Investigation of apparent diffusion coefficient and diffusion tensor anisotrophy in acute and chronic multiple sclerosis lesions.
Investigation of apparent diffusion coefficient and diffusion tensor anisotrophy in acute and chronic multiple sclerosis lesions.
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发表时间:
1999-09
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通讯作者:
A. Tievsky;T. Ptak;J. Farkas
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作者:
A. Tievsky;T. Ptak;J. Farkas
BACKGROUND AND PURPOSE The various stages of multiple sclerosis (MS) are characterized by de- and remyelination as well as by inflammation. Diffusion MR imaging is sensitive to tissue water motion, which might correspond to these pathologic processes. Our purpose was to demonstrate differences in apparent diffusion coefficient (ADC) and diffusion tensor anisotropy in acute and chronic MS plaques and in normal-appearing brain. METHODS Twelve MS patients underwent conventional and full-tensor diffusion MR imaging with B = 1221 s/mm2. Derivation of trace ADC and calculation of anisotropic scalars, including eccentricity, relative anisotropy (RA), and fractional anisotropy (FA) was performed on a per-pixel basis. Regions of interest of plaques and normal structures were determined on coregistered maps. MS lesions were classified as acute, subacute, or chronic on the basis of their appearance on conventional images and in relation to clinical findings. RESULTS Seven patients had acute plaques with a concentric arrangement of alternating high and low signal intensity on diffusion-weighted images. In nine acute lesions, plaque centers had high ADC with reduced anisotropy compared with rim, normal-appearing white matter (NAWM), and chronic lesions. The thin rim of diffusion-weighted hyperintensity surrounding the center showed variable ADC and anisotropic values, which were not statistically different from NAWM. Subacute and chronic MS lesions had intermediate ADC elevations/anisotropic reductions. Calculated FA pixel maps were superior to eccentricity or RA maps; however, quality was limited by signal-to-noise constraints. CONCLUSION ADC and diffusion anisotropic scalars reflect biophysical changes in the underlying pathology of the demyelinating process.