Pain Facilitation and Inhibition: Difference between revisions
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<br>'''Original Editor '''- [[User:Manisha Shrestha|Manisha Shrestha]] | |||
'''Original Editor '''- [[User:Manisha Shrestha|Manisha Shrestha]] | |||
'''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} | '''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}} | ||
endogenous pain inhibition-peri-acqueductal gray in mid brain. | endogenous pain inhibition-peri-acqueductal gray in mid brain. | ||
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== Objectives == | == Objectives == | ||
*Define and describe the differences between | *Define and describe the differences between facilitatory and inhibitory pathways, including their brain sites and neurotransmitters | ||
*Explain and describe how these pathways can be activated by non-pharmacological agents. | *Explain and describe how these pathways can be activated by non-pharmacological agents. | ||
== Ascending pain pathway == | == Ascending pain pathway == | ||
Ascending pain pathway is the pathway with afferent fibres. Lateral spinothalamic tract is the ascending tract which carry pain from pheriphery to central. Free nerve endings at tissue level are triggered by inflammatory mediators (Cytokines such as IL-1b, IL-6 and TNF ,prostaglandins) from immune cells of peripheral tissues after any injury. Aδ afferent fibers,which transmit impulses of fast pain secrete glutamate.The C type fibers, which transmit impulses of slow pain secrete substance P. Glutamate and Sustance p are two neurotrasmiters which help to transmit impluse from nerve endings i.e 1st order neuron to 2nd order neuron. 2nd order neuron run from dorsal horn of spinal cord (sustania gelatinosa) to opposite thalamus . Then 3rd order neuron from thalamus to cortex (primary and secondary somatosensory cortex (S1 and S2 respectively), anterior- and mid-cingulate cortex (ACC and MCC, respectively) and insula). | Ascending pain pathway is the pathway with afferent fibres. Lateral spinothalamic tract is the ascending tract which carry pain from pheriphery to central. Free nerve endings at tissue level are triggered by inflammatory mediators (Cytokines such as IL-1b, IL-6 and TNF ,prostaglandins) from immune cells of peripheral tissues after any injury. Aδ afferent fibers,which transmit impulses of fast pain secrete glutamate.The C type fibers, which transmit impulses of slow pain secrete substance P. Glutamate and Sustance p are two neurotrasmiters which help to transmit impluse from nerve endings i.e 1st order neuron to 2nd order neuron. 2nd order neuron run from dorsal horn of spinal cord (sustania gelatinosa) to opposite thalamus . Then 3rd order neuron from thalamus to cortex (primary and secondary somatosensory cortex (S1 and S2 respectively), anterior- and mid-cingulate cortex (ACC and MCC, respectively) and insula).<ref name=":0" /> | ||
== Descending pain pathway == | == Descending pain pathway == | ||
Supraspinal (or descending)pain control pathways arises from a number of supraspinal sites. Descending pain control pathways can be both facilitatory as well as inhibitory. Facilitatory pathways are the one which enhances pain perception where as inhibitory pathways suppresses pain perception. The balance between inhibition and facilitation is dynamic, and can be altered in different behavioral, emotional and pathological states. | Supraspinal (or descending)pain control pathways arises from a number of supraspinal sites. Descending pain control pathways can be both facilitatory as well as inhibitory. Facilitatory pathways are the one which enhances pain perception where as inhibitory pathways suppresses pain perception. The balance between inhibition and facilitation is dynamic, and can be altered in different behavioral, emotional, psychological and pathological states.<ref name=":0" /> Descending pain control pathways plays a critical role in determining the experience of both acute and chronic pain.<ref>Heinricher MM, Tavares I, Leith JL, Lumb BM. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894733/#!po=7.14286 Descending control of nociception: specificity, recruitment and plasticity.] Brain research reviews. 2009 Apr 1;60(1):214-25.</ref> Facilitatory and inhibitory pathways are further described below. | ||
=== Facilitatory pathways === | === Facilitatory pathways === | ||
Based on supraspinal sites: | |||
# thalamus, which seems to contribute to pain modulation via the mediodorsal (pain facilitation) and ventromedial (pain inhibition) nuclei | |||
# peri-acqueductal gray in mid brain. One seminal finding of endogenous pain inhi - bition, was the observation that focal electri - cal stimulation in the midbrain periaqueductal gray (PAG) produced profound analgesia in the awake rat [21], a finding that has been reproduced in human participants [22,23]. These results suggested that the PAG is an important brain area where ascending pain-related impulses are integrated with descending modulation from the midbrain and the limbic forebrain, includ - ing the amygdala, the rostral ACC, insula and orbitofrontal cortex | |||
# rostroventromedial medulla (RVM) play important roles in descending modulation of nociception, which can result either in inhibition and/or facilitation of nociceptive and non-nociceptive inputs. the rostro - ventromedial medulla (RVM) play important roles in descending modulation of nociception, which can result either in inhibition and/or facilitation of nociceptive and non-nociceptive inputs | |||
Based on Neurotransmitters | |||
=== Opioid pathway === | === Opioid pathway === | ||
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Direct stimulation of PAG or RVM does not only increase 5-HT but also norepinephrine concentrations in the cerebrospinal fluid, resulting in pain reductions | Direct stimulation of PAG or RVM does not only increase 5-HT but also norepinephrine concentrations in the cerebrospinal fluid, resulting in pain reductions | ||
Accumulating evidence supports the important role of CNS pain modulation for both analgesia and hyperalgesia. Multiple cortical and subcortical brain and brainstem regions integrate and process sensory, autonomic and emotional information, resulting in activation of the PAG and RVM, with subsequent inhibition or facilitation of pain-related dorsal horn neurons. This top–down modulation is relevant for experimental, as well as clinical pain, and influences the effects of pain-relieving drugs, such as opioids, NSAIDs, 5-HT–norepinephrine-reuptake inhibitors and gabapentinoids. These pain modulatory pathways are affected by memories and mood, as well as sociocultural background.<ref>Staud R. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904391/ The important role of CNS facilitation and inhibition for chronic pain.] International journal of clinical rheumatology. 2013 Dec 1;8(6):639.</ref> | Accumulating evidence supports the important role of CNS pain modulation for both analgesia and hyperalgesia. Multiple cortical and subcortical brain and brainstem regions integrate and process sensory, autonomic and emotional information, resulting in activation of the PAG and RVM, with subsequent inhibition or facilitation of pain-related dorsal horn neurons. This top–down modulation is relevant for experimental, as well as clinical pain, and influences the effects of pain-relieving drugs, such as opioids, NSAIDs, 5-HT–norepinephrine-reuptake inhibitors and gabapentinoids. These pain modulatory pathways are affected by memories and mood, as well as sociocultural background.<ref name=":0">Staud R. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904391/ The important role of CNS facilitation and inhibition for chronic pain.] International journal of clinical rheumatology. 2013 Dec 1;8(6):639.</ref> | ||
== Facilitatory Pathways == | == Facilitatory Pathways == | ||
Revision as of 04:36, 1 March 2020
Original Editor - Manisha Shrestha
Top Contributors - Manisha Shrestha, Lucinda hampton, Jo Etherton, Kim Jackson, Lauren Lopez, Tolulope Adeniji and Kirenga Bamurange Liliane
endogenous pain inhibition-peri-acqueductal gray in mid brain.
to affect pain modulation including the thalamus, which seems to contribute to pain modulation via the mediodorsal (pain facilitation) and ventromedial (pain inhibition) nuclei.
rostroventromedial medulla (RVM) play important roles in descending modulation of nociception, which can result either in inhibition and/or facilitation of nociceptive and non-nociceptive inputs.
Objectives[edit | edit source]
- Define and describe the differences between facilitatory and inhibitory pathways, including their brain sites and neurotransmitters
- Explain and describe how these pathways can be activated by non-pharmacological agents.
Ascending pain pathway[edit | edit source]
Ascending pain pathway is the pathway with afferent fibres. Lateral spinothalamic tract is the ascending tract which carry pain from pheriphery to central. Free nerve endings at tissue level are triggered by inflammatory mediators (Cytokines such as IL-1b, IL-6 and TNF ,prostaglandins) from immune cells of peripheral tissues after any injury. Aδ afferent fibers,which transmit impulses of fast pain secrete glutamate.The C type fibers, which transmit impulses of slow pain secrete substance P. Glutamate and Sustance p are two neurotrasmiters which help to transmit impluse from nerve endings i.e 1st order neuron to 2nd order neuron. 2nd order neuron run from dorsal horn of spinal cord (sustania gelatinosa) to opposite thalamus . Then 3rd order neuron from thalamus to cortex (primary and secondary somatosensory cortex (S1 and S2 respectively), anterior- and mid-cingulate cortex (ACC and MCC, respectively) and insula).[1]
Descending pain pathway[edit | edit source]
Supraspinal (or descending)pain control pathways arises from a number of supraspinal sites. Descending pain control pathways can be both facilitatory as well as inhibitory. Facilitatory pathways are the one which enhances pain perception where as inhibitory pathways suppresses pain perception. The balance between inhibition and facilitation is dynamic, and can be altered in different behavioral, emotional, psychological and pathological states.[1] Descending pain control pathways plays a critical role in determining the experience of both acute and chronic pain.[2] Facilitatory and inhibitory pathways are further described below.
Facilitatory pathways[edit | edit source]
Based on supraspinal sites:
- thalamus, which seems to contribute to pain modulation via the mediodorsal (pain facilitation) and ventromedial (pain inhibition) nuclei
- peri-acqueductal gray in mid brain. One seminal finding of endogenous pain inhi - bition, was the observation that focal electri - cal stimulation in the midbrain periaqueductal gray (PAG) produced profound analgesia in the awake rat [21], a finding that has been reproduced in human participants [22,23]. These results suggested that the PAG is an important brain area where ascending pain-related impulses are integrated with descending modulation from the midbrain and the limbic forebrain, includ - ing the amygdala, the rostral ACC, insula and orbitofrontal cortex
- rostroventromedial medulla (RVM) play important roles in descending modulation of nociception, which can result either in inhibition and/or facilitation of nociceptive and non-nociceptive inputs. the rostro - ventromedial medulla (RVM) play important roles in descending modulation of nociception, which can result either in inhibition and/or facilitation of nociceptive and non-nociceptive inputs
Based on Neurotransmitters
Opioid pathway[edit | edit source]
Descending projections from the RVM extend to spinal cord dorsal horns where they connect to primary afferent terminals, second- and third-order neurons, as well as interneurons.
Serotonergic pathway[edit | edit source]
serotonin (5-HT) and norepinephrine, are involved in endogenous pain modulation [51,52]. Norepinephrine and 5-HT can be released via descending pain pathways to modulate nociceptive signaling in the spinal cord. Norepinephrine inhibits pain through α2 adrenoceptors, while 5-HT seems to have pain facilitatory and inhibitory functions.
RVM neurons that have glycinergic or GABAergic projections to the spinal cord to mediate antinociception. It appears, that descending serotonergic projections from the RVM are relevant for pain facilitation in chronic pain, but they are not involved in opioid-mediated inhibition of acute pain.
Noradrenergic pathways[edit | edit source]
Direct stimulation of PAG or RVM does not only increase 5-HT but also norepinephrine concentrations in the cerebrospinal fluid, resulting in pain reductions
Accumulating evidence supports the important role of CNS pain modulation for both analgesia and hyperalgesia. Multiple cortical and subcortical brain and brainstem regions integrate and process sensory, autonomic and emotional information, resulting in activation of the PAG and RVM, with subsequent inhibition or facilitation of pain-related dorsal horn neurons. This top–down modulation is relevant for experimental, as well as clinical pain, and influences the effects of pain-relieving drugs, such as opioids, NSAIDs, 5-HT–norepinephrine-reuptake inhibitors and gabapentinoids. These pain modulatory pathways are affected by memories and mood, as well as sociocultural background.[1]
Facilitatory Pathways[edit | edit source]
Add text here...
Inhibitory Pathways[edit | edit source]
Add text here...
Descending pain modulation system[edit | edit source]
Non- pharmacological agents are the other agents which affect the pain modulation systems. for instance:
References[edit | edit source]
References will automatically be added here, see adding references tutorial.
- ↑ 1.0 1.1 1.2 Staud R. The important role of CNS facilitation and inhibition for chronic pain. International journal of clinical rheumatology. 2013 Dec 1;8(6):639.
- ↑ Heinricher MM, Tavares I, Leith JL, Lumb BM. Descending control of nociception: specificity, recruitment and plasticity. Brain research reviews. 2009 Apr 1;60(1):214-25.
- ↑ Armando Hasudungan. PAIN! Physiology - The Ascending Pathway, Descending Pain Pathway and the Substantia Gelatinosa. Available From: https://www.youtube.com/watch?v=5c8maFAhqIc [last accessed 22/2/2020]
