Abstract

The brain responds dynamically to transient episodes of ischemic insult. The standard brain imaging techniques, CT and conventional MRI, are insensitive to dynamic and regionally varying neural parenchymal responses to tissue ischemia. In contrast, perfusion and diffusion MRI permit visualization of these critical tissue processes and have afforded new insights into the pathophysiology of human cerebral ischemia. In addition, clinical studies have demonstrated that both conventional brain imaging and diffusion MRI are of substantial clinical use in patients with TIAs. The current conventional definition of TIA, which dates back to the 1950s, is onset of neurologic symptoms due to focal cerebral ischemia that resolve completely within 24 hours.1 Defects of this definition, which became apparent as early as the CT era (circa 1970s), have been demonstrated even more pointedly by recent MRI investigations. Nevertheless, all imaging studies discussed in this review have employed this conventional definition. Patients with clinical TIAs frequently have had previous cerebral ischemic events, both clinically manifest and silent. Conventional MRI is more sensitive than standard CT in identifying these preexisting lesions. In two different studies, MRI provided evidence of at least one infarct somewhere in the cerebrum in 77% to 81% of TIA patients.2,3⇓ Across 17 different studies, CT showed evidence of at least one infarct somewhere in the cerebrum in 0% to 68% of TIA patients. Many patients who meet conventional clinical criteria for TIA actually exhibit a new radiologic infarct on brain imaging, a phenomenon labeled by Waxman and Toole4 as “cerebral infarction with transient signs.” Conventional CT and MRI frequently demonstrate infarcts that are appropriately located to have accounted for the deficits observed during the TIA. Among patients meeting clinical criteria for TIA, 31% to 39% demonstrate neuroanatomically relevant infarcts on conventional MRI3,5⇓ and 2% to 48% …

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