Stroke Flashcards
What is the most common cause of MCA occlusion?
Atherosclerosis of CCA and ICA
What percentage of pts show CT abnormalities at 3-6 hours? 24 hours?
60%
100%
What CT findings preclude use of tPa?
Hemorrhage Involvement of >1/3rd MCA territory hypodensity >4.5 hours from onset Mass effect
What is the MRI appearance of acutre (
Earliest: Intravascular enhancement sign; seen w/in 2 hours
- Meningeal enhancement up to 3 days
- Cortical edema (increase signal on FLAIR) early as 3 hours
- Occluded arteries will be bright on FLAIR and low on GRE
What is the appearance of acute infarct on GRE?
Dilated veins with low signal in region of infarct
How do subacute MCA infarct appear on CT (2-21day)
- Hemorrhagic transformation most common 1-4 days
- Mass effect increases in first 3 days
- Wedge shaped hypodensity in area of infarct involving both grey and white matter
-Gyral enhancement 3-7 days after, better prognosis
When do most hemorrhagic transformations occur in infract? How many occur?
When does gyral enhancement occur? What is the significance?
1-4 days, 15%
3-7 days, denotes luxury perfusion and portends a better prognosis
What is the most common cause of hemorrhagic transformation of MCA stroke?
Thrombolytic therapy
What is the MR appearance of subacute infarct (2-21days)
Parenchymal enhancement 3-7days, persisting up to 6 months
Hyperintense on FLAIR and T2
At 14 days, T2 signal begins to drop
DWI fades around 7-10 days, gone by 14 days
when does DWI signal disappear in stroke?
7-10 days, gone by 14
What is the main cause of ACA stroke? Which other vessel is usually involved?
What is the imaging pattern?
Primary vessel disease, not emboli. Can be secondary to clipping of artery with subfalcine herniation
ICA
CT hypodensity and T2/FLAIR hyperintesnsity along the medial cerebral convexity
What is the common cause of PCA infarct? Where is the signal seen?
What is the symptom?
Downward transtentorial herniation secondary to compression of PCA between temporal lobe and edge of tentorium
Medial occiptal lobe
Homonymous hemianopsia
What are the considerations in stroke in a young person?
Trauma Drug overdose (cocaine, amphetamines) Coagulopathy (SCD, antiphospholipid) Vasculitides (lupus, wegeners) OCP Steroids
What are the two main associations with lacunar infarct?
What is the pathology? What arterial systems are mainly involved?
Age and HTN
Hyalinization of arteries leading to THROMBUS, not emboli
Lenticulostriate and thalamoperforators (basal ganglia, internal capsule, thalamus)
Also with basilar perforators, leads to brainstem infarct
Where are the watershed zones in the brain? What is a secondary consideration of watershed infarct other than hypotension or ICA occlusion
Between ACA and MCA territories Between PCA and MCA territories Parasagittal white matter Deep cerebellum Corpus Callosum
Fat emboli look the same as watershed infarcts
What is the difference between a hemorrhagic infarction and hemorrhagic transformation?
Infarct is when blood is present within 24 hours of symptom onset
Transformation is when blood is present between 2-14 days after onset
What is most common cause of hemorrhagic transformation?
Thrombolytic therapy (sudden reperfusion)
What percentage of infarcts are hemorrhagic?
What are indications of pending hemorrhagic transformation?
Poor pial collaterals, significant CT hypodensity, presence of microbleeds elsewhere
What shoudl be suspected with hemorrhage in nonarterial distribution?
Venous bleed
Which MR sequence is more sensitive for microbleeds?
GRE
What is wallerian degeneration?
What is it seen with?
Anterograde degeneration of axons and myelin; increased DWI signal following corticospinal tracts
MCA infarct
also seen with hemorrhage, tumor, trauma, WM disease
When does Wallerian degeneration occur after stroke?
How does it appear on MRI?
4 weeks; band of T2 hypointensity along ipsilateral corticospinal tract
2-3 months; ipsilateral corticospinal tract becomes hypERintense on T2 with associated ATROPHY
Can also see ipisilateral medial thalamic T2 hyperintensity
Brainstem atrophy and increased T2 signal
What cerebellar arteries are most commonly infarcted?
What are the associations?
What are the dreaded complications?
PICA»_space; SCA/AICA
Vertebral dissection (younger), Basilar disease (older)
Upward cerebellar herniation, downward tonsillar herniation with compression of brainstem
What is wallenburg syndrome? What vessel is associated?
Ipsilateral; pain/temp loss, ataxia, dysarthria/dysphagiapsilateral
Contralateral; pain and temp in trunk and limbs
vertigo (vestibular nucleus)
PICA
What is the risk increase with basilar occlusion vs ICA?
2.5x higher risk of death
What are the etiologies of basilar artery occlusion?
Embolism, atherosclerosis, vascular malformations
Syphillis, tuberculous, dehydration, fungal meningitis
What is infarcted with basilar occlusion?
Thalamus, posterior limb of internal capsule, midbrain
Median thalamic infarcts bilaterally suggest what?
Artery of percheron infarct
Pontine infarct produces what syndrome?
Locked in
What is the window for thrombolysis with basilar occlusion
24 hours
What are the etiologies of global brain hypoxia in adults? Kids?
Adults; trauma, severe HoTN/HTN, acute radiation, venous sinus occlusion
Children: dehydration, neonatal anoxia, abuse
What part of brain does hypoxia/ischemia predominantly involve?
Grey matter
deep nuclei, pericentral cortex, cortex, hippocampus, cerebellum
What is the initial CT appearance of brain hypoxia?
Diffuse cerebral edema with effacement of grey white junction
What is the acute MR appearance of hypoxia?
Subacute?
Chronic
Acute: Cortical enhancement (C+), restricted diffusion (basal ganglia, thalami, cortex)
Subacute; T2 edema with grey matter swelling, Cortical hyperintensity (T1)
Atrophy and cortical hypointensity (T2)
GLIOSIS: T2/FLAIR bright
What two imaging patterns can arise from generalized hypoxia?
Watershed infarct; parietoocciptal
Laminar necrosis
What is laminar necrosis? What is the common cause? How does it image on MR?
Ischemic changes to cerebellar/cerebral cortex
Gray matter layers 3, 5, 6
T1 hyperintense (presence of fatty macrophages)
DWI along gyri (perirolandic regions)
What is the main differential for globalized hypoxic changes in the brain? (IE grey white effacement, gyral DWI)
Hypoglycemia
Mitochondrial disease
Prion disease
Hepatic encephalopathy
What is the presentation of cortical vein thrombosis?
What are the predisposing factors?
Seizures
Inflammation/infection, trauma, dehydration, pregnancy, OCP, coagulopathies, collagen vascular diseases vasculitis
What is the cord sign?
Clot filled cortical vein
CT hyperdensity, T1 hyperintensity
What are the imaging findings in cortical vein thrombosis?
Hyperdense cortical vein (cord sign)
T1 hyperintense
Cortical/subcortical WM edema, hemorrhage, SAH overlying abnormality
Which venous occlusion is more common? Deep venous system or cortical/dural sinus?
Cortical/dural sinus
Who gets deep venous system occlusions? What are the etiologies?
Kids»_space; adults
Dehydration, paranasal sinus/mastoid infection, trauma, hypercoagulable state
What is the imaging appearance of deep venous sinus occlusion?
What is the main treatment difference between venous and arterial occlusion?
Simulates generalized anoxia
Thalamic/basal ganglia/midbrain abnormalities
Venous hemorrhage does not prevent use of thrombolytics
What are the etiologies of venous sinus occlusion (superior sagittal/transverse) in adults? kids?
Adults: paranasal/mastoid infection, OCP, hypercoagulable, CVD, pregnancy, malignancies, idiopathic
Kids: paranasal/mastoid infection, meningitis, trauma, dehydration
What is the appreance of superior sagittal/transverse sinus occlusion?
Delta sign; hypodense clot surrounded by enhanced venous blood in sinus
Noncon MR: hyperintensity and lack of flow void in vein with dural enhancement
What is the main cause of corpus callosal infarct?
What is the MR appearance?
Hypotensive - watershed area
DWI, contrast enhancement
What is the differential for a splenium (CC) lesion?
Seizure, vasculitis, irradiation, demyelination, trauma, viral infection, extrapontine osmotic myelinolysis
What are the etiologies of hypertensive encephalopathy?
Pregnancy, renal insufficiency, HUS, hypoalbuminemia, organ transplantation, TTP
Will be seen as T2/FLAIR hyperintensity due to elevated blood pressure causing leakage of fluid and proteins causing FOCAL CEREBRAL EDEMA
What is PRES?
Hypertensive encephalopathy in eclamptic pregnancy
Visual disturbances due to predominance for posterior circulation (lacks sympathetic innervation and autoregulation
What is the appearance of PRES?
What chemo drugs have a similar appearance on CT?
MR appearance?
Cortical swelling without hemorrhage- FOCAL EDEMA
Tacrolimus and cyclosporin
T2/FLAIR hyperintensity in posterior circulation, moderate DWI WITHOUT ADC, and minimal enhancement
What is the MR appearance of hypertensive encephalopathy? What is the differential?
T2/FLAIR hyperintensity in the basal ganglia, thalamus, midbrain
ADEM, venous thrombosis
What are the common causes of cerebral vasculitis?
Infection, giant cell arteritis, polyarteritis nodosa, temporal arteritis, wegeners, sarcoidosis, CVS, takayasu, chemical vasculitis (ergot, meth), postpartum
What is the appearance of cerebral vasculitis?
Focal areas of T2/FLAIR hyperintensity, nonarterial segmental DWI
can have normal MRA
Segmental narrowing, occlusion, slow vessel filling on DSA
What is moyamoya disease?
What is moyamoya syndrome?
Idiopathic progressive occlusive arteriopathy of childhood
Primary arterial disorder leading to occlusion of intracranial ICA
Similar imaging associated with SCD, CVD, NF1, menkes kinky hair syndrome, ASCVD, radiation
How does moyamoya look on angiogram?
Where are the infarcts? How does it look on FLAIR?
occlusion of supraclinoid ICA and proliferation of large and irregular perforating vessels as well as transdiploic ECA
Posterior cerebral arteries also affected with thalamoperforator enlargement
Deep and parasagittal watershed regions
High signal in sulci representing pial collaterals (Ivy sign)
What is the most common adult presentation of moyamoya?
Intraventricular hemorrhage
What is CADASIL?
What is the patient population? Where is the gene?
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarctions and Leukoencephalopathy
Young adults with TIA and strokes
Chromosome 19, smooth muscle cells of arterial walls (happens in young adults 19yo)
What is the MRI appearance of CADASIL? CT?
Patchy areas of T2 hyperintensity indistinguishable from small vessel disease.
Later will show T2 hyperintensity in TEMPORAL lobe white matter and internal capsule/subinsular region. Periventricular lesions become large and confluent
Nonspecific white matter changes in a young adult
What is the difference between stable and unstable plaque?
Stable - homogenous and calcified
Unstable - fibrous capsule, hemorrhage, lipid core
Where does FMD affect the carotid system?
95% high ICA
15-20% vertebral
bilateral in 60-75%
What is association with cerebral FMD?
Aneurysms (20-50%)
Which type of FMD is more common in the cranial circulation?
Medial > subadventitial
