ANTIALLODYNIC AND ANTIHYPERALGESIC EFFECTS OF NSAIDS COMBINATION IN SCIATIC NERVE LIGATION-INDUCED NEUROPATHIC PAIN IN THE RATS

Neuropathic pain (NP) has been considered as the most debilitating painful condition, the mechanisms underlying the neuropathic pain are not fully understood, but experiments on animal’s models indicate that both peripheral and central mechanisms have been involved in the pathogenesis of neuropathic pain. NP is characterized by behavioral symptoms of allodynia (pain in response to which actually do not evoke pain) and hyperalgesia (an exaggerated response to noxious stimuli). The NSAIDS are effective, inexpensive, and long-acting drugs, but their degree of analgesia is limited by the adverse effects at high doses,common ones are gastritis, gastrointestinal hemorrhage and ulceration. The prevalent belief that non-steroidal anti-inflammatory drugs (NSAIDs) lack efficacy for the treatment of neuropathic pain is so widely accepted that current neuropathic pain treatment guidelines either do not mention this class of medications or simply state that evidence of efficacy is limited or lacking. Yet, recent reports suggest that patients with neuropathic pain are at least as likely—and sometimes considerably more likely—to use NSAIDs than they are to use medications with wellestablished efficacy. There are growing evidence that central COX playsa key role in development and maintenance of neuropathic pain as evident by significantly increased immunoreactivity of COX-1 and COX-2 in superficial laminae cells in the ipsilateral spinal cord of rats with spinal nerve ligation.

[1]  Takeshi Kato,et al.  Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain , 2009, Journal of Molecular Neuroscience.

[2]  C. Hulsebosch,et al.  Mechanisms of chronic central neuropathic pain after spinal cord injury , 2009, Brain Research Reviews.

[3]  Tian-Le Xu,et al.  Reduced potassium-chloride co-transporter expression in spinal cord dorsal horn neurons contributes to inflammatory pain hypersensitivity in rats , 2008, Neuroscience.

[4]  R. Meli,et al.  AM404, an anandamide transport inhibitor, reduces plasma extravasation in a model of neuropathic pain in rat: Role for cannabinoid receptors , 2008, Neuropharmacology.

[5]  M. L. Sotgiu,et al.  Contribution by DRt descending facilitatory pathways to maintenance of spinal neuron sensitization in rats , 2008, Brain Research.

[6]  H. Ueda Peripheral mechanisms of neuropathic pain – involvement of lysophosphatidic acid receptor-mediated demyelination , 2008, Molecular pain.

[7]  J. Farrar,et al.  Pharmacologic management of neuropathic pain: Evidence-based recommendations , 2007, PAIN.

[8]  Philip Smith,et al.  Neuron type‐specific effects of brain‐derived neurotrophic factor in rat superficial dorsal horn and their relevance to ‘central sensitization’ , 2007, The Journal of physiology.

[9]  J. F. Herrero,et al.  The antinociceptive effect of systemic gabapentin is related to the type of sensitization-induced hyperalgesia , 2007, Journal of Neuroinflammation.

[10]  J. Stinson,et al.  Pharmacological management of chronic neuropathic pain - consensus statement and guidelines from the Canadian Pain Society. , 2007, Pain research & management.

[11]  T. Nurmikko,et al.  EFNS guidelines on pharmacological treatment of neuropathic pain , 2006, European journal of neurology.

[12]  R. Meyer,et al.  Mechanisms of Neuropathic Pain , 2006, Neuron.

[13]  Jun-Li Zhou,et al.  Analgesic effect of vitamin E is mediated by reducing central sensitization in neuropathic pain , 2006, PAIN.

[14]  S. Beggs,et al.  Neuropathic pain: symptoms, models, and mechanisms , 2006 .

[15]  C. Gravel,et al.  BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain , 2005, Nature.

[16]  George Havenith,et al.  Pain, thermal sensation and cooling rates of hands while touching cold materials , 2005, European Journal of Applied Physiology and Occupational Physiology.

[17]  C. Woolf,et al.  Cyclooxygenase 2 expression in the spared nerve injury model of neuropathic pain , 2004, Neuroscience.

[18]  H. Lee,et al.  Temporal expression of cytokines and their receptors mRNAs in a neuropathic pain model , 2004, Neuroreport.

[19]  H. Schaible,et al.  Descending control of persistent pain: inhibitory or facilitatory? , 2004, Brain Research Reviews.

[20]  S. Kulkarni,et al.  Differential effects of naproxen and rofecoxib on the development of hypersensitivity following nerve injury in rats , 2004, Pharmacology Biochemistry and Behavior.

[21]  H. Miranda,et al.  Isobolographic analysis of the antinociceptive interactions of clonidine with nonsteroidal anti-inflammatory drugs. , 2004, Pharmacological research.

[22]  V. Jevtovic-Todorovic,et al.  Redox modulation of peripheral T-type Ca2+ channels in vivo: alteration of nerve injury-induced thermal hyperalgesia , 2004, Pain.

[23]  G. Pasternak,et al.  The Synergistic Analgesic Interactions Between Hydrocodone and Ibuprofen , 2003, Anesthesia and analgesia.

[24]  Mario Saltarelli,et al.  Advances in neuropathic pain: diagnosis, mechanisms, and treatment recommendations. , 2003, Archives of neurology.

[25]  L. Sorkin,et al.  Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat , 2003, Neuroscience Letters.

[26]  L. Sorkin,et al.  Intramuscular injection of tumor necrosis factor-alpha induces muscle hyperalgesia in rats , 2003, Pain.

[27]  L. Landrum,et al.  The expression of Fos-labeled spinal neurons in response to colorectal distension is enhanced after chronic spinal cord transection in the rat , 2002, Neuroscience.

[28]  H. Kehlet,et al.  Comparative effect of paracetamol, NSAIDs or their combination in postoperative pain management: a qualitative review. , 2002, British journal of anaesthesia.

[29]  A. Lastra,et al.  Nociceptive reaction and thermal hyperalgesia induced by local ET-1 in mice: a behavioral and Fos study , 2002, Naunyn-Schmiedeberg's Archives of Pharmacology.

[30]  J. Chung,et al.  The changes in expression of three subtypes of TTX sensitive sodium channels in sensory neurons after spinal nerve ligation. , 2001, Brain research. Molecular brain research.

[31]  M. Zimmermann,et al.  Pathobiology of neuropathic pain. , 2001, European journal of pharmacology.

[32]  R. Raffa Pharmacology of oral combination analgesics: rational therapy for pain , 2001, Journal of clinical pharmacy and therapeutics.

[33]  N. Yonehara,et al.  Influence of painful chronic neuropathy on neurogenic inflammation , 2001, Pain.

[34]  J. Chung,et al.  Characteristics of ectopic discharges in a rat neuropathic pain model , 2000, PAIN®.

[35]  G. D. French,et al.  Wallerian degeneration is required for both neuropathic pain and sympathetic sprouting into the DRG , 1997, PAIN.

[36]  R. Coggeshall,et al.  Collateral Sprouting of Uninjured Primary Afferent A-Fibers into the Superficial Dorsal Horn of the Adult Rat Spinal Cord after Topical Capsaicin Treatment to the Sciatic Nerve , 1996, The Journal of Neuroscience.

[37]  J. Horn,et al.  Intrathecal ketorolac tromethamine produces analgesia after chronic constriction injury of sciatic nerve in rat , 1996, Canadian journal of anaesthesia = Journal canadien d'anesthesie.

[38]  A. Basbaum,et al.  Peripheral and central contributions to the persistent expression of spinal cord fos-like immunoreactivity produced by sciatic nerve transection in the rat , 1993, Brain Research.

[39]  Gary J. Bennett,et al.  A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man , 1988, Pain.

[40]  Iasp Subcommittee on Taxonomy Classification of chronic pain , 1986 .