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Seizure semiology represents the clinical expression of the activation of the several brain regions comprising an epileptic network. In mesial temporal lobe epilepsy (MTLE), this network includes the insular-opercular-neocortical temporal-hippocampal (IONTH) regions. In this study, we present the case of a patient with pharmacoresistant seizures characterized by nausea, lip-smacking, semipurposeful hand movements, and speechlessness, suggesting dominant hemisphere MTLE, with scalp video-EEG findings and left hippocampal sclerosis on brain MRI confirming the diagnosis. She underwent anterior temporal lobectomy with amygdalohippocampectomy and was seizure-free for 14 years before relapsing. Recurrent seizure semiology was similar to preoperative seizures, that is, consistent with left MTLE, despite the medial temporal lobe missing. Seizures were therefore assumed to arise from remnant portions of the IONTH network-the insula, operculum, and posterolateral temporal neocortex. Reinvestigation including MEG localization of spikes and acute MRI changes following a seizure cluster suggested a left opercular region epilepsy. Our patient thus demonstrated the principle that seizures with mesial temporal characteristics may arise from outside the mesial temporal lobe (MTL). MTLE semiology arises from the activation of a set of structures (the seizure network) associated with the MTL, which can be triggered by foci both within and outside the MTL itself, and indeed even in its absence. However, it is not necessary to resect the entire extended network to bring about extended periods of seizure freedom in patients with refractory MTLE.

Intracranial electroencephalography (iEEG) presents a unique opportunity to extend human neuroscientific understanding. However, typically iEEG is collected from patients diagnosed with focal drug-resistant epilepsy (DRE) and contains transient bursts of pathological activity. This activity disrupts performances on cognitive tasks and can distort findings from human neurophysiology studies. In addition to manual marking by a trained expert, numerous IED detectors have been developed to identify these pathological events. Even so, the versatility and usefulness of these detectors is limited by training on small datasets, incomplete performance metrics, and lack of generalizability to iEEG. Here, we employed a large annotated public iEEG dataset from two institutions to train a random forest classifier (RFC) to distinguish data segments as either 'non-cerebral artifact' (n = 73,902), 'pathological activity' (n = 67,797), or 'physiological activity' (n = 151,290). We found our model performed with an accuracy of 0.941, specificity of 0.950, sensitivity of 0.908, precision of 0.911, and F1 score of 0.910, averaged across all three event types. We extended the generalizability of our model to continuous bipolar data collected in a task-state at a different institution with a lower sampling rate and found our model performed with an accuracy of 0.789, specificity of 0.806, and sensitivity of 0.742, averaged across all three event types. Additionally, we created a custom graphical user interface to implement our classifier and enhance usability., (Copyright © 2023. Published by Elsevier Inc.)

Background: Pregabalin (PGB) is an effective adjunctive treatment for focal epilepsy and acts by binding to the alpha2-delta subunit of voltage-gated calcium channels to reduce excitatory neurotransmitter release. Limited data exist on its use in the neurocritical care setting, including cyclic seizures-a pattern of recurrent seizures occurring at nearly regular intervals. Although the mechanism underpinning cyclic seizures remains elusive, spreading excitation linked to spreading depolarizations may play a role in seizure recurrence and periodicity. PGB has been shown to increase spreading depolarization threshold; hence, we hypothesized that the magnitude of antiseizure effect from PGB is more pronounced in patients with cyclic versus noncyclic seizures in a critically ill cohort with recurrent seizures., Methods: We conducted a retrospective case series of adults admitted to two academic neurointensive care units between January 2017 and March 2019 who received PGB for treatment of seizures. Data collected included demographics, etiology of brain injury, antiseizure medications, and outcome. Continuous electroencephalogram recordings 48 hours before and after PGB administration were reviewed by electroencephalographers blinded to the administration of antiseizure medications to obtain granular data on electrographic seizure burden. Cyclic seizures were determined quantitatively (i.e., < 50% variation of interseizure intervals for at least 50% of consecutive seizures). Coprimary outcomes were decrease in hourly seizure burden in minutes and decrease in seizure frequency in the 48 hours after PGB initiation. We used nonparametric tests for comparison of seizure frequency and burden and segmented linear regression to assess PGB effect., Results: We included 16 patients; the median age was 69 years, 11 (68.7%) were women, three (18.8%) had undergone a neurosurgical procedure, and five (31%) had underlying epilepsy. All seizures had focal onset; ten patients (62.5%) had cyclic seizures. The median hourly seizure burden over the 48 hours prior to PGB initiation was 1.87 min/hour (interquartile range 1.49-8.53), and the median seizure frequency was 1.96 seizures/hour (interquartile range 1.06-3.41). In the 48 hours following PGB (median daily dose 300 mg, range 75-300 mg), the median number of seizures per hour was reduced by 0.80 seizures/hour (95% confidence interval 0.19-1.40), whereas the median hourly seizure burden decreased by 1.71 min/hour (95% confidence interval 0.38-3.04). When we compared patients with cyclic versus noncyclic seizures, there was a relative decrease in hourly seizure frequency (- 86.7% versus - 2%, p = 0.04) and hourly seizure burden (- 89% versus - 7.8%, p = 0.03) at 48 hours., Conclusions: PGB was associated with a relative reduction in seizure burden in neurocritically ill patients with recurrent seizures, especially those with cyclic seizures, and may be considered in the therapeutic arsenal for refractory seizures. Whether this effect is mediated via modulation of spreading depolarization requires further study., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.)