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 24-year-old man whose focal seizures began at age 7 presented for further evaluation. During his episodes, the patient was reported as having a surprised look on his face, covering his mouth with his hands, and laughing. These episodes happened several times per day and were followed by marching movements of the legs and grunting noises. The patient had no alteration of consciousness during his seizures. He also experienced hypermotor seizures arising out of sleep at least nightly and often had several per night. The patient sustained bilateral frontal lobe damage, intraparenchymal hemorrhages, and extra axial hemorrhages following a severe fall in 2006. He was seen by several neurologists before coming to WFBH.\nThe patient’s epilepsy was refractory to multiple antiseizure medications. His initial EMU admission in 2001 was unable to localize the seizure onset zone. The interictal EEG showed very frequent epileptiform discharges arising from the right frontal region, but PET showed mild decreased activity in the left medial temporal lobe which was consistent with an epileptogenic focus. Both ictal and interictal SPECT indicated slightly asymmetric activity within the temporal lobes with the right side greater than the left, also suggestive of an epileptogenic focus within the left temporal lobe. Because of the discordant findings, the patient proceeded to invasive monitoring. ICEEG pointed towards a right frontal lobe origin, but the pattern of spiking occurred almost simultaneously with patient’s clinical semiology. At that time, it was felt that the seizure focus was not clearly localized to warrant right frontal lobectomy. The patient then received a VNS in addition to medication, and this combination was effective for several years.\nThe patient began to experience more problems around 2012 and was recommended for a MEG scan. The patient’s MEG data were very noisy owing to metal hardware in his skull that covered the burr holes from his previous invasive monitoring, but SAM(g2) sufficiently removed these artifacts and revealed a single focus in the right middle frontal gyrus (A) with numerous, MEG-only spikes (B). (Because the head is magnetically transparent, MEG is not susceptible to breach effects from craniotomies or other defects.) The MRI obtained for the MEG scan also revealed a small focus of cortical thinning and irregularity with subtle T2 hypointensity in the right frontal lobe. Based on the MEG results, the patient underwent invasive monitoring with a stereo-EEG array placed over the MEG focus (C). The patient’s epileptiform activity (green arrowhead, D) was subsequently localized to the three ICEEG contacts (green arrows) nearest to the peak of the SAM focus (red sphere, C). The patient then received a right frontal lobe resection of the seizure focus and has been seizure free since.