Articles: hyperalgesia.
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Arthritis care & research · Aug 2010
Pressure pain sensitivity topographical maps reveal bilateral hyperalgesia of the hands in patients with unilateral carpal tunnel syndrome.
To assess topographical pressure pain sensitivity maps of the hand in patients with unilateral carpal tunnel syndrome (CTS) as compared with healthy subjects. ⋯ Our findings revealed bilateral generalized pressure pain hyperalgesia in unilateral CTS because lower PPT levels were found in all of the points. The pressure pain hyperalgesia was not uniformly distributed since PPTs were lower in points over the proximal phalanx of the fingers and the thenar eminency as compared with those points located over the distal phalanx of the fingers. The decrease in PPT levels was associated with the intensity and the duration of the pain symptoms, supporting a role of both peripheral and central sensitization mechanisms in this pain condition.
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Painful diabetic neuropathy may be due to impairments in descending modulation of nociceptive transmission at the spinal cord. In the present study, streptozotocin diabetic rats (STZ rats) with neuropathic symptoms (mechanical hypersensitivity) were used to perform a time-course evaluation of neuronal activity at the spinal dorsal horn and at the periaqueductal grey matter (PAG), a major brainstem area of pain modulation. The expression of Fos protein, a marker of nociceptive activation, progressively increased at the spinal dorsal horn at 4 and 10 weeks. ⋯ The present study shows that diabetic neuropathy is accompanied by a progressive increase of the spontaneous neuronal activity at the spinal cord. Changes in descending modulation of nociceptive transmission from the PAG are likely to occur during diabetic neuropathy, probably with exacerbation of facilitatory actions. The effects of gabapentin in reversing the behavioural signs of diabetic neuropathy and neuronal hyperactivity in the spinal cord and PAG reinforce the central causes of diabetic neuropathy and point to the central targets of the drug.
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Narcotic bowel syndrome (NBS) is a subset of opioid bowel dysfunctions that results from prolonged treatment with narcotics and is characterized by chronic abdominal pain. NBS is under-recognized and its molecular mechanisms are unknown. We aimed to (1) develop a rat model of NBS and (2) to investigate its peripheral and central neurobiological mechanisms. ⋯ We developed a rat model of narcotic bowel-like syndrome and showed that spinal microglia activation mediates the development of morphine-induced visceral hyperalgesia; peripheral neuroimmune activation and spinal dynorphin release represent an important mechanism in the delayed and long-lasting morphine-induced colonic hypersensitivity response to CRD.
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Exp Clin Psychopharmacol · Aug 2010
Repeated administration of pioglitazone attenuates development of hyperalgesia in a rat model of neuropathic pain.
Recent studies indicate the central neuroimmune and neuroinflammation activation play a critical role in the pathological states of pain. Pioglitazone, a potent synthetic agonists of PPARgamma, has shown to control neuroinflammation in many nervous system-related disorders. The present study was designed to explore the effects of pioglitazone in treating neuropathic pain and its possible neuroimmune mechanisms in the neuropathic pain using lumbar 5 (L5) spinal nerve transection rat model. ⋯ We found that pioglitazone (5 and 10 mg/kg) can markedly attenuate mechanical hyperalgesia produced by nerve transection, most significantly on the 14th day. The elevated TNF-alpha, IL-1beta, and NF-kappaB in brain were accordingly reduced. Our data could conclude that pioglitazone has ameliorative potential in attenuating the painful state associated with L5 nerve transection, which may further be attributed to inhibiting cerebral proinflammatory cytokines production and NF-kappaB activation in central nervous system.
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Lysophosphatidic acid (LPA) is released from injured tissue and cancer cells and is involved in the induction of neuropathic pain. The present study explores whether LPA plays a role in the development of osteocarcinoma-induced pain. ⋯ These data indicate that LPA is involved in the induction of bone cancer pain through mechanisms of peripheral C-fibers sensitization. LPA and its downstream molecules possibly are promising therapeutic targets for treatment of cancer pain.