Does electrode placement influence tens-induced antihyperalgesia in experimental inflammatory pain model?

BACKGROUND: Transcutaneous electrical nerve stimulation (TENS) is a treatment commonly used for managing pain; however, the ideal placement of the electrodes is not fully understood. OBJECTIVE: To investigate the best way to apply TENS electrodes in an experimental inflammatory pain model. METHOD: Knee joint inflammation was induced in rats, followed by administration of low-frequency TENS (4Hz) under anesthesia for five days. Animals were randomly allocated to five groups according to electrode placement (n=6, each): dermatome, contralateral, paraspinal, acupoint, and control. INTERVENTIONS: Low-frequency TENS at sensory intensity and 100µs pulse duration. Withdrawal thresholds to mechanical (von Frey) and thermal stimuli and joint edema were assessed before induction of inflammation and immediately before and after application of TENS. RESULTS: Reduced paw withdrawal threshold and thermal latency that occur 24h after the induction of inflammation were significantly reversed by the administration of TENS in all groups when compared with sham treatment or with the condition before TENS treatment. No difference was observed in the edema measurement. CONCLUSION: These results offer more options for practitioners to choose the area of the body most commodious for electrode placement, depending on the clinical condition of the patient, because the effect was similar at all sites. In addition, there was a loss of the effectiveness of TENS in reversing mechanical and thermal hyperalgesia on the fifth day, suggesting the development of the tolerance phenomenon.

Animal models of fibromyalgia.

Animal models of disease states are valuable tools for developing new treatments and investigating underlying mechanisms. They should mimic the symptoms and pathology of the disease and importantly be predictive of effective treatments. Fibromyalgia is characterized by chronic widespread pain with associated co-morbid symptoms that include fatigue, depression, anxiety and sleep dysfunction. In this review, we present different animal models that mimic the signs and symptoms of fibromyalgia. These models are induced by a wide variety of methods that include repeated muscle insults, depletion of biogenic amines, and stress. All potential models produce widespread and long-lasting hyperalgesia without overt peripheral tissue damage and thus mimic the clinical presentation of fibromyalgia. We describe the methods for induction of the model, pathophysiological mechanisms for each model, and treatment profiles.