Changes in serum levels of pain mediators in hemiplegic shoulder pain.

Abstract

To provide a new insight into the diagnosis and treatment of hemiplegic shoulder pain (HSP) by investigating changes in serum pain mediators. Cross-sectional study. Shoulder pain group (n=34) and control group (n=21). Pain-free shoulder mobility, anxiety status, depression status, and shoulder pain were measured by passive range of motion (PROM), self-rating anxiety scale, self-rating depression scale (SDS), and visual analog scale, respectively. The enzyme-linked immunosorbent assay was used to test the serum pain mediators, including interleukin (IL)-1β, IL-2, IL-6, IL-10, nerve growth factor (NGF), tumor necrosis factor-α (TNF-α), substance P (SP), calcitonin gene-related peptide (CGRP), bradykinin (BK), 5-hydroxytryptamine (5-HT), prostaglandin E2 (PGE2), and lysophosphatidic acid (LPA). Shoulder pain group pain-free PROM significantly lower than control (p<.01), and SDS index score of shoulder pain group was significantly higher than control (p<.05). The rate of spasticity in the flexor elbow muscles is higher in shoulder pain group (p<.01). CGRP, IL-10, and IL-2 were significantly upregulated in shoulder pain group compared with control (p<.01), whereas NGF, TNF-α, IL-6, 5-HT, PGE2, SP, LPA, BK, and IL-1β were significantly decreased (p<.01). Patients with HSP have a higher risk of joint mobility disorders and depression; spasticity may be an important factor in the development of shoulder pain; CGRP is thought to be the major pain mediator in HSP, and HSP may not be inflammatory.