Cerebral glucose metabolic response to combined total sleep deprivation and antidepressant treatment in geriatric depression

Objective: The treatment of geriatric depression is complicated by a variab le and delayed response to antidepressant treatment. The present study was undertaken to test the hypothesis that combined total sleep deprivation and paroxetine treatment would produce a persistent reduction in glucose metab olism in the anterior cingulate cortex similar to that reported after long- term antidepressant treatment. Method: Six elderly depressed patients who m et the DSM-IV criteria for major depressive disorder and six age-matched co mparison subjects underwent serial positron emission tomography (PET) studi es at baseline, after total sleep deprivation, after recovery sleep (after the initial paroxetine dose), and after 2 weeks of paroxetine treatment (pa tients only). The PET data were analyzed by using statistical parametric ma pping methods. Results: The patients' scores on a 13-item version of the Ha milton Depression Rating Scale were decreased after total sleep deprivation , after recovery sleep, and after 2 weeks of treatment. The Hamilton depres sion scores of the comparison subjects were not significantly altered. In t he patients, the greatest reductions in normalized, relative glucose metabo lism after sleep deprivation were observed in the anterior cingulate cortex (Brodmann area 24), and they persisted after recovery sleep and antidepres sant treatment. The comparison subjects demonstrated increased metabolism i n these areas. Conclusions: Improvement in the patients' depressive symptom s was accompanied by reduced glucose metabolism in the right anterior cingu late cortex and right medial frontal cortex. These preliminary data indicat e that in elderly depressed patients, total sleep deprivation may accelerat e the clinical and glucose metabolic response to antidepressant treatment.