Symptomatogenic zone and network of oroalimentary automatisms in mesial temporal lobe epilepsy

Oroalimentary automatisms (OAAs) are common clinical manifestations of medial temporal lobe epilepsy. Nevertheless, the location of the symptomatogenic zone of OAAs remains unclear. The generation mechanism of OAAs also has not been clarified. We attempt to explain these problems by analyzing interictal [¹⁸ F]-fluorodeoxyglucose positron emission tomography (¹⁸ FDG-PET) imaging and ictal stereo-electroencephalography (SEEG) recordings in patients with medial temporal lobe epilepsy.

Fifty-seven patients with mesial temporal lobe epilepsy were analyzed retrospectively. All underwent anterior temporal lobectomy (ATL) and were seizure-free. The patients were divided into OAA (+) and OAA (-) groups according to the occurrence of consistent stereotyped OAAs. The interictal PET data were compared with those of 18 healthy controls and were then compared between groups using statistical parametric mapping (SPM). Functional connectivity using linear regression analysis was performed between the target brain regions. To clarify the network of OAAs, ictal epileptogenicity index (EI) values, and the nonlinear correlation method h² were performed with SEEG on patients.

Compared to OAAs (-), the rolandic operculum was the only area with significant differences. Hippocampus and rolandic operculum showed significant correlations in the OAA (+) group (y = 0.758x+0.470, R²  = 0.456, P = 0.000). No correlation was found in the OAA (-) group (P = 0.486). The EI values of the OAA (+) group (median 0.20) were significantly higher (P < 0.0001) than those of the OAA (-) group (median 0). The h² in the OAA (+) group (h²  = 0.23 ± 0.13) showed stronger functional connectivity (t = 6.166, P < 0.0001) than that of the OAA (-) group (h²  = 0.08 ± 0.05).

The rolandic operculum is most likely to be the symptomatogenic zone of OAAs. In medial temporal lobe epilepsy, unilateral functional connection from the hippocampus to the rolandic operculum during seizure onset is the basis for the generation of OAAs.