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 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.