Sympathetic hyperinnervation in myofascial trigger points.

To evaluate the local distribution and activity of sympathetic nerves in myofascial trigger points (MTrPs) and explore the pathological mechanism of myofascial pain syndrome (MPS) using a rat model of disease.MPS was modeled in the model group (MG) by a combination of blunt trauma and eccentric exercise in Sprague-Dawley rats (n = 8). Eight rats were randomly assigned to the control group (CG). Histopathology was applied to detect the local conditions of the MTrPs. Tyrosine hydroxylase (TH), nerve growth factor (NGF), and norepinephrine (NE) were detected in the MTrPs to evaluate sympathetic remodeling.Muscle fiber rupture, atrophy and shape irregularity were universally observed in the MTrPs. TH expression was significantly increased in the MG, as detected by immunofluorescence, and NGF and TH expression was also higher in MTrPs in the MG than in MTrPs in the CG, as determined by immunohistochemistry. Furthermore, the expression of NE was significantly increased in MTrPs, as determined by ELISA.There was sympathetic hyperinnervation in MTrPs, which could partially explain the symptoms of MTrPs and is an interesting and useful new perspective regarding the diagnosis and treatment of MPS.The sympathetic nerves in MTrPs are remodeled, leading to sympathetic hyperinnervation. Sympathetic hyperinnervation can partially explain the symptoms of MPS. The pathological mechanism of sympathetic hyperinnervation may be a new perspective for the diagnosis and treatment of MPS.