Abstract
There has been recent interest in the basal ganglia as structural components of small-scale neural networks that may be strategically affected in cerebrovascular disease. The neural connectivity, blood and metabolic requirements of the caudate nucleus may make this structure particularly vulnerable to cerebrovascular disease related neurodegeneration. We have demonstrated cross-sectional caudate nucleus atrophy in a Stroke sample, and were interested to investigate whether longitudinal atrophy occurred in a cohort with cerebrovascular disease, to study the disease trajectory. Accordingly, we sought to compare two subsets of longitudinal epidemiological studies investigating confirmed cerebrovascular disease in the form of leukoaraiosis, and a group of healthy age-matched controls. We manually measured caudate nucleus volume via MRI at baseline and at three year follow-up, in the Stockholm subset of the Leukoaraioisis and Disability in the elderly Study (LADIS). We found that normalized bilateral caudate volume was significantly smaller on follow-up in the LADIS group; and there was an approximately twice higher annual rate of atrophy in LADIS than in healthy age and gender matched controls from Stockholm (Swedish National Study on Aging and Care - Kungsholmen subset) without white matter disease. Leukoaraiosis may be associated with increased caudate nucleus atrophy, a finding which has implications for cognitive and behavioural functions served by this structure. In the context of previous findings of reduced caudate volume associated with white matter hyperintensities in the Sydney Stroke Cohort, these findings support a potential aetiological role for the caudate in cerebrovascular disease.
Original language | English |
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Title of host publication | Vascular Dementia |
Subtitle of host publication | Risk Factors, Diagnosis and Treatment |
Publisher | Nova Science Publishers, Inc. |
Pages | 215-224 |
Number of pages | 10 |
ISBN (Print) | 9781611223132 |
Publication status | Published - 2011 |