Clinical Note

Regulation of Pain

It should be recognized that the perception of pain is not synonymous with activation of nociceptors. Pain is the feeling that normally accompanies irritating, aching, or burning sensations transmitted by nociceptive pathways; however, other factors such as stress, fright, or other strong emotional states may trigger the perception of pain in the absence of nociceptive activity. Similarly, nociception does not always lead to the perception of pain. Signals from nociceptors may be modified by two major mechanisms that can shunt or "gate" pain information so that it fails to reach conscious centers of the brain. The first component of the pain-gating mechanism is localized in the spinal cord and consists of inhibitory interneurons that link large-diameter mechanoreceptor axons with small-diameter nociceptive axons as they enter the dorsal horn of the cord. When the mechanoreceptor pathway is active, it causes the interneurons to inhibit nearby nociceptive axons, thus suppressing painful information before it projects up the spinal cord. This pathway presumably accounts for the fact that it feels less painful if you rub your toe after you stub it. It also forms the basis of electrical treatment for some kinds of chronic, intractable pain. Wires taped to the patient's skin can be used to electrically stimulate large-diameter sensory axons and thus suppress transmission of nocicep-tive information.

The second component of the pain-gating mechanism originates in an area of the brain stem called the periaqueductal gray matter (PAG), so named because it encircles the cerebral aqueduct. The PAG receives information from several brain regions regarding emotional status and then sends that information through descending projections to the dorsal horn of the spinal cord, where they effectively depress the activity of nociceptive neurons. Through this pathway, strong emotion, stress, or even stoic resolve can blunt the perception of pain. One type of neurotransmitter substance used within this pathway has been identified as an endogenous morphine-like substance called endorphin. Endorphin is manufactured in cells of the PAG, is released in the dorsal horn, and interacts with inhibitory endorphin receptors on nociceptive neurons. A number of drugs—notably, opium and similar compounds such as morphine, codeine, and heroin—are all capable of binding directly to the endorphin receptor, also called the opioid receptor. In this way, they produce profound analgesia when taken systemically. Through interactions with opioid receptors elsewhere in the brain, these potentially addictive drugs also cause mood changes, drowsiness, mental clouding, nausea, vomiting, and constipation.

process, termed primary hyperalgesia, occurs at the site of injury and is a result of a change within the receptor neuron itself, usually manifested as a decrease in the threshold response. In some cases, there is also a change from unimodal to bimodal responses, with more nerves becoming responsive to both mechanical and thermal stimuli. Similar changes may also occur in CNS neurons located within stimulated sensory pathways in brain and spinal cord. These higher order neurons can also exhibit decreased thresholds and in addition may show an increase in receptive field size. This condition is called secondary hyperalgesia (Fig. 4). Both primary and secondary hyperalgesia are linked to a greater than normal release of neuroactive substances that sensitizes nearby sensory receptors or central neurons. Bradykinin, histamine, serotonin, leukotrienes, prostaglandins, substance P, and cytokines have been implicated in primary hyperalgesia. Substance P, calcitonin-gene-related pep-tide (CGRP), and excitatory amino acids such as glutamate released from activated neurons in the brain and spinal cord may be involved in secondary hyperalgesia.

SENSORY RECEPTORS IN MUSCLES, JOINTS, AND VISCERAL ORGANS

Proprioceptors (from the Latinproprius, "one's own'') are so named because they provide information about body position and movement in space. Signals generated from proprioceptors generally do not reach cortical levels and thus do not contribute significantly to conscious perception. However, proprioceptive information is critically important in coordinating voluntary and reflex movement of skeletal muscle. Two major classes of muscle proprioceptors are involved in this process: (1) muscle spindles, which monitor length and rate of stretch of the innervated muscle; and (2) Golgi tendon organs, which gauge muscle force by monitoring muscle tension. Additional proprioceptive information is provided by a variety of mechanoreceptors in the connective tissue of joints. Some are rapidly adapting and provide information about limb movement; others are slowly adapting and continuously monitor body posture. These various sources of information work in an integrated manner so that loss of one input is compensated for by those remaining. For this reason, patients who have hip replacements and thus are devoid of proprioceptors in the affected joint still receive sufficient proprioceptive information from other sources to walk in a coordinated fashion.

Sensations from smooth muscle and from internal organs are much less discrete than those from somatic structures, such as skin and skeletal muscle. Visceral mechanoreceptors, thermoreceptors, and chemoreceptors are broadly distributed throughout the body and provide sensory information that activates local involuntary

1. local burn and reddening

2. weal (swelling)

3. action potentials in sensory fibers and all its branches releases substance P

3. action potentials in sensory fibers and all its branches releases substance P

4. flare: reddening and hyperalgesia (intense pain)

6. pain information passed to higher centers.

FIGURE 4 Hyperalgesia: increased sensitivity to a superficial burn on the forearm is shown here. (1) Injury of local tissue causes release of bradykinin and other pain-producing chemicals that also cause vasodilation and reddening. (2) Dilated capillaries leak fluid (edema), which produces a weal (swelling.) (3) Action potentials spread to all branches of the injured neuron and release neurotransmitters into the skin and spinal cord. (4) Substance P releases histamine from mast cells, causing additional vasodilation (reddening) and primary hyperalgesia (lower threshold). (5) Secondary hyperalgesia in the surrounding area is caused by sensitization of neurons in the CNS. (6) Pain information is transmitted through the spinal cord and passed to higher centers.

4. flare: reddening and hyperalgesia (intense pain)

5. secondary hyperalgesia due to neurotransmitters in the spinal cord and brain

6. pain information passed to higher centers.

FIGURE 4 Hyperalgesia: increased sensitivity to a superficial burn on the forearm is shown here. (1) Injury of local tissue causes release of bradykinin and other pain-producing chemicals that also cause vasodilation and reddening. (2) Dilated capillaries leak fluid (edema), which produces a weal (swelling.) (3) Action potentials spread to all branches of the injured neuron and release neurotransmitters into the skin and spinal cord. (4) Substance P releases histamine from mast cells, causing additional vasodilation (reddening) and primary hyperalgesia (lower threshold). (5) Secondary hyperalgesia in the surrounding area is caused by sensitization of neurons in the CNS. (6) Pain information is transmitted through the spinal cord and passed to higher centers.

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