Pain Modulation

Modulation of pain (inhibition of nociceptive impulses) can occur by a number of processes. Based on the gate-control theory, pain modulation might occur at the level of the dorsal horn.19 Because the brain can process only a limited number of signals at one time, other sensory stimuli at nociceptors might alter pain perception. This theory supports the effectiveness of counterirritants and transcutaneous electrical nerve stimulation (TENS) in pain management. Pain modulation can occur through several other complex processes. The endogenous opiate system consists of endorphins (enkephalins, dynorphins, and ß-endorphins) that interact with p-, ô-, and K-receptors throughout the CNS to inhibit pain impulses and alter perception. The CNS also includes inhibitory descending pathways from the brain that can attenuate pain transmission in the dorsal horn. Neurotransmitters involved in this descending system include endogenous opioids, serotonin, norepinephrine, y-aminobutyric acid (GABA), and neurotensin. The perception of pain involves not only nociceptive stimulation but physiologic and emotional input that contributes to the perception of pain. Con sequently, cognitive behavioral treatments such as distraction, relaxation, and guided imagery can reduce pain perception by altering pain processing in the cortex.

Peripheral Sensitization, Central Sensitization, and Wind-Up

Under normal conditions, a balance generally exists between excitatory and inhibitory neurotransmission. Changes in this balance can occur both peripherally and centrally, resulting in exaggerated responses and sensitization such as that observed in inflammatory, neuropathic, or functional chronic pain. Pain in these settings might occur spontaneously without any stimulus or might be evoked by a stimulus. Evoked pain might arise from a stimulus that normally does not cause pain (allodynia) such as a light touch in neuropathic pain. Hyperalgesia, an exaggerated and/or prolonged pain response to a stimulus that normally causes pain, can also occur as a result of increased sensitivity in the CNS.

During normal pain transmission, the AMPA receptors are activated, but the N-methyl-D-aspartate (NMDA) receptor is blocked by magnesium.16 Repeated nerve depolarization causes release of the magnesium block, allowing the influx of calcium and sodium, and results in excessive excitability and amplification of signals. Continued input from C-fibers and subsequent increases in substance P and glutamate causes the activation of the NMDA receptor, a process referred to as wind-up. Wind-up increases the number and responsiveness of neuron in the dorsal horn irrespective of the input from the periphery. Recruitment of neurons not normally involved in pain transmission or spread occurs, leading to allodynia, hyperalgesia, and spread to un-20

injured tissues. The wind-up phenomenon supports the observation that untreated acute pain can lead to chronic pain and the belief that pain processes are plastic and not static.

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