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.
A 37-year-old man with a VNS presented for further evaluation. The patient had focal seizures with dyscognitive symptoms and occasionally evolution to bilateral convulsive seizures since he was 18 years old. Several events were captured during an epilepsy monitoring unit (EMU) admission, all of which localized to the right temporal region. An MRI of his brain did not reveal any structural abnormalities. SPECT (F) and PET imaging (G) suggested a right temporal seizure focus. A MEG recording analyzed by SAM(g2) revealed a right mesial temporal focus centered on the hippocampus (B) and amygdala (C), with some occasional right ventral frontal, right posterior, and lateral temporal spread from this zone, and some additional spread to right insula. While the raw MEG sensor data exhibited artifacts due the VNS, the virtual electrode data from hippocampus and amygdala (A) displayed no evidence of VNS artifact. While clear spikes existed in the virtual electrode data, the EEG data only occasionally exhibited simultaneous interictal spikes. Invasive 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 (D), and several seizures arose from the anterior hippocampal and amygdalar electrodes, an example of which can be seen in E. Following 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 dose reduction in antiseizure medication, and another breakthrough of four seizures coincident with the onset of an illness.