颈动脉内膜切除术后高灌注或再灌注综合征

来源 :世界核心医学期刊文摘(神经病学分册) | 被引量 : 0次 | 上传用户:wanxueguan55
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Background and Purpose - Hyperperfusion syndrome (HS) after carotid endarterectomy (CEA) has been related to impaired cerebrovascular autoregulation in a chronically hypoperfused hemisphere. Our aim was to provide new insight into the pathophysiology of the HS using magnetic resonance imaging (MRI) studies with diffusion- weighted imaging (DWI) and perfusion- weighted imaging (PWI). Methods - Five out of 388 consecutive patients presented 2 to 7 days after CEA, partial seizures (n=5), focal deficits (n=5), and intracerebral hemorrhage (n=3). In 4 patients, using sequential examinations, we identified vasogenic or cytotoxic edema by DWI; we assessed relative interhemispheric difference (RID) of cerebral blood flow (CBF) by PWI; and we measured middle cerebral artery mean flow velocities (MCA Vm) by transcranial Doppler (TCD). Results - None of the patients presented pathological DWI hyperintensities, consistent with the absence of acute ischemia or cytotoxic edema. In 2 patients, we found an MRI pattern of reversible vasogenic edema similar to that observed in the posterior leukoencephalopathy syndrome. Middle cerebral artery (MCA) mean flow velocities (Vm) were not abnormally increased at any time. PWI documented a 20% to 44% RID of CBF in favor of the ipsilateral to CEA hemisphere. Conclusions - HS can occur in the presence of moderate relative hyperperfusion of the ipsilateral hemisphere. MCA Vm values may not accurately reflect RID of CBF over the cortical convexity. We suggest that the hemodynamic pathogenetic mechanisms of the HS are more complicated than hitherto believed and that they may be more accurately described by the term “ reperfusion syndrome“. u001a Background and Purpose - Hyperperfusion syndrome (HS) after carotid endarterectomy (CEA) has been related to impaired cerebrovascular autoregulation in a chronically hypoperfused hemisphere. Our aim was to provide new insight into the pathophysiology of the HS using magnetic resonance imaging (MRI) studies with Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI). Methods - Five out of 388 consecutive patients presented 2 to 7 days after CEA, partial seizures (n = 5), focal deficits (n = 5), and intracerebral In 4 patients, using sequential examinations, we identified vasogenic or cytotoxic edema by DWI; we assessed relative interhemispheric difference (RID) of cerebral blood flow (CBF) by PWI; and we measured middle cerebral artery mean flow Results - None of the patients presented pathological DWI hyperintensities, consistent with the absence of acute ischemia or cytotoxic edema. In 2 patients, we fou (MCA Vm) by transcranial Doppler nd an MRI pattern of reversible vasogenic edema similar to that observed in the posterior leukoencephalopathy syndrome. Middle cerebral artery (MCA) mean flow velocities (Vm) were not abnormally increased at any time. PWI documented a 20% to 44% RID of CBF in favor of the ipsilateral to CEA hemisphere. Conclusions-HS can occur in the presence of moderate relative hyperperfusion of the ipsilateral hemisphere. MCA Vm values ​​may not reflect RID of CBF over the cortical convexity. We suggest that the hemodynamic pathogenetic mechanisms of the HS are more complicated than hitherto believed and that they may be more accurately described by the term ”reperfusion syndrome". u001a
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