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Purpose: Anatomical localization of brain networks controlling post-stroke spasticity are not fully understood. The purpose of this study was to determine the relationship between the integrity of white matter tracts and severity of spasticity and how this relationship changes with mitigation of spasticity in response to motor learning therapy.Methods: Eleven stroke survivors (>6 months post-stroke) with arm sensorimotor deficits had 12-week (5 d/week, 5 hr/day) motor learning therapy. Outcome measures included modified Ashworth Scale (mAS), Fugl-Meyer Upper limb (FM) and Diffusion Tensor Imaging (DTI). mAS was scored for 9 arm muscles and summated. Using Freesurfer software, DTI was analyzed via longitudinal processing stream and white matter tracts were reconstructed according to a global probabilistic tractography algorithm. Fractional anisotropy (FA), axial diffusivity (AD), and radial diffusivity (RD) were averaged along the center of the 8 bilateral and 2 interhemispheric white matter tracts. We performed partial Spearman correlation (Bonferonni correction for multiple comparisons) to evaluate the relationship between mAS and DTI measures while controlling for change in Fugl-Meyer. Wilcoxon paired sign rank test was used to compare pre vs post rehab scores for mAS and FM.Results: Subjects were 59±8.3 years old, 46±30 months after stroke and 54% were female. mAS improved from 5.95±3 to 3.95±2.6 (p=0.002, paired sign rank test) and FM improved from 25.9±12.4 to 37.6±13.9 (p=0.00097). At baseline, lower spasticity correlated with higher AD in the ipsilesional cingulum angular bundle (rho=.86; p=0.0007). Greater improvement in spasticity correlated with lower AD in the contralesional uncinate fasciculus (rho=.79;p=0.004) at baseline. Both tracts are part of limbic system. Furthermore, lower spasticity at baseline correlated with lower FA in the contralesional corticospinal tract (rho=.81; p=0.004) at baseline.Conclusion: The results show the complex nature of anatomical localization for spasticity and its mitigation. Structural integrity of the contralesional corticospinal tract as well as bi-hemispheric limbic system tracts may be involved in post-stroke spasticity.