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14 Cards in this Set

  • Front
  • Back
etiology for supratentorial hemispheric parenchymal bleed
ruptured aneurysm
vascular malformation
cortical/dural venous thrombosis
amyloid
pathophys of amyloid angiopathy
amyloid deposits in media and intima of small arteries and arterioles or cortex/meninges
there is fibrinoid degeneration and microaneurysmal dilatation --> ruptured BV
pathologically how is amyloid angiopathy dx'd
stains red with congo red, wiht apple green birefringence under polarized light
describe pathogenesis of hemorrhagic transformation of infarct
altered BBB predisposes and then either pt had lysis, developed collateral flow, or there was correction of hypotension --> bleed
appearance of hemorrhagic transformation of infarct
cortical gray matter is almost always involved, +/- white matter involvement
appearance of WM if it is involved in a hemorrhagic transformation of infarct
WM is hypodense to nml WM on CT and is hetero in appearance (this + bleed being in a vascular distribution helps to distinguish it from lobar hemorrhage)
pathogenesis of dolichoectasia and fusiform aneurysm
they develop from ATH affecting media (as opposed to nml ATH dz, which affects the intima).
damage to the media --> arterial stretching, elongation extending over a long segment
do fusiform aneurysms rupture
rarely, but they do cause sx 2/2 mass effect --> hemiparesis, impaired eye mov't or other cranial neuoropathy
definition of a giant intracranial aneurysm
>25mm
BV most comonly involved in giant intracranial aneurysm
40-60% inovlve th ecavernous internal carotid artery
complications assoc with giant intracranial aneurysm
high risk o fhemorrhage, cerebral compression and thromboembolic events
classic appearance of partially thrombosed giant intracranial aneurysm
target appearance on CECT
appearance of giant intracranial aneurysm when not thrombosed
hyperdense on NECT and have marked enhancement
appearance of giant intracranial aneurysm on MR
variable