Abstract

To evaluate retrospectively quantitative diffusion tensor imaging (DTI) values of hyperintense lesions on nonenhanced T1-weighted magnetic resonance (MR) images in patients with multiple sclerosis (MS) to elucidate the degree of demyelination or remyelination associated with T1 hyperintense lesions and study their relationship to MR markers of tissue damage (brain atrophy). Institutional review board approval was obtained; informed consent was waived for this HIPAA-compliant study, including 76 patients with MS and 20 healthy control subjects without evidence of MS clinically or on imaging. T1 lesions were compared with normal white matter on nonenhanced images and judged to be hyperintense. Quantitative DTI metrics of T1 hyperintense lesions were examined, and the relationship between DTI parameters and brain atrophy were investigated in this study. At least one T1 hyperintense lesion was found in 16 patients (total, 28 lesions). Hyperintense lesions on T1-weighted imaging (T1WI) had lower mean diffusion (MD) than others signal intensity lesions on T1WI but higher MD than normal white matter (F = 3.931; P < 0.001); Fractional anisotropy (FA; F = 3.24; P < 0.001) and volume ratio (VR; F = 1.664; P < 0.001) were higher in hyperintense lesions on T1WI than hypointense/isointense lesions on T1WI, but were lower than normal-appearing white matter (NAWM) and normal white matter in controls. There was correlation between FA and VR (r = 0.678; P < 0.001) and inverse correlation between FA and MD (r = -0.437; P = 0.02), MD and VR (r = -0.423; P 0.025) for T1 hyperintense lesion. The MD values of T1 hyperintense lesions (r = -0.304; P < 0.001) and the VR values of T1 hyperintense lesions (r = 0.096; P = 0.042) were significantly (negative) correlated with Brain parenchymal fraction (BPF; higher BPF score); the FA values of T1 hyperintense lesions (r = -0.111; P = 0.018), the MD values of T1 hyperintense lesions (r = 0.379; P < 0.001) and the VR values of T1 hyperintense lesions (r = -0.142; P = 0.003) were significantly correlated with third ventricular width (lower width). However, the FA value of T1 hyperintense lesions was not significantly associated with BPF(r = 0.083; P = 0.08). The quantitative DTI values of T1 hyperintense MS plaques were between hypo-/isointense lesions and NAWM or normal white matter, and correlated with BPF and third ventricular width. Our results supports the notion that axonal remyelination may be the reason for T1 hyperintense lesions.

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