Sleep EEG Stages and Plasma Growth Hormone Concentration in States of Endogenous and Exogenous Hypercortisolemia or ACTH Elevation

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Abstract
Nocturnal sleep EEG stages and concomitant plasma growth hormone (GH) and cortisol concentrations were examined in subjects with endogenous or exogenous elevation of plasma corticosteroid or ACTH concentrations, and in patients with hypothalamic tumors. These studies were designed to determine whether central nervous system (CNS) function was uniquely altered in Cushing's disease, independent of the effects of hypercortisolemia per se. Marked reductions of sleep EEG stages III-IV and of the nocturnal GH rise were present in 4 treated (remission 5 months to 2 yr) and 6 untreated patients with Cushing's disease (clinically active 2 months to 10 yr duration) as well as in 4 “eu-corticoid” patients with hypothalamic tumors. In contrast, similar EEG and hormonal changes, present in a patient with Cushing's syndrome secondary to an adrenal adenoma, returned to normal 16 months following removal of the adenoma. These findings suggest that altered CNS function may be involved in the pathophysiology of Cushing's disease. The return of normal percentages of Stages III-IV sleep and normal nocturnal growth hormone increments following removal of the adrenal adenoma, suggest, however, that cortisol excess plays some role in the observed sleep EEG and GH changes. Suppression of Stage III-IV sleep in the patient with the adrenal adenoma prior to treatment, and lack of suppression in patients receiving chronic prednisone therapy (15–60 g. daily for 4 months to 10 yr) suggests either differential effects of synthetic and natural steroids, or different effects of intermittent exogenous steroid therapy as compared to continuous endogenous secretion. Normal sleep EEG stages in 4 patients with Cushing's disease who subsequently developed Nelson's syndrome also suggests a possible role for ACTH in the genesis of sleep EEG stages.

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