알츠하이머병에서 행동심리증상과 해부학적 영역의 연관성에 대한 VBM 영상분석Relationship between Neuroanatomical Location and Behavioral and Psychological Symptoms of Alzheimer’s Disease: A VBM Analysis
- Other Titles
- Relationship between Neuroanatomical Location and Behavioral and Psychological Symptoms of Alzheimer’s Disease: A VBM Analysis
- Authors
- 김희진; 박진석; 권혁성; 임성환; 김승현
- Issue Date
- Feb-2011
- Publisher
- 대한치매학회
- Keywords
- Behavioral psychiatric symptoms of dementia; Anatomical substrate; Voxel Based Morphometry; Alzheimer’s disease
- Citation
- Dementia and Neurocognitive Disorders(대한치매학회지), v.10, no.1, pp.27 - 33
- Indexed
- KCI
- Journal Title
- Dementia and Neurocognitive Disorders(대한치매학회지)
- Volume
- 10
- Number
- 1
- Start Page
- 27
- End Page
- 33
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/169028
- ISSN
- 1738-1495
- Abstract
- Background: Even though, behavioral and psychological symptoms of dementia (BPSD) is one of the most important problems in Alzheimer’s disease (AD), neuroanatomical substrates of BPSD have been much less understood than those of cognitive domains in AD. Objectives: The purposes of this study are to investigate whether BPSD of AD might be associated with atrophy in specific brain areas according to BPSD severity and compare the different patterns of the atrophic changes of brain in AD patients with severe BPSD group with mild BPSD group. Methods: Fifty three patients with or without neuropsychiatric symptoms of AD patients in mild and moderate stage were enrolled. All caregivers of the patients with AD conducted the Brief version of Neuropsychiatric Inventory Questionnaire (NPI-Q). Changes of brain according to the severities of BPSD were analyzed using Voxel Based Morphometry underlying Statistical Paramatric Mapping. Special patterns of atrophy were evaluated according to special sub-items of the NPI-Q. Results: NPI-Q total severity scores were correlated with the volume loss of bilateral frontal, temporal and left anterior cingulated gyri in AD (FDR corrected p< 0.05). Atrophy of left superior temporal region had meaningful correlations with positive symptoms of BPSD, such as delusion, hallucination, agitation/ aggression, euphoria and elation. Regional atrophy of right supramarginal gyri were correlated with negative symptoms of BPSD (e.g., Dysphoria/Depression) (uncorrected p< 0.001). Severe BPSD group showed atrophy in bilateral temporal cortices, predominantly right side (FDR corrected p< 0.05), not in white matter. Conclusions: BPSD in AD might be the results of degenerative changes in bilateral frontal and temporal corteces confined on the gray matter. White matter disruption did not significantly affect to BPSD. Changes in atrophic patterns might be different between the AD patients with positive and negative symptoms of BPSD.
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