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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*
Affiliation:
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Michael J. Firbank
Affiliation:
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Michelle Widdrington
Affiliation:
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
Andrew M. Blamire
Affiliation:
Institute of Cellular Medicine, Newcastle Magnetic Resonance Centre, Newcastle University, Newcastle upon Tyne, UK
Raj N. Kalaria
Affiliation:
Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
John T. O'Brien
Affiliation:
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: lopes.marcos.ant@gmail.com.

Abstract

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.

Type
Research Article
Copyright
Copyright © International Psychogeriatric Association 2011

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References

American Psychiatric Association (1987). Diagnostic and Statistical Manual of Mental Disorders DSM-IIIR. Washington, DC: American Psychiatric Association.Google Scholar
Bellebaum, C., Koch, B., Schwarz, M. and Daum, I. (2008). Focal basal ganglia lesions are associated with impairments in reward-based reversal learning. Brain, 131, 829841. doi:10.1093/brain/awn011.Google Scholar
Bokura, H., Kobayashi, S. and Yamaguchi, S. (1998). Distinguishing silent lacunar infarction from enlarged Virchow-Robin spaces: a magnetic resonance imaging and pathological study. Journal of Neurology, 245, 116122. doi:10.1007/s004150050189.Google Scholar
Borroni, B., Turla, M., Bertasi, V., Agosti, C., Gilberti, N. and Padovani, A. (2008). Cognitive and behavioral assessment in the early stages of neurodegenerative extrapyramidal syndromes. Archives of Gerontology and Geriatrics, 47, 5361. doi:10.1016/j.archger.2007.07.005.Google Scholar
Cohen, R. A. et al. (2002). The relationship of subcortical MRI hyperintensities and brain volume to cognitive function in vascular dementia. Journal of the International Neuropsychological Society, 8, 743752. doi:10.1017/S1355617702860027.Google Scholar
Cordoliani-Mackowiak, M.-A., Hénon, H., Pruvo, J.-P., Pasquier, F. and Leys, D. (2003). Poststroke dementia: influence of hippocampal atrophy. Archives of Neurology, 60, 585590. doi:10.1001/archneur.60.4.585.Google Scholar
Cousins, D. A., Burton, E. J., Burn, D., Gholkar, A., McKeith, I. G. and O'Brien, J. T. (2003). Atrophy of the putamen in dementia with Lewy bodies but not Alzheimer's disease: an MRI study. Neurology, 61, 11911195.Google Scholar
de Jong, L. W. et al. (2008). Strongly reduced volumes of putamen and thalamus in Alzheimer's disease: an MRI study. Brain, 131, 32773285. doi:10.1093/brain/awn278.Google Scholar
Du, A. T. et al. (2002). Effects of subcortical ischemic vascular dementia and AD on entorhinal cortex and hippocampus. Neurology, 58, 16351641.Google Scholar
Firbank, M. J. et al. (2007). Medial temporal atrophy rather than white matter hyperintensities predict cognitive decline in stroke survivors. Neurobiology of Aging, 28, 16641669. doi:10.1016/j.neurobiolaging.2006.07.009.Google Scholar
Firbank, M. J. et al. (2011). Cerebral blood flow by arterial spin labeling in poststroke dementia. Neurology, 76, 14781484. doi:10.1212/WNL.0b013e318217e76a.Google Scholar
Gold, G. et al. (2005). Cognitive consequences of thalamic, basal ganglia, and deep white matter lacunes in brain aging and dementia. Stroke, 36, 11841188. doi:10.1161/01.STR.0000166052.89772.b5.Google Scholar
Gootjes, L. et al. (2004). Regional distribution of white matter hyperintensities in vascular dementia, Alzheimer's disease and healthy aging. Dementia and Geriatric Cognitive Disorders, 18, 180188. doi:10.1159/000079199.Google Scholar
Grahn, J. A., Parkinson, J. A. and Owen, A. M. (2008). The cognitive functions of the caudate nucleus. Progress in Neurobiology, 86, 141155. doi:10.1016/j.pneurobio.2008.09.004.Google Scholar
Herrero, M. T., Barcia, C. and Navarro, J. M. (2002). Functional anatomy of thalamus and basal ganglia. Child's Nervous System, 18, 386404. doi:10.1007/s00381-002-0604-1.Google Scholar
Jokinen, H., Kalska, H., Mäntylä, R., Ylikoski, R., Hietanen, M. and Pohjasvaara, T. (2005). White matter hyperintensities as a predictor of neuropsychological deficits post-stroke. Journal of Neurology, Neurosurgery and Psychiatry, 76, 12291233.Google Scholar
Kokmen, E., Whisnant, J. P., O'Fallon, W. M., Chu, C. P. and Beard, C. M. (1996). Dementia after ischemic stroke: a population-based study in Rochester, Minnesota (1960–1984). Neurology, 46, 154159.Google Scholar
Lowery, K. et al. (2002). Cognitive decline in a prospectively studied group of stroke survivors, with a particular emphasis on the > 75's. Age and Ageing, 31, 2427. doi:10.1093/ageing/31.suppl_3.24.+75's.+Age+and+Ageing,+31,+24–27.+doi:10.1093/ageing/31.suppl_3.24.>Google Scholar
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D. and Stadlan, E. M. (1984). Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA work group under the auspices of Department of Health and Human Services Task Force on Alzheimer's disease. Neurology, 34, 939944.Google Scholar
Pasquier, F., Hénon, H. and Leys, D. (2000). Relevance of white matter changes to pre and poststroke dementia. Annals of the New York Academy of Sciences, 903, 466469. doi:10.1111/j.1749-6632.2000.tb06400.x.Google Scholar
Portas, C. M. et al. (1998). Volumetric evaluation of the thalamus in schizophrenic male patients using magnetic resonance imaging. Biological Psychiatry, 43, 649659. doi:10.1016/S0006-3223(97)00339-9.Google Scholar
Sachdev, P. S., Chen, X., Joscelyne, A., Wen, W., Altendorf, A. and Brodaty, H. (2007). Hippocampal size and dementia in stroke patients: the Sydney stroke study. Journal of the Neurological Sciences, 260, 7177. doi:10.1016/j.jns.2007.04.006.Google Scholar
Swartz, R. H. and Black, S. E. (2006). Anterior-medial thalamic lesions in dementia: frequent, and volume dependently associated with sudden cognitive decline. Journal of Neurology, Neurosurgery & Psychiatry, 77, 13071312. doi:10.1136/jnnp.2006.091561.Google Scholar
Swartz, R. H., Stuss, D. T., Gao, F. and Black, S. E. (2008). Independent cognitive effects of atrophy and diffuse subcortical and thalamico-cortical cerebrovascular disease in dementia. Stroke, 39, 822830. doi:10.1161/STROKEAHA.107.491936.Google Scholar
van der Werf, Y. D., Tisserand, D. J., Visser, P. J., Hofman, P. A. M., Vuurman, E. and Uylings, H. B. M. (2001). Thalamic volume predicts performance on tests of cognitive speed and decreases in healthy aging: a magnetic resonance imaging-based volumetric analysis. Cognitive Brain Research, 11, 377385. doi:10.1016/S0926-6410(01)00010-6Google Scholar
Vermeer, S. E., Prins, N. D., den Heijer, T., Hofman, A., Koudstaal, P. J. and Breteler, M. M. B. (2003). Silent brain infarcts and the risk of dementia and cognitive decline. New England Journal of Medicine, 348, 12151222. doi:10.1056/NEJMoa022066.Google Scholar
Wen, W. and Sachdev, P. S. (2004). Extent and distribution of white matter hyperintensities in stroke patients: the Sydney stroke study. Stroke, 35, 28132819. doi:10.1161/01.STR.0000147034.25760.3d.Google Scholar