ABSTRACT
Sleep deprivation (SD) is an effective and rapid antidepressant in a subset of depressed patients (1). The antidepressant and cerebral metabolic effects of total sleep deprivation (TSD) or partial sleep deprivation (PSD) for one night have been studied with functional neuroimaging. Despite the variations in methods and techniques, the overall findings were relatively consistent. First, in most studies, before SD, responders have significantly elevated metabolism compared with nonresponders and normal controls, in the orbital medial prefrontal cortex and especially the ventral portions of the anterior cingulate cortex. Second, after SD these hyperactive areas normalize in the responders. Ebert and colleagues (2) first reported this finding in a single photon emission computed tomography (SPECT) scan study of 10 patients (Table 1). Wu and colleagues (3) first reported this finding of higher glucose metabolic rate with PET scans in depressed responders in 1992. This initial finding was subsequently extended to a larger group of depressed patients (4). We reported that depressed responders were higher at baseline in the medial prefrontal cortex, ventral anterior cingulate, and posterior subcallosal gyrus than depressed nonresponders. However, Smith et al. (5) noted that geriatric depressed patients did not show higher anterior cingulate activity than normal controls prior to SD. One functional imaging study suggested that synaptic dopamine release was associated with the antidepressant effects of TSD;
the neurochemical implications of this finding are explored and possible neurotransmitter mechanisms are discussed.
