Cognitive impairments associated with morphological changes in cortical and subcortical structures in multiple system atrophy of the cerebellar type. (31st July 2015)

• Record Type: Journal Article
• Authors: Lee, M. J.; Shin, J.‐H.; Seoung, J.‐K.; Lee, J.‐H.; Yoon, U.; Oh, J.‐H.; Jung, D. S.; Kim, E.‐J.
• Is Part Of: European journal of neurology. Volume 23:Number 1(2016:Jan.)
• Page Start: 92
• Page End: 100
• Publication Date: 2015-07-31
• Subjects: cognitive impairment -- MRI -- multiple system atrophy -- surface based morphometry; Neurology -- Periodicals; Nervous system -- Diseases -- Periodicals; 616.8
• DOI: 10.1111/ene.12796
• Languages: English
• ISSNs: 1351-5101

Abstract

Abstract : Background and purpose: Patients with the cerebellar variant of multiple system atrophy (MSA‐C) often show cognitive deficits in various cognitive domains. The association between morphometric changes in cortical and subcortical structures and cognitive impairments in MSA‐C were investigated to explore the neural correlates responsible for cognitive deficits in MSA‐C patients. Methods: Using surface‐based morphometry, region‐of‐interest cortical thickness and the volumes and shapes of subcortical structures were examined in 18 patients who fulfilled the criteria of probable MSA‐C and were compared to 50 healthy controls. The association between regional changes and cognitive functions in MSA‐C were investigated by applying linear regression analyses after controlling for confounding factors. Results: Compared with controls, the patients with MSA‐C showed significant cortical thinning in the fronto‐temporo‐parietal regions and volume reduction in subcortical structures with shape changes. Cerebellar volume had no significant effect on cortical and subcortical volumes. The severity of atrophic changes in the bilateral thalamus, the left cerebellum and the left pericalcarine gyrus were significantly correlated with attentional, executive and visuospatial dysfunctions. Conclusion: Cognitive impairment in MSA‐C might result from functional disruption of the corticostriatal and pontocerebellar circuit mediated by primary cortical, cerebellar or thalamic pathology.