Thursday, 13 December 2012

Research: cognitive impairment. a grey and white matter problem

#MSBlog: Cognitive impairment correlates with both grey and white matter disease!

EpubPellicano et al. Cognitive Impairment and Its Relation to Imaging Measures in Multiple Sclerosis: A Study Using a Computerized Battery. J Neuroimaging. 2012 Dec. doi: 10.1111/j.1552-6569.2011.00687.x.

BACKGROUND AND PURPOSE: Cognitive impairment (CI) is an important component of MS disability. A complex biological interplay between white matter (WM) and gray matter (GM) disease likely sustains CI. This study aimed to address this issue by exploring the association between the extent of normal WM and GM disease and CI.

METHODS: Cognitive function of 24 MSers and 24 healthy volunteers (HVs) was studied using the Automated Neuropsychological Assessment Metrics (ANAM) battery. WM focal lesions and normal appearing WM (NAWM) volume in MSers, cortical thickness (CTh) and deep GM structure volumes in both MSers and HVs were measured by high field strength (3.0-Tesla; 3T) imaging.

RESULTS: An analysis of covariance showed that MSers performed worse than HVs on Code Substitution Delayed Memory (P= .04) and Procedural Reaction Time (P= .05) indicative of reduced performance in memory, cognitive flexibility, and processing speed. A summary score (Index of Cognitive Efficiency) indicating global test battery performance was also lower for the MSer group (P= .04). Significant associations, as determined by the Spearman rank correlation tests, were noted between each of these 3 cognitive scores and measures of NAWM volume [CDD-TP1(r= .609; P= .0035), PRO-TP1 (r= .456; P= .029) and ICE (r= .489; P= .0129)], CTh (r= .5; P≤ .05) and volume of subcortical normal appearing GM (NAGM) structures (r= .4; P≤ .04), but not WM lesions.

CONCLUSIONS: Both NAWM and NAGM volumes are related to CI in MS. The results highlight once again the urgent need to develop pharmacological strategies protecting MSers from widespread neurodegeneration as possible preventive strategies of CI development.

"Deja vu? Could early aggressive treatment be the answer to preventing cognitive impairment? A lot of neurologists are against this strategy because you may treat MSers destined to have a benign course with a high-risk treatment and expose them to the complications of this therapy. I agree this may be the likely outcome. If only we could develop better prognostic tools to identify MSers destined for a benign and more active course. By the time we do the individuals may have already accumulated irreversible damage. Surely MSers should be in the position to decide this for themselves?"

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