Cerebrovascular reactivity and subcortical infarctions

Citation
Lm. Cupini et al., Cerebrovascular reactivity and subcortical infarctions, ARCH NEUROL, 58(4), 2001, pp. 577-581
Citations number
41
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ARCHIVES OF NEUROLOGY
ISSN journal
00039942 → ACNP
Volume
58
Issue
4
Year of publication
2001
Pages
577 - 581
Database
ISI
SICI code
0003-9942(200104)58:4<577:CRASI>2.0.ZU;2-1
Abstract
Objectives: To investigate the association between different kinds of ische mic lesions and cerebrovascular reactivity (CR) and to evaluate their relat ionships with the major risk factors for stroke. Subjects and Methods: We evaluated CR using the breath-holding index techni que during bilateral transcranial Doppler monitoring of flow velocity in th e 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 follo wing 3 types of infarctions were identified: cortical (or territorial), sin gle subcortical, and subcortical with multiple silent subcortical infarctio ns. Patients with a condition of severe carotid artery stenosis or occlusio n, which in itself could account for altered CR, were excluded from this st udy. 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 s ubcortical infarctions group than in the control subjects (P<.001), single subcortical infarctions group (P<.01), and cortical infarctions group (P<.0 1). 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 C R. The multiple regression analysis indicated that the only significant fac tor able to influence the breath-holding index was the type of lesion. Conclusions: Nonstenotic patients with first-ever stroke who had a recent s ymptomatic subcortical infarction associated with multiple silent infarctio ns seem to have an impaired cerebrovascular reserve capacity. The strong as sociation 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 s ilent infarctions.