PAIN MANAGEMENT: DIFFERENT MODALITIES 3. Neuropathic Pain
Neuropathic pain may be described as “pain arising as a direct consequence of disease affecting the soma- tosensory nervous system.”9 Following nerve injury, changes in the sensory transmission of pain occur. The expression of neurotransmitters, changed pres- ence of neuromodulators, altered receptors, changes in ion channels, and altered structural proteins have been described.9 Following nerve injury, physiological changes can
occur. An increase in sodium ion channels at the site of injury and along the axon results in foci of hypersen- sitivity. Also, the development of a1-noradrenergic receptors in both affected as well as unaffected neurons in the vicinity of damage occurs. This mechanism ena- bles the sympathetic nervous system (via noradrener- gic neurons) to have an excitatory and therefore amplifying effect on pain-transmitting neurons. Following injury, afferent pain neurons may also
affect descending analgesic pathways that inhibit pain. The inhibitory neurons themselves become inhibited, accentuating the sensation of pain. The den- sity of both gamma-aminobutyric acid and opioid receptors may be reduced following injury to an affer- ent pain neuron.10 Hypertrophy and activation of glial cells may occur following injury to neurons, and the resulting activation leads the dorsal horn microglia to produce proinflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factora).11 Demyelination of nerves lead to hyperexcitability.
Damaged Schwann cells, similar to dorsal horn glial cells, may release proinflammatory mediators includ- ing the interleukins and tumor necrosis
factora.These contribute to regional activation of sensory fibers.12 Neuropathic pain may be induced by degenerative
lumbosacral lesions, spinal cord injuries, interverte- bral disc herniation, discospondylitis, vertebral os- teomyelitis, and immune-mediated nervous system inflammation.9
4. Visceral Pain
no distinction between Ad and C fibers.13 Visceral pain is also coupled with tonic increases in somatic muscle tone. Strong autonomic responses are gener- ated including changes in heart rate and blood pressure.14 Within the spinal cord, the dorsal col- umns (gracile and cuneate fasciculi) are more im- portant than the spinothalamic tract in trans- mitting nociceptive signals fromviscera.15
Visceral pain is often poorly localized in contrast to so- matic pain (pain related to skin, tissue, or muscles). Visceral pain is associated with mechanical stimuli such as stretching of the mesentery or visceral capsu- les, ischemia (with resulting hypoxia and regional lac- tic acid formation), or chemical or thermal stimulus. In contrast to somatic pain, visceral pain displays
5. Summary
Pain is complex in generation, transduction, percep- tion, and response. Animals vary in actions when suf- fering pain, this being a factor of individual tolerance and whether the pain is acute and unexpected or chronic with some degree of accommodation for the repeated stimulus. Multiple levels and components of the neurological systemare involved in the physiology of pain, these being subject to the effects of other body systems and events. The reader is referred to excel- lent reviews byMuir andWoolf16 and Lemke.17
Acknowledgments
Declaration of Ethics Inwriting this review, the Authors have adhered to the Principles of VeterinaryMedical Ethics of the AVMA.
Conflict of Interest The Authors have no conflicts of interest.
References
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4. Basbaum AI, Bautista DM, Scherrer G, et al. Cellular and molecular mechanisms of pain. Cell 2009;139:267–284.
5. Schmidt R, Schmelz M, Forster C, et al. Novel classes of re- sponsive and unresponsive C nociceptors in human skin. J Neurosci 1995;15:333–341.
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8. Porreca F, Ossipov MH, Gebhart GF. Chronic pain and med- ullary descending facilitation. Trends Neurosci 2002;25:319– 325.
9. Mathews KA. Neuropathic pain in dogs and cats: If only they could tell us if they hurt. Vet Clin North Am Small Anim Pract 2008;38:1365–1414.
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MannionRJ.Neuropathic pain:Aetiology, symp- toms,mechanisms, and management. The Lancet 1999;353: 1959–1964.
11. Gilron I, Watson CP, Cahill CM, et al. Neuropathic pain: A practical guide for the clinician. Can Med Assoc J 2006; 175:265–275.
12. Watkins LR,Milligan ED,Maier SF. Glial activation: A driving force for pathological pain. TrendsNeurosci 2001;24:450–455.
13. Cervero F, Laird JM. Visceral pain. The Lancet 1999;353:2145– 2148.
14. Hobson AR, Aziz Q. Central nervous system processing of human visceral pain in health and disease. News Physiol Sci 2003;18:109–114.
15. Palecek J. The role of dorsal columns pathway in visceral pain. Physiological Research 2004;53:S125–S130.
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