STROKE - IMAGING · infarction. However it should be followed by DWI of brain to early visualisation of acute infarct (about 30 min ) Further advanced imaging modalities like CT/MR

STROKE - IMAGING

Dr RAJASEKHAR REDDY

2nd Yr P.G. RADIODIAGNOSIS

KIMS,Narkatpalli.

STROKE

• Describes a clinical event that consists of sudden onset of neurological symptoms

Types

• Infarction - occlusion of cerebral arteries and veins(85%)

• Hemorrhage – intraparenchymal , subarachnoid

• Infarction without occlusion of cerebral arteries or veins may also occur-severe sustained hypotension,toxic ,anoxic insult

Imaging manifestations of ischemia -infarction

These vary with time

• Acute (upto-24hrs)

• Subacute –early,late ( 1-7 days. )

• Chronic (after 3 weeks )

CT

Hyperacute (<12hrs)

• 50 to 60 % normal

• Hyperdense middle cerebral artery

• Obscuration of lentiform nuclei

• Insular- ribbon sign

Acute(12 to 24hrs)

• Low density basal ganglia

• Loss of grey –white interface

• Sulcal effacement (gyral swelling)

Hyperdense MCA low density basal ganglia

CT axial plain

Subacute early (1 to 3 days)

• Wedge shaped low density area involving both grey and white matter

• Hemorrhagic transformation may occur

• Increasing mass effect

brain herniation

ventricular trapping(raised Intra Cranial Tension)

• If extensive can result in life threatening-malignant brain edema in cases of Internal Carotid Artery Occlusion,ICA dissection.

CT axial plain

SubAcute infarct

Subacute late (4 to 7 days)

• Gyral enhancement

• Mass effect,edema persist

Chronic

• Encephalomalacic changes,volume loss

• Calcification rare

MRI

• Diffusion weighted sequence is sensitive in acute infarcts

Hyperacute :- Immediate

• Absence of normal flow void

• <12 hrs- gyral edema, sulcal effacement , loss of grey white interface

• In hyperacute – diffusion restriction is seen with low ADC values (decrease to 30 to 40% below normal)

12 to 24hrs : -

• Hyperintensity on T2

• Meningeal enhancement, mass effect

• Intravascular contrast enhancement.

T1W E+ axial

coronal

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DIFFUSION WEIGHTED IMAGING

PRINCIPLE

IN Acute stroke – Due to alteration of

homeostasis results in excess intracellular

water accumulation - cytotoxic edema

- with an overall decreased rate of water

molecular diffusion within the affected tissue

Showing diffusion restriction which appers

bright.

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Late subacute

• Gs effect resolves

• T2 fogging

• Hemorrhagic changes

Chronic

• Enc

• Hemorrhagic residua

• Wallerian degener

T2W axial TIW E+axial

Subacute infarct on MRI

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C.T ANGIOGRAPHY

• C.T Angiography -widely available technique for assesement of both the intracranial and extracranial circulation.

• C.T Angiographic demonstration of a significant thrombus can guide appropriate therapy in the form of intra arterial or mechanical thrombolysis.

• Furthermore ,identification of the carotid disease and visualisation of the aortic arch can provide clues to the cause of the ishemic event and guidance for the I.R

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• Similar findings can be obtained by

MR Angiography.

• Like CT Angio MR Angio is useful for detection of intravascular occlusion due to thrombus and for evaluating the carotid bifurcation in patients with acute stroke.

• Time of Flight MR and contrast enhanced MR angio commonly used to evaluate intra cranial and extracranial circulation

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C.T PERFUSION IMAGING • Used in the assesement of ischemic penumbra

• This is done by measuring,

• -cerebral blood volume

• -cerebral blood flow

• Mean Transit Time - time difference between

arterial and venous (inflow and outflow )

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ARTERIAL

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VENOUS

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• The evaluation of the Brain perfusion is based on the central volume principle which is

• Cerebral Blood Flow= Cerebral Blood Volume /Mean Transition Time.

• Both the arterial and venous Region of Interest are optimally chosen in large vessels that course in a direction nearly perpendicular to the plane of C.T acquisition .

• Arterial ROI Is typically either of two A.C.A or unaffected M.C.A , Venous ROI is placed over the superior sagittal sinus , transverse sinus .

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• Comparision of DWI and PWI

• - The lesion appears smaller on DWI Than on

the Perfusion Weighted Images.This is typically

observed in large vessel strokes.

• -The lesion appears same size on DWI and PWI

when the tissue is irreversibly infarcted and

there is no penumbra.

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• The lesion appears larger on DWI than on PW

Images or the lesion seen only on DW Images

but not on Perfusion Weighted images.

• These findings are usually associated with

early reperfusion of ischemic tissue.

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TAKE HOME MESSAGE

• In case of suspected infarct C.T is the modality of choice to rule out Haemorrhage & to find early signs of infarction.

• However it should be followed by DWI of brain to early visualisation of acute infarct (about 30 min )

• Further advanced imaging modalities like CT/MR Angiography for localisation of Vascular Pathology.

• Perfusion study is done to look for Penumbra (salvagable brain parenchyma ) & planning of interventions.

THANK YOU

• THANK YOU