ArticleEuropean journal of neurology2026
Neural Correlates of Apathy in Multiple System Atrophy: A Clinical and Perfusion Imaging Study.
Article in European journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundApathy is a frequent nonmotor symptom of multiple system atrophy (MSA) that worsens quality of life. Although frontostriatal dysfunction has been implicated in apathy, its neural basis in MSA remains insufficiently characterized.
objectivesTo identify the neural substrates of apathy associated with MSA-specific neurodegenerative processes.
methodsThis retrospective cross-sectional study included 76 patients with cognitively preserved clinically established/probable MSA who underwent clinical and neuropsychological assessments, including the Apathy Scale and a separate depression measure, magnetic resonance imaging, and cerebral blood flow single-photon emission computed tomography. Clinical variables, gray matter volume, and voxel-wise perfusion were compared between apathy and non-apathy groups. Multivariate logistic regression was used to analyze the independent association of the significant perfusion cluster with apathy, and seed-based covariance analysis was used to explore network alterations.
resultsApathy was present in 55.3% of patients and did not differ between motor subtypes. Compared with the non-apathy group, the apathy group showed lower visuospatial scores and frequency of neurogenic orthostatic hypotension, similar depression scores and gray matter volume, and reduced perfusion in the medial prefrontal cortex on voxel-wise perfusion analysis. These findings remained independently associated with apathy after adjustment for clinical variables. Seed-based covariance analysis suggested reduced positive covariance between the medial prefrontal cortex and cerebellar regions, predominantly in the posterior lobe.
conclusionsApathy was common in MSA even with relatively preserved global cognition and distinct from depression. In addition to medial frontostriatal dysfunction, exploratory findings suggested that mechanisms related to cerebellar cognitive affective syndrome may contribute to its pathophysiology.
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