Brief reportP300 changes in major depressive disorders with and without psychotic features
Introduction
Psychotic features in depression not only change the clinical representation of the syndrome but also have very low response rate to antidepressant therapy (Glassman et al., 1975, Kocsis et al., 1990). In addition to hypofunctioning noradrenergic and serotonergic brain systems with low prefrontal brain perfusion, depressive patients with psychotic features have larger ventricles, poor neuropsychological performance, and a hyperdopaminergic state (Rothschild et al., 1989, van Praag and Verhoeven, 1980, Mazure et al., 1987, Tutus et al., 1998). Some authors (Schatzberg and Rothschild, 1992) have argued that depression with psychotic features should be a distinct syndrome in DSM although there is very limited electrophysiological information about this subject.
Initially a few reports have shown that the P300 (P3) wave was not different from those of controls in depressive patients, but recently a number of studies reported depressive patients have smaller P3 amplitude or longer latency (Bruder et al., 1991, Gordon et al., 1986, Pfefferbaum et al., 1984, Schlegel et al., 1991, Vandoolaeghe et al., 1998). Only Santosh et al. (1994) addressed the issue of psychosis in melancholic depression in their study which showed a significant negative correlation between psychotic features and P3 amplitude. But in that study the effect of treatment was not mentioned.
The aim of the present study was to investigate whether the P3 is a potential marker for psychotic subtype of depression and if so, whether it is a trait or state marker. Therefore, the study evaluated the possible P3 changes in depressive patients with psychotic (DwPF) and without psychotic features (DwoPF) both before medication and after remission.
Section snippets
Subjects
Thirty-six in-patients (20 male and 16 female) diagnosed as major depressive disorder according to DSM-IV criteria were included in the study (Table 1). None of the patients had a history of manic or hypomanic episode, heavy alcohol consumption or head trauma. A diagnosis was reached independently by at least two psychiatrists. Only the patients who had not taken any psychotropic drugs (including benzodiazepines) for at least 4 weeks were included in the study. All patients gave written
Results
There were no significant differences between the patient and control groups in age or education status (Table 1). HAM-D scores decreased significantly with treatment in both groups.
Discussion
The present study supports previous findings that P3 latency is longer in depressive patients (Bruder et al., 1991, Vandoolaeghe et al., 1998, Himani et al., 1999). In other studies this finding was more prominent in typical major depressive patients and correlated with retardation and insomnia (Bruder et al., 1991, Schlegel et al., 1991). Our results show that this delay is reversed with the treatment. The fact that we did not find any correlation between HAM-D scores and P3 latency might be
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