Gate control theory (관문통제이론)
- The gate control theory of pain was developed in the early 1960s by Ronald Melzack and Patrick Wall to account for some of the ways in which pain differs from other sensations. In particular, they were interested in the mechanisms by which other cutaneous stimuli and emotional states alter the level of pain felt. One site of interaction suggested by the theory is among the interneurons of the substantia gelatinosa in the spinal cord. The brain is also assumed to exert descending control on this system, since cognitive factors are known to influence even spinal withdrawal reflexes. For example, a hot cup of tea is likely to be dropped, but if the cup is made of fine Wedgewood china, one is less apt to drop it, and may even manage jerkily to put it back on the table before shaking the hand.
Although the anatomical possibility exists for large- and small-fiber interactions in the dorsal born, there is relatively little physiological evidence for hte gate control theory. At spinal level, the gate control theory predicts that somatic stimulation will produce presynaptic ingibition on both the small- and large-diameter dorsal root fibers that synapse on spinothalamic neurons. As several studies have failed to provide support for the gate control theory, it is appropriate to ask why the theory should be mentioned. There are two reasons. First, even if the theory is incorrect in detail, some of its clinical predictions are useful - for example, the suggestion that stimulation of the large-diameter dorsal column fibers should close the gate and thus diminish pain. Direct or even transcutaneous electrical stimulation of sensory nerves, particularly the dorsal column - which by itself is felt as tingling - does provide pain relief for long periods. The second reason is that the gate control theory reversed the historical research emphasis on pain as solely an afferent sensory experience. Pain also disrupts ongoing behavior, demands immediate attention, and serves an a primary negative reinforcer in a variety of situations. It suppresses behavior upon which it is contingent and supports a broad repertoire of avoidance and escape responses. To emphasize only the sensory features of pain in the study of its neural bases and to ignore its unigue affective and motivational properties is to confront only part of the problem. Similarly, to treat pain simply by trying to cut down the sensory input by pharmacological or surgical blocks disregards several useful modalities of treatment and can only delay the understanding of how the brain itself is organized to inhibit the perception of pain.