Answer
A third to a half of the patients presenting with a TIA have lesions on DWI. A significant proportion of these patients may not reveal a corresponding lesion on T2-WI. PWI may be more sensitive but has not been adequately tested in patients with TIA.
Although TIAs have been traditionally defined as transient (< 24 h) neurologic deficits of vascular origin, the advent of MRI has led to reconsideration of the definition. Recent tissue definitions of stroke emphasize that TIA with persistent ischemia on diffusion-weighted imaging is classified as stroke rather than a TIA. TIA, on the other hand, requires either a normal diffusion-weighted image without evidence of ischemia or reversible changes on DWI suggestive of ischemia rather than infarction. [13]
Recently, brain imaging (DWI) has been added to the clinical ABCD2 to identify patients with TIA with a high risk of stroke recurrence. The ABCD3-I score uses DWI and intracranial atherosclerosis detected by MRA to add prognostic value to the traditional ABCD2 score. It appears that DWI abnormality increases the ability to predict stroke at 7 and 90 days in patients presenting with clinical TIA. Intracranial disease on MRA seems to add to this score in a nonsignificant way. [14]
Go to Transient Ischemic Attack for more complete information on this topic.
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Magnetic resonance imaging in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: Apparent diffusion coefficient (ADC) map obtained from the same patient at the same time.
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Magnetic resonance imaging in acute stroke. Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean transfer time (MTT) map of the same patient.
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Magnetic resonance imaging in acute stroke. Diffusion-perfusion mismatch in acute ischemic stroke. The perfusion abnormality (right) is larger than the diffusion abnormality (left), indicating the ischemic penumbra, which is at risk of infarction.
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The diffusion-weighted MRI reveals a region of hypointensity in the distribution of the right middle cerebral artery. Flanking the anterior and posterior regions of this abnormality are regions of hyperintensities, which represent regions of new infarct. The contiguity of these regions suggests that they are extensions of the old infarct.
