Pain Facilitation and Inhibition
Tips for writing this page:
- Define and describe the differences between faciliatatory and inhibitory pathways, incluing their brain sites and neurotransmitters
- Explain and describe how these pathways can be activated by non-pharmacological agents.
Original Editor - Manisha Shrestha
Top Contributors - Manisha Shrestha, Lucinda hampton, Jo Etherton, Kim Jackson, Lauren Lopez, Tolulope Adeniji and Kirenga Bamurange Liliane
ascending and descending tracts for pain pathways.Ascending tract-lateral spinothalamic tract. 1st order neuron from pheripheral tissue ( prostaglandins) to dorsal horn of spinal cord(substania gelatinosa). neurotransmitter is Substance P. 2nd order neuron from sustania gelatinosa to 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.
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.
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) from immune cells of peripheral tissues after any injury. From the free nerve ending
1st order neuron from pheripheral tissue ( prostaglandins) to dorsal horn of spinal cord(substania gelatinosa). neurotransmitter is Substance P. 2nd order neuron from sustania gelatinosa to 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.
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 and pathological states. It plays a critical role in determining the experience of both acute and chronic pain.[1] Facilitatory and inhibitory pathways are further described below.
Facilitatory pathways[edit | edit source]
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.[2]
Facilitatory Pathways[edit | edit source]
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Inhibitory Pathways[edit | edit source]
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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]
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- ↑ 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.
- ↑ Staud R. The important role of CNS facilitation and inhibition for chronic pain. International journal of clinical rheumatology. 2013 Dec 1;8(6):639.
- ↑ 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]
