Change in illness perception is associated with short-term seizure burden outcome following video-EEG confirmation of psychogenic nonepileptic seizures.

OBJECTIVES: We aimed to evaluate whether potential changes in the patient's illness perception can significantly influence short-term seizure burden following video-electroencephalography (EEG) confirmation/explanation of psychogenic nonepileptic seizures (PNES). METHODS: Patients with PNES were dichotomized to two groups based on a five-point Symptom Attribution Scale: (a) those who prior to diagnosis perceived their seizures to be solely ("5") or mainly ("4") physical in origin (physical group) and (b) the remainder of patients with PNES (psychological group). The physical group (n=32), psychological group (n=40), and group with epilepsy (n=26) also completed the Brief Illness Perception Questionnaire (BIPQ) prior to diagnosis, and were followed up at 3months as well as at 6months postdiagnosis. RESULTS: At 3months postdiagnosis, the physical group experienced significantly greater improvement in seizure intensity (p=0.002) and seizure frequency (p=0.016) when compared with the psychological group. The physical group was significantly more likely to have modified their symptom attribution toward a greater psychological role to their seizures (p=0.002), and their endorsement on the BIPQ item addressing "consequences" (How much do your seizures affect your life?) was significantly less severe (p'=0.014) when compared with that of the psychological group and the group with epilepsy. At 6months postdiagnosis, the physical group continued to experience significantly greater improvement in seizure intensity (p=0.007) while their seizure frequency no longer reached significant difference (p=0.078) when compared with the psychological group. The physical group continued to be significantly more likely to have modified their symptom attribution toward a greater psychological role to their seizures (p=0.005), and their endorsement on the BIPQ item addressing "consequences" remained significantly less severe (p'=0.037) when compared with the psychological group and the group with epilepsy. CONCLUSIONS: Among patients with PNES, prediagnosis perception of seizures as "solely" or "mainly" physical in cause may be associated with greater likelihood of early postdiagnosis improvement in seizure burden. Within this physical group postdiagnosis, we uncovered preliminary evidence for significantly greater attribution toward psychological roles in seizures as well as reduction in cognitive distortion surrounding the adverse consequences of seizures. These findings portend particular impact of such changes in illness perception for this group.

Cardiac asystole associated with seizures of right hemispheric onset.

Ictal asystole is frequently underrecognized despite being a potentially lethal condition. We report two cases of ictal asystole with right hemispheric onset. These cases are unique since previous literature reports that seizures associated with bradyarrhythmias typically arise from left hemispheric foci. These cases further underscore the importance of clinical vigilance and the need of an enhanced diagnostic biomarker.

Neuroprotective effects of leptin following kainic acid-induced status epilepticus.

We investigated the potential neuroprotective effects of leptin (LEP) against cellular damage, long-term recurrent spontaneous seizures, and behavioral changes associated with kainate (KA)-induced status epilepticus (SE). Adult Sprague-Dawley rats were sacrificed 24 hours after KA injections, and hippocampi were subjected to histological analysis. In the acute condition, one group received 12 mg/kg KA intraperitoneally (KAac group), and another group received 12 mg/kg KA intraperitoneally, followed by two intraperitoneal LEP injections of 4 mg/kg each, 1 and 13 hours after KA (KALEPac group). For long-term outcomes, one group received KA (KA group), and the other group received three intraperitoneal LEP injections (4 mg/kg at 1 hour, and 2mg/kg at 13 and 24 hours) after KA (KALEP group). Controls were sham manipulated. Behavioral tests started 6 weeks after SE. All rats that received KA underwent behavioral seizures of comparable severity. Compared with the KAac group, the KALEPac group had significantly larger pyramidal cell surface areas and fewer black-stained degenerating neurons with silver stain. The KALEP and KA groups were comparable with respect to recurrent spontaneous seizures, aggression, hyperactivity, and impaired memory. We show that leptin reduces cellular injury associated with KA-induced SE, but does not prevent long-term recurrent spontaneous seizures and behavioral deficits.