Rationale: Patients who had seizures in the setting of acute encephalitis have a 22% risk to develop epilepsy by 20 years (3). Surgical
outcomes requires precise localization of epileptogenic focus in this population.
Methods: We discuss two patients with post-encephalitis intractable focal epilepsy. Data includes history, semiology, scalp EEG findings, MRI Brain, PET, SPECT and stereo-EEG findings.
Results: Patient 1 had GTC at age 36, after encephalitis and had 10 GTCs per year.
Treatments failed until surgery at age 50. There are two semiologies, one with no clinical signs for 14-40 seconds, nonsensical speech, non-versive left head turn, left facial tonic contraction with sign of four (extension left arm) and GTC. The second had an auditory aura of a familiar song, and GTC. MRI brain was negative. PET showed bilateral hypometabolism in perisylvian, insular and mesial temporal regions. SPECT showed hyperperfusion in posterior perisylvian regions and insula, mainly on the right, and in mesial temporal structures (Figure 1). Scalp EEG showed seizures arising from bilateral fronto-temporal regions. SEEG showed spikes in the right temporal operculum, STS, and mesial temporal structures. Ictal onset was in the lateral neocortical posterior perisylvian region, starting with STS and lateral contacts of MTG, anterior STS and involvement of ITG and mesial temporal structures (Figure 1).
Patient 2 seizures began after viral encephalitis at age 24. By 39 two prior epilepsy surgeries had failed. Semiology began with “hearing something from far away”, tingling of the right hand and/or leg, right face tonic contraction, right gaze deviation and GTC. The second had the auditory aura, oral automatisms, left face tonic, left hand dystonic posture, GTC.
MRI showed encephalomalacia in the right temporal region with perilesional gliosis. PET showed hypometabolism there and in the
contralateral temporal lobe. SPECT showed hyperperfusion in the right > left insular and perisylvian regions. Scalp EEG lateralized to the left hemisphere with typical seizures. SEEG showed spikes in bilateral temporal opercula, parahippocampal/fusiform gyrus, posterior insula, left amygdala, hippocampus and entorhinal cortex. Ictal onset was localized to independent bilateral Heschl’s gyri, posterior perysilvian regions followed by insula.
Conclusions: In post-encephalitic epilepsy, the network includes posterior perisylvian regions, STS, Heschl’s gyrus, posterior/anterior insula with spread to mesial temporal structures. Poor surgical outcomes can be due to misconceptions that mesial temporal structures are the main epileptogenic zone. Previous research has shown failure to achieve seizure freedom in 52% of patients.
These two patients have a wide epileptic network primarily involving the posterior perisylvian regions with spread to mesial temporal structures. Considering such complexity, hypotheses should include posterior perisylvian networks despite evidence of MTS involvement. Stereo-EEG is therefore critical to localize the epileptogenic zone, maximizing the efficacy of surgical treatment. Funding: None