Article
Cortical spreading depolarization triggers delayed ischemic neurological deficit in absence of proximal vasospasm in patients with aneurysmal subarachnoid hemorrhage
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Published: | September 16, 2010 |
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Objective: Cortical Spreading Depolarization (CSD) was measured in close association with delayed ischemic neuronal deficit (DIND) in patients with aneurysmal subarachnoid hemorrhage (aSAH). However, the assumed prime mechanism of DIND is the induction of proximal vasospasm triggered by breakdown products of erythrocytes during subarachnoid haemolysis. Nicardipine prolonged-release implants (NPRIs) have been proven to significantly reduce the incidence and degree of proximal vasospasm in patients with aSAH. In the present study we tested whether after treatment of proximal vasospasm with NPRIs CSD may still trigger DIND.
Methods: Therefore, we studied 13 patients with major aSAH. After surgical treatment of the ruptured aneurysm 10 NPRIs were placed closed to the proximal intracranial vessels. The degree of proximal vasospasm was assessed by digital subtraction angiography (DSA) on day 7 to 9. CSDs were recorded using a subdural 6-contact strip electrode in a total of 2,625 hours recording time. DIND was assessed by repeated neurological examination and repeated CT and/or MRI scans.
Results: 534 CSDs were assessed in 10 of 13 patients (77%). DSA revealed no vasospasm in 8 of 13 patients (62%) and mild, and moderate vasospasm in 3 and 2 of 13 patients, respectively (23% and 15%). Four Patients developed clinical and/or CT/MRI proven DIND, two of these patients in the absence of proximal vasospasm but time-locked to the occurrence of CSDs.
Conclusions: CSD may trigger DIND in the absence of proximal vasospasm in patients with aSAH.