Gate Control V9 Download

First proposed in 1965 by Ronald Melzack and Patrick Wall, the theory offers a physiological explanation for the previously observed effect of psychology on pain perception. Combining early concepts derived from the specificity theory and the peripheral pattern theory, the gate control theory is considered to be one of the most influential theories of pain. This theory provided a neural basis which reconciled the specificity and pattern theories -- and ultimately revolutionized pain research.[1]

Although there are some important observations that the gate control theory cannot explain adequately[which?], this theory remains the theory of pain which most accurately accounts for the physical and psychological aspects of pain perception.[2]

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When you experience a negative feeling, such as pain from a bump or an itch from a bug bite, a common reaction is an attempt to eliminate the feeling by rubbing the painful bump or scratching the itchy bite. Gate control theory asserts that activation of nerves that do not transmit pain signals, called nonnociceptive fibers, can interfere with signals from pain fibers, thereby inhibiting pain.[citation needed] It is proposed that both small-diameter (pain-transmitting) and large-diameter (touch-, pressure-, and vibration- transmitting) afferent nerve fibers carry information from the site of the injury to two destinations in the dorsal horn: 1. Transmission Cells that carry the pain signal up to the brain, and 2. Inhibitory Interneurons that impede transmission cell activity. Activation of transmission cells occurs from both excitatory small-diameter and excitatory large-diameter fibers.[citation needed] However, activation of the inhibitory interneurons varies: large-diameter fibers excite the interneuron, which ultimately reduces transmission cell firing[citation needed], whereas small-diameter fibers inhibit the inhibitory interneuron which lessens the inhibitory input to the transmission cell. Therefore, less pain is felt (via reduced transmission cell activity) when more activity in large-diameter fibers (touch-, pressure-, and vibration- transmitting) occurs relative to the activity in small-diameter (pain-transmitting) fibers.[citation needed]

The peripheral nervous system has centers at which pain stimuli can be regulated. Some areas in the dorsal horn of the spinal cord that are involved in receiving pain stimuli from A and C fibers, called laminae, also receive input from A fibers.[4] The nonnociceptive fibers indirectly inhibit the effects of the pain fibers, 'closing a gate' to the transmission of their stimuli.[4] In other parts of the laminae, pain fibers also inhibit the effects of nonnociceptive fibers, 'opening the gate'.[4]This presynaptic inhibition of the dorsal nerve endings can occur through specific types of GABAA receptors (not through the 1 GABAA receptor and not through the activation of glycine receptors which are also absent from these types of terminals). Thus, certain GABAA receptor subtypes but not glycine receptors can presynaptically regulate nociception and pain transmission.[5]

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, myelinated "A" fiber that carries messages quickly with intense pain, and a small, unmyelinated, slow "C" fiber that carries the longer-term throbbing and chronic pain. Large-diameter A fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by A and C fibers.

Ronald Melzack and Patrick Wall introduced their "gate control" theory of pain in the 1965 Science article "Pain Mechanisms: A New Theory".[8] The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the spinal cord: transmission cells that carry the pain signal up to the brain, and inhibitory interneurons that impede transmission cell activity. Activity in both thin and large diameter fibers excites transmission cells. Thin fiber activity impedes the inhibitory cells (tending to allow the transmission cell to fire) and large diameter fiber activity excites the inhibitory cells (tending to inhibit transmission cell activity). So, the more large fiber (touch, pressure, vibration) activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. The authors had drawn a neural "circuit diagram" to explain why we rub a smack.[9] They pictured not only a signal traveling from the site of injury to the inhibitory and transmission cells and up the spinal cord to the brain, but also a signal traveling from the site of injury directly up the cord to the brain (bypassing the inhibitory and transmission cells) where, depending on the state of the brain, it may trigger a signal back down the spinal cord to modulate inhibitory cell activity (and so pain intensity). The theory offered a physiological explanation for the previously observed effect of psychology on pain perception.[10]

In 1968, three years after the introduction of the gate control theory, Ronald Melzack concluded that pain is a multidimensional complex with numerous sensory, affective, cognitive, and evaluative components. Melzack's description has been adapted by the International Association for the Study of Pain in a contemporary definition of pain.[1] Despite flaws in its presentation of neural architecture, the theory of gate control is currently the only theory that most accurately accounts for the physical and psychological aspects of pain.[2]

The gate control theory attempted to end a century-old debate about whether pain is represented by specific neural elements (specificity theory) or by patterned activity (pattern theory) within a convergent somatosensory subsystem.[11] Although it is now considered to be oversimplified with flaws in the presentation of neural architecture, the gate control theory spurred many studies in pain research and significantly advanced our understanding of pain.[1]

The mechanism of gate control theory can be used therapeutically. 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.[4] In transcutaneous electrical nerve stimulation (TENS), nonnociceptive fibers are selectively stimulated with electrodes in order to produce this effect and thereby lessen pain.[4]

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.[citation needed]

The pain gate mechanism is located in the dorsal horn of the spinal cord, specifically in the Substantia gelatinosa. The interneurons within the Substantia gelatinosa are what synapse to the primary afferent neurons, and are where the gate mechanism occurs. [1] Thus, the substantia gelatinosa modulates the sensory information that is coming in from the primary afferent neurons. [3]

If the interneurons in the substantia gelatinosa are stimulated by the non-noxious large diameter A- fibers, an inhibitory response is produced and there are no pain signals sent to the brain, and in this instance the 'pain gate' is closed. [1][3]

This relates to the biopsychosocial model, and can help increase or decrease the pain perceived. If someone has worrisome or anxious thoughts, negative emotions or memories, poor past experiences, or receives negative social feedback, pain signals will be sent down from the brain passing through an 'open gate', and the pain perceived will be greater. However, positive thoughts, emotions, and memories about the painful experience, relaxation, or positive social feedback, will cause the gate to close, and the person will essentially experience less pain. [1]

The usage of TENS activates the pain gate mechanism to inhibit pain signals going up to the brain, and thus reduces the sensation of pain. Similar to as described above, the TENS activates non-noxious afferent fibers, which in turn activates the 'pain-inhibiting' interneurons in the spinal cord, and thus minimizes/reduces perceived pain as an output. This is because TENS can activate A- fibers, which helps facilitate the gate control mechanism. [2] The activation of the A- fibers will inhibit the input from the noxious A- and C fibers. [4]

Massage therapy also makes use of the gate control theory to reduce and inhibit pain, with the same reasoning of activating large diameter A- nerve fibers. This can be beneficial to many types of patients, and help with improving high blood pressure, sleep, relaxation, depression, stiffness, emotional well-being, recovery time, and many other conditions. Cardiac patients may benefit from massage to various painful body parts, which would help them minimize or eliminate the use of pharmaceuticals, and from experiencing possible side effects. [7]

Light mechanical stimulation of hairy skin can induce a form of itch known as mechanical itch. This itch sensation is normally suppressed by inputs from mechanoreceptors; however, in many forms of chronic itch, including alloknesis, this gating mechanism is lost. Here we demonstrate that a population of spinal inhibitory interneurons that are defined by the expression of neuropeptide Y::Cre (NPY::Cre) act to gate mechanical itch. Mice in which dorsal NPY::Cre-derived neurons are selectively ablated or silenced develop mechanical itch without an increase in sensitivity to chemical itch or pain. This chronic itch state is histamine-independent and is transmitted independently of neurons that express the gastrin-releasing peptide receptor. Thus, our studies reveal a dedicated spinal cord inhibitory pathway that gates the transmission of mechanical itch. 006ab0faaa