Abstract
BackgroundAs a refractory negative symptom, social anhedonia is prevalent in people with schizophrenia spectrum disorders. Furthermore, schizophrenia is conclusively correlated with disorganized functional brain network reflected by topological profile. However, studies on the relationship between social anhedonia and topological properties of functional brain network in schizophrenia were limited to a large extent. In the present study we explored the neurofunctional mechanism of social anhedonia in schizophrenia from the perspective of topological profile of functional brain network.MethodsSix-minute resting-state fMRI images were acquired from 65 patients with schizophrenia in a 3T SIMENS scanner. Topological properties of functional brain network derived from the resting-state fMRI image, including clustering coefficient, global efficiency and small-worldness were calculated. The social anhedonia of each participant was measured with the Chapman Social Anhedonia Scale. Due to the wide-range of duration of illness in patients with schizophrenia, we included the duration of illness, social anhedonia and their interaction into a generalized linear model to predict the three topological properties, with gender, age and education years as covariates.ResultsWe found that the clustering coefficient of brain functional network in schizophrenia increased (p = 0.032, beta = 0.000194 at the minimum network sparsity 35% in which all the nodes were fully connected), whereas the global efficiency decreased (p = 0.005, beta = -0.000022), as the progression of schizophrenia. Although the main effect of social anhedonia in predicting both the clustering efficient and the global efficiency were not significant, its interaction with the duration of illness was significant (p = 0.021, beta = 0.000038 for the clustering coefficient; p = 0.023, beta = -0.000003 for the global efficiency).DiscussionWith the development of schizophrenia, the increase of clustering coefficient and decrease of global efficiency of functional brain network may reflect the pathophysiology of schizophrenia since the onset of illness. Social anhedonia plays as a mediator between the altered topological profile of brain network and the progression of schizophrenia.
Highlights
Recent meta-analysis revealed that elevated presynaptic striatal dopaminergic function is a robust feature of psychosis like schizophrenia
Previous studies have examined the effects of clozapine on regional cerebral blood flow using radiotracer approaches in relatively small samples of patients, showing, in particular, frontal and limbic perfusion changes[1,2,3]
We evaluate the effects of clozapine on regional cerebral blood flow (rCBF), measured with a non-invasive MRI technique - pulsed continuous arterial spin labelling - which does not require radiotracer injection, as part of an ongoing study to identify neuroimaging predictors and mediators of clozapine response
Summary
Insufficient response to antipsychotics constitutes a challenge in the treatment of patients suffering from schizophrenia. Treatment resistances have been linked to a normal striatal dopamine system. We aim to stratify antipsychotic-naïve first-episode patients based on striatal dopamine synthesis capacity (DSC) measured with positron emission tomography (PET). We hypothesize that patients who respond to treatment have an increased DSC at baseline compared to non-responders and healthy controls (HC). Methods: The current data have been collected as a part of a multimodal first episode study. Patients are examined before and after 6 weeks treatment with flexible doses of Aripiprazole. PET: Dynamic scans are performed in an integrated PET-CT scanner using the tracer 3,4-dihydroxy-6-[18F]fluoro-L-phenylalanine (18F-FDOPA). Duration of scanning is two times one hour, with half an hour break
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