Abstract Details

Title Deep Gray Matter Atrophy Is Associated with DTI-Defined White Matter Tract Damage in Multiple Sclerosis

Topic MS and Related Diseases

Presentation(s) (-)

Poster/Presentation
Number 003

Objective

Background Previous MRI studies suggest a link between GM atrophy and WM damage in MS, however this relationship has not been fully elucidated.

Design/Methods 3T MRI images were acquired from 72 MS patients and 40 normal controls (NC). DGM volumes were derived from 3D-T1 images using FSL-FIRST software. DTI-derived WM metrics [fractional anisotropy (FA), mean diffusivity (MD), radial diffusivity (RD)] were aligned and skeletonized using FSL tract-based spatial statistics. Core WM tract metrics were averaged within 30 selected regions-of-interest (15 Left, 15 Right), representing specific WM tracts. Within hemispheres, a linear model assessed significantly differing correlations between regional WM tracts and DGM volumes in MS vs. NC, testing each of the DGM volumes against each of the 15 WM tracts.

Results All DGM areas showed atrophy and the majority of WM tracts were abnormal in MS vs. NC. Associations between WM tract damage and DGM atrophy were higher in MS vs. NC (p<0.05). In particular, MS patients showed reduced FA, increased RD and MD in the fornix and corona radiata, which were associated respectively with thalamic and caudate atrophy. Additionally, both increased RD, MD and selective increased RD or MD, but not decreased FA, in several WM tracts (cerebral peduncle, sagittal striatum, thalamic radiation, external and internal capsule) were associated with atrophy in adjacent DGM areas.

Conclusions This study shows a direct MS specific relationship between DGM atrophy and damage to connected WM tracts. Different patterns of WM tracts damage assessed by multiple DTI-derived metrics suggest diverse contributions of underlying WM pathology to DGM atrophy in MS. However, only a portion of the variance in DGM atrophy is explained by such WM changes, suggesting that other mechanisms contribute to such atrophy.

Authors/Disclosures
Antonia Ceccarelli, MD, PhD (Epicura Centre Hospitalier, VUB) PRESENTER	No disclosure on file
Mohit Neema, MD	No disclosure on file
Brian C. Healy	The institution of Mr. Healy has received research support from Analysis Group. The institution of Mr. Healy has received research support from Bristol-Myers Squibb. The institution of Mr. Healy has received research support from Verily Life Sciences. The institution of Mr. Healy has received research support from Novartis. The institution of Mr. Healy has received research support from Merck Serono. The institution of Mr. Healy has received research support from Genzyme.
Sung Lee	No disclosure on file
Shahamat Tauhid, MD (Brigham & Women's Hospital)	Dr. Tauhid has nothing to disclose.
Rohit Bakshi, MD, FAAN	Dr. Bakshi has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for EMD Serono. Dr. Bakshi has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Sanofi. The institution of Dr. Bakshi has received personal compensation in the range of $10,000-$49,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Journal of Neuroimaging. The institution of Dr. Bakshi has received research support from Bristol Myers Squibb. The institution of Dr. Bakshi has received research support from EMD Serono. The institution of Dr. Bakshi has received research support from Novartis.

��ɫ��

��ɫ��