Cerebrovascular reactivity and subcortical infarctions.

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Abstract
THE CORRELATION between an impaired functional blood flow reserve capacity and the occurrence of brain infarction was previously reported in patients with severe carotid artery disease.1-4 Patients with limited cerebrovascular reserve capacity have less adequate perfusion capacity than patients with normal reserves. An impaired cerebrovascular reserve capacity may increase the risk of cerebral ischemia in patients with major cerebral artery occlusion.5,6 Patients with severe carotid artery stenosis or occlusion often have a borderzone distribution of brain infarction in the cerebral hemisphere ipsilateral to internal carotid artery disease.7 Border-zone distribution of infarction has traditionally been attributed to hypoperfusion related to reduced blood flow in zones between major hemispheric vascular territories. Moreover, cerebrovascular reactivity (CR) was found to be significantly reduced in low-flow infarctions compared with thromboembolic infarctions in patients with ipsilateral carotid stenosis.8 An association was found between CR and white matter lesions. This supports the hypothesis that these kinds of lesions may be associated with hemodynamic ischemic brain injury.9 In addition, patients with major cerebral arterial occlusive diseases and misery perfusion have a high risk of recurrent ischemic stroke.6,10 These findings suggest that an impaired cerebrovascular reserve capacity is highly related to the occurrence of ischemic stroke. To our knowledge, the association between different types of ischemic lesions and CR has not been studied in patients who have had a stroke but who did not have severe carotid artery disease.