A 58-year-old man with VNS implantation 2 years prior to his MEG recording presented for further evaluation. The patient’s seizures began at age 1 year old after an episode of meningitis. His seizures began with staring and fidgeting with his hands and exclamations of “Thank you Jesus.” The seizures occasionally evolved to bilateral convulsive seizures. Seizure frequency did not improve with phenobarbital, phenytoin, primidone, carbamazepine, valproic acid, oxcarbazepine, topirimate, levetiracetam, zonisamide, or pregabalin. An MRI of his brain revealed left hippocampus sclerosis. Upon EMU admission, several seizures were captured, with localization to the left frontotemporal region.\nThe MEG recording captured the patient’s most frequent interictal epileptiform activity, a left frontal spike, as seen on the simultaneous scalp EEG. The original data analysis was complicated by the VNS-induced artifact, and the attempted localization was performed by marking spike times in the EEG, and ECDs were then computed from the MEG data on the corresponding times. The initial interpretation of spikes in the MEG recording analyzed with ECD was only that the spikes lateralized to the left hemisphere. However, later analysis of this MEG recording with SAM(g2) identified a peak in kurtosis in the left orbital frontal cortex in spite of the artifact from the patient’s VNS (Figure A). The source series reconstruction for this focus lacked the high-amplitude artifact present in the raw MEG sensor data, and epileptiform activity with an SNR of at least 35:1 was evident in the clean source signal series for this voxel, which was coincident with epileptiform activity seen by scalp EEG (Figure B).\nAs the localizing information from the beamformed MEG data was not available initially, placement of invasive monitoring was planned based on the abnormalities seen on MRI (left mesiotemporal sclerosis, Figure E) and positron emission tomography (PET) (left frontotemporal hypometabolism, Figure F). Three depth electrodes were placed into each temporal lobe. A total of seven strip electrodes were placed over the frontal and temporal cortex bilaterally, although the peak that was later identified from the MEG beamforming was not covered. Several seizures were captured with a possible focus in the left anterior temporal lobe, and the patient had a left anterior temporal lobectomy with amygdalohippocampectomy (Figure D). Following resection the patient’s seizure frequency improved slightly, from about four seizures monthly to two to three seizures monthly. His seizure semiology changed in that he no longer verbalized at the beginning of his seizures. However, the patient’s notable interictal epileptiform activity on scalp EEG, a left frontotemporal spike, remained unchanged following his resection. Further analysis of the MEG recording with source signal analysis at the sites of the left temporal depth electrodes and the right temporal depth electrodes identified MEG activity in the left temporal lobe that correlated with episodes of left temporal slowing on the scalp EEG and that appeared independent of the left frontotemporal spikes (Figure C).
A 63-year-old right-handed woman with VNS implantation 6 years prior to her MEG recording presented for further evaluation. Since age 18 months old the patient had focal seizures with impaired awareness and occasional evolution to bilateral convulsive seizures. Her auras were typified by staring off, ringing in her ears, and a nauseated feeling. The patient experienced feelings of déjà vu prior to bilateral convulsive seizures. Prior EEG evaluation had revealed bitemporal interictal spikes, more frequent over the left than the right hemisphere. Seizures were captured and appeared electrographically generalized. The patient had a choroid cyst adjacent to her right hippocampus, but otherwise the MRI of her brain was unremarkable. Primidone, lacosamide, and lamotrigine had not provided adequate seizure control. An MEG recording, beamformed with SAM(g2), indicated widespread activity with a left lateral temporal as well as left lateral frontal activity and a left mesial occipital–parietal focus. Source signal series from these areas displayed no evidence of VNS artifact and had an SNR of at least 35:1 for the interictal spikes relative to baseline activity.\nBased on information obtained from her EEG and MEG recordings, the patient underwent invasive monitoring. Bilateral subdural strips were placed in the orbitofrontal, lateral temporal, and inferior temporal regions. Bilateral depth electrodes were also placed in the amygdale and anterior and posterior hippocampi. Because, a resection of the occipital/parietal focus would have likely resulted in deficits, it was not covered by grids or strips.\nThe invasive monitoring captured six seizures arising from the right hemisphere and seven seizures arising from the left hemisphere. Of this total, five events were electrographic seizures and two were electro-clinical seizures. The monitoring revealed that the patient had independent seizures arising from broad fields in both hemispheres. On this basis, it was felt that the patient was a poor surgical candidate for seizure reduction or freedom, and the grids and strips were explanted.