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 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.