The mechanism and treatment strategy for immobilization-induced hypersensitivity in rats

Abstract

Cast immobilization is known to induce mechanical hypersensitivity, which disturbs rehabilitation. Some studies suggested that central neuronal sensitization may contribute to immobilizationinduced hypersensitivity. However, there is no research in eff ective treatment for immobilizationinduced hypersensitivity so far. We suggest that the lack of sensory input to peripheral tissue due to immobilization might induce changes to the nervous system, and cause immobilizationinduced hypersensitivity. Therefore, to prevent immobilization-induced hypersensitivity, sensory input should be delivered from peripheral tissue. We proposal the vibration therapy as the sensory input during immobilization: it has been reported that vibration therapy can reduce various types of pain. However, it is unclear whether vibration therapy reduce immobilization-induced hypersensitivity. To investigate the preventive and therapeutic effects of vibration therapy on immobilization-induced hypersensitivity, rats were immobilized for 8 weeks and divided randomly into 2 immobilization plus vibration groups (Im+Vib1 and Im+Vib2). Im+Vib1 group, for which vibration therapy was initiated immediately after the onset of immobilization, and Im+Vib2, for which vibration therapy was initiated 4 weeks after the onset of immobilization. To investigate central sensitization, calcitonin gene-related peptide (CGRP) expression in the spinal cord and dorsal root ganglion (DRG) was analyzed. As a result, immobilization-induced hypersensitivity was inhibited in the Im+Vib1 group but not in the Im+Vib2 group. Central sensitization, which was indicated by increases in CGRP expression in the spinal cord and the size of the area of CGRPpositive neurons in the DRG, was inhibited in only the Im+Vib1 group. Vibration therapy might be an effective technique to supplement the loss of sensory input and to inhibit hypersensitivity. These data suggest that initiation of vibration therapy in the early phase of immobilization may inhibit the development of immobilization-induced hypersensitivity.