When acute pain is inadequately treated, there is an increased risk of emergence of chronic pain. Several mechanisms are postulated to play a role in the development of chronic and enduring pain (see Table 2-4).
Ongoing abnormalities in peripheral tissues, with resultant inflammation, can result in activation of nociceptive pathways, rendering pain chronic. In such cases, treatment is best directed at the inflammatory mechanisms (e.g., aspirin or nonsteroidal anti-inflammatory agents). Peripheral nerves may become dysfunctional due to injury or disease (e.g., diabetes, infection, toxin exposure). Damaged neurons may fire spontaneously. Nociceptive fibers firing in this way are perceived in the CNS as signaling pain, yet in the peripheral tissues there may be no current injury. In such cases, antidepressants and anti-convulsants might be the most helpful treatment.
Trauma and injury can produce reflex motor activity in the vicinity of the injury, producing spasm. This process may initially serve a protective function in acute pain states, but in chronic pain states it can lead to aggravated muscle tension that exacerbates painful states (Zimmerman 1979).
The dorsal horn can become sensitized by a number of mechanisms that can potentiate chronic pain. Changes that occur within the dorsal horn may account for the maintenance of pain sensation that loses its relevance in its ability to signal danger. This sensitization appears to be related to changes mediated by CNS neurotransmitters, especially the excitatory neurotransmitter glutamate. With repeated stimulation (e.g., in poorly treated acute pain or in re-injury), glutamate activity can expand to include other receptors, including A-methyl-D-aspartate (NMDA) receptors. With expansion of glutamate activity, a series of intracellular processes occur that result in the heightened activation of dorsal horn cells, referred to as wind up. Such processes become difficult to interrupt from a therapeutic standpoint; however, NMDA receptor blockers (e.g., ketamine) can be helpful.
Ongoing NMDA activation can result in cell death. Death of neurons leaves areas of deafferentation in the spinal cord pathways. As a result, nearby sensory neurons often sprout collaterals into the deafferentated area to replace the synaptic connections lost after cell death. This replacement results in an innervation of pain pathways that correspond to the injured areas stimulated or activated by nearby undamaged areas.
The sympathetic nervous system can become a major contributor to ongoing pain (Zimmerman 1979). Trauma and injury trigger a sympathetic response that can effectively alter the neurochemical milieu of nociceptors in the periphery, along with causing changes in the microcirculation. This situation can alter the sensitivity of peripheral pain receptors, thereby augmenting pain sensitivity.
Pain can be maintained—despite lack of injury or even after effective healing—by the actions of the sympathetic nervous system. In such cases, protracted painful conditions can arise, such as reflex sympathetic dystrophy and complex regional pain disorder. Some of these disorders can be alleviated by blockade of sympathetic activity (i.e., sympatholysis); however, not all respond to sympatholytic techniques. Treatment for such disorders can include nerve blocks, sympathetic nerve blocks, and psychotropic medications (e.g., antidepressants and anticonvulsants).
Commensurate alterations in the thalamus and somatosensory cortex can occur after peripheral nerve injury. Thus, even after an amputation, the area of the somatosensory cortex corresponding to the amputated limb increases. Other cortical and limbic events can contribute to pain. The experience of pain can be shaped and influenced by the diffuse interconnections of the pain pathways with limbic and cortical pathways. In such cases, psychoactive medications, psychotherapy, and adjunctive therapeutic approaches such as relaxation training may be helpful modes of treatment.
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