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--- pain [2024/04/27 13:15] – created andrewtaustin
+++ pain [2024/12/26 16:50] (current) – [Melzack and Wall Gate Theory of Pain] andrewtaustin
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+{{tag>Related}}
 ====== Melzack and Wall Gate Theory of Pain ======
-The Melzack and Wall gate theory of pain, also known as the gate control theory, represents a seminal framework for understanding pain physiology. Proposed by Ronald Melzack and Patrick Wall in their 1965 paper published in "Science" journal, this theory revolutionised the scientific community's perception of pain by suggesting that pain perception involves complex interactions between different neural systems in the dorsal horns of the spinal cord.
+The Melzack and Wall gate theory of pain, also known as the gate control theory[(Gatecontroltheory>Gate control theory[[https://en.wikipedia.org/wiki/Gate_control_theory|Wikipedia]])], represents a seminal framework for understanding pain physiology. Proposed by Ronald Melzack[(Ronald_Melzack>Ronald Melzack[[https://en.wikipedia.org/wiki/Ronald_Melzack|Wikipedia]])] and Patrick Wall[(Patrick_D._Wall>Patrick D. Wall [[https://en.wikipedia.org/wiki/Patrick_D._Wall_(scientist)|Wikipedia]])] in their 1965 paper published in "Science" journal[( :harvard:Melzack1965>>
+authors   : Melzack R, Wall PD
+title     : Pain mechanisms a new theory
+publisher : Science
+published : November 1965
+url       : doi:10.1126/science.150.3699.971
+)][(PDF>Pain mechanisms: a new theory PDF [[http://www.hnehealth.nsw.gov.au/__data/assets/pdf_file/0012/70122/pain_mechanisms_20100315013844.pdf|archive.org]])], this theory revolutionized the scientific community's perception of pain by suggesting that pain perception involves complex interactions between different neural systems in the dorsal horns of the spinal cord.
 ==== Introduction ====
-The gate control theory was introduced to address inadequacies in the then-prevailing pain theories, which largely adhered to a linear model of pain transmission. According to this model, pain was thought to be directly proportional to the severity of the nociceptive stimulus. Melzack and Wall proposed a more nuanced mechanism wherein the spinal cord acts as a gate that blocks or allows pain signals to pass to the brain.
+The gate control theory was introduced to address inadequacies in the then-prevailing pain[(Pain>Pain[[https://en.wikipedia.org/wiki/Pain|Wikipedia]])] theories, which largely adhered to a linear model of pain transmission. According to this model, pain was thought to be directly proportional to the severity of the nociceptive stimulus. Melzack and Wall proposed a more nuanced mechanism wherein the spinal cord acts as a gate that blocks or allows pain signals to pass to the brain.
-<blockquote>**Ronald Melzack** was a Canadian psychologist born in 1929, renowned for his pioneering work in the study of pain. He earned his PhD from McGill University, where he later became a professor. Melzack's research significantly advanced the understanding of pain through the development of the McGill Pain Questionnaire and his co-creation of the gate control theory of pain with Patrick Wall. This theory revolutionised pain management and treatment practices. His contributions to the field earned him numerous awards and widespread recognition until his passing in 2019.
+<blockquote>**Ronald Melzack[(Ronald_Melzack>Ronald Melzack[[https://en.wikipedia.org/wiki/Ronald_Melzack|Wikipedia]])]** was a Canadian psychologist born in 1929, renowned for his pioneering work in the study of pain. He earned his PhD from McGill University, where he later became a professor. Melzack's research significantly advanced the understanding of pain through the development of the McGill Pain Questionnaire and his co-creation of the gate control theory of pain with Patrick Wall. This theory revolutionised pain management and treatment practices. His contributions to the field earned him numerous awards and widespread recognition until his passing in 2019.
-**Patrick David Wall** was a British neuroscientist and pain expert, born in 1925. He studied at the University of Cambridge and the University of Chicago. Wall is best known for co-developing the gate control theory of pain with Ronald Melzack, which provided a new framework for understanding pain as a dynamic interaction between physiological and psychological factors. His career was distinguished by his focus on the causes and treatment of chronic pain, and he held academic positions at several prestigious institutions including MIT and the University of London. Wall's work has had a lasting impact on both neuroscience and clinical approaches to pain management. He passed away in 2001.</blockquote>
+**Patrick David Wall[(Patrick_D._Wall>Patrick D. Wall [[https://en.wikipedia.org/wiki/Patrick_D._Wall_(scientist)|Wikipedia]])]** was a British neuroscientist and pain expert, born in 1925. He studied at the University of Cambridge and the University of Chicago. Wall is best known for co-developing the gate control theory of pain with Ronald Melzack, which provided a new framework for understanding pain as a dynamic interaction between physiological and psychological factors. His career was distinguished by his focus on the causes and treatment of chronic pain, and he held academic positions at several prestigious institutions including MIT and the University of London. Wall's work has had a lasting impact on both neuroscience and clinical approaches to pain management. He passed away in 2001.</blockquote>
 ==== Basic Mechanism ====
-At the heart of the gate control theory is the assertion that the dorsal horn of the spinal cord contains a neurological "gate" that modulates the pain signal before it is transmitted to the brain. This gate is influenced by the relative amount of activity in larger, faster nerve fibres (which carry non-painful sensory information) and smaller, slower nerve fibres (which carry pain signals).
+At the heart of the gate control theory is the assertion that the dorsal horn[(Posterior_grey_column>Posterior grey column [[https://en.wikipedia.org/wiki/Posterior_grey_column|Wikipedia]])] of the spinal cord contains a neurological "gate" that modulates the pain signal before it is transmitted to the brain. This gate is influenced by the relative amount of activity in larger, faster nerve fibres (which carry non-painful sensory information) and smaller, slower nerve fibres (which carry pain signals).
 ===== Interaction of Nerve Fibres =====
-  * **A-beta fibres**: Large, myelinated fibres transmit touch and vibration signals rapidly. They inhibit the transmission of pain signals by closing the gate.
+  * **A-beta fibres[(Group_A_nerve_fiber>Group A nerve fiber[[https://en.wikipedia.org/wiki/Group_A_nerve_fiber|Wikipedia]])]**: Large, myelinated fibres transmit touch and vibration signals rapidly. They inhibit the transmission of pain signals by closing the gate.
-  * **C fibres**: These small, unmyelinated fibres transmit slow, throbbing pain signals. Their activity opens the gate, allowing pain signals to ascend to the brain.
+  * **C fibres[(Group_C_nerve_fiber>Group C nerve fiber[[https://en.wikipedia.org/wiki/Group_C_nerve_fiber|Wikipedia]])]**: These small, unmyelinated fibres transmit slow, throbbing pain signals. Their activity opens the gate, allowing pain signals to ascend to the brain.
 ==== Modulation by Higher Brain Centres ====
 An innovative aspect of the gate control theory includes descending controls from the brain, which can amplify or dampen pain signals. These controls can be influenced by various factors, including psychological state—such as attention, anticipation, or emotional state—thus explaining why pain perception can vary in different situations.
+<blockquote>
+**Example Demonstrating the Gate Control Theory of Pain: The Soldier in Battle**
+Consider a clinical scenario involving a soldier who does not notice his injuries during an intense battle. This example highlights how the gate control theory of pain can explain variations in pain perception under different psychological states.
+**Background**
+During a heavy firefight, a soldier sustains injuries but continues to engage in combat without immediate awareness of his physical trauma. This phenomenon, often reported in military combat, underscores the complex nature of pain perception.
+**Situation Analysis**
+The soldier, despite having sustained injuries that would normally cause significant pain, reports no pain during the battle. This lack of pain perception can be attributed to the psychological and physiological responses under high-stress conditions.
+**Mechanism According to Gate Theory**
+According to the gate control theory, pain signals are modulated at the neurological gate in the spinal cord, where they can be inhibited or amplified. In the heat of battle, the soldier’s intense focus and high levels of stress hormones (like adrenaline) enhance the activity of descending pain inhibitory pathways from the brain. These pathways can effectively "close" the gate to pain signals, preventing them from ascending to the brain for perception.
+**Contributing Factors**
+**High Adrenaline Levels**: Adrenaline rush during intense situations increases heart rate and blood pressure and activates pain-suppressing mechanisms.
+**Fight or Flight Response**: The body’s acute stress response diverts attention from pain to more critical survival tasks.
+**Psychological Distraction**: The soldier's focused attention on battle and survival diverts his brain's processing away from pain sensations.
+**Outcome**
+Only after the battle, when the immediate danger has subsided and the psychological focus shifts, does the soldier begin to experience pain from the injuries. The decrease in adrenaline and the shift in mental focus open the gate for pain signals to reach the brain, leading to a delayed onset of pain perception.
+This example illustrates the profound effect of psychological state and physiological stress responses on pain perception through the lens of the gate control theory of pain. It highlights the dynamic and adaptable nature of the human pain processing system, which can temporarily suppress pain, providing a tactical advantage in survival situations.
+</blockquote>
 ==== Clinical Implications ====
 The theory has extensive implications for pain management and therapy. Understanding that pain signals can be modulated provides a basis for therapeutic approaches that aim to "close the gate," such as:
-  * **Transcutaneous Electrical Nerve Stimulation (TENS)**: This technique uses electrical stimulation to activate A-beta fibres, reducing pain perception.
+  * **Transcutaneous Electrical Nerve Stimulation (TENS)[(Transcutaneous_electrical_nerve_stimulation>Transcutaneous electrical nerve stimulation[[https://en.wikipedia.org/wiki/Transcutaneous_electrical_nerve_stimulation|Wikipedia]])]**: This technique uses electrical stimulation to activate A-beta fibres, reducing pain perception.
   * **Pharmacological interventions**: Certain medications can enhance inhibitory neurotransmitter levels at the gate, modulating pain transmission.
   * **Psychological interventions**: Techniques such as cognitive behavioural therapy (CBT) can modify the psychological factors influencing descending control pathways.
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 ==== References ====
-  * Melzack, R., & Wall, P.D. (1965). Pain Mechanisms: A New Theory. Science, 150(3699), 971-979.
+  * Melzack, R., & Wall, P.D. (1965). Pain Mechanisms: A New Theory. Science, 150(3699), 971-979.[( :harvard:Melzack1965>>
-  * Neuroscience Online: The Gate Control Theory of Pain [University of Texas Health Science Center at Houston (UTHealth)].
+authors   : Melzack R, Wall PD
+title     : Pain mechanisms a new theory
+publisher : Science
+published : November 1965
+url       : doi:10.1126/science.150.3699.971
+)][(PDF>Pain mechanisms: a new theory PDF [[http://www.hnehealth.nsw.gov.au/__data/assets/pdf_file/0012/70122/pain_mechanisms_20100315013844.pdf|archive.org]])]
+  * Neuroscience Online: The Gate Control Theory of Pain [University of Texas Health Science Center at Houston (UTHealth)][(Neuroscience_Online>Neuroscience Online [[https://nba.uth.tmc.edu/neuroscience/|UTHealth]])].
   * Pain Management and the Human Brain [Johns Hopkins Medicine].