P300 and symptom improvement in schizophrenia.

Psychopharmacology

PubMedID: 11685384

Gallinat J, Riedel M, Juckel G, Sokullu S, Frodl T, Moukhtieva R, Mavrogiorgou P, Nisslé S, Müller N, Danker-Hopfe H, Hegerl U. P300 and symptom improvement in schizophrenia. Psychopharmacology (Berl). 2001;158(1):55-65.
RATIONALE
A reduced amplitude of the auditory evoked P300 was interpreted as a trait marker of schizophrenia but reports about correlations between schizophrenic psychopathology and P300 amplitude indicate also a state character.

OBJECTIVES
To shed light upon these trait and state aspects a longitudinal study was performed to investigate the influence of symptom improvement and atypical neuroleptics on the amplitudes of the P300 and their subcomponents.

METHODS
P300 was recorded in 17 schizophrenic patients before and after 4 weeks under either clozapine or olanzapine in a double-blind controlled design. For comparison, 17 age- and sex-matched healthy subjects were investigated. Parietal and frontal P300 subcomponents were investigated separately using dipole source analysis.

RESULTS
Schizophrenic patients had smaller parietal (temporo-basal dipole) but not frontal subcomponent amplitudes (temporo-superior dipole) than controls. For the whole sample subcomponent amplitudes did not change over 4 weeks despite clinical improvement but patients with a pronounced improvement of the PANSS positive score showed a slight enhancement of both subcomponents. This was not significant when the P300 amplitude was measured at a single electrode (Pz). No significant difference between clozapine and olanzapine concerning effects on P300 amplitudes were observed.

CONCLUSIONS
The results indicate that P300 subcomponents are modulated by changes of positive but not by changes of negative symptoms or different neuroleptics. This result was obvious for P300 subcomponents but not for Pz electrode measurement, which may be due to a higher reliability of the dipole source activity. The results can be integrated into a hypothetical model containing two pathophysiological subgroups of schizophrenia.