Relationship between Neuroanatomical Location and Behavioral and Psychological Symptoms of Alzheimer's Disease: A VBM Analysis

알츠하이머병에서 행동심리증상과 해부학적 영역의 연관성에 대한 VBM 영상분석

  • Kim, Hee-Jin (Department of Neurology, College of Medicine, Hanyang University) ;
  • Park, Jin Seok (Department of Neurology, College of Medicine, Hanyang University) ;
  • Kwon, Hyuk Sung (Department of Neurology, College of Medicine, Hanyang University) ;
  • Lim, Sung-Hwan (Department of Neurology, College of Medicine, Hanyang University) ;
  • Kim, Seung H. (Department of Neurology, College of Medicine, Hanyang University)
  • 김희진 (한양대학교 의과대학 신경과학교실) ;
  • 박진석 (한양대학교 의과대학 신경과학교실) ;
  • 권혁성 (한양대학교 의과대학 신경과학교실) ;
  • 임성환 (한양대학교 의과대학 신경과학교실) ;
  • 김승현 (한양대학교 의과대학 신경과학교실)
  • Published : 2011.03.31

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.

Keywords

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