As negative symptoms represent a complex aggregate of emotional and motivational deficits, we expected correlations between functional activity during the task and negative symptom severity to vary by symptom subtype. Furthermore, functional magnetic resonance imaging (fMRI) studies have identified decreased functional activation and connectivity within these regions. Other studies have identified a negative correlation between the severity of negative symptoms and cortical thickness in prefrontal cortex, superior temporal cortex and medial temporal cortex, including the hippocampus. A review of 25 schizophrenia studies showed that blood oxygenation level-dependent (BOLD) activity in ventrolateral prefrontal cortex and ventral striatum was inversely associated with negative symptom severity during executive functioning and reward conditioning tasks, respectively. Įlucidating the neural correlates of negative symptom severity in schizophrenia and its modulatory effects on cognitive function in schizophrenia is a vital step towards identifying relevant endophenotypes, uncovering the pathophysiological mechanisms that underlie them and developing targeted interventions. Although improvements in negative symptoms are associated with improved functional outcomes, including independent living skills, social functioning and role functioning, and as such targeting them may have significant functional benefits, identification of reliable targets for the treatment of negative symptoms remains an unmet clinical need. Negative symptoms have a high internal consistency and vary in severity independently of positive symptoms such as hallucinations and delusions. The presence of negative symptoms in unaffected first-degree relatives further suggests that the neural underpinnings of these deficits may be associated with a genetic liability for schizophrenia. They are of particular interest due to their resistance to current antipsychotic treatments and their persistence over the course of the illness. Negative symptoms in schizophrenia patients include diminished motivation, affective responsiveness, speech, movement, social engagement and hedonic pleasure, and are associated with poor functional outcome and quality of life. This work has potential to inform interventions that target these symptom-related neural disruptions. Conclusions: Individual symptoms were related to different patterns of functional activation during the oddball task, suggesting that individual symptoms might arise from distinct neural mechanisms. Results: The severity of alogia, avolition/apathy and anhedonia/asociality was negatively correlated with BOLD activity in distinct sets of brain regions associated with processing of the target tone, including basal ganglia, thalamus, insular cortex, prefrontal cortex, posterior cingulate and parietal cortex. Blood oxygenation level-dependent (BOLD) signal during the target tone was correlated with severity of five negative symptom domains from the Scale for the Assessment of Negative Symptoms. Methods: Functional magnetic resonance imaging was conducted on 89 schizophrenia patients and 106 healthy controls during a two-tone auditory oddball task. We analyzed data from the Functional Biomedical Informatics Research Network dataset to explore the relationship between individual negative symptoms and functional brain activity during an auditory oddball task. Previous studies have focused on negative symptoms as a single category however, individual symptoms might be related to separate neurological disturbances. These deficits are stable over the course of illness and respond poorly to current medications. Background: The negative symptoms of schizophrenia include deficits in emotional expression and motivation.
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