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  • Acute pain can be produced from trauma sustained during surgery. This injury results in activation of the nociceptive system, including activation of primary afferent nerve fibers in the periphery, excitation of dorsal horn neurons in the spinal cord, and recruitment of key brain areas. It will further lead to the release of multiple inflammatory mediators, which then potentiate pain.
  • Persistent activation of the nociceptive system can lead to chronic pain. If nerves are damaged during surgery, this chronic pain can present in the form of neuropathy. In both instances, the chronic pain seems to be predominately centrally, as opposed to peripherally, mediated.
  • Analgesic interventions are generally effective for acute postoperative pain. However, for patients who develop chronic post-thoracotomy pain, pain relief is less easily achieved and may be best accomplished best by preemptive analgesia.

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Pain is a sensation that is normally associated with the application of noxious or injurious stimuli. In the context of thoracic surgery, pain can develop in multiple ways. Acute pain occurs as a direct result of physical trauma sustained during thoracic surgery. This trauma can include tissue damage from surgical incisions or manipulation, fractures to ribs, and hematomas.1 As will be discussed in this chapter, this acute pain may then develop into a chronic pain state in approximately half of all patients. Damage to nerves, most often the intercostal nerves, during surgery also contributes significantly to pain, as this damage manifests as a distinct form of chronic pain termed neuropathy. Thus, pain in thoracic surgery patients involves multiple components and mechanisms including those mediating acute somatic pain, hyperalgesia, and neuropathic pain. In the instance where these multiple components are all observed in a patient, the condition is referred to as chronic post-thoracotomy pain. To explain this condition in part or in its entirety, this chapter will review the basic physiology of pain, including pain pathways and neurochemistry, the neural mechanisms and neurochemical mediators of primary and secondary hyperalgesia, and the unique mechanisms of neuropathic pain.

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Peripheral Neural Mechanisms

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In general, pain begins in a distinct class of primary afferent fibers that respond selectively to noxious stimuli. These nociceptors are located in the periphery, with the cell bodies located in dorsal root ganglia (DRG) outside the spinal cord, and terminate in the dorsal horn. Nociceptors respond to a number of different stimulus modalities including thermal, chemical, and mechanical stimuli.2, 3 However, there are different classifications of nociceptors, generally based on the conduction velocity of the axons of these nociceptive neurons. The C fibers are generally unmyelinated fibers that conduct at velocities of less than 2 m/s and constitute over 75% of afferent fibers present in peripheral nerves. Several lines of evidence indicate that C-fiber nociceptors are essential for the normal perception of pain. For instance, intraneural electrical stimulation of identified C-fiber nociceptors in humans elicits the sensation of pain, and blockade of C-fiber transmission prevents thermal pain perception at the ...

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