Cerebellar atrophy in neurodegeneration-a meta-analysis
Cerebellar atrophy in neurodegeneration-a meta-analysis
Introduction The cerebellum has strong cortical and subcortical connectivity, but is rarely taken into account for clinical diagnosis in many neurodegenerative conditions, particularly in the absence of clinical ataxia. The current meta-analysis aims to assess patterns of cerebellar grey matter atrophy in seven neurodegenerative conditions (Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), progressive supranuclear palsy (MSP)).
Methods We carried out a systematic search in PubMed (any date: 14 July 2016) and a hand search of references from pertinent articles according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The authors were contacted to provide missing coordinate data. Peer-reviewed studies with direct comparison of patient and control groups, and availability of coordinate data of grey matter cerebellar atrophy in patients were included. These coordinates were used in an anatomical likelihood estimation meta-analysis.
Results Across 54 studies, clusters of cerebellar atrophy were found for AD, ALS, FTD, MSA, and PSP. Atrophy patterns were largely disease-specific, with overlap in certain areas of the cerebellar hemisphere, which showed marked atrophy in AD, ALS, FTD and PSP (Crus I/II), and MSA and PSP (lobules I–IV), respectively. Atrophy colocated with cerebellar areas implicated for motor (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) in the diseases.
Discussion Our findings suggest that cerebellar changes are largely disease-specific and correspond to cortical or subcortical changes in neurodegenerative conditions. High clinical variability in PD and HD samples may explain the absence of findings for consistent grey matter loss across studies. Our results have clinical implications for diagnosis and cerebellar neuroimaging referencing approaches.
780 - 788
HM, Gellersen
0659fbbb-d7a4-4b90-8600-d8d98e7f8df4
CC, Guo
85a02435-e391-4031-94ad-2e58bdfce659
O'Callaghan, C
f47ed92d-85af-42c8-b6db-3f75437f6147
RH, Tan
788414cc-eada-4d03-8d45-fe009d0a8696
Sami, S
93469bbd-03c0-4c39-b1ab-af7ef22bfa47
Hornberger, M
a48c1c63-422a-4c11-9a51-c7be0aa3026d
13 May 2017
HM, Gellersen
0659fbbb-d7a4-4b90-8600-d8d98e7f8df4
CC, Guo
85a02435-e391-4031-94ad-2e58bdfce659
O'Callaghan, C
f47ed92d-85af-42c8-b6db-3f75437f6147
RH, Tan
788414cc-eada-4d03-8d45-fe009d0a8696
Sami, S
93469bbd-03c0-4c39-b1ab-af7ef22bfa47
Hornberger, M
a48c1c63-422a-4c11-9a51-c7be0aa3026d
HM, Gellersen, CC, Guo, O'Callaghan, C, RH, Tan, Sami, S and Hornberger, M
(2017)
Cerebellar atrophy in neurodegeneration-a meta-analysis.
Journal of Neurology, Neurosurgery, and Psychiatry, 88, .
(doi:10.1136/jnnp-2017-315607).
Abstract
Introduction The cerebellum has strong cortical and subcortical connectivity, but is rarely taken into account for clinical diagnosis in many neurodegenerative conditions, particularly in the absence of clinical ataxia. The current meta-analysis aims to assess patterns of cerebellar grey matter atrophy in seven neurodegenerative conditions (Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), progressive supranuclear palsy (MSP)).
Methods We carried out a systematic search in PubMed (any date: 14 July 2016) and a hand search of references from pertinent articles according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The authors were contacted to provide missing coordinate data. Peer-reviewed studies with direct comparison of patient and control groups, and availability of coordinate data of grey matter cerebellar atrophy in patients were included. These coordinates were used in an anatomical likelihood estimation meta-analysis.
Results Across 54 studies, clusters of cerebellar atrophy were found for AD, ALS, FTD, MSA, and PSP. Atrophy patterns were largely disease-specific, with overlap in certain areas of the cerebellar hemisphere, which showed marked atrophy in AD, ALS, FTD and PSP (Crus I/II), and MSA and PSP (lobules I–IV), respectively. Atrophy colocated with cerebellar areas implicated for motor (PSP, MSA) or cognitive symptoms (FTD, ALS, PSP) in the diseases.
Discussion Our findings suggest that cerebellar changes are largely disease-specific and correspond to cortical or subcortical changes in neurodegenerative conditions. High clinical variability in PD and HD samples may explain the absence of findings for consistent grey matter loss across studies. Our results have clinical implications for diagnosis and cerebellar neuroimaging referencing approaches.
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Accepted/In Press date: 10 April 2017
Published date: 13 May 2017
Identifiers
Local EPrints ID: 505121
URI: http://eprints.soton.ac.uk/id/eprint/505121
ISSN: 0022-3050
PURE UUID: edca5344-8231-4cba-9759-78b1cbb82317
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Date deposited: 29 Sep 2025 17:49
Last modified: 30 Sep 2025 02:25
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Author:
Gellersen HM
Author:
Guo CC
Author:
C O'Callaghan
Author:
Tan RH
Author:
S Sami
Author:
M Hornberger
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