Stroke Flashcards
goal of stroke imaging
who benefits from therapy
hemorrhage precludes tPA
goal of stroke therapy
restore perfusion
AHA guidelines for stroke therapy
IV tPA within 3 hours of stroke onset
goal of perfusion imaging
characterize ischemic penumbra
perhaps predict area of vulnerable brain vs infarct core
insular ribbon sign
loss of gray-white differentiation
hyperdense artery sign
visualization of acute IV thrombus, typically in MCA
stroke MRI
restricted diffusion > mass effect/T2 and FLAIR hyperintensity > white matter changes > gyral enhancement/resolution of mass effect»_space; encephalomalacia
reason for restricted diffusion
shift from extracellular to intracellular water due to NA/K ATPase pump failure
increase viscosity of infarcted brain
AVM
congenital high flow vascular malformation
typically with seizures and bleeding
Spetzler Martin scale
evaluate AVM for surgical resection
AVM imaging characteristic
vascular nidus with multiple flow voids; adjacent gliosis, dystrophic calcifications and blood products (blooming)
vein of galen malformation
vascular malformation characterized by AV fistula from thalamoperforator branches
most common cause of extracardiac high output cardiac failure in kids
may cause parinaud in adults
dAVF
complex high flow lesions due to AV shunts between meningeal arterioles and dural venules
cognard classification
describes lesions with progressively increased risk of bleeding for dAVF
presence of cortical venous drainage and risk of hemorrhage
type V cognard classification
spinal dAVF; may cause myelopathy
carotid cavernous fistula
CCF; type of dAVF caused by trauma between cavernous carotid artery and cavernous sinus
enlargment of superior orbital vein and shunting within cavernous sinus; proptosis and CN palsy
low flow lesions
cavernous malformation/cavernoma; developmental venous anomaly; capillary telangiectasia
caput medusa morphology
developmental venous anomaly ; radially oriented vein
cavernoma
vascular hamartoma; small but definite bleed risk
can cause seizures
can be induced by radiation treatment
familial cavernomatosis
multiple cavernous malformations
cavernoma imaging manifestations
CT: hyperattenuating lesion (microcalcification within cavernoma)
MRI: popcorn like lobular mixed signal due to blood products of varying age; peripheral rim of hemosiderin (GREdark); no enhancement
CTA: occult
developmental venous anomaly/venous angioma
abnormal vein that provides functional venous drainage to normal brain
DO NOT TOUCH lesion; can cause venous infarct
capillary telangectasia
asymptomatic vascular lesion composed of dilated capillaries interspersed with normal brain
DO NOT TOUCH lesion
capillary telangectasia imaging
MRI: brush stroke like enhancing lesion in brainstem/pons; no mass effect or edema
GRE blooming
CTA/MRA: occult
SAH
commonly from trauma then aneurysm
thunderclap headache/meningismus
subarachnoid space hyperattenuation DDX
SAH, meningitis, leptomeningeal carcinomatosis, prior intrathecal contrast administration
also DDX increased FLAIR in subarachnoid space + recent oxygen/propofol administration
SAH work-up
noncontrast CT; lumbar puncture for xanthochromia if suspicion high despite negative CT
SAH locations/aneurysms
anterior interhemispheric fissure: ACA
suprasellar cistern: Pcomm
sylvian fissure: MCA
perimesencephalic cistern: basilar tip aneurysm or nonaneurysmal perimesencephalic SAH
grading scales for SAH
Hunt and Hess (clinical; no imaging/headaches)
Fisher: thickness of SAH
compliciations of SAH
vasospasm (peak 7 days after ictus)
acute hydrocephalus due to arachnoid granulations»_space; vetriculostomy
supericial siderosis: iron overload of pial membranes to to repeat bleeds; sensorineural deafness/ataxia
perimesencephalic SAH
nonaneurysmal SAH; occult venous bleeding
sandard care is to perform catheter angiography 2x, 1 week apart
mild to moderate vasospasm, better prognosis
reversible cerebral vasoconstriction syndrome
nontraumatic nonaneurysmal SAH and ischemia
thunderclap headache; prolonged but reversible vasoconstriction
saccular aneurysm
focal outpouching of arterial wall; typically at branch points; neck:body ratio affects treatment
sizes: small <1 cm, medium <2.5; giant >2.5 cm
may be caused by Takayasu/giant cell arteritis, HTN, marfan, ehlers-danlos, PCKD, NF1 (connective tissue diseases)
fusiform aneurysm
segmental arterial dilation without neck; due to atherosclerosis
do not occur at branch points
mycotic/infectious aneurysm
septic emboli; form in distal arterial circulation beyond circle of Willis
fragile; high risk of rupture
oncotic aneurysm
aneurysm caused by neoplasm
benign left atrial myxoma may peripherally embolize and cause distal oncotic aneurysm
traumatic pseudoaneurysm
do not contain all 3 layers of vessel wall; abnormal luminal narrowing proximal
occur distally
arteries close to bony structures (basilar/vertebral) prone to dissecting
dural sinuses
superior sagittal sinus > torcular herophili/confluence of sinuses
transverse sinus (left is usually hypoplastic)
sigmoid sinus < jugular bulb
deep cerebral veins
internal cerebral veins, basal vein of rosenthal, vein of galen
venous angle: septal/thalamostriate vein intersection (foramen of Monro)
superficial cerebral veins
vein of Trolard (superficial cortical to SSS)
vein of Labbe(drains temporal convexity to transvers/sigmoid sinus)
risk factors for venous thrombosis
pregnancy, OCP, thrombophilia, malignancy, infection
more common cause of stroke in younger patients
cortical vein thrombosis/deep venous sinus thrombosis
empty delta sign, cord sign, findings on MR venogram
cord sign: increased density in thrombosed sinus/cortical vein
empty delta sign: filling defect in SSS
MR venogram: lack of flow in thrombosed vein/dural venous sinus
thrombosis in SSS, deep venous system, transverse sinus»_space; venous infarction
superior sagittal sinus thrombosis: infarction of parasagittal high convexity cortex
deep venous system thrombosis: infarction bilateral thalami
transverse sinus thrombosis: infarction posterior temporal lobe
stages of iron in hemoglobin
intracellular oxyhemoglobin -> deoxygenation –> intracellular deoxyhemoglobin –> oxidation –> intracellular methemoglobin –> cell lysis –> extracellular methemoglobin –> chelation –> hemosiderin/ferritin
risk of posterior fossa hemorrhage >3cm
brainstem compression or hydrocephalus from 4th ventricular obstruction
hyperacute hematoma: blood product stage, T1/T2 signal
0-6 hrs
intracellular oxyhemoglobin
T1 isointense, T2 iso/hyperintense
peripheral rim on GRE
acute hematoma: blood product stage, T1/T2 signal
6-72 hrs
intracellular deoxyhemoglobin
T1 isointense, T2 dark
early subacute hematoma: blood product stage, T1/T2 signal
3 days -1 week
intracellualr methemoglobin
T1 hyperintense, T2 dark
late subacute hematoma: blood product stage, T1/T2 signal
1 week - months
extracellular methemoglobin
T1/2 bright
chronic hematoma: blood product stage, T1/T2 signal
extracellular iron/ferritin/hemosiderin
T1/2 dark
most common cause of spontaneous hemorrhage
chronic hypertension
common locations for hypertensive hemorrhage
basal ganglia, thalamus, cerebellum
imaging findings suggestive of hypertensive microangiopathy
periventricular white matter disease, prior lacunar infarcts
microhemorrhages on T2* in basal ganglia/brainstem
cerebral amyloid angiopathy
amyloid in small and medium artery walls that cause vessel weakness –> hemorrhage; can also cause occlusion and contribut to microangiopathy
exclusively in elderly adults (whites)
primary imaging feature of cerebral amyloid angiopathy
hematoma: lobar/cortical (parietal/occipital lobes)
multiple microhemorrhages seen on T2*; seen in cortex, not basal ganglia
aneurysmal hemorrhage
most common cause of nontraumatic SAH
AVM malformation hemorrhage
rupture of AVM; parenchymal hematoma
congenital abnormal high flow AV connection without intervening normal brain
tends to affect younger patients
dural AV fistula hemorrhage
fistulous connection between meningeal artery and venous sinus/cortical vein
most common types: cavernous-carotid fistula or posterior fossa dAVF
venous thrombosis hemorrhage
thrombosis of cortical veins/deep venous sinuses lead to venous hypertension which can cause infarction and parenchymal hemorrhage
hemorrhagic neoplasms in the brain
glioblastoma, mets (choriocarcinoma, melanoma, thyroid carcinoma, RCC; breast/lung based on most common)
pts treated with bevacizumab (Avastin)
cavernous malformation
vascular hamartoma that consists of low-flow endothelial lined blood vessels; no intervening brain
popcorn like lobular mixed high T1/2 signal; dark hemosiderin rim
however, once it bleeds hematoma is nonspecific
hemorrhagic transformation of infarct: risk factors
thrombolytic therapy, large region of hypoattenuation, dense artery sign
vasculitis hemorrhage
vasculitis typically causes cerebral ischemia, less likely frank emorrhage
moya moya
nonatherosclerotic vasculopathy; progressive stenosis of intracranial ICA –> proliferation of fragile lenticulostriate collaterals
susceptible to aneurysms in posterior circulaton; decreased flow in affected vascular regions
puff of smoke, ivy sign
puff of smoke: enlarged basal perforating arteries
ivy sign: FLAIR MRI; tubular branching hyperintense structures within sulci
types of intraparenchymal hemorrhage in elderly
hypertensive hemorrhage, amyloid angiopathy
