Generalised spike-wave discharges (GSW) in idiopathic generalised epilepsy (IGE) appear to have abrupt onset on EEG. However, in rodent models, GSW emerge during evolving brain network states. Using EEG-fMRI, Tangwiriyasakul et al. reveal that GSW onset in human IGE, as in rodent models, emerges during evolving brain network states.

Objective Slowing and frontal spread of the alpha rhythm have been reported in multiple epilepsy syndromes. We investigated whether these phenomena are associated with seizure control. Methods We prospectively acquired resting‐state electroencephalogram ( EEG ) in 63 patients with focal and idiopathic generalized epilepsy ( FE and IGE ) and 39 age‐ and gender‐matched healthy subjects (HS). Patients were divided into good and poor (≥4 seizures/12 months) seizure control groups based on self‐reports and clinical records. We computed spectral power from 20‐sec EEG segments during eyes‐closed wakefulness, free of interictal abnormalities, and quantified power in high‐ and low‐alpha bands. Analysis of covariance and post hoc t ‐tests were used to assess group differences in alpha‐power shift across all EEG channels. Permutation‐based statistics were used to assess the topography of this shift across the whole scalp. Results Compared to HS, patients showed a statistically significant shift of spectral power from high‐ to low‐alpha frequencies (effect size g = 0.78 [95% confidence interval 0.43, 1.20]). This alpha‐power shift was driven by patients with poor seizure control in both FE and IGE ( g = 1.14, [0.65, 1.74]), and occurred over midline frontal and bilateral occipital regions. IGE exhibited less alpha power shift compared to FE over bilateral frontal regions ( g = −1.16 [−0.68, −1.74]). There was no interaction between syndrome and seizure control. Effects were independent of antiepileptic drug load, time of day, or subgroup definitions. Interpretation Alpha slowing and anteriorization are a robust finding in patients with epilepsy and might represent a generic indicator of seizure liability.

The sensorimotor ERD quantifies activity of the brain during motor imagery tasks. Selection of the optimal baseline increases ERD.

ObjectiveCortical excitability differs between treatment responders and nonresponders in new‐onset epilepsy. Moreover, during the first 3 years of epilepsy, cortical excitability becomes more abnormal in nonresponders but normalizes in responders. Here, we study chronic active epilepsy, to examine whether cortical excitability continues to evolve over time, in association with epilepsy duration and treatment response.MethodsWe studied 28 normal subjects, 28 patients with moderately controlled epilepsy (≤4 seizures per year) and 40 patients with poorly controlled epilepsy (≥20 or more seizures per year). Resting motor threshold (RMT), active motor threshold (AMT), short‐interval intracortical inhibition (SICI), intracortical facilitation (ICF) and cortical silent period (CSP) were measured, using transcranial magnetic stimulation (TMS). Disease and treatment covariates were collected (age at onset of epilepsy, epilepsy duration, number of drugs prescribed, total drug load, sodium channel drug load).Results RMT and AMT were higher in patients than in normal subjects; RMT and AMT were higher in poorly controlled than moderately controlled patients. ICF at 12 msec and 15 msec were lower in poorly controlled patients than in normal subjects. Long‐interval intracortical inhibition (LICI) at 50 msec was higher in poorly controlled compared to moderately controlled patients. These differences were not explained by antiepileptic drug (AED) treatment or duration of epilepsy. RMT and AMT increased with duration in the poorly controlled group, but did not increase with duration in the moderately controlled group.InterpretationCortical excitability differs markedly between moderately controlled and poorly controlled patients with chronic epilepsy, not explained by disease or treatment variables. Moreover, the evolution of cortical excitability over time differs, becoming more abnormal in the poorly controlled group.

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