Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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J. Cereb. Blood Flow Metab. · Feb 2012
CommentCortical spreading ischemia in the absence of proximal vasospasm after aneurysmal subarachnoid hemorrhage: evidence for a dual mechanism of delayed cerebral ischemia.
There are longstanding inconsistencies in the evidence thought to link vasospasm in the major branches of the Circle of Willis with delayed cerebral ischemia and poor outcome from aneurysmal subarachnoid hemorrhage (aSAH). The demonstrations, first in the laboratory, and more recently in patients with aSAH, of cortical spreading ischemia based on an abnormal response of the cerebral microcirculation to spreading depolarization offer an additional possible mechanism for delayed ischemia. That such events can occur in the substantial absence of proximal vasospasm is compatible with this concept, but the preliminary evidence needs support from more extensive studies.
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J. Cereb. Blood Flow Metab. · Feb 2012
Delayed cerebral ischemia and spreading depolarization in absence of angiographic vasospasm after subarachnoid hemorrhage.
It has been hypothesized that vasospasm is the prime mechanism of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). Recently, it was found that clusters of spreading depolarizations (SDs) are associated with DCI. Surgical placement of nicardipine prolonged-release implants (NPRIs) was shown to strongly attenuate vasospasm. ⋯ Five patients developed DCI associated with clusters of SD despite the absence of angiographic vasospasm in three of those patients. The number of SDs correlated significantly with the development of DCI. This may explain why reduction of angiographic vasospasm alone has not been sufficient to improve outcome in some clinical studies.