Peripheral nerve injury

Sweitzer SM, Hickey WF et al (2002) Focal peripheral nerve injury induces leukocyte trafficking into the central nervous system potential relationship to neuropathic pain. Pain 100(1-2) 163-170... 

Zhang J, De Koninck Y (2006) Spatial and temporal relationship between monocyte chemoattractant protein-1 expression and spinal glial activation following peripheral nerve injury. J Neurochem 97 772-783... 

Pain sensation is modulated by glial cells communication with neuronal cells (reviewed by Scholz and Woolf 2007). The involvement of the CX3CL1/CX3CR1 pair in pain modulation has been recently demonstrated in different examples of experimental neuropathic pain induced by peripheral nerve injury or inflammation... 

An intriguing area of research on opioids has been the accumulating evidence for plasticity in opioid controls. The degree of effectiveness of morphine analgesia is snbject to modulation by other transmitter systems in the spinal cord and by pathological changes induced by peripheral nerve injury. Thus in neuropathic states, pain after nerve injury, morphine analgesia can be reduced (but can still be effective) and tactics other than dose-escalation to circumvent this will be briefly discussed in Chapter 21. 

Peripheral nerve injuries are caused by a variety of factors including acute trauma, chronic repetitive insults, and inheritable or acquired metabolic disorders (Ch. 36). As opposed to the CNS, which has traditionally been thought to be fixed, axonal injury in the PNS often results in some degree of spontaneous regeneration, although it... 

A broad variety of diseases may cause neuropathic pain 935 Injured axons may develop spontaneous and repetitive firing known as ectopic activity 935 Sensory neurons transform their phenotype 936 Spinal disinhibition allows more nociceptive signal input 936 Peripheral nerve injury provokes a marked neuroimmune reaction 937... 

Spinal disinhibition allows more nociceptive signal input. Following peripheral nerve injury there is a reduction in the GABAergic component of postsynaptic inhibitory currents caused by a degeneration of GABAergic interneurons [24] (Fig. 57-6). This loss of inhibition (disinhibition) results in an overall increase in the excitability of dorsal horn neurons. The degeneration of inhibitory interneurons is due to an excitotoxic effect of primary afferent ectopic activity on dorsal horn neurons [26]. 

Moore, K. A. et al. Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord. /. Neurosci. 22 6724-6731, 2002. 

Over the years, antidepressant drugs have become an important treatment option in chronic pain states, in their own right and as adjuncts to opiate treatment. In fact, tricyclic antidepressants are the mainstay of treatment of neuropathic pain conditions such as polyneuropathy, diabetic neuropathy, postherpetic neuralgia and peripheral nerve injury (Sindrup, 1997 Sindrup and Jensen, 1999). Other chronic pain states responsive to antidepressants include osteo- and rheumatoid arthritis, fibromyalgia, and chronic tension headache. 

Chabal, C., Jacobson, L., Mariano, A., Chaney, E., Britell, C. W.. The use of oral mexilitine for the treatment of pain after peripheral nerve injury, Anesthesiology 1992, 76, 513-517. 

Wallace, M.S., Dyck, J.B., Rossi, S.S., Yaksh, T.L. Computer-controlled lidocaine infusion for evaluation of neuropathic pain after peripheral nerve injury, Pain 1996, 66, 69-77. 

Mao, J., Price, D. D., Mayer, D. J.,Hayes, R. L. Pain-related increases in spinal cord membrane-bound proteinkinase C following peripheral nerve injury, Brain Res. 1992, 588, 144-149. 

Leem, J. W., Choi, E. J., Park, E. S., Paik, K. S. N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptor antagonists differentially suppress dorsal horn neuron responses to mechanical stimuli in rats with peripheral nerve injury, Neurosci. Lett. 1996, 211, 37-40. 

There is also evidence that AMPA/kainate receptors may be involved in chronic pain following peripheral nerve injury AMPA receptor expression is upregulated and peaks 2 weeks after nerve ligation (Harris et al., 1996). Furthermore, GYKI52466 potently inhibits hyperalgesia in Freund adjuvant-induced chronic arthritis (Szekely et al., 1997). 

Maeda, T., Kiguchi, N., Kobayashi, Y., Ozaki, M., and Kishioka, S. (2008). Pioglitazone attenuates tactile allodynia and thermal hyperalgesia in mice subjected to peripheral nerve injury. J. Pharmacol. Sci. 108, 341-347. 

Myers, R. R., Yamamoto, T., Yaksh, T. L., and Powell, H. C. (1993). The role offocal nerve ischemia and Wallerian degeneration in peripheral nerve injury producing hyperesthesia. Anesthesiology 78, 308-316. 

Arruda, J. L., Sweitzer, S., Rutkowski, M. D., and DeLeo, J. A. (2000). Intrathecal anti-IL-6 antibody and IgG attenuates peripheral nerve injury-induced mechanical allodynia in the rat Possible immune modulation in neuropathic pain. Brain Res. 879, 216—225. 

Dominguez, E., Rivat, C., Pommier, B., Mauborgne, A., and Pohl, M. (2008). JAK/STAT3 pathway is activated in spinal cord microglia after peripheral nerve injury and contributes to neuropathic pain development in rat. J. Neurochem. 107, 50—60. 

Siegan, J. B., Hama, A. T., and Sagen, J. (1996). Alterations in rat spinal cord cGMP by peripheral nerve injury and adrenal medullary transplantation. Neurosci. Lett. 215, 49-52. 

Wagner, R., and Deleo, J. A. (1996). Pre-emptive dynorphine and A-methyl-D-asparatate glutamate receptor antagonism alters spinal immunocytochemistry but not allodynia following complete peripheral nerve injury. Neurocsience 72, 527—534. 

Ultenius, C., Linderoth, B., Meyerson, B. A., and Wallin, J. (2006). Spinal NMDA receptor phosphorylation correlates with the presence of neuropathic signs following peripheral nerve injury in the rat. Neurosci. Lett. 399, 85—90. 

Hains, B. C., Saab, C. Y., Klein, J. P., Craner, M. J., and Waxman, S. G. (2004). Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury. J. Neurosci. 24, 4832-4839. 

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