Abstracts

Focal cortical dysplasia (FCD) is a common cause of surgically remediable focal epilepsy. The frequent occurrence of FCD in the perirolandic region makes a complete surgical resection without a permanent neurological deficit challenging. We aimed to identify the range of functional morbidity following this type of surgery, and identify variables associated with a worse outcome. We reviewed the clinical and invasive electroencephalographic (EEG) data of adult patients with perirolandic FCD who underwent invasive EEG and cortical mapping prior to surgery (N=16). Eleven patients had a new sensorimotor neurological deficit after surgical cortical resection. Using a detailed analysis of the subdural grid electrode mapping, the number of electrodes that showed; 1) interictal epileptiform activity, 2) EEG seizure onset, and 3) eloquent function during cortical electrical stimulation, were identified and correlated with the extent of the surgical resection. The neurological examination was performed and postoperative seizure outcome was examined at the 6 months, and latest postoperative visits. The average age at surgery was 22 years. Patients with type 2B pathology (64% vs. 20%), and a later age of epilepsy onset were more likely to have a postoperative deficit (median 5.9 vs. 0.6 years). The neurological examination before surgery was abnormal in only 2 of the 16 patients. The mean length of follow-up was 3.47 years. In patients with a postoperative neurological deficit, the mean number of electrodes involved in interictal and ictal epileptiform activity was 5.5 and 4.8 respectively. In patients without a postoperative neurological deficit, the mean number of electrodes involved in interictal and ictal epileptiform activity was 2.2 and 2.8, respectively. The mean number of electrodes with eloquent activity whose underlying cortex was removed was 3 in the deficit group compared to 0.4 in the normal group. Sixty percent of patients without a deficit had an Engel I outcome at latest follow-up, compared to 45% of the group with a deficit. Patients without a postoperative deficit were more likely to have a lesion on their MRI scan (80% vs. 45%), and a more localized epileptogenic focus as evidenced by EEG data. All patients with a postoperative deficit improved to a mild deficit (at least 4/5 MRC grade power) at follow-up, and in 3 patients the neurological deficit subsided completely. The identification of a more localized epileptogenic zone, by MRI or EEG criteria correlated with improved functional (and seizure) outcome after surgery. The removal of eloquent cortex defined by cortical stimulation was associated with an increased risk of deficit. However, despite the neurological deficits incurred postoperatively, the majority of patients regained functional use of the paretic limb at 6 months and later follow-up.