Articles: hyperalgesia.
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Am. J. Gastroenterol. · Nov 2008
Somatosensory hypersensitivity in the referred pain area in patients with chronic biliary pain and a sphincter of Oddi dysfunction: new aspects of an almost forgotten pathogenetic mechanism.
Somatosensory hyperalgesia in the referred pain area (RPA) in patients with acute or chronic abdominal pain syndromes may result from the convergence of nerve fibers from visceral and somatic tissues at the spinal and supraspinal levels. Chronic biliary pain in patients with the postcholecystectomy syndrome (i.e., biliary hypersensitivity) may be explained by persistent hyperexcitability of neurons in the central nervous system (CNS). The aim of this study was to evaluate the cutaneous neural sensory perception in the RPA in patients with chronic postcholecystectomy biliary pain and a sphincter of Oddi (SO) dysfunction (SOD). ⋯ Continuous visceral pain (biliary pain) caused by local inflammatory/sensitizing processes or a CNS malfunction could lead to significant hypersensitivity of the peripheral nociceptive nerve fibers in SOD patients. Postcholecystectomy pain may be explained by persistent hyperexcitability of the nociceptive neurons in the CNS with or without objective motility disorders of the SO.
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Journal of neurotrauma · Nov 2008
Capsular ligament involvement in the development of mechanical hyperalgesia after facet joint loading: behavioral and inflammatory outcomes in a rodent model of pain.
Whiplash injury can produce pain in the neck, arm, and hand, and has been associated with inflammation. However, the relationship between inflammatory responses and pain symptoms remains unknown, hindering the development of appropriate therapeutics for whiplash symptoms. Two joint loading paradigms were used separately in an established rat model of painful cervical facet joint distraction to apply: (1) gross failure, and (2) subfailure distraction of the facet capsular ligament. ⋯ Cytokine mRNA levels in the spinal cord and DRG were also significantly elevated after facet ligament failure, but not after painful subfailure loading. Findings suggest that different joint loading scenarios produced varied inflammatory responses in the CNS. These data support existing clinical reports suggesting that therapeutic interventions directed at the facet capsule may be effective in treating this painful injury.
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Migraine patients may have cutaneous allodynia during attacks. In order to investigate if pain physiology changes in the preattack phase we estimated heat pain and cold pain detection threshold (HPT and CPT) on three different days in 41 migraine patients and 28 controls. ⋯ Subclinical preattack thermal pain hypersensitivity seems to be a feature of the process that leads to a migraine attack.
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    Comparative Study
Pharmacological differences between static and dynamic allodynia in mice with herpetic or postherpetic pain.
In the present study, we investigated whether dynamic and static allodynia would be developed in the affected dermatome in murine models of herpetic pain and postherpetic neuralgia and pharmacologically characterized the allodynia. Inoculation with herpes simplex virus type-1 on the femur induced skin lesions in the dermatome including the plantar region of the hind paw from day 5 to day 21 after inoculation. Dynamic allodynia became apparent in the hind paw from day 3 to at least day 42. ⋯ Gabapentin (30 mg/kg, p.o.) markedly inhibited both static and dynamic allodynia. Developmental and pharmacological differences between static and dynamic allodynia suggest that independent mechanisms are responsible for dynamic and static allodynia. This murine model may be useful for the study of the mechanisms of dynamic allodynia of herpetic pain or postherpetic neuralgia and the development of new analgesics effective against the dynamic allodynia.
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To clarify the role of peroxisome proliferator activated receptor gamma (PPARgamma) in neuropathic pain, we examined the effect of pioglitazone, a PPARgamma agonist, on tactile allodynia and thermal hyperalgesia in a neuropathic pain model. Mice were subjected to partial sciatic nerve ligation (PSL) and given pioglitazone (1 - 25 mg/kg, p.o.) once daily. PPARgamma was distributed in the neurons of the dorsal root ganglion and the dorsal horn of the spinal cord and in the adipocytes at the epineurium of the sciatic nerve in naive mice. ⋯ A single administration of pioglitazone to mice on day 7 of PSL did not alter tactile allodynia and thermal hyperalgesia. PSL-induced upregulation of tumor necrosis factor-alpha and interleukin-6, which are essential for neuropathic pain, was suppressed by pioglitazone for the first week. This suggests that pioglitazone alleviates neuropathic pain through attenuation of proinflammatory cytokine upregulation by PPARgamma stimulation.