Original ArticlesSlow-wave sleep and ventricular size: a comparative study in schizophrenia and major depression
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.
Section snippets
Subjects
Twenty-eight inpatients were investigated. Fourteen patients (3 women, 11 men; age range: 21–43 years) had the first episode or an acute exacerbation of a schizophrenic disorder, paranoid type, according to DSM-III-R (American Psychiatric Association 1987; subchronic: n = 9; chronic: n = 5) and according to Research Diagnostic Criteria (RDC; Spitzer et al 1978). These patients had never been treated with psychoactive medications. The mean duration of illness was 26 ± 36 months (range: 7–144
Results
MANOVA applied to the EEG sleep parameters under investigation and the VBR revealed a significant main group effect (Wilks’ lambda = 2.65, p < .05). The univariate F tests within the MANOVA yielded the following results: as compared to the depressives, the schizophrenic patients had a significantly shorter sleep period time, a prolonged sleep onset latency, a shorter SWS latency, and a lower REM density index during the first REM period as well as averaged across all REM periods. The remaining
Discussion
The major findings in the present post hoc investigation were that the schizophrenic patients showed a more disturbed sleep continuity (shorter sleep period, longer sleep onset latency), a shorter SWS latency, and lower REM density indices than the depressed patients. Although the amount of SWS and the VBR values were well comparable in both disorders, a strong and positive association between SWS and VBR was ascertained in only the depressed patients.
Before discussing these findings in more
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