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