OBJECTIVE Theory of mind (ToM) is the ability to infer others' mental (Cognitive) and emotional (Affective) states, both being impaired in Parkinson's disease (PD). However, the clinical, neuropsychological, and neuropsychiatric… Click to show full abstract
OBJECTIVE Theory of mind (ToM) is the ability to infer others' mental (Cognitive) and emotional (Affective) states, both being impaired in Parkinson's disease (PD). However, the clinical, neuropsychological, and neuropsychiatric features underlying Affective and Cognitive ToM deficits in PD are unclear. Therefore, we performed a meta-analytic study to test whether PD demographical, clinical, neuropsychological, or neuropsychiatric changes related differently to both ToM processes. METHOD A systematic literature search was performed up to January 2022, including a total of 31 studies following our search terms. Data from each study were obtained from demographic (age, education), clinical (disease duration, Hoehn & Yahr staging system, Unified Parkinson's Disease Rating Scale-III, levodopa equivalent daily dose), neuropsychological (global cognitive functioning, memory subdomains, executive functions subdomains, processing speed/complex attention/working memory, visuospatial and constructional abilities, and language), and neuropsychiatric (depression, apathy, anxiety) variables. RESULTS Affective ToM impairment in PD was related to lower educational level and global cognition, deficits of generativity, decision making, attention/working memory, and language. Conversely, Cognitive ToM deficits were associated with advanced age, poorer global cognition, executive dysfunctions, and language impairments. Medication moderated the relationship between attention/working memory and Cognitive ToM, whereas age moderated the association of Affective ToM with language. No significant associations were found between ToM deficits and patients' neuropsychiatric or clinical states. CONCLUSIONS These findings clarify the neuropsychological and clinical features that explain ToM deficits in PD. Possibly, our results suggest the need to explore the complex neural networks involving frontostriatal and temporoparietal circuits behind changes in social cognition in PD. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
               
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