Abstract

<h3>Rationale</h3> There is evidence to suggest that COPD leads to cognitive impairment in patients both with and without hypoxaemia1; but the pathogenesis remains poorly understood. Also relevant to potential brain pathology in COPD are common vascular comorbidities including hypertension, diabetes and older age. Diffusion tensor imaging (DTI) is a novel MRI technique sensitive to subtle changes in white matter due to vascular damage. This is the first study to investigate white matter microstructure and tract pathology in COPD. <h3>Methods</h3> Participants (n=50) completed a full cognitive assessment (including executive function, working memory, episodic memory, processing speed, visuospatial ability) and 3T MRI scan. We compare 25 stable non-exacerbating COPD and 25 age-matched healthy controls. Volumes of grey matter (GMV), white matter (WMV), and white matter lesions (LV), were calculated. DTI data was analysed using tract based spatial statistics (TBSS).2 <h3>Results</h3> There are significant group differences between COPD patients and controls on all cognitive measures except episodic memory (executive function: F=15.39, p&lt;0.001; working memory: F=5.94, p=0.019; episodic memory: F=3.91, p=0.054; processing speed: F=11.64, p=0.001; visuospatial ability: F=10.10, p=0.003). COPD patients did not differ from healthy controls on measures of normalised GMV (t=0.229, p=0.820) or WMV (t=−0.727, p=0.471). Normalised Lesion Volume was significantly greater in patients vs controls (t=−2.27, p=0.029). DTI-TBSS revealed lower fractional anisotropy (FA) and higher mean diffusivity (MD) values throughout the brain in COPD patients vs Control subjects. Group differences in white matter integrity were observed throughout the temporal, frontal, parietal and occipital lobes and amounted to 60% of the total FA skeleton. See Abstract S92 figure 1. <h3>Conclusion</h3> This is the first paper to demonstrate that white matter integrity throughout the brain is significantly compromised in patients with COPD compared to age-matched Controls. This damage to white matter is also demonstrated by the significant group differences in white matter lesion load. No differences between patients and Controls were observed in brain volume, suggesting that group differences may be related to white matter integrity rather than atrophy.

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