Abstract TP319: Post-Stroke Shoulder Pain is Associated with Hyaluronan Deposition in Shoulder Muscles

Introduction: Shoulder pain occurs in 30-70% of patients with stroke and may persist in the chronic stage, interfering with motor recovery and quality of life. Reduced mobility and spasticity may result in the accumulation of hyaluronan (HA) in the extracellular matrix of muscles on the paretic side compared to non-paretic side, leading to dysfunctional gliding and reduced shoulder external rotation which is strongly correlated with post stroke shoulder pain (PSSP). Methods: 35 participants with PSSP and limitation in shoulder external rotation underwent MRI of the shoulder girdle musculature using T1, T2, T1ρ, and Dixon fat fraction imaging. HA concentration in the shoulder internal (pectoralis major) and external (infraspinatus) rotators was measured using T1ρ MRI relaxation time. Muscle atrophy and fat fraction were quantified using T1 closed surface volumetric analysis and Dixon imaging, respectively. Dynamic ultrasound shear strain mapping was used to quantify dysfunctional gliding of muscle. Pain was assessed using quantitative sensory testing. Results: T1ρ relaxation time was significantly increased in the infraspinatus on the paretic side (p) compared with the non-paretic (np) side (mean±SD: p, 29.1±3.0 vs. np, 27.2±2.2, Cohen’s d 0.75, p=0.002). Maximum shear strain was also reduced between the pectoralis major and minor muscles (p, 35.4±12.8% vs. np, 46.5±19.8%, Cohen’s d 0.66, p=0.008). Significant negative correlations were noted between maximum shear strain and T1ρ relaxation time difference between the paretic and non-paretic sides, (r=-0.6, p=0.0003), and pain severity (r=-0.5, p=0.03), suggesting that reduced muscle gliding is associated with increased HA accumulation and pain. There was greater atrophy in the infraspinatus (p, 94.1±45.6 vs. np, 122.1±54.1, p=0.0008), but fat fraction was not significantly increased. HA accumulation on T1ρ imaging was associated with greater muscle atrophy (r=-0.8, p=0.02). Conclusions: The results suggest that T1ρ MRI imaging is a valid structural biomarker for HA accumulation, and that ultrasound shear strain imaging is a valid functional biomarker for myofascial dysfunction. HA accumulation in paretic muscles may be a biologic cause of myofascial pain and dysfunction after stroke and is associated with muscle atrophy. Shoulder rehabilitation to prevent atrophy and HA accumulation in the shoulder muscles may disrupt the pathophysiology of post stroke shoulder pain.