Abstracts

The cause of seizures in patients with arachnoid cyst (AC) is thought to be secondary to the compression of adjacent cortex, associated cortical dysplasia (CD) or subpial gliosis according to anecdotal reports in the literature. The aim of our study is to systematically review the pathology around the cyst in patients with epilepsy treated with AC and cortical resection., We retrospectively reviewed patient data from epilepsy surgeries at the Cleveland Clinic Foundation between 1978 and 2006. Only those patients treated with resection of cyst and adjacent cortex were included in the study. Patients[apos] records were reviewed for demographic data, follow-up duration, EEG, MRI or CT imaging, and histopathology reports., Of 1880 patients, only 10 patients had AC and six were treated with cyst resection. There were five males and one female patient. The locations of the AC were in the left temporal fossa in four, left peri-rolandic region and right sylvian fissure in one each. Ictal onset zone was localized to the AC region in all patients. The mean duration of epilepsy was 12.2 + 8.8 years and the mean cyst size was 5.7 X 4.2 X 4 cms. Review of pathology showed mild subpial gliosis around the AC in all patients. Four of these showed normal adjacent cortex. However, one patient showed mild cortical dysplasia and another showed hippocampal sclerosis. At follow-up ranging from 9 [plusmn] 0.24 months, all 6 patients were seizure free (one patient had 3 seizures at 2 months and none thereafter). Patients with abnormal cortical pathology were found to have earlier onset, longer duration, and lower frequency of seizures., A cortical abnormality either independently or in association with subpial gliosis appears to be the cause of seizures in patients with AC. Identifying the cortical pathology preoperatively with the help of high-resolution MRI and a dedicated epilepsy imaging protocol could influence the type and extent of resection required. It is important to have proper orientation of the cyst and adjacent cortex in order to verify the pathological substrate for the seizures.,