Brief report
P300 changes in major depressive disorders with and without psychotic features

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Abstract

Background: Although there are many P300 studies in depressive patients, only a few studies have focused on the effects of psychotic features in depression and of response to antidepressant treatment on P300. This study was designed to investigate possible differences in the P300 component of event-related potentials in depressed patients with and without psychotic features and if any, to see whether these changes altered with treatment of depression. Methods: Thirty-six patients with major depressive disorder diagnosed according to DSM-IV, and 20 healthy control subjects were involved in the study. Sixteen of the patients had psychotic features. Auditory P300 was recorded before treatment and after remission. Results: Pretreatment P300 latencies were significantly prolonged both in patients with and without psychotic features compared to controls. Pretreatment P300 amplitudes were significantly decreased only in the patients with psychotic features. After treatment of depression, delayed P300 latencies in both patient groups and decreased P300 amplitude in the patient group with psychotic features were normalized. Limitations: The medication status of the patient was heterogeneous. Conclusion: Since the impairment seems to be improved by drug treatment, prolonged P300 latency might be a state marker for a major depressive episode, and decreased P300 amplitude which is correlated with paranoid ideation might be more associated with psychotic subtype.

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

References (25)

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