Relationship between DST Nonsuppression and Shortened REM Latency in Schizophrenia Rajiv Tandon, Catherine Lewis, Stephan F. Taylor, James E. Shipley, John R. DeQuardo, Michael Jibson, and Mona Goldman Key Words: Schizophrenia, sleep, REM latency, cortisol, dexamethasone suppression test, cholinergic BIOL PSYCHIATRY 1996;40:660-663 Introduction Nonsuppression of cortisol following dexamethasone adminis- tration (DST nonsuppression) and short REM latency were originally considered to be "biological markers" of major depres- sive disorder (MDD) (Carroll et al 1981; Rush et al 1982; Reynolds and Kupfer 1987). Several recent studies have, how- ever, documented both these abnormalities in a substantial number of schizophrenic patients (Zarcone et al 1987; Holsboer- Trachsler et al 1987; Tandon et al 1991a, 1992; Keshavan and Tandon 1993). Although many hypotheses have been advanced, the neurobiological basis of these abnormalities in MDD and schizophrenia is not precisely delineated. In MDD, a strong association between these findings has been observed in both correlational and categorical analyses (Asnis et al 1983; Rush et al 1983; Kerkhofs et al 1986), leading to the suggestion that a common pathophysiological mechanism or process may underlie the findings of short REM latency and DST nonsuppression in MDD (Poland et al 1989). The relationship between DST nonsuppression and shortened REM latency in schizophrenia has not been studied; knowledge about this relationship may be useful in defining the neurobiological underpinnings of these abnormalities in schizophrenia. The present study was conducted in order to evaluate this issue. The sleep data from most of these patients was summarized in a previous report (Tandon et al 1992) From the Schizophrenia Program, University of Michigan Medical Center, Ann Arbor, Michigan. Address reprint requests to Rajiv Tandon, MD, UH-8D-8806, University of Michigan Hospitals, Box 0116, Ann Arbor, M1 48109-0116. Received September 29, 1995; revised March 28, 1996. Presented at the 49th annual meeting of the Society of BioLogical Psychiatry, Philadelphia, May 20, 1994. as was the DST data (Tandon et al 1991a). The relationship between DST and sleep findings has not previously been re- ported. Methods The study sample consisted of inpatients hospitalized at the University of Michigan Schizophrenia Program over a four-year period (1988-1991) who had both sleep electroencephalographic (sleep-EEG) studies and a dexamethasone suppression test (DST) performed. Diagnostic evaluation included a structured interview using the Schedule for Affective Disorders and Schizo- phrenia, (SADS, Endicott and Spitzer 1978); all subjects had to meet DSM-III-R (American Psychiatric Association 1987) and Research Diagnostic Criteria (RDC, Spitzer et al 1978) for schizophrenia for inclusion in the study. Patients with a history of current or recent (< 6 months) alcohol or other substance abuse were excluded, as were those with current or recent evidence of a significant medical disorder. Patients were medication-free for a minimum of 2 weeks prior to the study. At medication-free baseline, all patients were rated on the brief psychiatric rating scale (BPRS, Overall and Gorham 1962), Scale for the Assess- ment of Negative Symptoms (SANS, Andreasen 1983), and the 17-item Hamilton Rating Scale for Depression (HRSD, Hamilton 1960) by a rater who was blind to the DST and sleep-EEG data. Positive symptom severity was assessed by the sum of four BPRS items: conceptual disorganization, suspiciousness, hallu- cinatory behavior, and unusual thought content (Kane et al 1988; Tandon et al 1990); negative symptoms were assessed by the SANS sum of global scores, and depressive symptoms by the HRSD total score. © 1996 Society of Biological Psychiatry 0006-3223/96/$15.00 PI1 S0006-3223(96)00205-3