4.0 Article

Cerebrovascular reactivity and subcortical infarctions

Journal

ARCHIVES OF NEUROLOGY
Volume 58, Issue 4, Pages 577-581

Publisher

AMER MEDICAL ASSOC
DOI: 10.1001/archneur.58.4.577

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Objectives: To investigate the association between different kinds of ischemic lesions and cerebrovascular reactivity (CR) and to evaluate their relationships with the major risk factors for stroke. Subjects and Methods: We evaluated CR using the breath-holding index technique during bilateral transcranial Doppler monitoring of flow velocity in the middle cerebral arteries of 41 consecutive patients attending our clinic for a recent, first-ever, ischemic stroke and in 15 control subjects. Based on the location of the lesion determined by computed tomography, the following 3 types of infarctions were identified: cortical (or territorial), single subcortical, and subcortical with multiple silent subcortical infarctions. Patients with a condition of severe carotid artery stenosis or occlusion, which in itself could account for altered CR, were excluded from this study. All physiological and pathologic conditions that could possibly cause an impairment in CR were recorded. Results: The breath-holding index was significantly lower in the multiple subcortical infarctions group than in the control subjects (P<.001), single subcortical infarctions group (P<.01), and cortical infarctions group (P<.01). In all of the groups male sex (P<.05) and a history of hypertension (P<.05), regardless of whether hypertension was treated, correlated with low CR. The multiple regression analysis indicated that the only significant factor able to influence the breath-holding index was the type of lesion. Conclusions: Nonstenotic patients with first-ever stroke who had a recent symptomatic subcortical infarction associated with multiple silent infarctions seem to have an impaired cerebrovascular reserve capacity. The strong association of subcortical infarctions with multiple silent infarctions with low CR indicates the role of small vessel vasculopathy and hypoperfusion as possible pathogenetic mechanisms of subcortical infarctions ith multiple silent infarctions.

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