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 21-year-old man with an onset of seizures in 2004 presented for further evaluation. He had one febrile seizure in infancy and has a history of headaches. His events consisted of staring off for a few minutes, being unaware of surroundings, and exhibiting abnormal behavior and incomprehensible speech. He felt tired afterwards and typically had an aura of a right frontal headache. The patient’s seizure frequency was 1–2 per week, and his longest seizure-free interval was two years. The patient had tried multiple antiseizure medications but his seizures were insufficiently controlled under them. During a subsequent EMU admission, scalp EEG recorded several seizures originating in the left temporal region, and his interictal EEG was notable for occasional left temporal slowing and left temporal epileptiform activity. Ictal SPECT exhibited left occipital and left temporal hyperperfusion during one of these seizures, and a later interictal SPECT uncovered two possible anterior and posterior left temporal foci that were considered worrisome for seizure foci. The PET scan was negative. Structural MRI indicated a possible subtle form of hippocampal malrotation as well as two small foci of T2 hyperintensity in the bilateral frontal white matter that were nonspecific, but were thought to be the sequelae of prior ischemia, inflammation/infection, trauma or demyelination. In contrast, the patient’s MEG scan revealed a left occipital focus (A) with hundreds of MEG-only spikes visible on the virtual electrode (B). Based on the collective results, the patient received invasive monitoring with inter-hemispheric and left lateral occipital grids and left temporal depth electrodes. ICEEG confirmed the left occipital MEG focus as the seizure generator. The patient had a left occipital resection and had a few seizures shortly after surgery in the setting of medication nonadherence. Following this, he has been seizure-free for over a year.