Contribution of Brain Imaging to the Understanding Of Gait Disorders in Alzheimer’s Disease

Author:

Annweiler Cédric1234,Beauchet Olivier4,Celle Sébastien5,Roche Frédéric5,Annweiler Thierry6,Allali Gilles7,Bartha Robert3,Montero-Odasso Manuel12

Affiliation:

1. Division of Geriatric Medicine, Department of Medicine, Parkwood Hospital, St. Joseph’s Health Care, London, Ontario, Canada

2. Gait and Brain Lab, Lawson Health Research Institute, Western University, London, Ontario, Canada

3. Department of Medical Biophysics, Center for Functional and Metabolic Mapping, Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada

4. Department of Neuroscience, Division of Geriatric Medicine, Angers University Hospital, University Memory Center of Angers, UPRES EA 2646, University of Angers, UNAM, Angers, France

5. Service de Physiologie Clinique et de l’Exercice, CHU Saint-Etienne, Faculté de Médecine Jacques Lisfranc, Université Jean Monnet, Saint-Etienne, France

6. Department of Radiology, University Hospital, Saint-Etienne, France

7. Department of Neurology, Geneva University Hospitals, Switzerland

Abstract

Although gait disorders are common in Alzheimer’s disease (AD), determining which brain structures and related lesions are specifically involved is a goal yet to be reached. Our objective was to systematically review all published data that examined associations between gait disorders and brain imaging in AD. Of 486 selected studies, 4 observational studies met the selection criteria. The number of participants ranged from 2 to 61 community dwellers (29%-100% female) with prodromal or dementia-stage AD. Quantitative gait disorders (ie, slower gait velocity explained by shorter stride length) were associated with white matter lesions, mainly in the medial frontal lobes and basal ganglia. The nigrostriatal dopamine system was unaffected. Qualitative gait disorders (ie, higher stride length variability) correlated with lower hippocampal volume and function. Gait disorders in AD could be explained by a high burden of age-related subcortical hyperintensities on the frontal–subcortical circuits (nonspecific) together with hippocampal atrophy and hypometabolism (specific).

Publisher

SAGE Publications

Subject

Psychiatry and Mental health,Geriatrics and Gerontology,Clinical Psychology,General Neuroscience

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