10. In vivo cortical spreading depression in epilepsy patients is not limited to clinically significant trauma

Abstract

Cortical spreading depression (CSD) – initially considered a correlate for migraine auras – has also been related to other neurologic diseases in vitro. In vivo it has been shown in stroke and trauma patients and was considered to be a sign of poor outcome (Strong, 2002; Fabricius 2006; Dreier et al., 2012). The aim of our study was to investigate CSD in epilepsy patients undergoing invasive presurgical video-EEG-monitoring, allowing to collect CSD-data in patients without severe brain damage. Data of 18 patients with pharmacoresistant epilepsy undergoing invasive video-EEG-monitoring with 44 up to 106 subdural electrodes and with a high pass filter of 0,02 Hz filter settings were evaluated. CSD was defined as a slow wave in the range of 1–5 mm/min with suppression of the normal EEG-activity. Data were related to the extent of periprocedural hemorrhage, the origin and number of seizures and histopathologic findings. In 7/18 patients we could detect CSD. Two of them developed a clinically symptomatic subdural hematoma (SDH), paralleled by an increase of CSD-frequency; in 4/7 subclinical hemorrhage or minor lesions could be demonstrated on MRI, while one patient showed no abnormality on MRI. In comparison, minor hemorrhage was documented in 5/11 patients without CSD. There was no obvious spatial or temporal relation of CSD to seizure onset. The main histopathological finding both in patients with and without CSD was focal cortical dysplasia. Our data show CSD for the first time in vivo in patients without major brain trauma in patients with epilepsy. The main finding was that CSD is not limited to major brain damage but might also appear after mild trauma without clinical relevance or even without detectable trauma. Out data did not show a temporal or spatial correlation of CSD to seizure onset or histopathological findings. However, larger numbers and a longer follow-up are necessary to draw conclusions about the clinical relevance of CSD in epilepsy patients.