A 31-year-old right-handed woman with implantation of a VNS 3 years prior to her MEG recording presented for further evaluation. Since age 5 years old the patient had focal seizures that began with a “funny feeling,” flushing, and head turning to the right. Some seizures terminated at this point, while at other times her seizures progressed to impair awareness and/or evolved into a bilateral convulsive seizure. Treatment with acetazolamide, carbamazepine, valproic acid, and levetiracetam failed to improve the woman’s seizure frequency. An MRI did not demonstrate any structural brain abnormalities. An epilepsy monitoring unit (EMU) evaluation captured seizures with a broad, right hemispheric onset. An initial MEG recording prior to VNS implantation captured epileptiform activity, which was originally and unsuccessfully analyzed using ECD modeling. The interpretation at the time was that the MEG study did not provide localizing information.\nSynthetic aperture magnetometry (g2) was used to analyze a second MEG recording after the VNS implantation, as well as the previous recording performed prior to VNS implantation. Even though the second recording was separated from the first by 6 years and the raw MEG sensor data were strongly contaminated by artifact from the VNS during the second recording, an equivalent right frontal focus was identified on both recordings (Figure A). This indicates that SAM can reproducibly localize interictal epileptiform activity despite the presence of large artifacts due to the VNS implant. Examination of the source signal series reconstructed from the focus demonstrated MEG discharges that correlated with the simultaneously recorded scalp EEG during the second recording (Figure C), and, importantly, that lacked the high-amplitude fluctuations present in the raw MEG data that were induced by the VNS (Figure B). (For comparison, the raw MEG sensor data prior to VNS implantation are depicted in the top part of Figure B.) Furthermore, during the patient’s second MEG recording an electrographic seizure was recorded by EEG, with a preceding MEG-recorded discharge detected in the source signal series (Figure D). The SNR for the virtual electrodes was at least 50:1.\nGiven the new localizing information provided by the MEG recordings, the patient was determined to be a candidate for invasive monitoring and possible resection. A subdural grid was placed over the right frontal lobe, covering the focus identified on MEG (Figure F). Seizures captured during the invasive monitoring demonstrated electrographic onset (Figure E) very close to the focus of peak kurtosis identified by SAM(g2) on the MEG recordings (Figure F). Following resection, which included the focus identified by SAM(g2), the patient experienced a significant improvement in her seizures, improving from four to six focal seizures with loss of awareness and sometimes evolution to bilateral convulsive seizures monthly to two to four focal seizures with retained awareness monthly. Her scalp EEG recordings demonstrated a greatly reduced frequency of interictal epileptiform activity.
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).