Multimodal Interactions: Pain-Touch

While injecting local anesthetic into a patient's gum, the dentist may grab the patient's cheek and shake it with his or her other hand. This greatly reduces the pain of the injection. The sensory signals produced by shaking, which may be considered a rather vigorous form of touch, are somehow blocking the pain the patient would otherwise feel. Patrick Wall and Ronald Melzack explained this suppression by proposing that pain signals must pass through a neural “gate” in the spinal cord if they are to reach the brain, and that touch signals are sometimes able to close this gate. Later work has broadly confirmed this gate control theory, while refining our understanding of how gating works.

Pain gating is possible because of the distinctive anatomy of the sensory pathways for touch and pain. The details of these pathways and their functioning for the perception of pain and touch are discussed in this entry. Separate sensory nerve fibers, called mechanoreceptors and nociceptors, respond to tactile stimulation and to noxious stimulation, respectively. These two types of signals are therefore kept separate from one another as they travel, in neighboring axons, from peripheral tissues to the spinal cord. (Sensory fibers from the face go to the brain stem instead of the spinal cord, but the rules are otherwise the same.)

Once in the spinal cord, the two types of axons follow different paths. Mechanoreceptors split, with a long branch reaching all the way up to the brain, while a short branch terminates in the cord. Nociceptors, on the other hand, all terminate in the cord. Therefore, only by being synaptically transmitted to second-order neurons can pain signals reach the brain. As they cross these synapses, pain signals are especially vulnerable to being suppressed or otherwise modified.

Remarkably, the short branches of mechanoreceptors are able to influence pain intensity by interfering with the ability of nearby nociceptors to activate second-order neurons. Mechanoreceptors bring about this interference by activating special inhibitory neurons with short axons. This segmental inhibition (so named because it occurs when the tactile and noxious stimuli are close enough together for their signals to interact within individual or adjacent cord segments) is the primary physiological process underlying pain gating.

We make use of pain gating in everyday life, when we gently rub a bruise, press our forehead during a headache, or (because itch is closely related to pain) scratch an insect bite. But research has shown that vibration, as when the dentist shakes a patient's cheek, is the most effective form of touch for closing the gate. Vibration activates mechanoreceptors vigorously because they are stimulated anew by each cycle; their messages reach the central nervous system and strongly prod inhibitory neurons to block pain messages. Drugstore vibrators relieve an aching back or shoulder through a combination of pain gating and their effect on muscle tension.

Pain can also be suppressed in other ways. For example, a mild pain may be reduced or eliminated when the person has a more intense pain in another part of the body. This phenomenon is called diffuse noxious inhibitory controls, or DNIC. An example is that a person with arthritis in several joints may note that his or her pain seems to “travel around the body” from day to day, affecting primarily one joint at a time. Emotional state can also affect pain. In one recent case, a woman severely cut her hand. As she drove herself to the emergency room, bleeding profusely and fearing for the consequences, she felt no pain. Only when the doctor assured her that she would be fine did severe pain envelop her hand.

...