Article
Spreading depolarizations in clusters affect cerebral metabolism in patients with aneurysmal subarachnoid hemorrhage
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Authors
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Edgar Santos
- University Hospital Heidelberg, Department of Neurosurgery, Heidelberg, Germany
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Alexandra Nagel
- Charité University Medicine Berlin, Department Neurology and Neurosurgery, Berlin, Germany
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Kara L. Krawenski
- Charité University Medicine Berlin, Department Neurology and Neurosurgery, Berlin, Germany
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Daniel Hertle
- University Hospital Heidelberg, Department of Neurosurgery, Heidelberg, Germany
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Asita S. Sarrafzadeh
- Charité University Medicine Berlin, Department Neurology and Neurosurgery, Berlin, Germany
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Jens P. Dreier
- Charité University Medicine Berlin, Department Neurology and Neurosurgery, Berlin, Germany
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Andreas Unterberg
- University Hospital Heidelberg, Department of Neurosurgery, Heidelberg, Germany
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Oliver W. Sakowitz
- University Hospital Heidelberg, Department of Neurosurgery, Heidelberg, Germany
| Published: | September 16, 2010 |
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Outline
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Objective: Spreading depolarizations (SDs) contribute to infarct expansion in experimental brain injury. SDs also propagate in the injured human brain, whether they contribute to secondary brain damage is not clear yet. Cerebral microdialysis may be used to assess metabolic changes in patients with acute brain injury and at risk for further deterioration. We studied dynamics of glucose, lactate, pyruvate and glutamate during the occurrence of SDs in patients with aneurismal subarachnoid haemorrhage.
Methods: In a prospective observation study in 42 patients with aneurismal subarachnoid haemorrhage multimodal cerebral monitoring was performed. All patients underwent craniotomy for early (<72 h) aneurysm obliteration. All patients received an invasive intracranial pressure probe and a cerebral microdialysis probe (CMA70/71, CMA, Solna, Sweden) in the vascular territory of the aneurysm-bearing vessel. In addition to routine monitoring, patients had subdural 6–8 contact linear electrode strips (Wyler, 5/10 mm platinum; Ad-Tech Medical Instrument Corp., Racine, WI) placed adjacent to the injured cortex in a centrifugal orientation.
Results: Out of 42 patients, 15 patients exhibited SDs. Of these, 7 patients presented with acute neurological deficits and displayed 118 SDs. Eighty-nine occurred as single SDs and 29 as part of a cluster (more than two SDs in 120 minutes). Patients without acute neurological deficits exhibited 94 single SDs and 82 as part of a cluster. The baseline level of lactate and glutamate were significantly higher in the group with acute neurological deficits. Relative to these baseline values, we found both a significant transient decrease in glucose and a transient increase in lactate in the group of clustered SDs but not in the case of single SDs. Pyruvate and glutamante were not significantly affected by either type of SD.
Conclusions: SDs occur in non-ischemic brain tissue. Clusters of SD are related to metabolic changes suggestive of ongoing secondary damage in primarily non-ischemic brain tissue.
