Article
Clusters of spreading depression is an electrophysiological correlate of delayed neurological deterioration after subarachnoid hemorrhage
Spreading-Depression-Clusters sind elektrophysiologische Korrelate für verzögerte neurologische Defizite nach Subarachnoidalblutung
Search Medline for
Authors
Published: | May 8, 2006 |
---|
Outline
Text
Objective: Aneurysmal subarachnoid hemorrhage (SAH) has a mortality rate around 45%. Delayed ischemic neurological deficit (DIND) is the predominant in-hospital complication. In animal experiments it was found that products of hemolysis in the subarachnoid space induced prolonged cortical spreading depressions (SD) which triggered waves of severe vaso-constriction. This process led to widespread cortical necrosis similar to the predominant infarct pattern of DIND in human autopsy studies. Therefore, we prospectively studied the occurrence of SD in patients with SAH.
Methods: 18 patients were consecutively recruited by four centers, members of the Co-operative Study on Brain Injury Depolarizations (COSBID) study group. Research consents were obtained after clinical decision for surgical treatment. A linear, 6-contact electrocorticography (ECoG) recording strip (Wyler) was placed on the cortex accessible through the craniotomy. Thereafter, the electrocorticogram was continuously monitored for periods up to 10 days. SD was defined by the sequential onset of a rapidly developing reduction of the power of ECoG amplitude of at least 50% associated with a propagating, polyphasic slow potential shift.
Results: During a recording period of 2265.5 hours 13 of 18 patients developed a total of 298 SD. Six patients showed a delayed decrease of consciousness (GCS, fall from GCS 14 (12, 15) to 9 (8, 11), P<0.05, Wilcoxon test). This correlated significantly with the occurrence of new clusters of SD. Evolution of new CT-proven brain infarcts was characterized by a pattern change of SD towards very prolonged depression.
Conclusions: 72% of patients with SAH in this study showed recurrent SD. Delayed neurological deterioration was associated with new clusters of SD. Brain infarcts were associated with a characteristic pattern change of SD.