Background and aims: Recent data have revealed that clinically generalised tonic–clonic seizures do not involve all brain regions electrophysiologically. The hippocampus in particular could be protected from epileptic activity by putative filtering properties of the dentate gyrus. Here we investigated if simple or complex focal seizures (SFS/CFS) and in particular secondarily generalised tonic–clonic seizures (SGS) of extrahippocampal onset (EHO) spare the hippocampus and if there are promotive factors.
Methods: We retrospectively assessed clinical, electrophysiological, imaging and histopathological data from patients undergoing presurgical evaluation of focal epilepsy with hippocampal depth and extrahippocampal subdural electrodes and selected those suffering from SGS of EHO. We further subdivided this patient sample according to qualitative MRI criteria into a HL(−) group, with an extrahippocampal lesion only, and a HL(+) group, displaying an extrahippocampal and additional hippocampal lesion.
Results: 14 patients (seven in each group) fulfilling the inclusion criteria had a total of 43 SGS, of which 35 were of EHO. Whereas only 68% of SFS/CFS of EHO propagated into the hippocampus, all SGS of EHO invaded the hippocampi independently of the ictal propagation pattern or degree of hippocampal pathology. All hippocampi in the HL(−) group displayed interictal epileptiform activity and even seizure onset in two patients.
Conclusions: In our patient sample, the human hippocampus was not spared during SGS of EHO, but was invariably invaded by epileptic activity. The presence of spontaneous epileptic activity in the HL(−) group revealed persistent modifications in hippocampal excitability that might be due to secondary epileptogenesis in the hippocampus following repeated seizures of EHO.
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Competing interests: None.
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