Authors: Laila Malani Mohammad, MD; Mohammad Abbas, MD; Rosstin Ahmadian, BS; C. Shuttleworth, PhD; Andrew Carlson (Albuquerque, NM)

Introduction: Most patients who undergo chronic subdural hematoma (cSDH) evacuation recover with a straightforward course. There is a subset of patients who do not improve or even worsen after evacuation. We hypothesize that worsening in some cases may be related to temporary brain dysfunction caused by cortical spreading depolarizations (CSD). Methods: Prospective observational study of 40 patients who underwent cSDH evacuation. At the time of surgery, a 1x6 subdural electrode strip was placed on the cortex parallel to the drain. CSD was scored using standard criteria of propagating DC shift, with associated depression of high frequency electrocorticography (ECog) activity. Results: Definite CSD occurred in 6/40 subjects (15%). There were no statistical differences in demographics between the populations, including age, gender, subdural characteristics, or pre-operative presentation. 4/6 subjects (67%) had resolution of their pre-operative symptoms. A clinical EEG was ordered in 2/6 subjects (33%), with no findings of seizures or epileptiform activity. One subject’s new deficit was observed 40 hours following the appearance of the first CSD, after the electrode strip was removed. The other subject, with clinical deterioration, had fluent speech immediately post-operatively but had documented aphasia 28 hours later, as reported by nursing. This correlated precisely with the first spreading depolarization seen on the patient’s electrode recording. The patient continued to have both aphasia and the presence of CSD until the removal of the strip electrode. Conclusion: This is the first observation of CSD occurring after cSDH evacuation, at a rate of 15%, in our series. One subject demonstrated delayed clinical deterioration after the electrode had been removed, and another subject demonstrated a time-locked clinical deterioration that correlated precisely with their first CSD. This data supports our hypothesis that CSD may be responsible for some cases of protracted recovery. This may represent a new therapeutic target in these patients.