Abstract
Neurocognitive deficits and negative symptoms (NS) have a pivotal role in subjects with schizophrenia (SCZ) due to their impact on patients’ functioning in everyday life and their influence on goal-directed behavior and decision-making. P3b is considered an optimal electrophysiological candidate biomarker of neurocognitive impairment for its association with the allocation of attentional resources to task-relevant stimuli, an important factor for efficient decision-making, as well as for motivation-related processes. Furthermore, associations between P3b deficits and NS have been reported. The current research aims to fill the lack of studies investigating, in the same subjects, the associations of P3b with multiple cognitive domains and the expressive and motivation-related domains of NS, evaluated with state-of-the-art instruments. One hundred and fourteen SCZ and 63 healthy controls (HCs) were included in the study. P3b amplitude was significantly reduced and P3b latency prolonged in SCZ as compared to HCs. In SCZ, a positive correlation was found between P3b latency and age and between P3b amplitude and the Attention-vigilance domain, while no significant correlations were found between P3b and the two NS domains. Our results indicate that the effortful allocation of attention to task-relevant stimuli, an important component of decision-making, is compromised in SCZ, independently of motivation deficits or other NS.
Highlights
IntroductionA mild to severe impairment in neurocognitive skills is present in the majority of subjects with schizophrenia, independently of the severity of symptoms
The outcomes of the analysis revealed a reduction in P3b amplitude and a delayed peak in response to target stimuli in subjects with schizophrenia as compared to healthy controls
P3b was noticeably affected in subjects with schizophrenia
Summary
A mild to severe impairment in neurocognitive skills is present in the majority of subjects with schizophrenia, independently of the severity of symptoms This impairment can be detected throughout different phases of schizophrenia, such as the premorbid, prodromal and remission stages of the illness or even in non-affected relatives of subjects with schizophrenia [15,16,17,18,19,20,21,22,23,24,25,26,27]. Impairments in these functions might be explained as the cumulative effect of abnormalities in processes such as early neurodevelopment, neuronal maturation and neuroplasticity, leading to faulty cortico–cerebellar–thalamic–cortical circuits [30,31,32,33,34,35,36]
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