- Gate control theory of pain
The gate control theory of pain, put forward by
Ronald Melzack (a Canadian psychologist) andPatrick David Wall (a British physician) in 1962, [P.D. Wall, R. Melzack, "On nature of cutaneous sensory mechanisms," Brain, 85:331, 1962.] and again in 1965, [R. Melzack, P.D. Wall, "Pain mechanisms: A new theory," Science, 150:171-9, 1965.] is the idea that the perception of physicalpain is not a direct result of activation ofnociceptor s, but instead is modulated by interaction between differentneuron s, both pain-transmitting and non-pain-transmitting. The theory asserts that activation of nerves that do not transmit pain signals can interfere with signals from pain fibers and inhibit an individual's perception of pain.Physiology
Gate control theory asserts that activation of nerves which do not transmit pain signals, called nonnociceptive fibers, can interfere with signals from pain fibers, thereby inhibiting pain. Afferent pain-receptive nerves, those that bring signals to the brain, comprise at least two kinds of fibers - a fast, relatively thick,
myelin ated "Aδ" fiber that carries messages quickly with intense pain, and a small, unmyelinated, slow "C" fiber that carries the longer-term throbbing andchronic pain . Large-diameter Aβ fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibers.The
peripheral nervous system has centers at which pain stimuli can be regulated. Some areas in thedorsal horn of thespinal cord that are involved in receiving pain stimuli from Aδ and C fibers, called laminae, also receive input from Aβ fibers. The nonnociceptive fibers indirectly inhibit the effects of the pain fibers, 'closing a gate' to the transmission of their stimuli. In other parts of the laminae, pain fibers also inhibit the effects of nonnociceptive fibers, 'opening the gate'.An inhibitory connection may exist with Aβ and C fibers, which may form a
synapse on the sameprojection neuron . The same neurons may also form synapses with aninhibitory interneuron that also synapses on the projection neuron, reducing the chance that the latter will fire and transmit pain stimuli to thebrain (image at right). The inhibitory interneuron fires spontaneously.cite book | last=Kandel | first=Eric R. | authorlink=Eric R. Kandel | coauthors= James H. Schwartz, Thomas M. Jessell | title=Principles of Neural Science | publisher=McGraw-Hill | location=New York | year=2000 | edition=4th edition | isbn=0-8385-7701-6 |pages=482–486] The C fiber's synapse would inhibit the inhibitory interneuron, indirectly increasing the projection neuron's chance of firing. The Aβ fiber, on the other hand, forms an "excitatory" connection with the inhibitory interneuron, thus "decreasing" the projection neuron's chance of firing (like the C fiber, the Aβ fiber also has an excitatory connection on the projection neuron itself). Thus, depending on the relative rates of firing of C and Aβ fibers, the firing of the nonnociceptive fiber may inhibit the firing of the projection neuron and the transmission of pain stimuli.Gate control theory thus explains how stimulus that activates only nonnociceptive nerves can inhibit pain. The pain seems to be lessened when the area is rubbed because activation of nonnociceptive fibers inhibits the firing of nociceptive ones in the laminae. In
transcutaneous electrical stimulation (TENS), nonnociceptive fibers are selectively stimulated withelectrode s in order to produce this effect and thereby lessen pain.One area of the brain involved in reduction of pain sensation is the
periaqueductal gray matter that surrounds thethird ventricle and thecerebral aqueduct of theventricular system . Stimulation of this area producesanalgesia (but not total numbing) by activating descending pathways that directly and indirectly inhibit nociceptors in the laminae of the spinal cord. It also activatesopioid receptor-containing parts of the spinal cord.Afferent pathways interfere with each other constructively, so that the brain can control the degree of pain that is perceived, based on which pain stimuli are to be ignored to pursue potential gains. The brain determines which stimuli are profitable to ignore over time. Thus, the brain controls the perception of pain quite directly, and can be "trained" to turn off forms of pain that are not "useful". This understanding led Melzack to assert that "pain is in the brain".
Comparison to other theories
Prior theories of the
neurochemistry of pain had not taken the brain into account - pain was thought to be simply a direct response to a stimulus, a one-way "alarm system" like that proposed byRené Descartes . This did not, for instance, explain why a carpenter can hit his thumb and not feel much pain, while a novice is in agony, nor did it explainphantom limb pain , when the signal is in fact impossible to receive, since the wiring for it is gone.Consequences
The impact of this theory on medical treatment for pain has been profound, and has made it a multi-disciplinary field. Those being taught pain control techniques can actually be told why they work. This seems to play a major role in achieving results - which is explained most readily by
psychoneuroimmunology , in which the nerves are seen as the link between theimmune system and sensory and cognitive experience.Corroboration
This theory is corroborated by Reynold's comparative study on rats. By stimulating a certain area of the brain (the periaqueductal area in the midbrain), Reynolds could induce
analgesia to such an extent that the animal subjects of the experiment could undergo painless abdominal surgery while awake. This ties in with the Gate Control Theory, which posits that brain activity can affect the level of pain experienced.References
Further reading
cite book
last = Banyard
first = Philip
title = Psychology in Practice: Health
publisher =Hodder & Stoughton
date = 2002
isbn = 0-340-84496-5External links
* [http://www.library.ucla.edu/biomed/his/painexhibit/panel6.htm The Gate Control Model Opens a New Era in Pain Research]
* http://www.lib.mcg.edu/edu/eshuphysio/program/section8/8ch5/s8ch5_56.htm
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