Abstracts

Rationale: Autoimmunity is a rising etiology for chronic focal epilepsy of unknown origin. Glutamic acid decarboxylase 65 antibodies (GAD65Abs) have been associated with both encephalitis and late-onset chronic temporal lobe epilepsy (TLE). Mesial temporal sclerosis (MST) is frequently seen at the time of diagnosis of patients. Methods: Retrospective Unicenter study of a cohort of patients with chronic temporal lobe epilepsy (TLE) and high GAD65Abs levels (RIA levels higher than 2000 UI) referred to the Neuroimmunology or Epilepsy Unit between 2003 and 2017. All patients underwent a 3T MRI study and we used FreeSurfer 6.0 automated pipeline for hippocampus segmentation into 12 bilateral subregions. Normalized volumes were analyzed. Mean diffusivity and fractional anisotropy was measured in each hippocampal segments and compared to 8 control patients with TLE of other etiologies. We aim to report hippocampal changes in the neuroimage of adult patients diagnosed with GAD65Abs related TLE. Results: Among 16 patients with TLE and high GAD65Abs levels, 11 fulfilled the criteria. Out of the 11 patients 8 had a 3 Tesla MRI with a median of 48 diffusion directions and were included for analysis, 6 of them females (75%). The median age was 29.5 (IQR: 32-26.5) and 5 suffered autoimmune comorbidities, mainly type 1 diabetes mellitus (n:4; 50%). The median duration of epilepsy was 7.92 years (IQR: 11.7-3.1). One of the patients had a unilateral and 2 had a bilateral MST. Seizure onset was characterized by focal aware sensory and autonomic seizures in 7 of the patients followed by impaired awareness in 6 of them. Average seizure frequency was daily in 3 patients, weekly in 1 patient, monthly in 2 patients and yearly in 1 patient. The difference in sex and age was not statistically significant between patients and controls. Significant reductions (p: 0.046) in left cornu ammonis area (CA 3-4) volume was found in patients (0.00013) compared to the control group (0.000094). No other hippocampal segment was significantly different. Conclusions: Anti-GAD TLE may be associated with specific structural hippocampal damage with higher neuronal loss and gliosis CA 3-4. This differs from classic MTS associated with febrile seizures and atrophy involving mainly CA1. Advanced imaging studies may allow outlining disease etiology. Funding: No funding