A 37-year-old man with a VNS presented for further evaluation. The patient had focal seizures with impaired awareness and occasionally evolution to bilateral convulsive seizures since he was 18 years old. Several events were captured during an EMU admission, all of which localized to the right temporal region. An MRI of his brain did not reveal any structural abnormalities. Single-photon emission computed tomography (SPECT) (Figure F) and PET imaging (Figure G) suggested that a right temporal seizure focus. An MEG recording analyzed by SAM(g2) revealed a right mesial temporal focus centered on the hippocampus (Figure B) and amygdala (Figure C), with some occasional right ventral frontal, right posterior, and lateral temporal spread from this zone, and some additional spread to right insula. [While MEG is less sensitive to deep sources, others have successfully imaged hippocampus and amygdala (–), and given the invasive monitoring results and resection outcome listed below, the hippocampal and amygdalar sources seem reasonable.] While the raw MEG sensor data exhibited artifacts due the VNS, the source signal reconstructions from hippocampus and amygdala (Figure A) displayed no evidence of VNS artifact, with an SNR of 35:1 for the interictal spikes. While clear spikes existed in the source signal data, the EEG data only occasionally exhibited simultaneous interictal spikes.\nInvasive monitoring was planned on the basis of the concordant findings between MEG, SPECT, and PET. Subdural grids were placed over the lateral and mesial aspects of the right temporal lobe, and depth electrodes were inserted into the right amygdala and right anterior and posterior hippocampus. Frequent interictal spikes were seen on the hippocampal and amygdalar electrode contacts (Figure D), and several seizures arose from the anterior hippocampal and amygdalar electrodes, an example of which can be seen in Figure E.\nFollowing the invasive monitoring the patient received a right anterior temporal lobectomy with amygdalohippocampectomy. Prior to his surgery, the patient experienced ~2 seizures per month. Following surgery, the patient was seizure-free for several months, but experienced a breakthrough of two seizures following a reduction in lacosamide dosage, and another breakthrough of four seizures coincident with the onset of an illness.
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).