Slow-wave sleep and ventricular size: a comparative study in schizophrenia and major depression

Abstract

Background: A slow-wave sleep (SWS) deficit and a shortened rapid eye movement (REM) sleep latency are commonly described in schizophrenia and depression. In addition, a close association between ventricular system measurements and SWS are reported in both disorders; however, a comparative, combined polysomnographic and computed tomographic investigation is lacking.

Methods: In the present post hoc study we analyzed the electroencephalographic sleep pattern and the ventricular brain ratio (VBR) of 14 drug-naive schizophrenic patients and of 14 depressed patients who were drug-free for a sufficient time period.

Results: Whereas the depressives showed the often described SWS and REM sleep changes, these measurements were quite normal in the schizophrenics. The VBR values were similar in both patient groups and exceeded in 71% of the schizophrenics and in 50% of the depressives the cutoff point of a “normal” VBR value. A close association between SWS and VBR was found in the depressives but not in the schizophrenics.

Conclusions: The results of the present study of drug-naive schizophrenic patients and of depressed patients indicate only a minor overlap between the pathophysiological changes observed in both disorders. Therefore, the present investigation adds evidence for the assumption that schizophrenia and depression are etiopathogenetically distinct entities, rather than representing points on a continuum of liability.

Introduction

In schizophrenia, a slow-wave sleep (SWS) deficit has been suggested to be the prevailing alteration in the electroencephalographic (EEG) sleep pattern, to be stable across nights, and to represent an abnormality of traitlike character Benson and Zarcone 1989, Keshavan et al 1992, Benson et al 1996. An elegant theoretical model relates this SWS deficit to a pronounced elimination of cortical synapses, which act in synchrony to produce the high-amplitude, low-frequency EEG activity typical for slow-wave sleep Feinberg 1983, Keshavan et al 1992, Benson et al 1996. This theory is supported by findings that an enlargement of the ventricular system in schizophrenia is negatively interrelated with slow-wave activity in the waking brain (Takeuchi et al 1994) and with visually scored SWS van Kammen et al 1988, Benson et al 1996. In addition, a shortened rapid eye movement (REM) latency is also a frequently cited EEG sleep finding in schizophrenia and has also been reported to be associated with an enlarged ventricular system (Keshavan et al 1991).

In major depression, a SWS deficit and a shortened REM latency have also been claimed as characteristic sleep changes for this disorder, in which, however, the most robust EEG sleep finding is an elevated index of rapid eye movements during REM sleep (REM density index; see Lauer et al 1991, Lauer et al 1995, Benca et al 1992). Furthermore, ventricular enlargement has been seen in about 30–40% of depressives (Jeste et al 1988), and ventricular brain ratio has been described to be closely associated with SWS measurements in depressed patients (Lauer et al 1992).

Thus, a number of polysomnographic and brain imaging observations appear to coincide well in patients with schizophrenia and with major depression, supporting the concept that both psychiatric disorders are not etiopathogenetically distinct entities, but represent points on a continuum of liability (e.g., Crow 1986); however, comparative studies addressing both EEG sleep and brain imaging in schizophrenia and depression are lacking, and even comparative sleep studies are rare and, moreover, provide conflicting results Ganguli et al 1987, Zarcone et al 1987, Kempenaers et al 1988, Hudson et al 1993, Benson and Zarcone 1993, Riemann et al 1994.

Based on our EEG sleep and cranial computed tomography (cCT) findings in depressed patients (Lauer et al 1992) and in drug-naive patients with schizophrenia (Lauer et al 1997), we hypothesized that the pattern of SWS and of REM sleep as well as their relationship to morphological brain alterations do not correspond in both psychiatric disorders. To test this hypothesis, we performed the present post hoc analyses, whereby the patients’ groups compared were part of our larger and independently performed sleep studies mentioned above.