Hyperalgesia allodynia

Clinical manifestation Primary hyperalgesia, allodynia, spontaneous pain Secondary hyperalgesia, allodynia, spontaneous pain, aberrantly referred pain ... 

Nociceptive neurons in the spinal cord as well as in higher centres such as the thalamus and cortex can also undergo alterations in activity following chronic peripheral changes and trauma (Table 1). These changes are typically long-term in nature and lead to the clinical syndromes of centrally maintained pain (secondary hyperalgesia, allodynia, spontaneous pain). Alterations... 

H. Kawahara, A. Sakamoto, S. Takeda, H. Onodera, J. Imaki, R. Ogawa, A prostaglandin E2 receptor subtype EP1 receptor antagonist (ONO-8711) reduces hyperalgesia, allodynia, and c-fos gene expression in rats with chronic nerve constriction, Anesth. Analg. 93 (2001) 1012. 

DeLeo, J. A., Colburn, R. W., Nichols, M., and Malhotra, A. (1996). Interleukin-6-mediated hyperalgesia/allodynia and increased spinal IL-6 expression in a rat mononeuropathy model. J. Interferon Cytokine Res. 16, 695—700. 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Clinical pain is characterized by the presence of spontaneous pain or hypersensitivity to pain-provoking stimuli. Hypersensitivity includes pain produced by low-intensity stimuli that normally only elicit an innocuous sensation (allodynia), or an exaggerated response to a noxious stimulus (hyperalgesia). There are two distinct forms of clinical pain, the pain that occurs after tissue injury or inflammatory diseases (inflammatory pain) and the pain associated with a lesion or disease of the nervous system (neuropathic pain). Although the mechanisms responsible for the initiation and maintenance of these pains differ, they are both characterized by heightened... 

Neuropathic pain is often chronic, not well described, and not easily treated with conventional analgesics. There may be exaggerated painful responses to normally noxious stimuli (hyperalgesia) or painful responses to normally nonnoxious stimuli (allodynia). 

The uncompetitive NMDA receptor antagonist ketamine has been available for clinical use as an anaesthetic for 40 years (Domino et al. 1965). Ketamine is effective in various animal models of hyperalgesia and allodynia and has been reported to have antinociceptive effects in some of these models at doses devoid of obvious side-effects. Others, however, have reported that the effects of ketamine are only seen at doses producing ataxia (see Parsons 2001 for review). Ketamine reportedly inhibits the area of secondary hyperalgesia induced by chemical (Park et al. 1995) or thermal stimuli (Ilkjaer et al. 1996 Warncke et al. 1997) and inhibits temporal siunmation of repeated mechanical (Warncke et al. 1997) and electrical stimuli (Arendtnielsen et al. 1995 Andersen et al. 

Fundytus ME, Osborne MG, Henry JL, et al (2002) Antisense oligonucleotide knockdown of mGluR(l) alleviates hyperalgesia and allodynia associated with chronic inflammation. Pharmacol Biochem Behav 73 401-410... 

Chronic constriction injury (CCI) models (Bennett and Xie, 1988 Kim and Chung, 1992 Mosconi and Kruger, 1996) have been used to examine chronic pain states in experimental animals. In these models, intrathecally administered a2-agonists reduced mechanical allodynia and thermal hyperalgesia that developed following nerve constriction (Levy et al., 1994 Yaksh et al., 1995). This... 

Antagonism of group I mGluRs appears to be particularly useful in the reduction of hyperalgesia and allodynia associated with chronic pain... 

Fisher, K., Fundytus, M. E., Cahill, C. M., Coderre, T. J. Intrathecal administration of the mGluR compound, (S)-4CPG, attenuates hyperalgesia and allodynia associated with sciatic nerve constriction injury in rats, Pain 1998, 77, 59-66. 

Chaplan, S. R., Malmberg, A. B., Yaksh, T. L. Efficacy of spinal NMDA-receptor antagonism in formalin hyperalgesia and nerve injury evoked allodynia in the rat, J. Pharmacol. Exp. Ther. 1997, 280, 829-838. 

Sutton, J.L., Maccecchini, M.L., Kajander, K.C. The kainate receptor antagonist 2S,4R-4-methylglutamate attenuates mechanical allodynia and thermal hyperalgesia in a rat model of nerve injury, Neuroscience 1999, 91, 283-292. 

Ta, L.E., Dionne, R.A., Fricton, J.R., Hodges, J., Kajander, K C. SYM-2081 a kainate receptor antagonist reduces allodynia and hyperalgesia in a freeze injury model of neuropathic pain, Brain Res. 2000, 858, 106-120. 

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