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Updated: Sep 12, 2026

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
Alterations in white matter integrity in patients with postherpetic neuralgia evidenced by peak width of skeletonized
Daeseok Oh1, Dong Ah Lee2, Ho-Joon Lee3
1Department of Anesthesiology, Haeundae Paik Hospital, Inje University College of Medicine, Busan, Korea.
Background:
Postherpetic neuralgia (PHN) causes chronic neuropathic pain and reduced quality of life. The peak width of skeletonized mean diffusivity (PSMD), based on MD histogram along the fractional anisotropy skeleton, has shown robustness and clinical relevance in other neurological disorders.
Methods:
This single-center cross-sectional study included 83 participants: 42 patients with PHN and 41 age- and sex-matched healthy controls. All participants underwent diffusion tensor imaging (DTI), and data were analyzed using the FMRIB Software Library software. PSMD and conventional DTI metrics were computed and compared between groups.
Results:
Patients with PHN exhibited marked increase in PSMD relative to healthy controls (2.862 ± 0.436 × 10-4 vs. 2.369 ± 0.407 × 10-4 mm2/s, P < 0.001). Additionally, MD and axial diffusivity (AD) were significantly elevated in the PHN group compared with controls (0.854 ± 0.035 vs. 0.836 ± 0.030, P = 0.012; 1.292 ± 0.036 vs. 1.264 ± 0.033, P < 0.001; respectively). Receiver operating characteristic analysis demonstrated that PSMD provided the greatest discriminative ability between groups (area under the curve = 0.816, P < 0.001). Furthermore, multivariable logistic regression including PSMD, MD, and AD identified PSMD as the sole independent predictor of PHN status (P = 0.002).
Conclusions:
This study demonstrated that patients with PHN showed altered white matter integrity, with increased PSMD, MD, and AD values compared to healthy controls. PSMD showed superior diagnostic performance over most conventional DTI metrics and may serve as promising marker of widespread white matter disruption in PHN at the group level.
