Abstracts

Abnormal hippocampal shape and orientation have been previously reported in patients with focal epilepsy (Baulac et al. [italic]Ann Neurol[/italic] 1998:44:223-233). Typical MRI appearance consisted of incomplete folding of the hippocampus (Hc) with abnormal medial location along the choroid fissure, globular shape or verticalization. The purpose of this study is to assess the epileptogenicity of HcDC through evaluation of depth electrode recording (SEEG). We retrospectively analyzed all epileptic patients (n=69) who had at least bilateral temporal lobe depth electrode implantation between 1995 and 2003. We performed hippocampal volumetric study and analysis of the hippocampal shape and orientation abnormalities and reviewed interictal and ictal SEEG findings. Fifteen of 69 patients were found to have abnormal shape and orientation of the Hc (unilateral in 10 cases and bilateral in 5, hence there were 20 Hc with HcDC and 10 without). Eleven had extratemporal depth or peg electrodes in addition to temporal implantation. Fifteen patients (7 men) with HcDC were studied. Eight had only HcDC on MRI. Seven also had extraHc lesions: three had ischemic lesions in the posterior quadrant and four periventricular nodular heterotopia. There was concomitant hippocampal atrophy in nine (unilateral in 6 and bilateral in 3). Ictal semiology suggested widespread or multifocal neocortical involvement with temporal predominance in nine and extra-temporal in six patients. Surface EEG interictal findings were mainly temporal, but ictal onsets were predominantly bilateral or widespread.
Eighteen (90%) of 20 Hc with developmental abnormality showed active interictal epileptiform abnormalities (IEA) during SEEG whereas five of 10 without such abnormality had IEA (p=0.02, Fischer[rsquo]s exact test). All patients showed in addition extraHc IEA: amygdala, 12 (6, bilateral); temporal neocortex, 10 (2, bilateral); and extratemporal, 3 (1, bilateral). Eleven (55%) Hc with HcDC had ictal onset restricted to the abnormal Hc whereas only one (10%) without HcDC showed this (p=0.02). All patients except one however had in addition seizure onsets involving other temporal or extratemporal structures. In a highly selected group of patients with intractable focal epilepsy we found abnormal shape and orientation of Hc in 21.7%. Although we recorded interictal and ictal SEEG epileptiform activity coming from the HcDC in the majority of patients, large and multiple epileptogenic zones were found in most (14/15). These findings suggest that HcDC have intrinsic epileptogenicity, but very likely as part of a more extensive disturbance of brain development. (Supported by the Savoy Foundation for Epilepsy and EK by the Preston Robb fellowship (MNI).)