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 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.