ObjectiveWe conducted a retrospective, case–control study of neurocysticercosis patients to ascertain early markers that identify subjects likely to develop treatment‐resistant seizures.MethodsClinical histories and imaging studies from 38 neurocysticercosis patients who had been followed for 18 months after treatment were evaluated. Both pairwise and multifactorial analyses were conducted to identify factors associated with continued seizures.ResultsEleven of 38 patients continued to have seizures during the follow‐up period. On univariate analysis, the number of neurocysticercosis lesions, number of bands on the baseline neurocysticercosis western blot, edema volumes on follow‐up MRI scans, edema volume changes between baseline and follow‐up images, and proportion of calcified lesions with perilesional edema were all significantly increased in subjects who had persistent seizures during the 18‐month follow‐up period. On multivariate analyses using recursive partition and random forest algorithms, variables associated with persistent seizures included: the number of total and calcified lesions, presence of perilesional edema, the rate of change in the lesion and edema volumes from baseline to follow‐up, and the number of bands on the neurocysticercosis western blot.InterpretationMeasures of both inflammation and disease burden are key risk factors for persistent seizures despite anticonvulsant treatments in patients with neurocysticercosis. Inflammation is therefore a potentially modifiable risk factor for the frequently seen severe seizure disorders in patients with neurocysticercosis.

Objective: Interictal spikes are a biomarker of epilepsy, yet their precise roles are poorly understood. Using long-term neocortical recordings from epileptic patients, we investigated the spatial-temporal propagation patterns of interictal spiking.Methods: Interictal spikes were detected in 10 epileptic patients. Short time direct directed transfer function was used to map the spatial-temporal patterns of interictal spike onset and propagation across different cortical topographies.Results: Each patient had unique interictal spike propagation pattern that was highly consistent across times, regardless of the frequency band. High spiking brain regions were often not spike onset regions. We observed frequent spike propagations to shorter distances and that the central sulcus forms a strong barrier to spike propagation. Spike onset and seizure onset seemed to be distinct networks in most cases. Conclusions:Patients in epilepsy have distinct and unique network of causal propagation pattern which are very consistent revealing the underlying epileptic network. Although spike are epileptic biomarkers, spike origin and seizure onset seems to be distinct in most cases.Significance: Understanding patterns of interictal spike propagation could lead to the identification patient-specific epileptic networks amenable to surgical or other treatments.

Background: Traumatic brain injury (TBI) remains a significant risk factor for post-traumatic epilepsy (PTE). The pathophysiological mechanisms underlying the injury-induced epileptogenesis are under investigation. The dentate gyrus—a structure that is highly susceptible to injury—has been implicated in the evolution of seizure development. Methods: Utilizing the murine unilateral focal control cortical impact (CCI) injury, we evaluated seizure onset using 24/7 EEG video analysis at 2–4 months post-injury. Cellular changes in the dentate gyrus and hilus of the hippocampus were quantified by unbiased stereology and Imaris image analysis to evaluate Prox1-positive cell migration, astrocyte branching, and morphology, as well as neuronal loss at four months post-injury. Isolation of region-specific astrocytes and RNA-Seq were performed to determine differential gene expression in animals that developed post-traumatic epilepsy (PTE+) vs. those animals that did not (PTE−), which may be associated with epileptogenesis. Results: CCI injury resulted in 37% PTE incidence, which increased with injury severity and hippocampal damage. Histological assessments uncovered a significant loss of hilar interneurons that coincided with aberrant migration of Prox1-positive granule cells and reduced astroglial branching in PTE+ compared to PTE- mice. We uniquely identified Cst3 as a PTE+-specific gene signature in astrocytes across all brain regions, which showed increased astroglial expression in the PTE+ hilus. Conclusions: These findings suggest that epileptogenesis may emerge following TBI due to distinct aberrant cellular remodeling events and key molecular changes in the dentate gyrus of the hippocampus.

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