Abstract
BackgroundMany reports have emphasized that watershed infarcts are the consequence of hemodynamic compromise, but other reports have suggested that this is not always the case and have suggested that embolization plays a major role in the development of watershed infarcts. Impaired cerebral vasomotor reactivity has certain correlates in watershed hypoperfusion strokes.ObjectivesThis study aimed to assess the role of vasomotor reactivity impairment in watershed infarcts by transcranial Doppler. It also recorded correlates associated with impaired vasomotor reactivity in such patients.MethodologySixty patients with watershed infarction after more than 1 month from onset were studied and grouped into three groups (14 patients with mixed internal and external watershed, 28 patients with internal watershed and 18 patients with external watershed infarcts). Magnetic resonant imaging and angiography of brain, carotid duplex, and echocardiography were done. CO2 reactivity to assess vasomotor reactivity was determined using Doppler.ResultsCerebral vasomotor reactivity was impaired significantly among the internal watershed group compared with the external watershed group (P value = 0.040). In external watershed infarcts, the anterior external watershed group showed significant impairment of vasomotor reactivity compared to posterior external watershed group (P value = 0.046). Impaired cerebral vasomotor reactivity was more evident in diabetic patients and not statistically related with other risk factors. It was also associated with middle cerebral artery stenosis.ConclusionThe hemodynamic impairment is related to internal watershed more than external watershed infarcts, also it is more associated with anterior than posterior external watershed infarcts. Diabetes mellitus is the most correlated cerebrovascular risk factor associated with impaired vasomotor reactivity in such patients.
Highlights
Border zone or watershed (WS) hypoperfusion infarcts occur in cerebral areas between adjacent nonanastomosing arterial territories
Many studies have concluded that watershed infarcts occur due to hemodynamic compromise, but other reports have stated that this is not always the case and have suggested that embolization plays a major role in the development of watershed infarcts, some studies have indicated that both mechanisms play a role in the pathogenesis of border zone infarction [2]
middle cerebral artery (MCA) stenosis was more among internal watershed (IWS) group (35.7%) than external watershed (EWS) group (22.2%), yet the results did not reach a statistical significance
Summary
Border zone or watershed (WS) hypoperfusion infarcts occur in cerebral areas between adjacent nonanastomosing arterial territories. The other one lies in the deep areas along and slightly above the lateral ventricle, between the deep and the superficial branches of the MCA The former, cortical areas were named as the external watershed (EWS), and the latter were named as the internal watershed (IWS) [1]. Many studies have concluded that watershed infarcts occur due to hemodynamic compromise, but other reports have stated that this is not always the case and have suggested that embolization plays a major role in the development of watershed infarcts, some studies have indicated that both mechanisms play a role in the pathogenesis of border zone infarction (reduced cerebral perfusion may impair the washout of micro-emboli) [2]. Impaired cerebral vasomotor reactivity has certain correlates in watershed hypoperfusion strokes
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