The structural involvement of the cingulate cortex in premanifest and early Huntington's disease
The impact of Huntington's disease neuropathology on the structure of the cingulate is uncertain, with evidence of both cortical enlargement and atrophy in this structure in early clinical disease. We sought to determine differences in cingulate volume between premanifest Huntington's dise...
Saved in:
Published in: | Movement disorders Vol. 26; no. 9; pp. 1684 - 1690 |
---|---|
Main Authors: | , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01-08-2011
Wiley |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | The impact of Huntington's disease neuropathology on the structure of the cingulate is uncertain, with evidence of both cortical enlargement and atrophy in this structure in early clinical disease. We sought to determine differences in cingulate volume between premanifest Huntington's disease and early Huntington's disease groups compared with controls using detailed manual measurements. Thirty controls, 30 subjects with premanifest Huntington's disease, and 30 subjects with early Huntington's disease were selected from the Vancouver site of the TRACK‐HD study. Subjects underwent 3 Tesla magnetic resonance imaging and motor, cognitive, and neuropsychiatric assessment. The cingulate was manually delineated and subdivided into rostral, caudal, and posterior segments. Group differences in volume and associations with performance on 4 tasks thought to utilize cingulate function were examined, with adjustment for appropriate covariates. Cingulate volumes were, on average, 1.7 mL smaller in early Huntington's disease (P = .001) and 0.9 mL smaller in premanifest Huntington's disease (P = .1) compared with controls. Smaller volumes in subsections of the cingulate were associated with impaired recognition of negative emotions (P = .04), heightened depression (P = .009), and worse visual working memory performance (P = .01). There was no evidence of associations between volume and ability on a performance‐monitoring task. This study disputes previous findings of enlargement of the cingulate cortex in Huntington's disease and instead suggests that the cingulate undergoes structural degeneration during early Huntington's disease with directionally consistent, nonsignificant differences seen in premanifest Huntington's disease. Cingulate atrophy may contribute to deficits in mood, emotional processing, and visual working memory in Huntington's disease. © 2011 Movement Disorder Society |
---|---|
Bibliography: | Relevant conflicts of interest/financial disclosures: Josephine Barnes is funded by an Alzheimer's Research Trust UK research fellowship with the kind support of the Kirby Laing Foundation. Blair R. Leavitt is a clinician-scientist supported by the Canadian Institutes of Health Research, the Michael Smith Foundation for Health Research, and the CHDI Foundation. The Dementia Research Centre is an Alzheimer's Research Trust Co-ordinating Centre. David Craufurd acknowledges the support of the NIHR Biomedical Research Centre in Manchester. Full financial disclosures and author roles may be found in the online version of this article. istex:AF3B865F30DD0E54535373EB390C50FABB171433 ArticleID:MDS23747 ark:/67375/WNG-6FRGS6M5-2 Funding agencies: TRACK-HD is supported by the CHDI Foundation, a not-for-profit organization dedicated to finding treatments for Huntington's disease. This work was undertaken at UCLH/UCL which received a proportion of funding from the Department of Health's NIHR Biomedical Research Centres' funding scheme. Funding agencies: TRACK‐HD is supported by the CHDI Foundation, a not‐for‐profit organization dedicated to finding treatments for Huntington's disease. This work was undertaken at UCLH/UCL which received a proportion of funding from the Department of Health's NIHR Biomedical Research Centres' funding scheme. Relevant conflicts of interest/financial disclosures: Josephine Barnes is funded by an Alzheimer's Research Trust UK research fellowship with the kind support of the Kirby Laing Foundation. Blair R. Leavitt is a clinician‐scientist supported by the Canadian Institutes of Health Research, the Michael Smith Foundation for Health Research, and the CHDI Foundation. The Dementia Research Centre is an Alzheimer's Research Trust Co‐ordinating Centre. David Craufurd acknowledges the support of the NIHR Biomedical Research Centre in Manchester. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0885-3185 1531-8257 |
DOI: | 10.1002/mds.23747 |