• Maria Sueiras, Vanessa Thonon, Estevo Santamarina, Ángela Sánchez-Guerrero, Marilyn Riveiro, Maria-Antonia Poca, Manuel Quintana, Dario Gándara, and Juan Sahuquillo.
• Department of Clinical Neurophysiology, Vall d'Hebron University Hospital, Paseo Vall d'Hebron 119-129, 08035, Barcelona, Spain. msueiras@vhebron.net.
• Neurocrit Care. 2021 Jun 1; 34 (3): 876-888.

ObjectiveSpreading depolarizations (SDs) have been described in patients with ischemic and haemorrhagic stroke, traumatic brain injury, and migraine with aura, among other conditions. The exact pathophysiological mechanism of SDs is not yet fully established. Our aim in this study was to evaluate the relationship between the electrocorticography (ECoG) findings of SDs and/or epileptiform activity and subsequent epilepsy and electroclinical outcome.MethodsThis was a prospective observational study of 39 adults, 17 with malignant middle cerebral artery infarction (MMCAI) and 22 with traumatic brain injury, who underwent decompressive craniectomy and multimodal neuromonitoring including ECoG in penumbral tissue. Serial electroencephalography (EEG) recordings were obtained for all surviving patients. Functional disability at 6 and 12 months after injury were assessed using the Barthel, modified Rankin (mRS), and Extended Glasgow Outcome (GOS-E) scales.ResultsSDs were recorded in 58.9% of patients, being more common-particularly those of isoelectric type-in patients with MMCAI (p < 0.04). At follow-up, 74.7% of patients had epileptiform abnormalities on EEG and/or seizures. A significant correlation was observed between the degree of preserved brain activity on EEG and disability severity (R [mRS]: + 0.7, R [GOS-E, Barthel]: - 0.6, p < 0.001), and between the presence of multifocal epileptiform abnormalities on EEG and more severe disability on the GOS-E at 6 months (R: - 0.3, p = 0.03) and 12 months (R: - 0.3, p = 0.05). Patients with more SDs and higher depression ratios scored worse on the GOS-E (R: - 0.4 at 6 and 12 months) and Barthel (R: - 0.4 at 6 and 12 months) disability scales (p < 0.05). The number of SDs (p = 0.064) and the depression ratio (p = 0.1) on ECoG did not show a statistically significant correlation with late epilepsy.ConclusionsSDs are common in the cortex of ischemic or traumatic penumbra. Our study suggests an association between the presence of SDs in the acute phase and worse long-term outcome, although no association with subsequent epilepsy was found. More comprehensive studies, involving ECoG and EEG could help determine their association with epileptogenesis.

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