Abstracts

RATIONALE: Stress is a common seizure precipitant in patients with epilepsy (Klein P, 2000). Pathophysiology of possible seizure facilitation by stress is unknown. In animal seizure models, cortisol exerts a proconvulsant effect. In the present pilot study, we examined the hypothesis that stress-related acute elevation of serum cortisol increases neuronal excitability in 3 patients with stress-related epilepsy.
METHODS: 3 patients with subjectively defined stress-sensitive localization-related epilepsy (LRE) of temporal lobe focus (TLE) underwent ACTH stimulation testing with simultaneous long term ambulatory EEG monitoring (AEEG). 250 mcg of ACTH was administered at 8 a.m. Serum cortisol and ACTH levels were drawn at times 0, 30, 60, and 90 miinutes, and 2, 3, 4, 5, and 6 hours after ACTH injection. AEEG monitoring was done continuously for 24 hours before and 24 hours after ACTH injection. EEG spikes frequency and spatial distribution was analyzed during 24 hours before and after ACTH injections.
RESULTS: In two patients, ACTH injection resulted in no spike frequency or distribution change. In the third patient, spike frequency was also unchanged. However, the spatial distribution of spikes widened. Spikes which had been reproducibly confined to the left sphenoidal and anterior temporal electrodes before the injection spread to involve the whole temporal area. This was seen from 30-180 minutes after ACTH injection and co-incided with serum cortisol elevation that ranged from 38.6-46.3 mcg/dl.
CONCLUSIONS: Acute elevation of cortisol may be associated with EEG spike facilitation in some patients with stress-sensitive TLE, indicating possible increase in neuronal excitability. Further studies are needed to determine the significance of this preliminary finding.
Support: No current funding.