Apathy and Impulsivity Co-Occur in Huntington's Disease.


Journal

Brain and behavior
ISSN: 2162-3279
Titre abrégé: Brain Behav
Pays: United States
ID NLM: 101570837

Informations de publication

Date de publication:
Oct 2024
Historique:
revised: 13 08 2024
received: 28 05 2024
accepted: 01 09 2024
medline: 30 9 2024
pubmed: 30 9 2024
entrez: 30 9 2024
Statut: ppublish

Résumé

Apathy is a debilitating behavioral change in Huntington's disease (HD), but impulsivity in HD has not been well documented, and the co-occurrence of these behaviors in HD has not been investigated. Our objective was to determine whether apathy and impulsivity co-occur in people with HD and their associations with quality of life. Carriers of Huntington's gene expansion (premanifest to mild motor manifest disease; n = 42) along with healthy controls (n = 20) completed measures of apathy (Apathy Evaluation Scale and Apathy Motivation Index) and impulsivity (Barratt Impulsiveness Scale-11 and UPPS-P impulsivity scale), along with mood, cognition, clinical, and quality of life measures. Apathy and impulsivity measures were each reduced to a single metric per patient using principal component analysis. Correlations and multiple linear regression models determined associations between apathy and impulsivity and the potential influence of other covariates. Apathy and impulsivity were significantly correlated (r = 0.6, p < 0.001, 95% CI [0.36, 0.76]) in HD, with this association remaining after controlling for depressive symptoms, motor disease severity, and cognitive function. Furthermore, apathy and depressive symptoms were associated with poorer quality of life. Apathy and impulsivity co-occur in individuals with premanifest to mild manifest HD and have a significant impact on wellbeing. We add to a growing evidence body that apathy and impulsivity may be intrinsically linked.

Sections du résumé

BACKGROUND BACKGROUND
Apathy is a debilitating behavioral change in Huntington's disease (HD), but impulsivity in HD has not been well documented, and the co-occurrence of these behaviors in HD has not been investigated.
OBJECTIVE OBJECTIVE
Our objective was to determine whether apathy and impulsivity co-occur in people with HD and their associations with quality of life.
METHODS METHODS
Carriers of Huntington's gene expansion (premanifest to mild motor manifest disease; n = 42) along with healthy controls (n = 20) completed measures of apathy (Apathy Evaluation Scale and Apathy Motivation Index) and impulsivity (Barratt Impulsiveness Scale-11 and UPPS-P impulsivity scale), along with mood, cognition, clinical, and quality of life measures. Apathy and impulsivity measures were each reduced to a single metric per patient using principal component analysis. Correlations and multiple linear regression models determined associations between apathy and impulsivity and the potential influence of other covariates.
RESULTS RESULTS
Apathy and impulsivity were significantly correlated (r = 0.6, p < 0.001, 95% CI [0.36, 0.76]) in HD, with this association remaining after controlling for depressive symptoms, motor disease severity, and cognitive function. Furthermore, apathy and depressive symptoms were associated with poorer quality of life.
CONCLUSIONS CONCLUSIONS
Apathy and impulsivity co-occur in individuals with premanifest to mild manifest HD and have a significant impact on wellbeing. We add to a growing evidence body that apathy and impulsivity may be intrinsically linked.

Identifiants

pubmed: 39344371
doi: 10.1002/brb3.70061
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e70061

Subventions

Organisme : Division of Health Sciences, University of Otago
Organisme : Canterbury Medical Research Foundation

Informations de copyright

© 2024 The Author(s). Brain and Behavior published by Wiley Periodicals LLC.

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Auteurs

Lee-Anne Morris (LA)

Department of Medicine, University of Otago, Christchurch, New Zealand.
New Zealand Brain Research Institute, Christchurch, New Zealand.

Kyla-Louise Horne (KL)

Department of Medicine, University of Otago, Christchurch, New Zealand.
New Zealand Brain Research Institute, Christchurch, New Zealand.

Laura Paermentier (L)

New Zealand Brain Research Institute, Christchurch, New Zealand.

Christina M Buchanan (CM)

Department of Neurology, Auckland City Hospital, Te Whatu Ora Health, Auckland, New Zealand.
Centre for Brain Research Neurogenetics Research Clinic, University of Auckland, Auckland, New Zealand.

Michael MacAskill (M)

New Zealand Brain Research Institute, Christchurch, New Zealand.

Daniel Myall (D)

New Zealand Brain Research Institute, Christchurch, New Zealand.

Masud Husain (M)

Department of Experimental Psychology, University of Oxford, Oxford, UK.
Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.

Richard Roxburgh (R)

Department of Neurology, Auckland City Hospital, Te Whatu Ora Health, Auckland, New Zealand.
Centre for Brain Research Neurogenetics Research Clinic, University of Auckland, Auckland, New Zealand.

Tim Anderson (T)

Department of Medicine, University of Otago, Christchurch, New Zealand.
New Zealand Brain Research Institute, Christchurch, New Zealand.
Department of Neurology, Christchurch Hospital, Te Whatu Ora Health, Christchurch, New Zealand.

Campbell Le Heron (CL)

Department of Medicine, University of Otago, Christchurch, New Zealand.
New Zealand Brain Research Institute, Christchurch, New Zealand.
Department of Neurology, Christchurch Hospital, Te Whatu Ora Health, Christchurch, New Zealand.

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