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Disruptions of frontoparietal control network and default mode network linking the metacognitive deficits with clinical symptoms in schizophrenia

The metacognitive deficit in awareness of one's own mental states is a core feature of schizophrenia (SZ). The previous studies suggested that the metacognitive deficit associates with clinical symptoms. However, the neural mechanisms underlying the relationship remain largely unknown. We here...

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Detalles Bibliográficos
Autores principales: Jia, Wenbin, Zhu, Hong, Ni, Yinmei, Su, Jie, Xu, Rui, Jia, Hongxiao, Wan, Xiaohong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267896/
https://www.ncbi.nlm.nih.gov/pubmed/31789478
http://dx.doi.org/10.1002/hbm.24887
Descripción
Sumario:The metacognitive deficit in awareness of one's own mental states is a core feature of schizophrenia (SZ). The previous studies suggested that the metacognitive deficit associates with clinical symptoms. However, the neural mechanisms underlying the relationship remain largely unknown. We here investigated the neural activities associated with the metacognitive deficit and the neural signatures associated with clinical symptoms in 38 patients with SZ using functional magnetic resonance imaging with a perceptual decision‐making task accompanied with metacognition, in comparison to 38 age, gender, and education matched healthy control subjects. The metacognitive deficit in patients with SZ was associated with reduced regional activity in both the frontoparietal control network (FPCN) and the default mode network. Critically, the anticorrelational balance between the two disrupted networks was substantially altered during metacognition, and the extent of alteration positively scaled with negative symptoms. Conversely, decoupling between the two networks was impaired when metacognitive monitoring was not required, and the strength of excessive neural activity positively scaled with positive symptoms. Thus, disruptions of the FPCN and the default mode network underlie the metacognitive deficit, and alternations of network balance between the two networks correlate with clinical symptoms in SZ. These findings implicate that rebalancing these networks holds important clinical potential in developing more efficacious therapeutic treatments.