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Physiology of the Pain System
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Projections from the rostral ventromedial medulla (RVM) directly synapse with the dorsal horn of the spinal cord. These cells are both serotonergic and non-serotonergic. In addition, there are cells from the RVM that project back to the dorsolateral pons, utilizing enkephalin as inhibitory and SP as excitatory neurotransmitters.
Opioid Medications and Correct Medical Usage—An Update
Published in Gary W. Jay, Clinician’s Guide to Chronic Headache and Facial Pain, 2016
Data shows that opioids can increase pain through activation of the bul-bospinal facilitation from the rostral ventromedial medulla (RVM); increased pain can decrease spinal opioid antinociceptive potency and finally blockade of restores the (63).
Opioid Medications and Correct Medical Usage—An Update
Published in Gary W. Jay, Practical Guide to Chronic Pain Syndromes, 2016
Data shows that opioids can increase pain through activation of the bul-bospinal facilitation from the rostral ventromedial medulla (RVM); increased pain can decrease spinal opioid antinociceptive potency and finally blockade of pain restores the antinociceptive potency (63).
Transcranial direct current stimulation combined with peripheral stimulation in chronic pain: a systematic review and meta-analysis
Published in Expert Review of Medical Devices, 2023
Rayssa Maria Do Nascimento, Rafael Limeira Cavalcanti, Clécio Gabriel Souza, Gabriela Chaves, Liane Brito Macedo
The combination of peripheral stimulation and transcranial stimulation could act priming the brain, that is, one therapy would increase the brain’s receptiveness to receive the other therapy. This occurs due to the capacity of these techniques to neuromodulate the cortex, increasing or decreasing its excitability [46]. Besides that, their top-down and bottom-up approaches could act together by bombarding the pain system and inducing a summative effect [45,47]. It is worth to remember that tDCS acts on motor cortex and its mechanisms for pain are related to neurophysiological changes, such as decrease in thalamic hyperactivity and neurochemical mediation of neurotransmitters and central receptors involved with the inhibitory control of descending pain pathways [48,49]. On the other hand, the most used forms of peripheral electrical stimulation for pain treatment, in theory, act through two main mechanisms: 1) selective stimulation of large-diameter non-nociceptive neural fibers at the level of spinal dorsal horn, activating inhibitory neurons of pain and suppressing nociceptive fibers (gait control theory of pain) [50,51] and 2) release of endogenous opioids and inhibition of nociceptive markers through activation of specific receptors in areas of pain control, such as rostral ventromedial medulla and periaqueductal gray [52,53].
A potential paradigm shift in opioid crisis management: The role of pharmacogenomics
Published in The World Journal of Biological Psychiatry, 2022
David Eapen-John, Ayeshah G. Mohiuddin, James L. Kennedy
Opioids and opiates are a class of analgesic drugs widely used in a clinical setting for pain management, especially in the post-operative context. Opioid class drugs target both the ascending (sensory) and descending (modulatory) pain pathways to produce analgesia. At the level of the brainstem, opioids act on GABAergic interneurons in the Periaqueductal Grey (PAG) to disinhibit the antinociceptive activity of projection neurons to the rostral ventromedial medulla (RVM) which blocks the ascending transmission of pain signals from the spinal cord (Jalabert et al. 2011; Matsui et al. 2014; Owusu Obeng et al. 2017; Burns et al. 2019). At the level of the spinal cord, opioids act on pain transmission neurons in the dorsal horn, reducing their activity and subsequently the ascending transmission of nociceptive signals (Jalabert et al. 2011; Matsui et al. 2014; Owusu Obeng et al. 2017; Burns et al. 2019).
Modulation of sensitization processes in the management of pain and the importance of descending pathways: a role for tapentadol?
Published in Current Medical Research and Opinion, 2020
Filippo Caraci, Flaminia Coluzzi, Franco Marinangeli, Sebastiano Mercadante, Giuseppe Rinonapoli, Patrizia Romualdi, Mariaflavia Nicora, Anthony H. Dickenson
Supraspinal involvement is central to the experiential aspects as well as in the affective components of pain. Multiple regions are involved, such as the hypothalamus, amygdala and cortex, as well as the nucleus accumbens and the periaqueductal grey5,8. Pathways run back from the brain to the spinal cord and many of the descending tracts are monoaminergic: at spinal synapses, the descending pathways induce the release of several mediators, including endogenous opioids, NA, serotonin (5-HT) and gamma-aminobutyric acid (GABA), thus modulating the transmission between primary and secondary neurons9. Remarkably, NA pathways exert an inhibitory effect on the transmission of acute and chronic pain, thus counteracting the establishment of chronic pain9. Conversely, serotoninergic pathways may have a facilitatory effect in the advanced stages of chronicity and therefore, might play a pro-nociceptive role10. The imbalance between amplified spinal ascending signals and inadequate activation of the descending inhibitory pathways plays a key role in the development and maintenance of many chronic pain syndromes9. Activity in the descending noradrenergic system can be gauged in animals and humans by diffuse noxious inhibitory controls (DNIC) and conditioned pain modulation (CPM), respectively, whereby one painful stimulus can inhibit another11. This control mechanism often fails in persistent pain states, allowing descending facilitation from the rostral ventromedial medulla (RVM) to dominate.