Early effects of risperidone (2.5 ? 1 mg/day) on auditory information processing were investigated in 9 neuroleptic naive patients with schizophrenia spectrum disorders and 9 healthy controls by using event-related potentials (ERPs). ERPs were elicited during active auditory 'oddball' paradigm and were recorded before and after two weeks of treatment. Baseline P3 latencies were significantly delayed in patient group. Risperidone treatment did not change P3 amplitudes and latencies. However, P2 amplitudes were reduced in parallel with the clinical improvement measured by Positive and Negative Syndrome Scale (PANSS). Although risperidone did not change neural bases of active attention after two weeks of treatment, the reduction of P2 amplitude suggests that risperidone may affect auditory information processing in patients with schizophrenia spectrum disorders who never have been exposed to antipsychotic treatment.
ERPs could be helpful in the objectification of many psychological measures. In the last few decades one of the most commonly used ERPs has been the mismatch negativity (MMN) potential. It may be used to detect cognitive dysfunction in patients suffering from schizophrenia, dementia, depression, and can also be successfully applied in treatment monitoring. Nevertheless, changes of MMN parameters (prolongation of latency or reduction of amplitude) are not sufficiently specific to help to diagnose particular diseases. In this study we looked for more strict and specific MMN characteristics selective for schizophrenia. Fifteen healthy human subjects and twelve suffering from schizophrenia spectrum disorders were studied. Two new parameters were considered: the speed of ascending part of MMN slope (SAS) and the half area of the MMN wave. These two measures could differentiate the early stages of cognitive processing disturbances in schizophrenia spectrum disorders.
Correlations between measures of attention and topographical abnormalities of evoked cortical potentials elicited during the Continuous Attention Test (CAT) were assessed in 50 schizophrenic patients, compared to 50 healthy subjects. For each group and for each CAT condition evoked responses consisted of six successive epochs (segments) of stable spatially configured potentials. Quantitative descriptors of those configurations (Lehmann 1987) were referred to the CAT data. In patients: (1) segments III-V were delayed, (2) in the non-target condition, diminished global field power (GFP) emerged, coexisting either with lower amplitude of posterior potentials in segment I and II or with lower amplitude of a central positive potential in segment V, (3) an altered topographic pattern of responses to the target stimulus occurred. In healthy subjects detection of the target (as compared to the non-target condition) was associated with a shift of the location of the positive potential in segments IV and V from a central towards the prefrontal area. In patients, in segment V a similar shift reached frontal, but not prefrontal areas, and additionally, the central areas remained active. Delayed latency and low GFP in segment V in the non-target condition in patients correlated with poor CAT performance. A more posterior location of the positive centroid in segment V during detection of the target correlated with better CAT results, and the associated GFP increase with less prolonged reaction time. The data revealed a possible compensatory role of central and frontal areas in the face of weakened prefrontal functions in schizophrenia.
This study was designed to compare the performance of 50 chronic schizophrenics (CS) to that of 30 right brain-damaged patients (R), and 50 healthy controls (N) on several facial perception measures: Emotion Labelling and Recognition, and the Benton Facial Recognition Test. CSs were diagnosed according to DSM-IV criteria and their psychiatric state was assessed using the PANSS scale. All subjects were right handed. Their cognitive state was assessed using the MMSE. Subjects rated their current mood on a visual analogue scale. The results showed that the CSs and Rs were significantly impaired compared to Ns for the emotional tasks but did not differ from each other. Moreover, the patient groups were significantly less accurate in recognising emotionally neutral facial stimuli. Each subject group had more difficulty processing negative relative to positive affect. The deficit in schizophrenia was found to be stable, which may reflect a trait-like, rather than a state-dependent, characteristic. Moreover, some support is provided for the notion that facial affect perception in chronic schizophrenia is associated with right hemisphere dysfunction.
There is some evidence that the pathophysiology of schizophrenia is related to changes in the innate and adaptive immune systems. In an attempt to define a potential immunological dysfunction in schizophrenia, we measured the serum levels of several cytokines in the sera of 24 patients with paranoid schizophrenia and investigated the cytokine production in whole blood assays after stimulation in vitro with virus (Newcastle disease), phytohemagglutinin (PHA) or bacterial lipopolysaccharide (LPS) and compared them with healthy, normal controls. A significant increase of IL-6, IL-8 and IFN- gamma levels, but a decreased IL-10 level were observed in the sera of patients with schizophrenia. No significant changes in the serum levels of IL-2, IL-4, IFN-alpha and TNF-alpha were detected in these patients. When cytokine production in vitro was examined, a significant defect in PHA-induced IL-2, IL-4 and IFN-gamma, and in virus-induced IFN-alpha production, but no significant alterations in LPS-induced IL-6, IL-10 and TNF-alpha production were observed. In summary, increased serum levels of some cytokines such as IL-6, IL-8 and IFN-gamma indicate an activation of the inflammatory response in schizophrenia, while the in vitro assay indicates significant changes in the Th1 (decreased production of IL-2 and IFN-gamma) and Th2 (decreased production of IL-4) cell system responses. The role of the defective IFN-apha production in the regulation of the imbalance between Th1 and Th2 cell system responses is suggested.
Sensory gating in rats can be measured with a double click paradigm. The diminished response towards the second click is a physiological manifestation of reduced sensory input. This physiological process seems to be disturbed in human psychoses. It is thought that gating, as measured with this paradigm, is a preattentive, involuntary phenomenon which is not modulated by attention. If this is indeed the case, than it is hypothesized that gating should not be modulated by non-REM sleep. In the present experiment pairs of clicks (500 ms interval) were presented during wakefulness, non-REM as well as REM sleep and cortical auditory evoked potentials (AEP's) were recorded in chronically implanted rats. Rather similar AEP's were found after the first and second stimulus. However, the amplitudes of the various components of the second AEP were smaller than those of the first AEP, suggesting a gated response. This was the case during all three levels of vigilance. The amplitudes of both AEP's showed the more often reported changes in amplitude during sleep and REM sleep. Clear differences were seen in gating: compared to wakefulness a decrease in gating was found during REM sleep while gating was unchanged during non-REM sleep. The latter outcome seems to confirm that gating in rats is indeed a preattentive process. Finally, results were discussed in terms of neuronal properties of thalamic relay cells and it is suggested that firing properties of thalamic relay cells are not involved in this type of sensory gating.
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