Dr R. Anjan Dr R. Anjan BharathiBharathi

3rd leading cause of mortality & morbidity.

Goal of imaging• Early and accurate diagnosis• Information about the intracranial

vasculature and brain perfusion to guide appropriate therapy.

Goals of Acute Stroke Imaging

4 Ps of acute stroke imaging

Parenchyma Assess early signs of acute stroke, ruleout hemorrhage

Pipes Assess extra cranial & intra cranial circulation for intravascular thrombus

Perfusion Assess cerebral blood volume, cerebral blood flow, and mean transit time

Penumbra Assess tissue at risk of dying if ischemia continues without recanalization of intravascular thrombus

Rowley HA. The four Ps of acute stroke imaging: parenchyma, pipes, perfusion, and penumbra.AJNR Am J Neuroradiol 2001;22:599–601

Modality UtilityUnenhanced CT Quick/ identify early signs of

stroke /rule out h’gge.

CT angiography Depict intravascular thrombi/ stenosis/occlusion

CT perfusion Salvageable tissue →penumbra

DWI Hyper acute ischemia

Gradient- echo H’gge

MR angiography Status of neck and intracranial vessels

Diffusion and perfusion mismatch

Presence of a penumbra

DWI• Sensitive to random motion of water

molecules by a value called ADC which is measured.

• As the water molecules moved in the direction of the field gradient, in transverse the accumulate a phase shift magnetization which is related to that of a stationary one; this results in signal attenuation.

• ADC in ischemic areas is < 50% than the brain and appear hyperintense on DWI

• Ischemia Na-K pump failure Cytotoxic edema with in tissue water by 3-5%.

• The ADC values are rarely reversible though IAT may occasionally cause disappearance of the diffusion defect.

• Acute drop in ADC -- normalizes to baseline at 5-10 days after ischemia [pseudonormalization].

• ADC values can be > normal levels at the time passes does aiding in differentiation between acute, subacute and chronic infarcts.

PWIPWI• Principle of dynamic susceptibility

contrast (DSC) imaging. --Bolus-contrast ie tracking a nondiffusible paramagnetic (gadolinium) which is passing through brain tissue on a T2*

• 0.2 mmol/kg (roughly double at a high flow rate (3-5 cc/sec) 10 to 12 s after scan initiation.

• Blood oxygen level and arterial spin tagging.

• The signal intensity declines as contrast material passes through the infarcted area and returns to normal as it exits this area.

• A curve is derived from this tracing data (ie, signal washout curve), which represents and estimates the cerebral blood volume (CBV).

Diffusion and perfusion mismatch

Take home msg

Copyright ©2005 American Heart Association

Topakian, R. et al. Stroke 2005;36:e162-e164

Before After thrombolysis

• Although conventional MRI sequences often do not show evidence of stroke in the acute phase, conventional MRI may show signs of intravascular thrombus such as absence of flow void on T2-WI, vascular hyperintensity on FLAIR.

80 yr old male with right TIA

T2

MRI in acute stroke – Acute phase (1-7 d)

• Edema maximizes at 48-72 h and MRI signals become more prominent and well demarcated.

• Hypo intensity on T1-WI and as a hyperintense area on T2-WI.

• Mass effect.• Arterial enhancement usually persists

throughout the acute phase• Parenchymal enhancement appreciated at

the end of this phase in complete infarction.

• In incomplete infarction, the parenchymal enhancement is usually earlier.

• Reperfusion occurs and both petechial and frank hemorrhage can be observed, typically 24-48 hours after the onset of the stroke.

• Usually, petechial hemorrhages cause the "fogging" phenomenon, due to hemoglobin degradation products, that masks the infarction on both T1-WI and T2-WI.

30 yr femaleAcute demyelination

Acute infarct in a background of chronic small vessel disease

Comatose 64 yr old

Hyperacute infarct

Time MRI Finding Etiology

2-3 min DWI - Reduced ADCDecreased motion of protons

2-3 minPWI - Reduced CBF, CBV, MTT

Decreased CBF

0-2 hT2-WI - Absent flow void signal

Slow flow or occlusion

0-2 hT1-WI - Arterial enhancement

Slow flow

2-4 hT1-WI - Subtle sulcal effacement

Cytotoxic edema

2-4 hT1-WI - Parenchymal enhancement

Incomplete infarction

8 hT2-WI - Hyperintense signal

Vasogenic and cytotoxic edema

16-24 hT1-WI - Hypointense signal

Vasogenic and cytotoxic edema

5-7 dParenchymal enhancement

Complete infarction