Articles: hyperalgesia.
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To address the mechanisms of hyperalgesia and dorsal horn plasticity following peripheral tissue inflammation, the effects of adjuvant-induced inflammation of the rat hindpaw on behavioral nociception and nociceptive neuronal activity in the superficial dorsal horn were examined in neonatally capsaicin-treated rats 6-8 weeks of age. Capsaicin treatment resulted in an 82% loss of unmyelinated fibers in L5 dorsal roots, a dramatic reduction of substance P-like immunoreactivity in the spinal cord, and a significant decrease in the percentage of dorsal horn nociceptive neurons that responded to C-fiber stimulation and noxious heating of the skin. The thermal nociceptive threshold was significantly increased in capsaicin-treated rats, but behavioral hyperalgesia to thermal stimuli still developed in response to inflammation. ⋯ There was no difference in stimulation-induced expansion of the receptive fields for WDR neurons between vehicle- or capsaicin-treated rats. An N-methyl-D-aspartate receptor antagonist, MK-801, attenuated the behavioral hyperalgesia and reduced the receptive field size of dorsal horn neurons in inflamed capsaicin- and vehicle-treated rats. The data suggest that while capsaicin-sensitive primary afferents may be involved in neuronal plasticity induced by peripheral tissue inflammation, changes in the capsaicin-insensitive WDR and NS populations are sufficient to produce thermal and mechanical hyperalgesia after the loss of capsaicin-sensitive primary afferents.
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The experimental arthritis of the knee joint used in the present study leads to joint swelling, increased joint temperature, limping, guarding, and a decrease in paw withdrawal latency (PWL) to radiant heat (hyperalgesia) within hours in rats. Unexpectedly, administration of the non-NMDA receptor antagonist, CNQX, in the spinal cord 4 h after initiation of the arthritis significantly reduced the degree of joint inflammation and returned PWL times to baseline. Therefore, the present results indicate that established joint swelling and hyperalgesia can be reduced significantly by CNQX.
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In rheumatology, all of the more than 400 specified syndromes are associated with pain. In the conceptual discussion on the multidimensional influences postulated to explain the development of chronic pain, fibromyalgia has gained increasing interest. Fibromyalgia (fibrositis) is an unspecific soft-tissue disorder with chronic wide-spread musculoskeletal pain and palpable hypersensitivity at fibrositic tender points. ⋯ Histochemical investigations on muscle biopsy and biochemical tests have revealed unspecific changes but no characteristic muscle abnormality. It is supposed that the clinical features may result from central neurohumoral dysfunction combining with peripheral mechanisms to result in hyperalgesia. An integrated therapeutic concept with a reassuring and positive doctor-patient relationship can be helpful in achieving satisfactory treatment results.
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Nerve lesions producing extensive axonal loss can induce painful hyperalgesic states in man. The affect of axonal regeneration and end-organ reinnervation on hyperalgesia and pain is controversial. This study used two axonotmetic models, the sciatic crush injury (CI) and the sciatic chronic constrictive injury (CCI), to investigate the affects of nerve regeneration and reinnervation on hyperalgesia and presumed painful behavior in rats. ⋯ Motor function recovery occurred primarily over days 23-59 post-ligature. During this prolonged period of motor function recovery there was a resolution of the sciatic-mediated plantar surface heat hyperalgesia and the saphenous-mediated heat ANH. The above data support the hypothesis that the successful regeneration of distal axons after axonotmetic lesions can initiate the resolution of neuropathic hyperalgesia.
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Braz. J. Med. Biol. Res. · Aug 1994
The induction of des-Arg9-bradykinin-mediated hyperalgesia in the rat by inflammatory stimuli.
1. The B1 receptor agonist des-Arg9-BK does not induce mechanical hyperalgesia when injected into the rat knee joint at 1-100 nmol, or thermal hyperalgesia when injected intravenously up to 1 mumol/kg. 2. Bradykinin (BK), administered into the joint, (1 nmol-1 mumol) induces a mechanical hyperalgesia, which is maximal by 4 h. ⋯ After interleukin-1 beta pre-treatment (1 unit into the joint or paw) des-Arg9-BK induced both thermal and mechanical hyperalgesia. Co-administration of des-Arg9-Leu8-BK 0.5 nmol with des-Arg9-BK 0.5 nmol into the joint prevented development of hyperalgesia and co-administration of des-Arg9-Leu8-BK (200 nmol/kg, iv) with des-Arg9-BK 10 nmol/kg prevented reduction of thermal withdrawal latencies. 6. These data suggest that after an inflammatory insult B1 receptors may play a role in the transduction of nociceptive information.