MAGNETIC-RESONANCE RELAXATION-TIME MAPPING IN MULTIPLE-SCLEROSIS - NORMAL APPEARING WHITE-MATTER AND THE INVISIBLE LESION LOAD

Citation
S. Barbosa et al., MAGNETIC-RESONANCE RELAXATION-TIME MAPPING IN MULTIPLE-SCLEROSIS - NORMAL APPEARING WHITE-MATTER AND THE INVISIBLE LESION LOAD, Magnetic resonance imaging, 12(1), 1994, pp. 33-42
Citations number
NO
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging
Journal title
ISSN journal
0730725X
Volume
12
Issue
1
Year of publication
1994
Pages
33 - 42
Database
ISI
SICI code
0730-725X(1994)12:1<33:MRMIM->2.0.ZU;2-0
Abstract
Prolonged T-1 and/or T-2 relaxation times (RT) in the normal appearing white matter (NAWM) of patients with multiple sclerosis (MS) have bee n attributed either to a diffuse abnormality, or to ''small lesions'' undetected by visual inspection of conventional MR images. In a compar ison of brain slices from five MS patients and five healthy control su bjects, we have confirmed that the average T-1 and T-2 RTs obtained fr om NAWM in patients with MS are significantly prolonged (p <.04). Quan titative pixel-by-pixel mapping shows that this overall prolongation i s due to the averaging of RTs from two subfractions of NAWM. In all pa tients a proportion (average 54% for T-1 and 63% for T-2) of the total white matter pixel sample from each MR brain slice had RT values indi stinguishable from those found in the white matter of matched healthy control subjects (i.e., ''normal normal appearing white matter,'' NNAW M). Scattered throughout the NAWM were multiple small areas, often of only one or two pixels, with abnormal RT values. These lesions, which were revealed only by pixel-by-pixel mapping of RT, made up a signific ant proportion (average 47% for T-1 or 57% for T-2 estimates) of the t otal (visible plus ''invisible'') lesion load per slice, and of the NA WM (average 36% for T-1, 27% for T-2), with wide interpatient variabil ity. Further studies of these minute lesions are required to determine their total volume in the brain, their precise nature, evolution and relevance to the functional deficit in MS.