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 6-year-old girl with a VNS implantation for pharmaco-resistant seizures presented from an outside institution for further evaluation. The patient was known to have a cortical dysplasia. The patient’s EEG revealed numerous distributed spikes, suggesting that the presence of multiple foci. Beamforming of the MEG recording with SAM(g2) revealed bilateral orbitofrontal activity with a much more kurtotic signal on the left than the right. SAM(g2) also identified bilateral temporal activation with a much greater involvement of the right hemisphere. There was an additional focus of lesser kurtosis encompassing the left insula and spreading to the left occipitoparietal cortex. The source signal reconstructions corresponding to these foci possessed an SNR of about 35:1 and exhibited numerous interictal spikes with simultaneous EEG spikes.