Flashcards in Vascular Malformations Deck (24):
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
1) no blood. 2) diffuse blood 3) clot 4) intraventricular or intraparenchymal blood. for SAH.
pupil/CN3 involved severe sudden HA
think PCA aneurysm
all admitted to ICU for monitor for signs of respiratory distress of neuro deterioration.
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.
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.
drug use (cocaine, amphetamine, cigarettes, alcohol). fx, HTN, polycystic kidney disease, marina's, ehlers-danlos syndrome, fibromuscular dysplasia.
aneurysm size v rupture rate
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
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
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
occlusive arteriopathy that affect terminal ICA + proximal ACA and MCA. in asia. look like puff of smoke