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Neuroradiology > Stroke > Flashcards

Stroke Flashcards

1
Q

What is the most common cause of MCA occlusion?

A

Atherosclerosis of CCA and ICA

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2
Q

What percentage of pts show CT abnormalities at 3-6 hours? 24 hours?

A

60%

100%

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3
Q

What CT findings preclude use of tPa?

A 
Hemorrhage
Involvement of >1/3rd MCA territory
hypodensity
>4.5 hours from onset
Mass effect
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4
Q

What is the MRI appearance of acutre (

A

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
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5
Q

What is the appearance of acute infarct on GRE?

A

Dilated veins with low signal in region of infarct

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6
Q

How do subacute MCA infarct appear on CT (2-21day)

A
  • 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

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7
Q

When do most hemorrhagic transformations occur in infract? How many occur?

When does gyral enhancement occur? What is the significance?

A

1-4 days, 15%

3-7 days, denotes luxury perfusion and portends a better prognosis

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8
Q

What is the most common cause of hemorrhagic transformation of MCA stroke?

A

Thrombolytic therapy

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9
Q

What is the MR appearance of subacute infarct (2-21days)

A

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

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10
Q

when does DWI signal disappear in stroke?

A

7-10 days, gone by 14

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11
Q

What is the main cause of ACA stroke? Which other vessel is usually involved?

What is the imaging pattern?

A

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

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12
Q

What is the common cause of PCA infarct? Where is the signal seen?

What is the symptom?

A

Downward transtentorial herniation secondary to compression of PCA between temporal lobe and edge of tentorium

Medial occiptal lobe

Homonymous hemianopsia

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13
Q

What are the considerations in stroke in a young person?

A 
Trauma
Drug overdose (cocaine, amphetamines)
Coagulopathy (SCD, antiphospholipid)
Vasculitides (lupus, wegeners)
OCP
Steroids
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14
Q

What are the two main associations with lacunar infarct?

What is the pathology? What arterial systems are mainly involved?

A

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

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15
Q

Where are the watershed zones in the brain? What is a secondary consideration of watershed infarct other than hypotension or ICA occlusion

A 
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

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16
Q

What is the difference between a hemorrhagic infarction and hemorrhagic transformation?

A

Infarct is when blood is present within 24 hours of symptom onset

Transformation is when blood is present between 2-14 days after onset

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17
Q

What is most common cause of hemorrhagic transformation?

A

Thrombolytic therapy (sudden reperfusion)

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18
Q

What percentage of infarcts are hemorrhagic?

A
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19
Q

What are indications of pending hemorrhagic transformation?

A

Poor pial collaterals, significant CT hypodensity, presence of microbleeds elsewhere

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20
Q

What shoudl be suspected with hemorrhage in nonarterial distribution?

A

Venous bleed

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21
Q

Which MR sequence is more sensitive for microbleeds?

A

GRE

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22
Q

What is wallerian degeneration?

What is it seen with?

A

Anterograde degeneration of axons and myelin; increased DWI signal following corticospinal tracts

MCA infarct

also seen with hemorrhage, tumor, trauma, WM disease

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23
Q

When does Wallerian degeneration occur after stroke?

How does it appear on MRI?

A

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

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24
Q

What cerebellar arteries are most commonly infarcted?

What are the associations?

What are the dreaded complications?

A

PICA&raquo_space; SCA/AICA

Vertebral dissection (younger), Basilar disease (older)

Upward cerebellar herniation, downward tonsillar herniation with compression of brainstem

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25
Q

What is wallenburg syndrome? What vessel is associated?

A

Ipsilateral; pain/temp loss, ataxia, dysarthria/dysphagiapsilateral

Contralateral; pain and temp in trunk and limbs

vertigo (vestibular nucleus)

PICA

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26
Q

What is the risk increase with basilar occlusion vs ICA?

A

2.5x higher risk of death

27
Q

What are the etiologies of basilar artery occlusion?

A

Embolism, atherosclerosis, vascular malformations

Syphillis, tuberculous, dehydration, fungal meningitis

28
Q

What is infarcted with basilar occlusion?

A

Thalamus, posterior limb of internal capsule, midbrain

29
Q

Median thalamic infarcts bilaterally suggest what?

A

Artery of percheron infarct

30
Q

Pontine infarct produces what syndrome?

A

Locked in

31
Q

What is the window for thrombolysis with basilar occlusion

A

24 hours

32
Q

What are the etiologies of global brain hypoxia in adults? Kids?

A

Adults; trauma, severe HoTN/HTN, acute radiation, venous sinus occlusion

Children: dehydration, neonatal anoxia, abuse

33
Q

What part of brain does hypoxia/ischemia predominantly involve?

A

Grey matter

deep nuclei, pericentral cortex, cortex, hippocampus, cerebellum

34
Q

What is the initial CT appearance of brain hypoxia?

A

Diffuse cerebral edema with effacement of grey white junction

35
Q

What is the acute MR appearance of hypoxia?

Subacute?

Chronic

A

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

36
Q

What two imaging patterns can arise from generalized hypoxia?

A

Watershed infarct; parietoocciptal

Laminar necrosis

37
Q

What is laminar necrosis? What is the common cause? How does it image on MR?

A

Ischemic changes to cerebellar/cerebral cortex

Gray matter layers 3, 5, 6

T1 hyperintense (presence of fatty macrophages)

DWI along gyri (perirolandic regions)

38
Q

What is the main differential for globalized hypoxic changes in the brain? (IE grey white effacement, gyral DWI)

A

Hypoglycemia
Mitochondrial disease
Prion disease
Hepatic encephalopathy

39
Q

What is the presentation of cortical vein thrombosis?

What are the predisposing factors?

A

Seizures

Inflammation/infection, trauma, dehydration, pregnancy, OCP, coagulopathies, collagen vascular diseases vasculitis

40
Q

What is the cord sign?

A

Clot filled cortical vein

CT hyperdensity, T1 hyperintensity

41
Q

What are the imaging findings in cortical vein thrombosis?

A

Hyperdense cortical vein (cord sign)

T1 hyperintense

Cortical/subcortical WM edema, hemorrhage, SAH overlying abnormality

42
Q

Which venous occlusion is more common? Deep venous system or cortical/dural sinus?

A

Cortical/dural sinus

43
Q

Who gets deep venous system occlusions? What are the etiologies?

A

Kids&raquo_space; adults

Dehydration, paranasal sinus/mastoid infection, trauma, hypercoagulable state

44
Q

What is the imaging appearance of deep venous sinus occlusion?

What is the main treatment difference between venous and arterial occlusion?

A

Simulates generalized anoxia

Thalamic/basal ganglia/midbrain abnormalities

Venous hemorrhage does not prevent use of thrombolytics

45
Q

What are the etiologies of venous sinus occlusion (superior sagittal/transverse) in adults? kids?

A

Adults: paranasal/mastoid infection, OCP, hypercoagulable, CVD, pregnancy, malignancies, idiopathic

Kids: paranasal/mastoid infection, meningitis, trauma, dehydration

46
Q

What is the appreance of superior sagittal/transverse sinus occlusion?

A

Delta sign; hypodense clot surrounded by enhanced venous blood in sinus

Noncon MR: hyperintensity and lack of flow void in vein with dural enhancement

47
Q

What is the main cause of corpus callosal infarct?

What is the MR appearance?

A

Hypotensive - watershed area

DWI, contrast enhancement

48
Q

What is the differential for a splenium (CC) lesion?

A

Seizure, vasculitis, irradiation, demyelination, trauma, viral infection, extrapontine osmotic myelinolysis

49
Q

What are the etiologies of hypertensive encephalopathy?

A

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

50
Q

What is PRES?

A

Hypertensive encephalopathy in eclamptic pregnancy

Visual disturbances due to predominance for posterior circulation (lacks sympathetic innervation and autoregulation

51
Q

What is the appearance of PRES?

What chemo drugs have a similar appearance on CT?

MR appearance?

A

Cortical swelling without hemorrhage- FOCAL EDEMA

Tacrolimus and cyclosporin

T2/FLAIR hyperintensity in posterior circulation, moderate DWI WITHOUT ADC, and minimal enhancement

52
Q

What is the MR appearance of hypertensive encephalopathy? What is the differential?

A

T2/FLAIR hyperintensity in the basal ganglia, thalamus, midbrain

ADEM, venous thrombosis

53
Q

What are the common causes of cerebral vasculitis?

A

Infection, giant cell arteritis, polyarteritis nodosa, temporal arteritis, wegeners, sarcoidosis, CVS, takayasu, chemical vasculitis (ergot, meth), postpartum

54
Q

What is the appearance of cerebral vasculitis?

A

Focal areas of T2/FLAIR hyperintensity, nonarterial segmental DWI

can have normal MRA

Segmental narrowing, occlusion, slow vessel filling on DSA

55
Q

What is moyamoya disease?

What is moyamoya syndrome?

A

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

56
Q

How does moyamoya look on angiogram?

Where are the infarcts? How does it look on FLAIR?

A

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)

57
Q

What is the most common adult presentation of moyamoya?

A

Intraventricular hemorrhage

58
Q

What is CADASIL?

What is the patient population? Where is the gene?

A

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)

59
Q

What is the MRI appearance of CADASIL? CT?

A

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

60
Q

What is the difference between stable and unstable plaque?

A

Stable - homogenous and calcified

Unstable - fibrous capsule, hemorrhage, lipid core

61
Q

Where does FMD affect the carotid system?

A

95% high ICA

15-20% vertebral

bilateral in 60-75%

62
Q

What is association with cerebral FMD?

A

Aneurysms (20-50%)

63
Q

Which type of FMD is more common in the cranial circulation?

A

Medial > subadventitial

Neuroradiology (15 decks)

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