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People with epilepsy often report seizures precipitated by stress. This is believed to be due to effects of stress hormones, such as cortisol, on neuronal excitability. Cortisol, regardless of stress, is released in hourly pulses, whose effect on epileptic activity is unknown. We tested the relation between cortisol levels and the incidence of epileptiform abnormalities in the electroencephalogram of people with focal epilepsy. Morning cortisol levels were measured in saliva samples obtained every 15 min. Interictal epileptiform discharges were determined in the same time periods. We investigated the relationship between cortisol levels and the epileptiform discharges distinguishing persons with from those without stress-precipitated seizures (linear mixed model), and analysed the contribution of individual, epilepsy and recording characteristics with multivariable analysis. Twenty-nine recordings were performed in 21 individuals. Cortisol was positively related to incidence of epileptiform discharges (β = 0.26, P = 0.002) in people reporting stress-sensitive seizures, but not those who did not report stress sensitivity (β = -0.07, P = 0.64). The relationship between cortisol and epileptiform discharges was positively associated only with stress sensitivity of seizures (β = 0.31, P = 0.005). The relationship between cortisol levels and incidence of interictal epileptiform discharges in people with stress-sensitive seizures suggests that stress hormones influence disease activity in epilepsy, also under basal conditions.

SUMMARYPurpose: To evaluate the effect of stress on seizure frequency in childhood epilepsy, and to assess possible differences between children in whom seizures are precipitated by stress and those in whom they are not. Methods: Parents or caregivers of children with active epilepsy (aged 2-16 years) were sent questionnaires on developmental and epilepsy characteristics, life-time stress exposure, and the effect of stressful periods and moments of acute stress on seizure frequency in their child. Further information was extracted from patient files. Key Findings: Parents or caregivers of 153 children with a median age of 8.8 years responded to the questionnaires. Thirty-nine percent reported an increase in seizure frequency during periods of stress, with a median increase of 2.5 times the frequency compared to nonstressful periods.Thirty-seven percent reported that seizures were precipitated by acute stress, with stress being a precipitating factor in 33% (median value) of the seizures. Overall, 51% of the patients reported stress sensitivity of seizures. A higher number of negative life events experienced in total life was related to an increase in seizure frequency in stressful periods (odds ratio [OR] 1.3, p = 0.01) as well as to the precipitation of seizures by acute stress (OR 1.3, p = 0.02). Significance: Stress sensitivity is reported in half of the children with epilepsy. Results of this study suggest a relation between experienced negative life events and stress sensitivity of childhood epilepsy. One possible explanation could be that experiencing negative life events may cause a larger response to daily stressors, thereby increasing the likelihood to induce epileptic activity.

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SummaryObjective: The most common reported seizure-precipitant is stress. We recently showed a biologic basis for stress sensitivity of seizures: cortisol levels in people with stress-sensitive epilepsy correlated with focal interictal epileptiform discharges (IEDs) on electroencephalography (EEG). Here we aimed to determine whether the effect of cortisol on the epileptic brain is global or focal, and whether cortisol affects all brains or just those of stress-sensitive people. Because epilepsy is associated with changes in functional brain connectivity, we studied the relationship between cortisol and changes in global and focal (node-centered) functional connectivity measures for individuals with stress-sensitive and non-stresssensitive epilepsy. Methods: Seventeen people with epilepsy underwent long-term (>24 h) EEG recording. During the first 5 h after waking, saliva was collected every 15 min for cortisol measurements. Theta-band functional connectivity was assessed for every 15 min of the recording. We calculated the average phase-lag index (PLI) between all channels as a measure of global functional connectivity. We used network Strength, the averaged PLI per channel, as focal functional connectivity measure. We correlated cortisol, global, and focal functional connectivity (Strength) with IED frequency using linear mixed models. Analyses were split for people with and without stress-sensitivity of seizures. Results: Cortisol was negatively correlated with global functional connectivity in people with stress-sensitive seizures (estimate À0.0020; P < .01), whereas not in those without stress-sensitivity (estimate À0.0003; P = .46). This relationship occurred irrespective of the presence of IEDs on a channel (channels without IEDs and stress-sensitivity: estimate À0.0019; P < .01, non-stress-sensitive À0.0003; P = .41). Global and focal functional connectivity were negatively correlated with IED frequency, irrespective of stress sensitivity of seizures or channel type. Significance: People with stress-sensitive epilepsy have a whole-brain neuronal response to cortisol that is different from that of people with non-stress-sensitive epilepsy. This offers a basis for understanding seizure genesis in stress-sensitive epilepsy, which might require a different treatment approach.