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Post-stroke dementia: the contribution of thalamus and basal ganglia changes

Published online by Cambridge University Press:  12 December 2011

Marcos Antonio Lopes*
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Michael J. Firbank
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Michelle Widdrington
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Andrew M. Blamire
Institute of Cellular Medicine, Newcastle Magnetic Resonance Centre, Newcastle University, Newcastle upon Tyne, UK
Raj N. Kalaria
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
John T. O'Brien
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Correspondence should be addressed to: Marcos Antonio Lopes, MD, PhD, Universidade Federal de Santa Catarina, Hospital Universitário, Departamento de Clínica Médica, Rua Maria Flora Pausewang, Campus Universitário, CEP 88040-970, Florianópolis, SC, Brasil. Phone: +55 48 3721 9014. Email:


Background: The neurobiological basis of increased risk of dementia in stroke patients is unclear, though there are several related pathological changes, including white matter hyperintensities (WMH), and medial temporal atrophy. Subcortical gray matter structures have also been implicated in dementia resulting from vascular pathology, particularly vascular dementia. This study aimed to investigate the contribution of changes in subcortical gray matter structures to post-stroke dementia (PSD).

Methods: T1- and T2-weighted images and T2-weighted fluid-attenuated inversion recovery (FLAIR) images were obtained on a 3-Tesla magnetic resonance (MR) system, in four groups aged over 75 years: post-stroke with dementia (PSD; 8), post-stroke no dementia (PSnoD; 33), Alzheimer's disease (AD; 26) and controls (30). Automated software was used to measure the volume of thalamus, putamen, caudate nucleus, and hippocampus as well as total WMH volume. The number of subcortical lacunes was also counted.

Results: The number of caudate lacunes was higher in the PSnoD group, compared with AD (p = 0.029) and controls (p = 0.019). The putamen volume was smaller in the stroke and AD groups, when compared with controls. In the whole stroke group, putamen lacunes were correlated with impairment in memory (Rey test; ρ = −0.365; p = 0.031), while WMH and hippocampal volume both correlated with global dysfunction.

Conclusion: Our findings implicate a variety of neurobiological substrates of dementia, such as small vessel disease and Alzheimer pathology, which develop after stroke in an old older population, with a contribution from subcortical brain structures.

Research Article
Copyright © International Psychogeriatric Association 2011

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