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74 Cards in this Set

  • Front
  • Back
does gray or white matter receive more blood flow
gray matter (3-4x greater)
2 types of cerebral edema
vasogenic edema (white matter is exclusively involved); usually from a mass

cytotoxic - involves gray matter and GWJ, usually seen in CVA
describe what happens at a cellular level during acute ischemia
Na-K pump stops working, influx of sodium, efflux of K. Water follows NA and cytotoxic edema results
timing of insular ribbon sign
situation where this is seen
within 6 hrs after infarct
MCA occlusion
what is the lentiform nucleus edema sign
early edema in putamen seen in proximal MCA occlusions
what is the time-frame of T2 hyperintensity in infarct
6-12 hrs
what CT findings (other than hemorrhage) are contraindications to TPA
extensive edema on initial CT (may be associated with increased risk of hemorrhage)
edema affecting >1/3 MCA territory
masses
what does encephalomalacia mean
"brain softening"
pathophys of hemorrhagic transformation of infarction
reperfusion into infarcted capillary beds can lead to microscopic or gross hemorrhage
why are pts often asx if they have had a hemorrhagic transformation of infarct
b/c usually the hemorrhage is in an area of brain that is already dead or dysfxnal
how to differentiate primary vs secondary hemorrhage
hemorrhagic infarction is confined to involved vascular territory
primary hemorrhage does not usually respect vascular boundaries
intraventricular hemorrhage is uncommon in hemorrhagic transformation
petechial gyral pattern is only seen in secondary hemorrhage
time-frame of hemorrhagic transformation of acute infarct
1-2 wks
how does hemorrhagic transformation of acute infarct usually look

CT
MR
serpiginous line of petechial blood that follows gyral contours of infarcted cortex

on CT: linear hyperattenuating area
MR: bright signal along affected gyrus on TI 2/2 methemoglobin
what % of stenosis has shown to benefit from CEA
70% or greater
in ischemic infarct, what is the first sign of infarct, and how soon can it be seen
restricted diffusion
within minutes
when is maximal intracranial swelling seen after infarct
3-7 days
sx of a vertebrobasilar stroke
syncope
ataxia
CN dysfxn
homonymous visual field defects
facial droop
occlusion of what BV --> amaurosis fugax
ophthalmic branch of ICA
main branches of ACA
medial lenticulostriate
pericallosal
hemispheric
what territory does the medial lenticulostriate artery serve
rostral portions of BG
(ant/inf internal capsule,
putamen,
GP,
caudate head,
portions of hypothal,
optic chiasm
what is the largest branch of medial lenticulostriate branches

what does it serve
recurrent artery of Heubner
serves caudate head and anterior internal capsule region
sx if there is infarction of medial lenticulostriate territory
motor aphasia
facial weakness
disturbances of mood and judgement
what arteries are the hemispheric branches of the ACA
oribtofrontal and frontopolar arteries
termination of ACA
collasomarginal (upper)
pericallosal (lower)

this bifurcation occurs just distal to takeoff of the orbitofrontal and frontopolar arteries
sx if unilateral damage to ACA hemispheric branches

if b/l?
leg weakness on opposite side of
body
incontinence, akinetic mutism
main branches of MCA
lateral lenticulostriate branches
hemispheric branches
pathophys of insular ribbon sign
when prox MCA is occluded, the insular region is the furthest away from any potential collateral supply
what do the lateral lenticulostriate branches serve
putamen
lateral GP
superior half of internal capsule and adjacent corona radiata
majorityof caudate
posteriori hemispheric branches of MCA
posterior parietal artery (supplies parietal lobe post to sensory strip)
angular artery (post-latl parietal and lateral occipital lobes)
posterior temporal artery (majority of temporal lobE)
occlusion of what --> broca's aphasia
anterior MCA branches of dominant hemisphere
occlusion of what --> wernicke's aphasia
posterior branches of MCA in dominant hemisphere
occlusion of what --> contralateral homonymous field defects
posterior temporal branch of MCA
what gyrus is involved --> weakness of face, arm, leg
contralateral precentral gyrus
occlusion of what --> global aphasia
total MCA infarct on dominant side
where does the vertebral artery arise from
subclavian artery
at what level of the brain does the basilar artery bifurcate
midbrain
major branches of the PC A
midbrain and thalamic perforating vessels
posterior choroidal arteries
cortical branches to medial temporal and occipital lobes
sx oifi there is infarction of midbrain
loss of pupoillary light response (damage to quadrigeminal plate)
impaired upgaze (damage to CN III)
somnolence (damage to reticular activating formation)
sx in thalamic infarction
contralateral sensory loss
what do the posterior choroidal arteries serve
choroid plexus
pineal gland
regions contiguous with 3rd vent
what do the PCA cortical branches supply
inferomedial temp lobe (via the inferior temp artery)
superior occipitalgyrus (par-occ artery)
visual cortex and occipital lobe (via calcarine artery)
fetal origin of PCA
20% of pts 'have 1 or both of the prox PCA segments that are hypoplastic or absent
flow instead comes from ICA via a prominent PCOM
why does fetal origin of PCA exist
embryologically, PCA develops with the ICA
t or f: cbl hemorrhage with any significant mass effect is a surgical emergency
true --> requires post fossa decompression
what are the branches of BV to cbl from bottom to top
PICA
AICA
Sup Cbl art
what does PICA arise from
vertebral arteries
superior cbl artery territory
superior vermis
middle and superior cbl peduncles
"roof" of cbl
AICA territory
ant-med cbl
occassionally part of the middle cbl peduncle
PICA territory
dorsolat medulla
inf vermis
posteriolat cbl hemispheres
which cbl branch is most commonly infarcted
PICA
triggering events for border zone infarct
cardiac arrest
shock
when is unilateral border zone infarct seen
when carotid occlusion is unmasked by global hypotension
clinical findings of border zone infarct
weakness isolated to upper arms
cortical blindness
memory loss
most common location for venous infarction
transverse , superior sag sinus, and cavernous sinus
what are the blood breakdown products
oxyHb
deoxyHb
metHb (intra-, then extracellular)
hemosiderin
under nml conditions, what state is HB in
oxygb and deoxyhb
(O2 is extracted from oxy-Hb converting it to deoxy-Hb)
what do oxy and deoxy Hb look like on T2
oxyHb - bright (Fe2+ but in a diamagnetic state)
deoxy-Hb - dark (Fe2+ but in a paramagnetic state)
classic presentation of PCOM aneurysm

ICA/parasellar aneurysm

Bitemporal field defect
u/l 3rd nerve palsy
cavernous sinus syndrome
ACA aneurysm
pathophys of congenital cerebral aneurysm
congenital absence of arterial media
size of aneurysm that has increased risk of rupture
3-5 mm
most commmon location for aneurysm
ACOM >
MCA >
PCOM >
Basilar
what should be considered if a distal branch aneurysm is seen
mycotic aneurysm
4 main types of vascular malformations
AVM
cavernous malformation
telangiectasia
venous malf
most comon type of vasc malf

how do they present
AVM (arteries and veins connected to each other without intervening capillaries)

sz, hemorrhage
complications of cerebral AVM
10% will develop assoc aneurysm
2% annual risk of bleeding
histology of cavernous malf
thin walled sinusoidal vessel (neither artery nor vein)
presentation of cavernous malf
sz or small parenchymal hemorrhage
dva
congenitally anamolous vein that drains nml brain
appearance of dva
enlarged enhancing stellate venous complex that extends to ventricular or cortical surface
managment of dva
unclear- they are often the only venous drainage for an area of brain
pts usually asx
telangiectasia
capillary sized vessel, usually small and solitary
how does amyloid angiopathy often present
frequently have lobar hemorrhage
can present with progressive senile dementia in 30% pts
appearance of amyloid angiopathy
amyloid deposits in media and adventitia of medium and small BV
when to think of amyloid angiopathy
elderly, demented pt with new or recurrent superficial hemorrhage