8. Pain Modulation and Mechanisms
Part 3 of 3

Nachum Dafny, Ph.D.
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Stress-Induced Analgesia (SIA)

Analgesia may be produced in certain stressful situations. Exposure to a variety of painful or stressful events produces an analgesic reaction. This phenomenon is called stress induced analgesia (SIA). SIA has been thought to provide insight into the psychological and physiological factors that activate endogenous pain control and opiate systems. For example, soldiers wounded in battle or athletes injured in sports events sometimes report that they do not feel pain during the battle or game; however, they will experience the pain later after the battle or game has ended. It has been demonstrated (in animals) that electrical shocks cause stress-induced analgesia. Based on these experiments, it is assumed that the stress the soldiers and the athletes experienced suppressed the pain which they would later experience.

It has been suggested that endogenous opiates are released in response to stress and inhibit pain by activating the midbrain descending system. Moreover, some SIA exhibited cross tolerance with opiate analgesia, which indicates that this SIA is mediated via opiate receptors. Experiments using different parameters of electrical shock stimulation demonstrate that such stress produces analgesia and some of these stresses that produce analgesia could be blocked by the opioid antagonist naloxone, whereas others were not blocked by naloxone. These observations lead to the conclusion that both opiate and non-opiate forms of SIA exist.

The modulation of pain by electrical brain stimulation results from the activation of descending inhibitory fibers, which modulate (block) the input and output of laminae I, II, V and VII neurons. The route from the PAG to the spinal cord is not direct. It appears to involve a link with the 5-HT-rich raphe nuclei, as well as norepinephrine (NE) from the locus coeruleus (LC) and dopamine (DA) from the ventral tegmental area (VTA). Axons from the raphe nuclei, locus coeruleus and VTA project to the spinal cord dorsal horn by way of the DLF to terminate in lamina I, II and IV to VII (i.e., stimulation of NRM, VTA and LC inhibits the neuronal activity of lamina I, II and IV to VII neurons).

Opioid and serotonergic antagonists reverse both local opiate analgesia and brain-stimulation produced analgesia. This suggests that OA and SPA are produced via the same descending inhibitory system.

In conclusion, in the CNS, much of the information from the nociceptive afferent fibers results from excitatory discharges of multireceptive neurons. The pain information in the CNS is controlled by ascending and descending inhibitory systems, using endogenous opioids, or other endogenous substances like serotonin as inhibitory mediators. In addition, a powerful inhibition of pain-related information occurs in the spinal cord. These inhibitory systems can be activated by brain stimulation, intracerebral microinjection of morphine, and peripheral nerve stimulation. Centrally acting analgesic drugs activate these inhibitory control systems. However, pain is a complex perception that is influenced also by prior experience and by the context within which the noxious stimulus occurs. This sensation is also influenced by emotional state. Therefore, the response to pain varies from subject to subject.

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