Pain Modulation
Pain Modulation The process by which pain signaling changes along the pain transmission pathway, which explains why individuals respond differently to the same stimulus, and explains the mechanism of action when clinical analgesia is used. Pain control and regulation is a complex endeavor, often Top reasons why patients seek the services of rehabilitation specialists. Pain modulation begins with an understanding of the different levels of pain regulation and extends to clinical interventions and programs aimed at reducing pain. For example, opioids can increase and Reduce pain experience.
Levels of Pain Modulation
Pain modulation is easily divided into 5 discreet interaction levels. These levels correspond to important synaptic connections or important chemical processes involved in pain transmission.
Level 1: Periphery
Grade 1 pain modulation refers to events that occur in the periphery of the body to the source of the pain. Somatosensory is defined as sensation from mucus in the skin extremities and joints and is divided into: touch and pressure) and proprioception.
Nociceptors are peripheral cell nerve endings that initiate pain sensation in response to noxious stimuli (thermo-mechanical or chemical), which in turn trigger action potentials in the spinal cord and higher centers. It is divided into A-delta and C fibers.
- A-delta fibers are large (larger than C-fibers), myelinated, fast-conducting fibers associated with localized sharp and rapid pain sensations.
- C fibers are small unmyelinated slow-conducting nerve fibers involved in dull and slow pain perception.
Under normal conditions, when noxious stimuli (tissue damage) are present, nociceptors are inactive, and these nociceptors respond according to the type of stimulus, and cyclooxygenase 2 is activated to release more PG (prostaglandin ), nociceptors will transmit signals to In the dorsal horn of the spinal cord (first-order neurons), the first neuron releases the chemical P to transmit a signal.
A-beta is the large diameter of the myelin sheath and has the fastest conduction velocity. These fibers respond to non-painful stimuli, such as touch, mild pressure, and vibration. The beta stimulated by deep touch may explain why rubbing the painful area can reduce pain [1][2].
Level 2: Dorsal Horn
Grade 2 pain modulation refers to events in the dorsal horn of the spinal cord. Regulation at the spinal cord level occurs under Ronaldo SG’s Substantial Gelatenosa gating theory GCT theory first proposed by Ronald Melzack and Patrick Wall in 1965 This theory explains pain transmission and modulation dependent on large (A-Beta) and small (C-fiber) sensory fibers. Under steady-state conditions, the gait is closed and no pain signal is transmitted (inhibitory interneuron I blocks the projection neurons that transmit pain signals and connections them to the brain).
When noxious stimuli stimulate small nociceptor fibers, an action potential signal is transmitted, which in turn inhibits inhibitory interneurons (I) and projection neurons are activated, the gate is opened, and pain signals are transmitted to the brain. When the action potential is delivered Pain signals are propagated through the release of substance P by activating vesicles through first-order neurons.
For example, if large sensory fibers (A-Beta) are activated by deep touch, the transmitted signal activates inhibitory interneurons and blocks projection neurons, the gate closes and there is no pain [3]. Disruption of pain signaling from the spinothalamic tract to the cortex in the dorsal horn.
gate opened
gate closed
Modulation at the level of the spinal cord produces local analgesia, which receives another control from descending pathways, resulting in a diffuse inhibition of pain.
Level 3: Fast neuronal descendants and endogenous
The descending inhibitory pathway/mechanism of pain modulation depends on the release of opioids on the SG which controls/inhibits signaling between first and second order neurons. The descending pathway begins in the periaqueductal gray PAG of the midbrain and proceeds to the raphe nucleus of the midbrain. medulla to the dorsal horn of the spinal cord, where:
These pathways release serotonin and noradrenergic neurons to inhibit substance P release from the presynaptic cleft of first-order neurons.
Stimulation of inhibitory interneurons releases opioids (endorphins enkephalins), which in turn inhibit the release of substance P from the presynaptic form and inhibit postsynaptic transmission of signals by secondary neurons.
[4]
Level 4: Cortical
Anterior cingulate cortex.
Noxious stimuli are transmitted to the cortex via the spinothalamic tract, which acts as a third interneuron relay in the somatosensory area. Pain signals in the cortex induce pain modulation through two mechanisms:
- The cortex activates the PAG in the midbrain to activate the descending pathway (top-down control of pain), which, as previously described, interrupts and inhibits pain signals in the dorsal horn, thus inhibiting the spinothalamic tract by extension [5].
- Interactions between different domains; cortex-limbic forebrain structures basal ganglia This interaction is important for perceiving noxiousness but not pain. For example activation of the anterior cingulate cortex (ACC) and rostral agranular insular cortex (RAIC) Noxious stimulation showed activation of these regions and increased regional cerebral blood flow (rCBF) to these regions. ACC plays a role in pain transmission, is thought to be involved in placebo analgesia, and in conditioned learning [6][7].
Insular cortex.
Rostral agranular insular cortex also affects descending inhibitory pathways and is responsible for pain learning and memory. One study showed that the paraventricular nucleus of the hypothalamus emits oxytocin projections that support GABA neurotransmission and activate descending spinal cord Noradrenergic mechanism [8].
Physiotherapy interventions for pain regulation.
A systematic review by Arribas-Romano A et al in 2020 showed that physical therapy modalities can alert pain perception in chronic musculoskeletal pain CMP by reducing temporal summation, increasing conditioned pain modulation and slightly improving central sensitization Manual therapy and strength training are the most effective methods for producing these changes [9]. A combination of techniques demonstrated a significant increase in conditioned pain modulation.
Manual Therapy
Manual therapy has shown increased activity in cortical pain-modulating regions such as the RAIC in the insular cortex and the PAG in the periaqueductal gray [9].
- Myofascial release and Message.
- Joint mobilization and low-speed mobilization [9].
- Spinal manipulative therapy: reduces anticipated pain and tension during exercise[10].
Modalities
- Transcranial magnetic stimulation/ mprempren nkanyan tẽẽ.
an important way to reduce perception in chronic pain conditions and demonstrated a significant difference compared to sham techniques [11]. The precentral cortical area of the motor cortex is the most targeted area for pain modulation.
Transcutaneous Electrical Nerve Stimulation (TENS). The TENS mechanism relies on the gating theory and the release of endorphins and enkephalins.
- Low Level Laser Therapy.
- Acupuncture
Acupuncture is used as a complementary modality for pain management, the mechanism of which depends on the release of endogenous opioids serotonin and norepinephrine [12]. The variability in its effect may refer to the method of application, the number of needles and the duration of application. have Low-to-moderate quality studies have shown reductions in pain intensity with modest benefits, especially for chronic pain (chronic low back pain tension headaches chronic headaches migraine and myofascial pain) [13] Acute conditions and this improvement is modest There is no clinical significance, placebo effect and other randomized controlled trials can be referred to, there is no difference between sham acupuncture and real acupuncture, and it can be used for patients who cannot tolerate other standard therapies [12].
- Dry needling.
- Interferential Therapy
Exercise
For information on the effect of exercise on pain and recommended forms of exercise, you can read: Exercises and Activities for Pain Management
Resources
Wikibooks, what is pain?
UTHealth, the University of Texas
References
- ↑ Purves D, Augustine GJ, Fitzpatrick D, Katz LC, LaMantia AS, McNamara JO, Williams SM. Nociceptors. Sunderland, MA. 2001.
- ↑ Yam MF, Loh YC, Tan CS, Khadijah Adam S, Abdul Manan N, Basir R. General pathways of pain sensation and the major neurotransmitters involved in pain regulation. International journal of molecular sciences. 2018 Aug;19(8):2164.
- ↑ Yam MF, Loh YC, Tan CS, Khadijah Adam S, Abdul Manan N, Basir R. General pathways of pain sensation and the major neurotransmitters involved in pain regulation. International journal of molecular sciences. 2018 Aug;19(8):2164.
- ↑ Armando Hasudungan. PAIN! Physiology – The Ascending Pathway, Descending Pain Pathway, and the Substantia Gelatinosa. Available from: http://www.youtube.com/watch?v=5c8maFAhqIc[last accessed 11/12/2021]
- ↑ Ohara PT, Vit JP, Jasmin L. Cortical modulation of pain. Cellular and Molecular Life Sciences CMLS. 2005 Jan;62(1):44-52.
- ↑ Xie YF, Huo FQ, Tang JS. Cerebral cortex modulation of pain. Acta Pharmacologica Sinica. 2009 Jan;30(1):31-41.
- ↑ Steeds CE. The anatomy and physiology of pain. Surgery (Oxford). 2009 Dec 1;27(12):507-11.
- ↑ Gamal-Eltrabily M, de Los Monteros-Zúñiga AE, Manzano-García A, Martínez-Lorenzana G, Condés-Lara M, González-Hernández A. The rostral agranular insular cortex, a new site of oxytocin to induce antinociception. Journal of Neuroscience. 2020 Jul 15;40(29):5669-80.
- ↑ Jump up to:9.0 9.1 9.2 Arribas-Romano A, Fernández-Carnero J, Molina-Rueda F, Angulo-Diaz-Parreño S, Navarro-Santana MJ. Efficacy of physical therapy on nociceptive pain processing alterations in patients with chronic musculoskeletal pain: a systematic review and meta-analysis. Pain Medicine. 2020 Oct;21(10):2502-17.
- ↑ Ellingsen DM, Napadow V, Protsenko E, Mawla I, Kowalski MH, Swensen D, O’Dwyer-Swensen D, Edwards RR, Kettner N, Loggia ML. Brain mechanisms of anticipated painful movements and their modulation by manual therapy in chronic low back pain. The journal of pain. 2018 Nov 1;19(11):1352-65.
- ↑ Mylius V, Borckardt JJ, Lefaucheur JP. Noninvasive cortical modulation of experimental pain. Pain. 2012 Jul 1;153(7):1350-63.
- ↑ Jump up to:12.0 12.1 Kelly RB, Willis J. Acupuncture for pain. American family physician. 2019 Jul 15;100(2):89-96.
- ↑ Skelly AC, Chou R, Dettori JR, Turner JA, Friedly JL, Rundell SD, Fu R, Brodt ED, Wasson N, Winter C, Ferguson AJ. Noninvasive nonpharmacological treatment for chronic pain: a systematic review.
