Referred Somatic Hyperalgesia Mediates Cardiac Regulation by the Activation of Sympathetic Nerves in a Rat Model of Myocardial Ischemia.

Myocardial ischemia (MI) causes somatic referred pain and sympathetic hyperactivity, and the role of sensory inputs from referred areas in cardiac function and sympathetic hyperactivity remain unclear. Here, in a rat model, we showed that MI not only led to referred mechanical hypersensitivity on the forelimbs and upper back, but also elicited sympathetic sprouting in the skin of the referred area and C8-T6 dorsal root ganglia, and increased cardiac sympathetic tone, indicating sympathetic-sensory coupling. Moreover, intensifying referred hyperalgesic inputs with noxious mechanical, thermal, and electro-stimulation (ES) of the forearm augmented sympathetic hyperactivity and regulated cardiac function, whereas deafferentation of the left brachial plexus diminished sympathoexcitation. Intradermal injection of the α2 adrenoceptor (α2AR) antagonist yohimbine and agonist dexmedetomidine in the forearm attenuated the cardiac adjustment by ES. Overall, these findings suggest that sensory inputs from the referred pain area contribute to cardiac functional adjustment via peripheral α2AR-mediated sympathetic-sensory coupling.

Referred Somatic Hyperalgesia Mediates Cardiac Regulation by the Activation of Sympathetic Nerves in a Rat Model of Myocardial Ischemia / 神经科学通报·英文版

Myocardial ischemia (MI) causes somatic referred pain and sympathetic hyperactivity, and the role of sensory inputs from referred areas in cardiac function and sympathetic hyperactivity remain unclear. Here, in a rat model, we showed that MI not only led to referred mechanical hypersensitivity on the forelimbs and upper back, but also elicited sympathetic sprouting in the skin of the referred area and C8-T6 dorsal root ganglia, and increased cardiac sympathetic tone, indicating sympathetic-sensory coupling. Moreover, intensifying referred hyperalgesic inputs with noxious mechanical, thermal, and electro-stimulation (ES) of the forearm augmented sympathetic hyperactivity and regulated cardiac function, whereas deafferentation of the left brachial plexus diminished sympathoexcitation. Intradermal injection of the α2 adrenoceptor (α2AR) antagonist yohimbine and agonist dexmedetomidine in the forearm attenuated the cardiac adjustment by ES. Overall, these findings suggest that sensory inputs from the referred pain area contribute to cardiac functional adjustment via peripheral α2AR-mediated sympathetic-sensory coupling.

Electroacupuncture at Neurogenic Spots in Referred Pain Areas Attenuates Hepatic Damages in Bile Duct-Ligated Rats.

Visceral pain frequently produces referred pain at somatic sites due to the convergence of somatic and visceral afferents. In skin overlying the referred pain, neurogenic spots characterized by hyperalgesia, tenderness and neurogenic inflammation are found. We investigated whether neurogenic inflammatory spots function as acupoints in the rat model of bile duct ligation-induced liver injury. The majority of neurogenic spots were found in the dorsal trunk overlying the referred pain and matched with locations of acupoints. The spots, as well as acupoints, showed high electrical conductance and enhanced expression of the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP). Electroacupuncture at neurogenic spots reduced serum hepatocellular enzyme activities and histological patterns of acute liver injury in bile duct ligation (BDL) rats. The results suggest that the neurogenic spots have therapeutic effects as acupoints on hepatic injury in bile-duct ligated rats.

Does the addition of visceral manipulation improve outcomes for patients with low back pain? Rationale and study protocol.

OBJECTIVES: There has been no randomised controlled trial conducted to investigate the effectiveness of visceral manipulation (VM) for the treatment of low back pain (LBP). The primary aim of this study would be to investigate whether the addition of VM, to a standard physiotherapy treatment regimen, improves pain 6 weeks post treatment commencement in people with LBP. Secondary aims would be to examine the effect of VM on disability and functional outcomes at 2, 6 and 52 weeks post-treatment commencement and pain at 2 and 52 weeks. METHODS: This paper describes the rationale and design of a randomised controlled trial investigating the addition of VM to a standard physiotherapy treatment algorithm which includes manual therapy, specific exercise and functional exercise prescription. Analysis of data would be carried out by a statistician blinded to group allocation and by intention-to-treat.

Myofascial trigger points, pain, disability, and sleep quality in individuals with mechanical neck pain.

OBJECTIVE: The purpose of this study was to investigate the presence of active myofascial trigger points (MTrPs) in a greater number of muscles than previous studies and the relation between the presence of MTrPs, the intensity of pain, disability, and sleep quality in mechanical neck pain. METHODS: Fifteen patients with mechanical neck pain (80% women) and 12 comparable controls participated. Myofascial trigger points were bilaterally explored in the upper trapezius, splenius capitis, semispinalis capitis, sternocleidomastoid, levator scapulae, and scalene muscles in a blinded design. Myofascial trigger points were considered active if the subject recognized the elicited referred pain as a familiar symptom. Myofascial trigger points were considered latent if the elicited referred pain was not recognized as a symptom. Pain was collected with a numerical pain rate scale (0-10); disability was assessed with Neck Disability Index; and sleep quality, with the Pittsburgh Sleep Quality Index. RESULTS: Patients exhibited a greater disability and worse sleep quality than controls (P < .001). The Pittsburgh Sleep Quality Index score was associated with the worst intensity of pain (r = 0.589; P = .021) and disability (r = 0.552; P = .033). Patients showed a greater (P = .002) number of active MTrPs (mean, 2 ± 2) and similar number (P = .505) of latent MTrPs (1.6 ± 1.4) than controls (latent MTrPs, 1.3 ± 1.4). No significant association between the number of latent or active MTrPs and pain, disability, or sleep quality was found. CONCLUSIONS: The referred pain elicited by active MTrPs in the neck and shoulder muscles contributed to symptoms in mechanical neck pain. Patients exhibited higher disability and worse sleep quality than controls. Sleep quality was associated with pain intensity and disability. No association between active MTrPs and the intensity of pain, disability, or sleep quality was found.

Nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points.

OBJECTIVE: The aim of the study was to evaluate whether or not there exists nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points (MTrPs). METHODS: Eleven healthy volunteers participated in this study, which consisted of 3 sessions of electromyography-guided intramuscular injection with a minimum of a week interval in between. In each session, a bolus of either hypertonic saline (6%, 0.1 mL, each), glutamate (0.1 mL, 0.5 M, each), or isotonic saline (0.9%, 0.1 mL, each) was randomly injected into a latent MTrP and a non-MTrP located in the right or left gastrocnemius medialis muscles. After each injection, participants were asked to rate the perceived pain intensity on an electronic visual analog scale (VAS) and to mark the pain areas on pain drawings. Maximal pain intensity (VAS(peak)), the area under the curve (VAS(auc)), and local and referred pain areas were extracted. RESULTS: Injections of either hypertonic saline, glutamate, or isotonic saline into the latent MTrPs induced a higher VAS(peak) and larger VAS(auc) than the non-MTrPs (all, P<0.05). Furthermore, the MTrPs with referred pain after painful injections were found to show higher VAS(peak) and larger VAS(auc) than those without referred pain (both, P<0.001). CONCLUSIONS: These results confirm the existence of nociceptive hypersensitivity at latent MTrPs and provide the first evidence that there exists non-nociceptive hypersensitivity (allodynia) at latent MTrPs. Finally, the occurrence of referred muscle pain is associated with higher pain sensitivity at latent MTrPs.