Cortical spreading depression and peri-infarct depolarisation in human ischaemic stroke: a multicentre study (Co-operative Study on Brain Injury Depolarisations, COSBID)

• Published in: Aktuelle Neurologie
• Main Authors: Dohmen, C, Sakowitz, O, Fabricius, M, Bosche, B, Reithmeier, T, Ernestus, RI, Brinker, G, Dreier, JP, Woitzik, J, Strong, AJ, Graf, R
• Format: Conference Proceeding
• Language: English
• Published: 11.09.2007
• ISSN: 0302-4350; 1438-9428
• DOI: 10.1055/s-2007-987499

Objective: Cortical spreading depression (CSD) and peri-infarct depolarisation (PID) have been shown in various experimental models of stroke to cause infarct expansion and secondary neuronal damage. For many years it has been speculated that CSD/PID occur in patients with ischaemic stroke. Recently, CSD and PID have been documented in patients with subarachnoid hemorrhage and traumatic brain injury. In the present study, we report for the first time on CSD/PID in human ischaemic stroke. Methods: Patients were recruited by centres of the Co-operative Study on Brain Injury Depolarisations (COSBID). The study was approved by local ethics Committees. All patients suffered from complete or subtotal infarction of the MCA territory (malignant MCA infarction) and underwent decompressive hemicraniectomy. During the operation, a subdural electrode strip with 6 linear contacts were placed over the peri-infarct region of 16 patients. From these electrodes, 4 ECoG channels were acquired in a bipolar fashion; one electrode was used as ground. CSD was defined as gradually developing depression of ECoG activity with simultaneous slow potential changes (SPC) spreading between at least 2 channels. If local ECoG activity was suppressed at the time of the SPC, the event was defined as PID. Results: Monitoring was started between 24 and 109h after stroke and performed for up to 120h. The first patient had to be excluded from data analysis due to technical failure during the recording. From the following 15 patients, a total recording time of 1638h was scanned for depolarisation events. In 3 patients, no depolarisation events occurred. In these patients, the electrode strip was placed over infarcted tissue, i.e. hypodense tissue on CCT. Local ECoG activity was not present in these patients throughout the measurement. In the remaining 12 patients (80%), a total of 165 episodes of depolarisation events were recorded (147 CSD, 18 PID). Seizure activity did not occur in any patient. Conclusion: Similar to findings in experimental stroke models, CSD and PID are found with high incidence in patients with MCA infarction suggesting that this phenomenon is a relevant factor in the pathophysiology of ischaemic tissue damage and thus a target for treatment development.