Pain Descending Pathways: Difference between revisions

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== Introduction ==
== Introduction ==
'''The Descending Pain Modulatory System:''' The ''"top down"'' modulation of pain has been in evidence since the early work of Sherrington<ref name="Sherrington">Sherrington CS. The Integrative Action of the Nervous System. New Haven, CT: Yale Univ. Press,1906.</ref>&nbsp;showing that [[Nociception|nociceptive]] reflexes were enhanced after transection of the [[Spinal cord anatomy|spinal cord]]. This was further elaborated on by Fields<ref name="Fields">Fields HL. Pain modulation: expectation, opoid analgesia and virtual pain. Prog Brain Res 2000; 122:245-253;</ref>&nbsp;and Milan<ref name="Milan">Milan MJ. Descending control of pain. Prog Neurobiology 2002; 66:355-474;</ref>&nbsp;who, based upon observations in the 1960's that electrical stimuation of the periaqueductal gray (PAG) area can produce analgesia, demostrated through electrophysiological and pharmacological studies that descending influences on spinal nociceptive processing involves the PAG and the rostral ventromedial medulla (RVM).
Once a pain signal from the ascending pathway reaches the somatosensory cortex, it triggers the descending pain modulatory system. The goal of this pathway is to allow the organism to function enough to respond to the pain source by reducing the pain signal through neuronal inhibition ie the ''"top down"'' modulation of pain. It begins in the periaqueductal gray (PAG), an area of grey matter in the midbrain that is involved in a descending pain control pathway. The periaqueductal gray, or PAG, receives pain information via the spinomescencephalic tract and processes the nociceptive information and relays it to the rostral ventral medulla (RVM). These neurons in the RVM then send a signal down the spinal cord and activate the endogenous opiate system to suppress pain.<ref>Neuroscientifically Challenged PAG Available:https://neuroscientificallychallenged.com/glossary/periaqueductal-gray (accessed 18.4.2022)</ref><ref name=":0">Tufts Available: Opioid peptides<nowiki/>https://sites.tufts.edu/opioidpeptides/pathways-and-receptors/classical-opioid-signaling/ (accessed 18.4.2022)</ref>[[Image:Descending-inhibitory-pathway.jpg|border|center|558x558px|alt=]]Our body produces natural (endogenous) opioids, which comprise endorphins, dynorphins, and enkephalins. On a molecular level, both these and synthetic opioids inhibit pain signals by interfering with intracellular signaling and preventing ascending pain-causing neurons from sending action potentials. <ref name=":0" /> Opioids have actions at two sites, the presynaptic nerve terminal and the postsynaptic neuron. The postsynaptic actions of opioids are usually inhibitory. The presynaptic action of opioids is to inhibit neurotransmitter release, and this is considered to be their major effect in the nervous system<ref>NPS medicine  Opioids Available: https://www.nps.org.au/australian-prescriber/articles/opioids-mechanisms-of-action<nowiki/>(accessed 18.4.2022)</ref>.


The PAG is an area of grey matter in the midbrain that is involved in a descending pain control pathway. The periaqueductal gray, or PAG, receives pain information via the spinomescencephalic tract and then can activate the endogenous opiate system to suppress pain.<ref>Neuroscientifically Challenged PAG Available:https://neuroscientificallychallenged.com/glossary/periaqueductal-gray (accessed 18.4.2022)</ref>
Opioid receptors are located in the: brain (highest densities found in the thalamus, the PAG, and the RVM); spinal cord (high density in the dorsal horn region) and; peripheral organs, eg heart, blood vessels, kidneys, sympathetic ganglia, and the adrenal medulla)<ref>Decaillot F, Abul-Husn NS, Devi L. Opioid and Opioid-like Receptors.Available: https://www.sciencedirect.com/science/article/pii/B9780080552323601035 (accessed 8.4.2022)</ref><br>
 
== Why is the System Useful?  ==
Work by Hadjipavlou et al<ref name="Hadjipavlou">Hadjipavlou G, Dunckley P, Behrens TE, Tracey I. Determining anatomical connectives between cortical and brainstem pain processing regions in humans: a diffusion tensor imaging study in healthy controls. Pain 2006; 123: 169-178</ref>&nbsp;used functional and anatomical studies to link the descending pain modulatory system from the [[brainstem]] (where the PAG and RVM reside) to a number of higher level brain areas including; cingulofrontal regions, the amygdalae and the hypothalamus (figure 3<ref name="bingel">Bingel U, Tracey I. Imaging CNS Modulation of Pain in Humans. Physiology 2008; 23:371-380</ref>). This may go someway to help explain the role that emotions and cognition have in processing [[Nociception|nociceptive]] information.&nbsp;  
 
[[Image:Descending-inhibitory-pathway.jpg|border|center|300px]]<br>
 
Underpinning the descending pain modulatory system is the endogenous [[Opioids|opioid]] system<ref name="Akil">Akil H, Watson SJ, Young E, Lewis ME, Khachaturian H, Walker JM. Endogenous opioids: biology and function. Annu Rev Neurosci 1984; 7: 223-255</ref>&nbsp;and according to Willer<ref name="Willer">Willer JC, Dehen H, Cambier J. Stress induced analgesia in humans: endogenous opiods and naloxone-reversible depression of pain reflexes. Science 1981; 212:689-691</ref>&nbsp;this system may be activated by a variety of reflex and cognitively trigged states. At the spinal cord (dorsal horn) level, the opiod system causes inhibition of substance P from peripheral noxious <u>mechanical</u> stimulation<ref name="Kuraishi">Kuraishi, Y. Neuropeptide-mediated transmission of nociceptive information and its regulation. Novel mechanisms of analgesics 2008; 110(10),711-772</ref>&nbsp;via release of noradrenaline from the dorsalateral PAG (dPAG) and <u>thermal</u> nociceptive stimuli via the release of serotonin from the ventrolateral PAG (vPAG)<ref name="Kuraishi 1983">Kuraishi Y, Harada Y, Aratani S. Seperate involvement of the spinal noradrenergic and serotonergic systems in morphine analgesia: the differences in mechanical and thermal algesic tests. Brain Res 1983;273, 245-252</ref>.


== Why is the System Useful?  ==
Evidence for pain modulalatory mechanisms were first recorded by Beecher<ref name="Beecher">Beecher HK. Pain in men wounded in battle. Ann Surg. 1946;123(1):96-105</ref>. Beecher, a physician serving the US Army during World War II, observed as many as three quarters of badly wounded soldiers reported none to only moderate pain and did not require pain relief medication. According to his report the men were alert and responsive and the injuries were not trivial, including compound fractures and penetrating wounds. This led him to the conclusion that "strong emotions" block pain. This clearly opposess the classical Cartesian view where pain was considered to be a hard-wired system that passively transmitted noxious inputs to the brain.


Evidence for pain modulalatory mechanisms were first recorded by Beecher<ref name="Beecher">Beecher HK. Pain in men wounded in battle. Ann Surg. 1946;123(1):96-105</ref>. Beecher, a physician serving the US Army during World War II, observed as many as three quarters of badly wounded soldiers reported none to only moderate pain and did not require pain relief medication. According to his report the men were alert and responsive and the injuries were not trivial, including compound fractures and penetrating wounds. This led him to the conclusion that "strong emotions" block pain. This clearly opposess the classical Cartesian view where pain was considered to be a hard-wired system that passively transmitted noxious inputs to the brain. It is now generally accepted that the experience of pain does not soley rely on noxious inputs, but many variables interplay with the experience, including memory, mood, environment, attention and expectation. Ultimatley, this means the resultant pain experienced to the same sensory input can vary considerably<ref name="Bingel">Bingel U, Tracey I. Imaging CNS modulation of pain in humans. Physiolohy 2008;23:371-380</ref>. It is the brain's job to weigh all the information and decide whether creating pain is the most appropraite reponse. This provides a necessary '''survival function''' since it allows the pain experience to be altered according to the situation rather than having pain always dominate<ref name="Bingel" />.&nbsp;  
It is now generally accepted that the experience of pain does not solely rely on noxious inputs, but many variables interplay with the experience, including memory, mood, environment, attention and expectation. Ultimatly, this means the resultant pain experienced to the same sensory input can vary considerably<ref name="Bingel">Bingel U, Tracey I. Imaging CNS modulation of pain in humans. Physiolohy 2008;23:371-380</ref>. It is the brain's job to weigh all the information and decide whether creating pain is the most appropriate response. This provides a necessary '''survival function''' since it allows the pain experience to be altered according to the situation rather than having pain always dominate<ref name="Bingel" />.&nbsp;  


== Implications for Physiotherapists  ==
== Implications for Physiotherapists  ==
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Thirdly,&nbsp;<span style="line-height: 1.5em;">&nbsp;manual techniques such as [[Manual Therapy|joint mobilisations]], manipulations have been proposed to activate &nbsp;the system and significantly contribute to their therapeutic effects<ref name="Wright">Wright A. Hypoalgesia post manipulative therapy: a review of a potential neurophysiological mechanism. Man Ther 1995;1(1), 11-16</ref>. &nbsp;</span><span style="line-height: 1.5em;">Noxious stimuli can activate the system</span><ref name="Yaksh">Yaksh TL, Elde RP. Factors governing release of methionine enkephalin-like immunoreactivity from mesencephalon and spinal cord of the cat in vivo. J.Neurophysiol 1981;46 (5), 1056-1075</ref><ref name="Fields 2">Fields HL, Basbaum AL. Central Nervous System mechanisms of pain modulation, In: Wall PD, Melzack R. Textbook of pain, 4th ed.Churchill Livingstone, Edinburgh; 1999</ref>&nbsp;<span style="line-height: 1.5em;">and this&nbsp;</span><span style="line-height: 19.9200000762939px;">can help explain why manual</span><span style="line-height: 1.5em;">&nbsp;techniques that may elicit some pain (to some degree) can be helpful to reduce pain overall. </span><span style="line-height: 1.5em;">&nbsp;This knowledge can aid the physiotherapist with careful selection and use of techniques with a </span>''"top down"''<span style="line-height: 1.5em;"> philosphy, freeing them from selecting interventions based merely on proposed local tissue reponses such as inhibiting reflex muscle contraction, reducing intra-articular pressure and reducing the level of joint afferent activity</span><ref name="Zusman">Zusman M. Spinal manipulative therapy: a review of some proposed mechanisms, and a new hypothesis. Aust J. Physiotherapy 1986;32(2),89-99</ref>  
Thirdly,&nbsp;<span style="line-height: 1.5em;">&nbsp;manual techniques such as [[Manual Therapy|joint mobilisations]], manipulations have been proposed to activate &nbsp;the system and significantly contribute to their therapeutic effects<ref name="Wright">Wright A. Hypoalgesia post manipulative therapy: a review of a potential neurophysiological mechanism. Man Ther 1995;1(1), 11-16</ref>. &nbsp;</span><span style="line-height: 1.5em;">Noxious stimuli can activate the system</span><ref name="Yaksh">Yaksh TL, Elde RP. Factors governing release of methionine enkephalin-like immunoreactivity from mesencephalon and spinal cord of the cat in vivo. J.Neurophysiol 1981;46 (5), 1056-1075</ref><ref name="Fields 2">Fields HL, Basbaum AL. Central Nervous System mechanisms of pain modulation, In: Wall PD, Melzack R. Textbook of pain, 4th ed.Churchill Livingstone, Edinburgh; 1999</ref>&nbsp;<span style="line-height: 1.5em;">and this&nbsp;</span><span style="line-height: 19.9200000762939px;">can help explain why manual</span><span style="line-height: 1.5em;">&nbsp;techniques that may elicit some pain (to some degree) can be helpful to reduce pain overall. </span><span style="line-height: 1.5em;">&nbsp;This knowledge can aid the physiotherapist with careful selection and use of techniques with a </span>''"top down"''<span style="line-height: 1.5em;"> philosphy, freeing them from selecting interventions based merely on proposed local tissue reponses such as inhibiting reflex muscle contraction, reducing intra-articular pressure and reducing the level of joint afferent activity</span><ref name="Zusman">Zusman M. Spinal manipulative therapy: a review of some proposed mechanisms, and a new hypothesis. Aust J. Physiotherapy 1986;32(2),89-99</ref>  
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== References  ==
== References  ==

Revision as of 02:08, 18 April 2022

Original Editor - Adrian Mallows.

Top Contributors - Adrian Mallows, Lucinda hampton, Jo Etherton, Admin and Lauren Lopez  

Introduction[edit | edit source]

Once a pain signal from the ascending pathway reaches the somatosensory cortex, it triggers the descending pain modulatory system. The goal of this pathway is to allow the organism to function enough to respond to the pain source by reducing the pain signal through neuronal inhibition ie the "top down" modulation of pain. It begins in the periaqueductal gray (PAG), an area of grey matter in the midbrain that is involved in a descending pain control pathway. The periaqueductal gray, or PAG, receives pain information via the spinomescencephalic tract and processes the nociceptive information and relays it to the rostral ventral medulla (RVM). These neurons in the RVM then send a signal down the spinal cord and activate the endogenous opiate system to suppress pain.[1][2]

Our body produces natural (endogenous) opioids, which comprise endorphins, dynorphins, and enkephalins. On a molecular level, both these and synthetic opioids inhibit pain signals by interfering with intracellular signaling and preventing ascending pain-causing neurons from sending action potentials. [2] Opioids have actions at two sites, the presynaptic nerve terminal and the postsynaptic neuron. The postsynaptic actions of opioids are usually inhibitory. The presynaptic action of opioids is to inhibit neurotransmitter release, and this is considered to be their major effect in the nervous system[3].

Opioid receptors are located in the: brain (highest densities found in the thalamus, the PAG, and the RVM); spinal cord (high density in the dorsal horn region) and; peripheral organs, eg heart, blood vessels, kidneys, sympathetic ganglia, and the adrenal medulla)[4]

Why is the System Useful?[edit | edit source]

Evidence for pain modulalatory mechanisms were first recorded by Beecher[5]. Beecher, a physician serving the US Army during World War II, observed as many as three quarters of badly wounded soldiers reported none to only moderate pain and did not require pain relief medication. According to his report the men were alert and responsive and the injuries were not trivial, including compound fractures and penetrating wounds. This led him to the conclusion that "strong emotions" block pain. This clearly opposess the classical Cartesian view where pain was considered to be a hard-wired system that passively transmitted noxious inputs to the brain.

It is now generally accepted that the experience of pain does not solely rely on noxious inputs, but many variables interplay with the experience, including memory, mood, environment, attention and expectation. Ultimatly, this means the resultant pain experienced to the same sensory input can vary considerably[6]. It is the brain's job to weigh all the information and decide whether creating pain is the most appropriate response. This provides a necessary survival function since it allows the pain experience to be altered according to the situation rather than having pain always dominate[6]. 

Implications for Physiotherapists[edit | edit source]

Knowledge of the descending pain modulatory system  and its components can help physiotherapists in several ways. Firstly, it helps physiotherapists explain why the amount of pain a patient is experiencing does not neccesarily relate to the amount of tissue damage they have sustained[5]. Physiotherapists can educate their patients about the role of the descending pain modulatory system and how the central nervous sytem weighs all the information before deciding if a pain experience is the most approriate action for survival. Neuroscience education has been shown to be effective in several studies[7][8][9][10] [11][12].

Secondly, knowledge of the anatomy (see above) involved in the descending pain modulatory system can help physiotherapists utilise management strategies to that access and activate the system. These could include adding distractions to exercises and perfoming exercises in different emotional states and or in different environments.

Thirdly,  manual techniques such as joint mobilisations, manipulations have been proposed to activate  the system and significantly contribute to their therapeutic effects[13].  Noxious stimuli can activate the system[14][15] and this can help explain why manual techniques that may elicit some pain (to some degree) can be helpful to reduce pain overall.  This knowledge can aid the physiotherapist with careful selection and use of techniques with a "top down" philosphy, freeing them from selecting interventions based merely on proposed local tissue reponses such as inhibiting reflex muscle contraction, reducing intra-articular pressure and reducing the level of joint afferent activity[16]

References[edit | edit source]

References will automatically be added here, see adding references tutorial.

  1. ↑ Neuroscientifically Challenged PAG Available:https://neuroscientificallychallenged.com/glossary/periaqueductal-gray (accessed 18.4.2022)
  2. ↑ 2.0 2.1 Tufts Available: Opioid peptideshttps://sites.tufts.edu/opioidpeptides/pathways-and-receptors/classical-opioid-signaling/ (accessed 18.4.2022)
  3. ↑ NPS medicine Opioids Available: https://www.nps.org.au/australian-prescriber/articles/opioids-mechanisms-of-action(accessed 18.4.2022)
  4. ↑ Decaillot F, Abul-Husn NS, Devi L. Opioid and Opioid-like Receptors.Available: https://www.sciencedirect.com/science/article/pii/B9780080552323601035 (accessed 8.4.2022)
  5. ↑ 5.0 5.1 Beecher HK. Pain in men wounded in battle. Ann Surg. 1946;123(1):96-105
  6. ↑ 6.0 6.1 Bingel U, Tracey I. Imaging CNS modulation of pain in humans. Physiolohy 2008;23:371-380
  7. ↑ Moseley G Combined physiotherapy and education is efficacious for chronic low back pain. Australian Journal of Physiotherapy 2002; 48:297–302
  8. ↑ Louw A, Louw Q, Crous LCC. Preoperative Education for Lumbar Surgery for Radiculopathy. South African Journal of Physiotherapy. 2009;65(2):3-8.
  9. ↑ Moseley, GL. A randonmised controlled trial of intensive neurophysiology education in chronic low back pain. Clin J Pain 2002;20:324-330
  10. ↑ Meeus MJ. Pain physiology education improves pain beliefs in patients with chronic fatigue syndrome compared with pacing and self-management education:a double-blind randomised controlled trial. Arch Phys Med Rehabil 2010;91:1153-1159
  11. ↑ Clarke CL. Pain Neurophysiology education for the management for the management of individuals with chronic low back pain: systematic review and meta-analysis. Manual Therapy 2011;16:544-549
  12. ↑ Louw A. The effect of neuroscience education on pain and disability, anxiety, and stress in chronic musculoskeletal pain. Archives of Physical Medicine and Rehabilitation 2011;92:2041-2056
  13. ↑ Wright A. Hypoalgesia post manipulative therapy: a review of a potential neurophysiological mechanism. Man Ther 1995;1(1), 11-16
  14. ↑ Yaksh TL, Elde RP. Factors governing release of methionine enkephalin-like immunoreactivity from mesencephalon and spinal cord of the cat in vivo. J.Neurophysiol 1981;46 (5), 1056-1075
  15. ↑ Fields HL, Basbaum AL. Central Nervous System mechanisms of pain modulation, In: Wall PD, Melzack R. Textbook of pain, 4th ed.Churchill Livingstone, Edinburgh; 1999
  16. ↑ Zusman M. Spinal manipulative therapy: a review of some proposed mechanisms, and a new hypothesis. Aust J. Physiotherapy 1986;32(2),89-99

 

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