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Traditionally, the opioid analgesics and the nonsteroidal anti-inflammatory drugs have been the mainstay for primary analgesia. Numerous other agents, however, are available in our vast pharmacopeia that are beneficial as primary or adjuvant analgesics, particularly for chronic nonmalignant pain that is neuropathic in origin. This vast array of drugs includes the antidepressants, the anticonvulsants, systemic local anesthetics, psychostimulants, neuroleptics, autonomic drugs, calcium channel blockers, skeletal muscle relaxants, N-methyl-d-aspartate (NMDA) receptor antagonists, corticosteroids, capsaicin, cannabinoids, and various other miscellaneous agents (e.g., tramadol, lithium, magnesium, neuronal nicotinic acetylcholine receptor ligands, butyl-p-amino benzoate, bupivacaine microspheres, and SNX-111).

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Classically, the nociceptive pathway consists of a three neuron chain, dual-ascending system, which can transmit pain signals from the periphery to the cerebral cortex. The cell bodies for the first-, second-, and third-order neurons reside in the dorsal root ganglion, dorsal horn, and thalamus, respectively. The dual-ascending system runs in parallel and consists of the Aδ and C fibers. The thinly myelinated Aδ fibers transmit “first pain,” which tends to be sharp, stinging, and discriminatory in nature. The unmyelinated C fibers transmit “second pain,” which is more diffuse, has a persistent burning quality, and carries an affective-motivational component to it. Injury to this neuronal pathway is believed to precipitate neuropathic pain. Examples of chronic neuropathic pain are listed in Table 62-1, and surgical procedures associated with neuropathic pain are shown in Table 62-2.

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Table 62-1 Examples of Chronic Neuropathic Pain
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Table Graphic Jump Location
Table 62-2 Surgical Procedures Associated with Neuropathic Pain
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The pathophysiologic mechanisms that theoretically underlie neuropathic pain are numerous and may involve ectopic impulses, neurogenic inflammation, changes in protein expression associated with gene-regulated c-fos, neuropeptide changes, ephaptic connections, sympathetic dysfunction, death of inhibitory spinal neurons, peripheral and central neuronal sprouting, central sensitization, and inflammation of nervi nevorum.1 On physical examination, patients with neuropathic pain classically display allodynia, hyperalgesia, and hyperpathia.

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Attenuation of nociceptive transmission can be accomplished at various points along this pain pathway, which includes transduction, transmission, modulation, and perception. The purpose of this chapter is to discuss the numerous drugs available to achieve this. The goal is to tailor the patient’s analgesic regimen by administering the appropriate drug, in the correct dose, and by the most appropriate route of administration so as to maximize analgesia and minimize side effects. Frequently, additive or even synergistic effects can be obtained by combining different types of drugs. ...

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