Gate control theory

Last updated August 28, 2024

The gate control theory of pain asserts that non-painful input closes the nerve "gates" to painful input, which prevents pain sensation from traveling to the central nervous system.

The gate control theory of pain describes how non-painful sensations can override and reduce painful sensations. A painful, nociceptive stimulus stimulates primary afferent fibers and travels to the brain via transmission cells. Increasing activity of the transmission cells results in increased perceived pain. Conversely, decreasing activity of transmission cells reduces perceived pain. In the gate control theory, a closed "gate" describes when input to transmission cells is blocked, therefore reducing the sensation of pain. An open “gate” describes when input to transmission cells is permitted, therefore allowing the sensation of pain.

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]

Willem Noordenbos (1910–1990), a Dutch researcher at the University of Amsterdam, proposed in 1959 a model which featured interaction between small (unmyelinated) and thick (myelinated) fibers. In this model, the fast (myelinated) fibers block the slow (unmyelinated) fibers: "fast blocks slow".^[3]

Proposed mechanisms

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 Aδ and C fibers, called laminae, also receive input from Aβ 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 GABA_A receptors (not through the α1 GABA_A receptor and not through the activation of glycine receptors which are also absent from these types of terminals). Thus, certain GABA_A receptor subtypes but not glycine receptors can presynaptically regulate nociception and pain transmission.^[5]

An inhibitory connection may exist with Aβ and C fibers, which may form a synapse on the same projection neuron. The same neurons may also form synapses with an inhibitory interneuron that also synapses on the projection neuron, reducing the chance that the latter will fire and transmit pain stimuli to the brain (image on the right). The inhibitory interneuron fires spontaneously.^[4] 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.^[4]

History and legacy

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 "Aδ" 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 Aβ fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibers.

When it was first proposed in 1965, the theory was met with considerable skepticism.^[6] Despite having to undergo several modifications, its basic conception remains unchanged.^[7]

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]

Therapeutic uses

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 mild electrical currents through electrodes in order to produce this effect and thereby lessen pain.^[4]

One area of the brain involved in reduction of pain sensation is the periaqueductal gray matter that surrounds the third ventricle and the cerebral aqueduct of the ventricular system. Stimulation of this area produces analgesia (but not total numbing) by activating descending pathways that directly and indirectly inhibit nociceptors in the laminae of the spinal cord.^[4] Descending pathways also activate opioid receptor-containing parts of the spinal cord.^{[ citation needed ]}

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 ]}

Gate control theory influenced the development of mindfulness-based pain management (MBPM).^[12]

Related Research Articles

A neuron, neurone, or nerve cell is an excitable cell that fires electric signals called action potentials across a neural network in the nervous system. Neurons communicate with other cells via synapses, which are specialized connections that commonly use minute amounts of chemical neurotransmitters to pass the electric signal from the presynaptic neuron to the target cell through the synaptic gap.

In biology, the nervous system is the highly complex part of an animal that coordinates its actions and sensory information by transmitting signals to and from different parts of its body. The nervous system detects environmental changes that impact the body, then works in tandem with the endocrine system to respond to such events. Nervous tissue first arose in wormlike organisms about 550 to 600 million years ago. In vertebrates, it consists of two main parts, the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS consists of the brain and spinal cord. The PNS consists mainly of nerves, which are enclosed bundles of the long fibers, or axons, that connect the CNS to every other part of the body. Nerves that transmit signals from the brain are called motor nerves (efferent), while those nerves that transmit information from the body to the CNS are called sensory nerves (afferent). The PNS is divided into two separate subsystems, the somatic and autonomic, nervous systems. The autonomic nervous system is further subdivided into the sympathetic, parasympathetic and enteric nervous systems. The sympathetic nervous system is activated in cases of emergencies to mobilize energy, while the parasympathetic nervous system is activated when organisms are in a relaxed state. The enteric nervous system functions to control the gastrointestinal system. Nerves that exit from the brain are called cranial nerves while those exiting from the spinal cord are called spinal nerves.

The somatic nervous system (SNS) is made up of nerves that link the brain and spinal cord to voluntary or skeletal muscles that are under conscious control as well as to skin sensory receptors. Specialized nerve fiber ends called sensory receptors are responsible for detecting information within and outside of the body.

Muscle spindles are stretch receptors within the body of a skeletal muscle that primarily detect changes in the length of the muscle. They convey length information to the central nervous system via afferent nerve fibers. This information can be processed by the brain as proprioception. The responses of muscle spindles to changes in length also play an important role in regulating the contraction of muscles, for example, by activating motor neurons via the stretch reflex to resist muscle stretch.

The grey columns are three regions of the somewhat ridge-shaped mass of grey matter in the spinal cord. These regions present as three columns: the anterior grey column, the posterior grey column, and the lateral grey column, all of which are visible in cross-section of the spinal cord.

A reflex arc is a neural pathway that controls a reflex. In vertebrates, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This allows for faster reflex actions to occur by activating spinal motor neurons without the delay of routing signals through the brain. The brain will receive the input while the reflex is being carried out and the analysis of the signal takes place after the reflex action.

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending "possible threat" signals to the spinal cord and the brain. The brain creates the sensation of pain to direct attention to the body part, so the threat can be mitigated; this process is called nociception.

<span class="mw-page-title-main">Periaqueductal gray</span> Nucleus surrounding the cerebral aqueduct

The periaqueductal gray (PAG), also known as the central gray, is a brain region that plays a critical role in autonomic function, motivated behavior and behavioural responses to threatening stimuli. PAG is also the primary control center for descending pain modulation. It has enkephalin-producing cells that suppress pain.

A neural circuit is a population of neurons interconnected by synapses to carry out a specific function when activated. Multiple neural circuits interconnect with one another to form large scale brain networks.

In neuroscience, Golgi cells are the most abundant inhibitory interneurons found within the granular layer of the cerebellum. Golgi cells can be found in the granular layer at various layers. The Golgi cell is essential for controlling the activity of the granular layer. They were first identified as inhibitory in 1964. It was also the first example of an inhibitory feedback network in which the inhibitory interneuron was identified anatomically. Golgi cells produce a wide lateral inhibition that reaches beyond the afferent synaptic field and inhibit granule cells via feedforward and feedback inhibitory loops. These cells synapse onto the dendrite of granule cells and unipolar brush cells. They receive excitatory input from mossy fibres, also synapsing on granule cells, and parallel fibers, which are long granule cell axons. Thereby this circuitry allows for feed-forward and feed-back inhibition of granule cells.

Allodynia is a condition in which pain is caused by a stimulus that does not normally elicit pain. For example, sunburn can cause temporary allodynia, so that usually painless stimuli, such as wearing clothing or running cold or warm water over it, can be very painful. It is different from hyperalgesia, an exaggerated response from a normally painful stimulus. The term comes from Ancient Greek άλλος (állos) 'other' and οδύνη (odúnē) 'pain'.

<span class="mw-page-title-main">Nucleus raphe magnus</span> Cluster of nuclei in the brain stem

The nucleus raphe magnus (NRM) is one of the seven raphe nuclei. It is situated in the pons in the brainstem, just rostral to the nucleus raphe obscurus.

The apex of the posterior grey column, one of the three grey columns of the spinal cord, is capped by a V-shaped or crescentic mass of translucent, gelatinous neuroglia, termed the substantia gelatinosa of Rolando, which contains both neuroglia cells, and small neurons. The gelatinous appearance is due to an abundance of neuropil with a very low concentration of myelinated fibers. It extends the entire length of the spinal cord and into the medulla oblongata where it becomes the spinal trigeminal nucleus.

The spinoreticular tract is a partially decussating (crossed-over) four-neuron sensory pathway of the central nervous system. The tract transmits slow nociceptive/pain information from the spinal cord to reticular formation which in turn relays the information to the thalamus via reticulothalamic fibers as well as to other parts of the brain. Most (85%) second-order axons arising from sensory C first-order fibers ascend in the spinoreticular tract - it is consequently responsible for transmiting "slow", dull, poorly-localised pain. By projecting to the reticular activating system (RAS), the tract also mediates arousal/alertness in response to noxious (harmful) stimuli. The tract is phylogenetically older than the spinothalamic ("neospinothalamic") tract.

Group C nerve fibers are one of three classes of nerve fiber in the central nervous system (CNS) and peripheral nervous system (PNS). The C group fibers are unmyelinated and have a small diameter and low conduction velocity, whereas Groups A and B are myelinated. Group C fibers include postganglionic fibers in the autonomic nervous system (ANS), and nerve fibers at the dorsal roots. These fibers carry sensory information.

The Golgi tendon reflex (also called inverse stretch reflex, autogenic inhibition, tendon reflex) is an inhibitory effect on the muscle resulting from the muscle tension stimulating Golgi tendon organs (GTO) of the muscle, and hence it is self-induced. The reflex arc is a negative feedback mechanism preventing too much tension on the muscle and tendon. When the tension is extreme, the inhibition can be so great it overcomes the excitatory effects on the muscle's alpha motoneurons causing the muscle to suddenly relax. This reflex is also called the inverse myotatic reflex, because it is the inverse of the stretch reflex.

As long as humans have experienced pain, they have given explanations for its existence and sought soothing agents to dull or cease painful sensations. Archaeologists have uncovered clay tablets dating back as far as 5,000 BC which reference the cultivation and use of the opium poppy to bring joy and cease pain. The Greek writer Homer's The Odyssey, written in 800 BC, features the character of Telemachus using opium to soothe his pain and forget his worries. While some cultures researched analgesics and allowed or encouraged their use, others perceived pain to be a necessary, integral sensation. Physicians of the 19th century used pain as a diagnostic tool, theorizing that a greater amount of personally perceived pain was correlated to a greater internal vitality, and as a treatment in and of itself, inflicting pain on their patients to rid the patient of evil and unbalanced humors.

A spinal interneuron, found in the spinal cord, relays signals between (afferent) sensory neurons, and (efferent) motor neurons. Different classes of spinal interneurons are involved in the process of sensory-motor integration. Most interneurons are found in the grey column, a region of grey matter in the spinal cord.

Tactile induced analgesia is the phenomenon where concurrent touch and pain on the skin reduces the intensity of pain that is felt.

Presynaptic inhibition is a phenomenon in which an inhibitory neuron provides synaptic input to the axon of another neuron to make it less likely to fire an action potential. Presynaptic inhibition occurs when an inhibitory neurotransmitter, like GABA, acts on GABA receptors on the axon terminal. Or when endocannabinoids act as retrograde messengers by binding to presynaptic CB1 receptors, thereby indirectly modulating GABA and the excitability of dopamine neurons by reducing it and other presynaptic released neurotransmitters. Presynaptic inhibition is ubiquitous among sensory neurons.

References

1 2 3 Moayedi, M.; Davis, K. D. (3 October 2012). "Theories of pain: from specificity to gate control". Journal of Neurophysiology . 109 (1): 5–12. doi:10.1152/jn.00457.2012. PMID 23034364. S2CID 11260950.
1 2 Meldrum, Marcia L. "Physiology of pain". Encyclopædia Britannica . Retrieved 27 April 2014. The theory of pain that most accurately accounts for the physical and psychological aspects of pain is the gate-control theory
↑ Mander, Rosemary (2010). Pain in Childbearing and its Control: Key Issues for Midwives and Women. John Wiley & Sons. ISBN 9781444392067.
1 2 3 4 5 6 7 8 9 10 Kandel, Eric R.; James H. Schwartz; Thomas M. Jessell (2000). Principles of Neural Science (4th ed.). New York: McGraw-Hill. pp. 482–486. ISBN 0-8385-7701-6.
↑ Lorenzo LE, Godin AG, Wang F, St-Louis M, Carbonetto S, Wiseman PW, Ribeiro-da-Silva A, De Koninck Y (June 2014). "Gephyrin Clusters Are Absent from Small Diameter Primary Afferent Terminals Despite the Presence of GABA_A Receptors". J. Neurosci. 34 (24): 8300–17. doi: 10.1523/JNEUROSCI.0159-14.2014 . PMC 6608243 . PMID 24920633.
↑ "Patrick Wall, 76, British Authority on Pain". The New York Times . 21 August 2001. Retrieved 27 April 2014.
↑ Craig, James C.; Rollman, Gary B. (February 1999). "SOMESTHESIS". Annual Review of Psychology. 50 (1): 305–331. doi:10.1146/annurev.psych.50.1.305. PMID 10074681.
↑ Melzack R, Wall PD (November 1965). "Pain mechanisms: a new theory" (PDF). Science. 150 (3699): 971–9. Bibcode:1965Sci...150..971M. doi:10.1126/science.150.3699.971. PMID 5320816. Archived from the original (PDF) on 2012-01-14.{{cite journal}}: CS1 maint: date and year (link)
↑ Melzack R, Katz J (2004). "The Gate Control Theory: Reaching for the Brain". In Craig KD, Hadjistavropoulos T (ed.). Pain: psychological perspectives. Mahwah, N.J: Lawrence Erlbaum Associates, Publishers. ISBN 0-8058-4299-3.
↑ Skevington, Suzanne (1995). Psychology of pain. New York: Wiley. p. 11. ISBN 0-471-95771-2.
↑ Craig, A.D. (Bud) (March 2003). "Pain Mechanisms: Labeled Lines Versus Convergence in Central Processing". Annual Review of Neuroscience . 26 (1): 1–30. doi:10.1146/annurev.neuro.26.041002.131022. PMID 12651967.
↑ Burch, Vidyamala (2016). "Meditation and the management of pain". The Psychology of Meditation. Oxford University Press. pp. 153–176. doi:10.1093/med:psych/9780199688906.003.0007. ISBN 978-0-19-968890-6.

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[theories-1] 1 2 3 Moayedi, M.; Davis, K. D. (3 October 2012). "Theories of pain: from specificity to gate control". Journal of Neurophysiology . 109 (1): 5–12. doi:10.1152/jn.00457.2012. PMID 23034364. S2CID 11260950.

[Meldrum-2] 1 2 Meldrum, Marcia L. "Physiology of pain". Encyclopædia Britannica . Retrieved 27 April 2014. The theory of pain that most accurately accounts for the physical and psychological aspects of pain is the gate-control theory

[3] Mander, Rosemary (2010). Pain in Childbearing and its Control: Key Issues for Midwives and Women. John Wiley & Sons. ISBN 9781444392067.

[KandelPrin-4] 1 2 3 4 5 6 7 8 9 10 Kandel, Eric R.; James H. Schwartz; Thomas M. Jessell (2000). Principles of Neural Science (4th ed.). New York: McGraw-Hill. pp. 482–486. ISBN 0-8385-7701-6.

[pmid24920633-5] Lorenzo LE, Godin AG, Wang F, St-Louis M, Carbonetto S, Wiseman PW, Ribeiro-da-Silva A, De Koninck Y (June 2014). "Gephyrin Clusters Are Absent from Small Diameter Primary Afferent Terminals Despite the Presence of GABA_A Receptors". J. Neurosci. 34 (24): 8300–17. doi: 10.1523/JNEUROSCI.0159-14.2014 . PMC 6608243 . PMID 24920633.

[6] "Patrick Wall, 76, British Authority on Pain". The New York Times . 21 August 2001. Retrieved 27 April 2014.

[7] Craig, James C.; Rollman, Gary B. (February 1999). "SOMESTHESIS". Annual Review of Psychology. 50 (1): 305–331. doi:10.1146/annurev.psych.50.1.305. PMID 10074681.

[pmid5320816-8] Melzack R, Wall PD (November 1965). "Pain mechanisms: a new theory" (PDF). Science. 150 (3699): 971–9. Bibcode:1965Sci...150..971M. doi:10.1126/science.150.3699.971. PMID 5320816. Archived from the original (PDF) on 2012-01-14.{{cite journal}}: CS1 maint: date and year (link)

[MelzackKatz-9] Melzack R, Katz J (2004). "The Gate Control Theory: Reaching for the Brain". In Craig KD, Hadjistavropoulos T (ed.). Pain: psychological perspectives. Mahwah, N.J: Lawrence Erlbaum Associates, Publishers. ISBN 0-8058-4299-3.

[Skevington11-10] Skevington, Suzanne (1995). Psychology of pain. New York: Wiley. p. 11. ISBN 0-471-95771-2.

[11] Craig, A.D. (Bud) (March 2003). "Pain Mechanisms: Labeled Lines Versus Convergence in Central Processing". Annual Review of Neuroscience . 26 (1): 1–30. doi:10.1146/annurev.neuro.26.041002.131022. PMID 12651967.

[Burch_2016-12] Burch, Vidyamala (2016). "Meditation and the management of pain". The Psychology of Meditation. Oxford University Press. pp. 153–176. doi:10.1093/med:psych/9780199688906.003.0007. ISBN 978-0-19-968890-6.

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