Pain Management and Somatosensory Function

Pain Management and Somatosensory Function, Pain may be debilitating and unpleasant because it interferes with job, spending time with family, and rest. Medication and non-pharmaceutical therapy may be used to treat both acute and chronic pain. Non-pharmacological treatments attempt to lessen patients’ fear, worry, and anxiety, and to alleviate their pain, therefore giving them a feeling of agency (El Geziry et al., 2018). This includes the use of physical treatments such as heat or cold packs, psychological therapies such as the use of relaxation methods, and occupational therapies. This debate focuses on heat and cold pain management techniques, as well as the usage of nonsteroidal anti-inflammatory drugs (NSAIDs), in order to discover the pain management processes.

Pain Management and Somatosensory Function

Thermal Impact

Pain is a somatic feeling comprised of an intricate constellation of unpleasant sensory, emotional, and cognitive responses triggered by tissue injury. Nociceptors are neurons in the periphery that detect the presence of noxious chemical stimuli as a consequence of damage or pain infliction (Malanga et al., 2015). These neurons detect temperature and pressure extremes and convert these inputs into long-distance electrical impulses that are sent to the brain to produce pain feeling (Dubin & Patapoutian, 2010). The impact of heat on the perception of pain is mediated through calcium channels, wherein heat raises the intracellular calcium concentration. Increased calcium channels create action potentials that provide a sensation of heat in the brain. Heat treatment activates heat-sensitive sensory receptors including TRPV1, TRPV2, and TRPV4 (Dubin & Patapoutian, 2010). Once active, these channels occupy many binding sites, reducing pain perception. Activation of these receptors also suppresses the activity of P2X2 and P2Y2 purine pain receptors, hence directly reducing peripheral pain.

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Influence on Endogenous Compounds

Endogenous opioids are a family of opioids that are generated in the brain and circulate broadly throughout the body. These substances are referred to as opioids because they have been shown to bind to opioid receptors in the brain. Endogenous opioids are neuropeptides generated from either proenkephalin A or proopiomelanocortin, and owing to their neural-related actions, they are often known as neuromodulators (Winters et al., 2017). Common endogenous molecules include enkephalins and endorphins, which control anxiety, pain, decision-making, drug dependency, and memory. Enkephalins and endorphins are opioid receptor agonists which bind to the brain’s mu, delta, and kappa receptors.

The functions of endogenous opioids are determined by their agonistic or antagonistic properties. For instance, beta-endorphins connect to various opioid receptors to alleviate pain, regulate cardiovascular function, and balance food metabolism. Through their influence on higher-order emotional and neurological processes, these substances are also reported to cause euphoria (Winters et al., 2017). Enkephalins have been shown to exert conventional effects on pain control and neurotransmission. These drugs change calcium influx to directly hyperpolarize neurons. Their action is best evident in the areas of the spinal cord where enkephalins in the periaqueductal gray region resolve analgesia and prevent the release of excitatory neurotransmitters.

In the endocrine system, endogenous opioids serve diverse functions. According to studies, a high concentration of enkephalins in the hypothalamus modulates endocrine function (Winters et al., 2017). Enkephalin contributes to the regulation of growth factors as one such function. There is speculation that enkephalins control the proliferation of normal and pathological cells and tissues.

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Due to its role in growth control, enkephalins are also known as opioid growth factor (OGF) and are physiologically paracrine and exocrine generated, rapidly degraded, and subject to the circadian rhythm (Winters et al., 2017). Through their action on the amygdala, endogenous opioids have also been discovered to play a crucial role in the control of fear and emotional responses. According to studies, eliminating one family of endogenous opioids, such as the enkephalins, enhances behavioral indicators of dread and anxiety. Endogenous opioids also influence motor activity, intestinal tract motility, peristalsis, and limbic system control.

Pain Management and Somatosensory Function NSAID Analgesics

Nonsteroidal anti-inflammatory medications are the most prevalent over-the-counter pain relievers in the world. These medications, which include aspirin, ibuprofen, and naproxen, function chemically to control pain in the body. By having an impact on the cyclooxygenase (COX) enzyme, the medicines suppress the generation of prostaglandins (Osafo et al., 2017). COX-1 is a constitutive component of normal cells, whereas COX-2 is induced in inflammatory cells. The most plausible mechanism for producing analgesia, according to studies, is the suppression of COX-2 (Osafo et al., 2017). Inhibition of the COX-1 and COX-2 enzymes reduces the generation of the inflammatory mediator prostaglandins. This indicates that the body’s inflammatory response is suppressed, resulting in reduced swelling and discomfort. Furthermore, certain NSAIDs block the lipoxygenase pathway, which leads in the generation of algogenic compounds. These metabolites interfere with proteins that mediate pain-relieving signals, hence inducing analgesia. Emerging research indicates that NSAIDs have a central mechanism of action that enhances the peripheral suppression of prostaglandin release (Osafo et al., 2017). NSAIDS influence the creation and production of prostaglandins through CNS action, in conjunction with the release of endogenous opioids.

References

Dubin, Alan E., and Alex Patapoutian (2010). Nociceptors are the pain receptors in the nervous system. Journal of Clinical Investigation, 120(11), pages 3760-3772. doi: 10.1172/JCI42843

El Geziry, A., Toble, Y., Al Kadhi, F., Pervaiz, M., & Al Nobani, M. (2018). Pain treatment without medication. 1-14 of Pain Management in Special Circumstances. DOI: 10.5772/intechopen.79689

Malanga, G. A., Yan, N., & Stark, J. (2015). Mechanisms and effectiveness of cold and heat therapy for musculoskeletal injuries. Postgraduate Medicine, 127(1), 57-65. DOI: 10.1080/00325481.2015.992719

Osafo, N., Agyare, C., Obiri, D. D., & Antwi, A. O. (2017). Nonsteroidal anti-inflammatory medication mechanism of action Nonsteroidal Anti-Inflammatory Medication, 1 to 15. DOI: 10.5772/68090

Gregoriou, G. C., Winters, B. L., Kissiwaa, S. A., Wells, O. A., Medagoda, D. I., Hermes, S. M.,… & Bagley, E. E. (2017). Moment-by-moment neuronal transmission and excitability are governed by endogenous opioids. Nature Communications, 8(1), pages 1-15. https://doi.org/10.1038/ncomms14611

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