
homonymous hemianopia denser inferiorly, marked impairment of cortical sensory functions - graphesthesia, sterognosis and disorders of spacial thought, anosagnosia, neglect, dressing apraxia, constructional apraxia If dominant hemisphere, Wernicke's aphasia |
|
What ares are supplied by the lenticulostriate arteries?
|
basal ganglia, motor fibers related to face, hand, arm, leg as they descend in genu and posterior limb of internal capsule.
|
|
How does clinical syndrome produced by occlusion of the trifurcation/bifurcation of MCA differ from that produced by occlusion of the stem of the MCA?
|
motor/sensory fibers of the leg are affected as well in the IC and so contralateral hemiplegia nd sensory loss
|
|
What areas does the PCA supply?
|
occipital cerebral cortex, medial temporal lobes, thalamus, rostral midbrain
|
|
Clinical syndrome of posterior cerebral artery occlusion?
|
hmonymous hemianopia of contralateral visual field, sometimes sparing of macular vision
Vision defects may be denser superioroly (in contrast to MCA lesions) Ocular abnormalities - vertical gaze palsy, oculomotor nerve palsy, INO, vertical skew deviation of eyes anomic aphasia, alexia without agraphia, visual agnosia |
|
Clinical syndrome produced by bilateral psoterior cerebral artery infarction?
|
cortical blindness, memory impairement, inability to recognize familiar faces, other exotic visual and behavioral syndromes
|
|
Infarct causing locked-in syndrome?
|
ventral portion of pons (basis pontis) is infarcted and tegmentum is spared.
|
|
Syndrom produced by embolism to the tip of the basilar artery?
|
unilateral or bilateral oculomotor nerve palsies, hemiplegia or quardiplegia with decerebrate or decorticate posturing from involvement of cerebral peduncles in midbrain, impairment in consciousness
may be confused with uncal herniation syndrome |
|
Wallenberg syndrome?
|
Ipsilateral cerebellar ataxia, Horner syndrome, facial sensory deficit
Contralateral impaired pain and temperature nystagmus, vertigo, nausea, vomiting, dysphagia, dysarthria, hiccup |
|
Anterior inferior cerebellar artery occlusion syndrome?
|
Ipsilateral facial weakness, gaze palsy, deafness, tinnitus
|
|
Superior cerebellar artery occlusion syndrome?
|
Impaierd optokinetic nystagmus or skew deviation of eeys
contralateral sensory disturbance involving touch, vibration, position sense, pain and temperature |
|
What are the structures supplied by the long penetrating paramedian arteries?
|
Medial cerebral peduncle, sensory pathways, rednucleus, reticular formation, midline cranial nerve nuclei (III, IV, VI, XII)
|
|
Lacunar infarct syndromes?
|
Pure motor
Pure sensory Clumsy hand dysarthria - dysarthria facial weakness, mild weakness and clumsiness of hand on side of facial involvment (contralateral IC or pons) Ataxic hemiparesis - hemiparesis and ataxia usually of the leg. |
|
What should be done for ppx for further stroke when stroke on aspirin?
|
Raise dose, add plavix or other antiplatelet, or 3 month course of warfarin
Maintain INR in 3-4 range |
|
Which levels of the spinal cord are most vulnerable to drops in perfusion pressure?
|
upper and lower levels of thoracic cord
|
|
Pupils in thalamic compression?
|
slightly smaller - maybe from sympathetic pathway interruption
|
|
What do pinpoint pupils indicate?
|
Focal damage at pontine level, opioid overdose
less likely - organophosphate toxociity, miotic eye drops, neurosyphilis |
|
What sort of limb movements are never associated with posturing or reflex?
|
limb abduction
|
|
Describe decorticate response to pain
|
flexion of arm at elbow, adduction at shoulder, extension of leg and ankle
|
|
Describe decerebrate response to pain
|
extension at elbow, internal rotation at sholder and forearm, leg extension
|
|
What metabolic disturbances also impair pupil reactivity?
|
massive barbiturate overdose with apnea, hypotension
acute anaoxia hypothermia anticholinergic poisoning opioid overdose |
|
How long can hypoglycemic coma be tolerated with expectation for significant recovery?
|
60-90 minutes
|