FDG-PET patterns associated with ideomotor apraxia and imitation apraxia in patients with corticobasal syndrome. (July 2021)

• Record Type: Journal Article
• Authors: Jo, Sungyang; Oh, Jungsu S.; Cheong, E-Nae; Kim, Hyung Ji; Lee, Sunju; Oh, Minyoung; Kim, Jae Seung; Chung, Sun Ju; Lee, Chong S.; Kwon, Miseon; Kang, Dongwha; Lee, Jae-Hong
• Is Part Of: Parkinsonism & related disorders. Volume 88(2021)
• Page Start: 96
• Page End: 101
• Publication Date: 2021-07
• Subjects: Imitation apraxia -- Ideomotor apraxia -- Corticobasal syndrome -- FDG positron emission tomography; Parkinson's disease -- Periodicals; Movement disorders -- Periodicals; Movement Disorders -- Periodicals; Nerve Degeneration -- Periodicals; Nervous System Diseases -- Periodicals; Parkinson Disease -- Periodicals; Tremor -- Periodicals; Parkinson, Maladie de -- Périodiques; Parkinson's disease; 616.833
• DOI: 10.1016/j.parkreldis.2021.06.006
• Languages: English
• ISSNs: 1353-8020

Abstract

Abstract: Introduction: Apraxia is a core clinical feature of corticobasal syndrome (CBS). Among the subtypes of apraxia, ideomotor and imitation apraxia are frequently found in CBS. However, little is known about the brain networks that are characteristic of each apraxia subtype or their clinical implication. In this study, we used 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) to explore the specific patterns of glucose hypometabolism that are characteristic of apraxia subtypes by focusing on ideomotor and imitation apraxia. Methods: We compared the areas of glucose hypometabolism in the brains of 52 patients with CBS and 13 healthy controls, both as a whole and according to apraxia subtypes. In addition, we investigated the relationship between the apraxia subtypes and the clinical phenotype of CBS. Results: In patients with CBS, common hypometabolism was observed in the frontal gyrus, precentral gyrus and caudate regardless of apraxia subtypes. In particular, ideomotor apraxia was associated with hypometabolism in the angular gyrus, while imitation apraxia was associated with hypometabolism in the posterior part including the postcentral gyrus, precuneus, and posterior cingulate gyrus. Patients who showed both ideomotor and imitation apraxia were more likely to show the typical features of CBS and progressive supranuclear palsy compared with patients showing only one type of apraxia. Conclusion: Group comparison analysis using FDG-PET revealed distinct pathways of ideomotor and imitation apraxia in CBS. These findings add to our understanding of the brain networks underlying apraxia in association with the clinical features of CBS. Highlights: Ideomotor apraxia was related to hypometabolism in the angular gyrus. Imitation apraxia was related to hypometabolism in the posterior area. Common hypometabolism was observed in the frontal and precentral gyri and caudate. Patients with both apraxias had more features of PSP than those with one apraxia.