Abstract
The aim of this study was to clarify the mechanism of disuse-induced muscle hyperalgesia through the evaluation of the pharmacological behaviour of muscle hyperalgesia profiles in chronic post-cast pain (CPCP) rats with acute and chronic-phase mirror-image muscle hyperalgesia treated with diclofenac (NSAID), pregabalin (an inhibitor of Ca2+ channel α2δ), and duloxetine (SNRI). After 2 weeks of cast immobilization, the peak cross-sectional area and muscle wet weight of the ipsilateral soleus and gastrocnemius muscles decreased more significantly in CPCP rats than in untreated rats. Histological findings revealed disuse-induced muscle atrophy in CPCP rats. The blood biochemical parameters of CPCP rats in acute and chronic phases did not differ significantly from those of untreated rats. The diclofenac and pregabalin-treated groups exhibited no improvement in acute or chronic muscle hyperalgesia. In contrast, the duloxetine-treated group exhibited an improvement in acute muscle hyperalgesia, but showed no apparent effect on chronic muscle hyperalgesia on ipsilateral or contralateral sides. However, the chronic muscle hyperalgesia was reversed by intrathecal administration of DAMGO (a μ-opioid receptor agonist). The results suggest that chronic muscle hyperalgesia in CPCP rats did not result from an inflammatory mechanism, and there is only a low probability that it’s caused by a neuropathic mechanism.
Highlights
IntroductionKinesiophobia is the fear of movement and physical activity, which is (wrongfully) assumed to cause (re)injury[1]
Kinesiophobia is the fear of movement and physical activity, which is assumed to causeinjury[1]
The purpose of the present study was to evaluate the effects of diclofenac, pregabalin, and duloxetine—on acute and chronic-phase muscle hyperalgesia in chronic postcast pain (CPCP) rats in order to verify the pharmacological behaviour of muscle hyperalgesia profiles in these rat models
Summary
Kinesiophobia is the fear of movement and physical activity, which is (wrongfully) assumed to cause (re)injury[1]. To our knowledge, no study has demonstrated the efficacy of SNRIs in CRPS They have, been demonstrated to be effective in fibromyalgia[24], which involves extensive chronic muscle hyperalgesia similar to that in CRPS, and in low-back pain[25,26], which— to CRPS—involves complex causes of pain[20,27]. These results strongly suggest that pain is caused by transformations in the central nervous system (such as reduced functioning of the descending-pain inhibitory system) as well as psychosocial factors[24,25,28]. As has been stated in many reports, the chronic phase especially involves plastic changes in the central nervous system[18,19,30]; phase changes in pain are expected to cause changes in the mechanism of pain induction
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