A 31-year-old woman with spells preceded by visual symptoms of macropsia and micropsia and olfactory auras presented for further evaluation. Following the auras, the patient often exhibited right eye deviation and tonic flexion of the right upper extremities followed by a loss of awareness and generalized tonic-clonic events of 2–3 min in length. Afterwards, the patient experienced mild confusion and was tired for tens of minutes. She also had jerking of her arms and legs during sleep and the patient’s husband was unable to arouse her. The patient’s auras occurred every few days. She had 1–2 daytime spells a month, and she estimated that she had several more nighttime spells. These spells had been captured on routine EEG and during two EMU admissions and no electrographic change suggestive of seizure was noted. Neither a CT nor an MRI demonstrated any structural brain abnormalities. Treatment with several antiseizure medicines failed to provide adequate relief, and the patient had allergic reactions to some of the medicines. Despite the significant concern that her spells were nonepileptic in nature, given the severity of her events the patient received a diagnostic MEG scan.\nSAM(g2) identified three foci of epileptiform activity during her MEG scan: one focus in the left posterior temporal/lateral occipital cortex (A), and bilateral mesial temporal foci (not shown). The left posterior temporal/lateral occipital cortical focus was likely responsible for her visual symptoms, and the bilateral mesial temporal foci were likely responsible for her olfactory auras as the irritable zones encompassed entorhinal cortex. The irritability of the mesial temporal cortices was initially supported by bilateral sphenoidal electrodes, which detected interictal epileptiform activity. Importantly, MEG captured two seizures during the recording which originated within the posterior temporal/lateral occipital cortex, and neither of these seizures was discernable on EEG (B). Based on the MEG localizing information, ICEEG was performed as part of a presurgical evaluation. During a recorded seizure, ICEEG demonstrated early epileptiform activity (red channel, D) at electrodes (green) near the SAM(g2) peaks (red crosses, C). While ICEEG confirmed the localization of the three SAM(g2) foci, it also corroborated the MEG finding that the posterior temporal/lateral occipital focus was indeed the seizure initiator. Interestingly, the morphology of the ICEEG seizure was very similar to the morphology of the MEG seizure; both started with an initial spike, then exhibited a period of fast activity, and then evolved into a rhythmic discharge. Because the patient’s primary focus encompassed part of visual cortex, she decided against surgery to avoid a potential visual field defect. However, the MEG findings were still useful as they definitively identified the patient as having epilepsy. The patient is currently being considered for responsive neurostimulation device (RNS) placement.
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).