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Flashcards in Vascular Malformations Deck (24):

popcorn MRI

multiple cavernomas. intractable seizures. bright on CT bc of pooling blood. blood product of dif age= characteristic. hyper intensity is methemoglobin. hypo intense ring-hemosiderin on T2. Predisposing gene -CCM1/2/3. most in superficial in cortex ad jot subarachnoid space. can be anywhere


Fischer scale

1) no blood. 2) diffuse blood 3) clot 4) intraventricular or intraparenchymal blood. for SAH.


pupil/CN3 involved severe sudden HA

think PCA aneurysm


SAH management

all admitted to ICU for monitor for signs of respiratory distress of neuro deterioration.


SAH complciations

1) rebleeding 2) vasosplasm 3) hyponatremia 4) cardiac dysfunction 5)hydrocephalus


rebleeding v SAH

rerupture rate of untreated aneurysm is 30%. highest risk is 1st week. 50% of pt with 2nd aneurysm die.


hyponatremia SAH

due to inappropriate secretion of vasopressin- "cerebral salt wasting." occurs btw 3-7d. should not be treated with free water restriction bc that can cause cerebral ischemia. tx with intravenous normal saline, sodium tablets or hypertonic saline


cardiac dysfunc SAH

often dev T wave inversion or ST elevation ~ MI. SHF from myocardial damage due to catecholamine surge. normalizes over 3-4wks.


aneurysm RF

drug use (cocaine, amphetamine, cigarettes, alcohol). fx, HTN, polycystic kidney disease, marina's, ehlers-danlos syndrome, fibromuscular dysplasia.


aneurysm size v rupture rate

10mm-1%. >25mm-6%


fusiform aneurysm

uniform dilation of an entire artery


hydrocephalus v SAH

occur wks to mo post aneurysm rupture due to obstruction of CSF reabsorption within arachnoid granulations and presents with classic triad of gait, apraxia, dementia and urinary incontinence. ventricular shunting is needed. may be acute-obtundation or coma. = need emergent ventricle drainage


vasospasm v SAH

dx by doppler US(show incr flow due to narrowing) or CT angio. prevent with triple H therapy (HTN, hypervolemia, hemodilution)



apear as multiple flow voids


capillary telaniectasia

seen in MS. rarely of clinical sig. formed by network of dialed capillaries. surround brain tissue is normal. most commonly in pons


developmental venous anomalies (DVA)

most common vascular malformation. composed of enlarged collection of veins. rarely bleed. no surgical resection bc can cause venous infarction


kissing carotids

carotids deviate medially in sella. can compress pituitary gland or stalk. relevant in pt who need transphenoidal surgery



elongation and distention of artery due to deterioration of tunica intimate and weakening of vessel wall usually due to HTN. indivi present with cranial N dysfunction. most likely effect basilar- present with multi CN dysfunc due to mass effect.



rare neuroendocrine neoplasm. most are benign. arise from carotid body- painless mass in neck or mass effect on vagus/hypoglossal. surgical removal. rarely secrete hormone


congenital absence of ICA

rare. collateral flow through circle of wills from persistent embryonic vessel or transcranial collateral from external carotid artery.


embryonic cxn btw ICA and vertebrobasilar system

trigeminal, otic and hypoglossal artery. persistence in adult associated with higher rate of vascular malformation like aneurysm and AVM. can dev CN def or trigeminal neuralgia


posterior reversible encephalopathy syndrome (PRES)

rated incr in BP or due to ummunosuppresant use like tacrolimus or cyclosporin. path- disordered cerebral auto regulation of vasculature in posterior regions of brain.
present: visual sx, seizure, HA, altered mental status. reversible with normalization of BP or discontinue med. some left with permanent visual deficit


moyamoya disease

occlusive arteriopathy that affect terminal ICA + proximal ACA and MCA. in asia. look like puff of smoke


vasculitis labs

incr CRP. confirm with mining's biopsy