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 21-year-old man with an onset of seizures in 2004 presented for further evaluation. He had one febrile seizure in infancy and has a history of headaches. His events consisted of staring off for a few minutes, being unaware of surroundings, and exhibiting abnormal behavior and incomprehensible speech. He felt tired afterwards and typically had an aura of a right frontal headache. The patient’s seizure frequency was 1–2 per week, and his longest seizure-free interval was two years. The patient had tried multiple antiseizure medications but his seizures were insufficiently controlled under them. During a subsequent EMU admission, scalp EEG recorded several seizures originating in the left temporal region, and his interictal EEG was notable for occasional left temporal slowing and left temporal epileptiform activity. Ictal SPECT exhibited left occipital and left temporal hyperperfusion during one of these seizures, and a later interictal SPECT uncovered two possible anterior and posterior left temporal foci that were considered worrisome for seizure foci. The PET scan was negative. Structural MRI indicated a possible subtle form of hippocampal malrotation as well as two small foci of T2 hyperintensity in the bilateral frontal white matter that were nonspecific, but were thought to be the sequelae of prior ischemia, inflammation/infection, trauma or demyelination. In contrast, the patient’s MEG scan revealed a left occipital focus (A) with hundreds of MEG-only spikes visible on the virtual electrode (B). Based on the collective results, the patient received invasive monitoring with inter-hemispheric and left lateral occipital grids and left temporal depth electrodes. ICEEG confirmed the left occipital MEG focus as the seizure generator. The patient had a left occipital resection and had a few seizures shortly after surgery in the setting of medication nonadherence. Following this, he has been seizure-free for over a year.