Visual P3 abnormalities in patients with first-episode schizophrenia, unaffected siblings of schizophrenia patients and individuals at ultra-high risk for psychosis.

Cued version of the continuous performance test (AX-CPT) assesses sustained attention, working memory and cognitive control processes, which have been reported as impaired in schizophrenia. This study investigated visual P3 event-related potential elicited during cued CPT in patients with schizophrenia and in individuals who were at clinical or genetic high risk for psychosis to determine whether any abnormality may provide a marker of vulnerability for psychosis. Visual P3 elicited during cued CPT have not been reported in individuals at high risk for psychosis. Visual Go and NoGo P3 potentials were assessed in 34 antipsychotic-naive patients with first-episode schizophrenia (FES), 25 clinically unaffected siblings of these patients (familial high-risk for psychosis, FHR), 49 antipsychotic-naive individuals at ultra-high risk for psychosis (UHR) and 37 healthy control (HC) participants. FES patients had overall smaller P3 amplitudes than all other groups. P3 amplitude of the UHR participants was in-between the HC participants and FES patients. The anteroposterior P3 topography differed between the groups, with FES patients and FHR participants showing a more frontally distributed P3 compared with the HC participants. These findings suggest that the reduction in visual P3 amplitude may provide a vulnerability marker for psychosis in individuals who are at clinical high risk for psychosis and that a more frontally distributed visual P3 may be a marker of genetic liability for psychosis.

Relationship of negative symptom severity with cognitive symptoms and functioning in subjects at ultra-high risk for psychosis.

AIM: Negative symptoms and cognition are related with functioning in schizophrenia. However, it is not clear whether they have a similar effect in individuals at ultra-high risk (UHR) for psychosis. In this study, we aimed to explore relationship of negative symptoms with cognition and functioning cross-sectionally in people with UHR for psychosis. METHODS: In total, 107 people participated in this study. We assessed negative symptoms with Scale for Negative Symptoms (SANS). We applied a cognitive battery including seven tests. We evaluated functioning by using Global Assessment of Functioning Scale and work/study status as an indicator of role functioning. RESULTS: SANS scores were correlated to global functioning cross-sectionally. SANS total score was correlated to cognitive test scores related to cognitive flexibility and attention. Only Trail Making Test B (TMT B) was negatively correlated to global functioning. SANS-affective blunting and SANS-avolition scores were independently related to global functioning. There was a significant indirect effect of the TMT B and composite attention scores on global functioning through negative symptoms indicating a complete mediation. CONCLUSION: Our findings suggest that negative symptoms, particularly avolition have an impact on functioning and the association of cognition with functioning was mediated by negative symptoms in UHR.

Deficits in Go and NoGo P3 potentials in patients with schizophrenia.

Cognitive control processes elicited during a cued continuous performance test were evaluated using event-related potentials in 46 patients who were within the first 5 years of diagnosis of schizophrenia, and 29 healthy controls. Patients had longer reaction times, lower hit rates, and higher false alarm rates compared with controls. Patients had an overall P3 amplitude reduction that was more prominent on NoGo compared with Go trials. This greater P3 reduction on NoGo trials was present in central and parietal regions, but was absent in the frontal region, where the P3 reduction was comparable on NoGo and Go trials. Our findings suggest that the neural activity contributing to Go and NoGo P3s are both deteriorated in schizophrenia, but those contributing to central and parietal NoGo P3s are the most severely affected ones. We conclude that the cognitive control processes engaged during execution, and particularly during inhibition of a prepared motor response were disturbed in the early course of schizophrenia. Our findings might be related to our sample being in relatively early stages of schizophrenia and/or related to the use of atypical antipsychotics by most of our patients.

Lack of progressive reduction in P3 amplitude after the first-episode of schizophrenia: A 6-year follow-up study.

P3 event-related potential may track the course of neurophysiological pathology in schizophrenia. Reduction in the amplitude of the auditory P3 is a widely replicated finding, already present at the first psychotic episode, in schizophrenia. Whether a progressive deficit is present in auditory P3 in schizophrenia over the course of illness is yet to be clarified. Previous longitudinal studies did not report any change in P3 over time in schizophrenia. However, these studies have been inconclusive, because of their relatively short follow-up periods, lack of follow-up data on controls, and assessment of patients already at the chronic stages of schizophrenia. Auditory P3 potentials, elicited by an oddball paradigm, were assessed in 14 patients with first-episode schizophrenia and 22 healthy controls at baseline and at the 6-year follow-up. P3 amplitudes were smaller in patients with first-episode schizophrenia than in controls. Importantly, over the 6-year interval, the P3 amplitudes were reduced in controls, but they did not change in patients. The lack of P3 reduction over time in patients with schizophrenia might be explained by the maximal reduction in P3 already at baseline or by the alleviation of P3 reduction over time.

N2 and P3 potentials in early-onset and late-onset patients with obsessive-compulsive disorder.

BACKGROUND: Impaired cognitive control processes may be central in the pathogenesis of obsessive-compulsive disorder (OCD). Our objective was to evaluate cognitive control processes with event-related potentials in early-onset OCD (EO) and late-onset OCD (LO), which are suggested to have distinct characteristics. METHODS: Participants were unmedicated EO (n = 26) and LO patients (n = 33) without comorbid psychopathology and healthy controls (n = 54). Go/No-go tasks with 50 and 80% Go trial probabilities were implemented to manipulate the strength of response conflict and inhibitory demands. RESULTS: LO patients had shorter N2 latencies than controls and did not show the N2 amplitude increase seen in controls with the increase in Go trial probability as suggestive of abnormal conflict monitoring processes. Both EO and LO patients showed smaller P3 increase than controls with the increase in Go trial probability, suggesting problems in modifying attentional control with changes in task demands. P3 was more anteriorly distributed in LO patients than controls. Additionally, P3 increase, with the increase in Go trial probability, was larger in frontal and central sites than in parietal sites in controls, whereas in EO patients it was almost homogenous across anteroposterior sites. CONCLUSIONS: N2 processes were affected only in LO, whereas P3 processes were affected in both EO and LO, although, somewhat differently. P3 distributions suggest that EO and LO patients have differences concerning the contributions of frontal and parietal components of attentional networks to the execution of Go/No-go tasks. Our results imply that EO and LO are distinct subtypes affecting the cognitive control systems differently.

Cognitive deficits in clinical and familial high risk groups for psychosis are common as in first episode schizophrenia.

The aim of this study is to compare the neurocognitive functions in individuals with clinical or genetic risk for psychosis, in patients with first-episode schizophrenia (FES) and in healthy controls. We compared cognitive functions of 52 individuals at ultra high risk (UHR) for psychosis, 53 patients with FES, their 30 healthy siblings (familial high risk group, FHR) and controls. FES group had worse neuropsychological performance than controls in all of the domains. UHR group had worse performance in verbal learning, attention, and working memory than controls. Additionally, individuals at UHR with familial risk had worse performance on executive functions than the control group. FES group had lower global composite score than UHR group, and worse sustained attention than FHR group. FHR group had worse performance on executive functions and attention than controls. We found no difference in cognitive performances of UHR and FHR groups. Cognitive deficits in UHR and FHR groups were largely similar to those with FES. These findings support that cognitive deficits may arise before the first episode of schizophrenia.

P50 gating at acute and post-acute phases of first-episode schizophrenia.

Deficit in P50 sensory gating has repeatedly been shown in schizophrenia. In order to determine the contribution of trait and/or state features to P50 gating deficit in schizophrenia we evaluated the P50 gating in patients with first-episode schizophrenia (FES) at acute and post-acute phases. Subject groups comprised 16 patients with FES and 24 healthy controls. Patients were tested at the acute phase of the illness and retested at the post-acute phase when their positive symptoms improved. During the testing at the acute phase five patients were neuroleptic-naive and the others were taking atypical antipsychotics which were started recently in order to control the acute excitation. Patients were receiving risperidone, olanzapine or quetiapine treatment at the post-acute phase. P50 gating was impaired in patients at the acute phase compared to controls. However, at the post-acute phase P50 gating was increased compared to the acute phase, reaching to the gating values of controls. P50 gating improvement might be emerged from atypical antipsychotic medication, although this can only be definitively determined by randomized studies including different antipsychotics.

Mismatch negativity at acute and post-acute phases of first-episode schizophrenia.

The objective of this study was to evaluate the mismatch negativity (MMN) in patients with first-episode schizophrenia at acute and post-acute phases in order to determine the contribution of trait and/or state features to MMN disturbances in schizophrenia. Subject groups comprised 30 patients with first-episode schizophrenia at the acute phase and 34 healthy controls. Ten patients were neuroleptic-naive during testing at the acute phase. Twenty-one patients were retested at the post-acute phase when their symptoms improved. All patients were taking antipsychotic medication at the post-acute retest session. MMN amplitude of the patients at acute phase did not differ from controls. However, MMN amplitude at post-acute phase was reduced compared to both controls and acute phase. Similar results were obtained when the analyses were confined to neuroleptic-naive patients. The sensory memory functions indexed by MMN seem to be unaffected at the onset of schizophrenia but deteriorated during the post-acute illness phase. MMN reduction at the post-acute phase might be emerged from antipsychotic medication.

Novelty P3 and P3b in first-episode schizophrenia and chronic schizophrenia.

The objective of this study was to evaluate P3b and novelty P3 responses in patients with first-episode schizophrenia (FES) and chronic schizophrenia (CS). P3b is consistently reported to be reduced in CS. However, novelty P3 results in CS are controversial. Novelty P3 is not studied, and there are only a few P3b studies in patients with FES. Subject groups comprised 31 patients with FES and 36 younger control subjects, and 26 patients with CS and 35 older control subjects. Automatically elicited auditory novelty P3 and effortfully elicited auditory P3b potentials were assessed. P3b amplitudes were reduced in both patients with FES and CS relative to their controls. CS and FES patients did not differ in P3b amplitude. Novelty P3 amplitude was reduced in patients with CS. Novelty P3 amplitude in patients with FES did not differ from their controls. P3b amplitude reduction may be a trait marker of schizophrenia and may not progress over the course of illness, although this can only be definitively determined by longitudinal studies. Novelty P3 amplitude reduction present in patients with CS, is not found at the onset of illness. Novelty P3 seems unaffected early in the disease process.