Somatosensory Function and Treatment of Pain. Pain may be incapacitating and aggravating since it interferes with work, family time, and sleep. There are a variety of treatment options for both acute and chronic pain, including pharmacological and nonpharmacological therapy. Non-pharmacological treatments try to relieve fear, discomfort, and anxiety, as well as pain, in order to provide patients a feeling of control (El Geziry et al., 2018).
Somatosensory Function and Treatment of Pain
These include physical treatments such as heat or cold packs, psychological therapies such as relaxation methods, and occupational therapies. This topic focuses on heat and cold pain management techniques as well as the usage of nonsteroidal anti-inflammatory drugs (NSAIDs) to uncover the processes behind pain management.
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- Function of the senses and pain management.
Somatosensory Function and Treatment of Pain Result of Heat
Pain is a complex constellation of unpleasant sensory, emotional, and cognitive sensations resulting from tissue injury. Nociceptors are peripheral neurons that detect the presence of noxious chemical stimuli caused by tissue damage or pain (Malanga et al., 2015). These neurons detect temperature and pressure extremes and convert them into long-range electrical impulses that are sent to the brain to produce pain feeling (Dubin & Patapoutian, 2010). The impact of heat on pain perception is mediated by calcium channels, with heat increasing intracellular calcium levels. Increased calcium channels create action potentials that result in a sensation of heat in the brain. When heat treatment is administered, heat-sensitive receptors such as TRPV1, TRPV2, and TRPV4 are activated (Dubin & Patapoutian, 2010). Once active, these channels occupy several binding sites, resulting in a reduction in pain sensitivity. In addition, activation of these receptors decreases the function of P2X2 and P2Y2 purine pain receptors, reducing peripheral pain directly.
Impact on Endogenous Substances
Endogenous opioids are a family of opioids generated in the brain and broadly distributed throughout the body. These substances are referred regarded as opioids because they attach to opioid receptor sites in the brain. Endogenous opioids are neuropeptides generated from proenkephalin A or proopiomelanocortin; owing to their neural-related actions, they are often referred to as neuromodulators (Winters et al., 2017). Enkephalins and endorphins are widespread endogenous hormones that govern fear, pain, decision making, drug dependency, and memory. Enkephalins and endorphins bind to the mu, delta, and kappa opioid receptors in the brain.
Somatosensory Function and Treatment of Pain
The functions of endogenous opioids depend on whether the molecules are agonistic or antagonistic. Beta-endorphins, for instance, bind to various opioid receptors to alleviate pain, control cardiovascular function, and balance food metabolism. It has also been discovered that these substances induce bliss through their influence on higher-order emotional and neurological processes (Winters et al., 2017). It has been established that enkephalins have conventional effects on pain control and neurotransmission. These compounds affect calcium influx, resulting in direct neuronal hyperpolarization. Enkephalins in the periaqueductal gray region of the spinal cord resolve analgesia and inhibit the release of excitatory neurotransmitters. This effect is best observed in regions of the spinal cord where enkephalins in the periaqueductal gray region inhibit the release of excitatory neurotransmitters.
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Within the endocrine system, endogenous opioids have unique functions. According to studies, a high enkephalin content in the hypothalamus leads to endocrine regulation (Winters et al., 2017). Enkephalin contributes to the regulation of growth factors, for example. It is hypothesized that enkephalins control the development of normal and pathological cells and tissues. Enkephalins are also known as opioid growth factor (OGF) due to their role in growth control. They 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 are also found to play a crucial role in the regulation of fear and emotional responses. Studies show that eliminating one family of endogenous opioids, such as the enkephalins, enhances fear and anxiety-related behaviors. Motor activity, digestive tract motility, peristalsis, and limbic control are also influenced by endogenous opioids.
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, manage pain in the body on a molecular level. The medications suppress the formation of prostaglandins by inhibiting the cyclooxygenase (COX) enzyme (Osafo et al., 2017). Cyclo-oxygenase enzyme 1 (COX-1) is an inherent component of normal cells, while cyclo-oxygenase 2 (COX-2) is increased in inflammatory cells. According to studies, suppression of COX-2 is the most plausible mechanism for producing analgesia (Osafo et al., 2017). Inhibition of COX-1 and COX-2 enzymes reduces the formation of prostaglandins, which are inflammatory mediators. This indicates that the body’s inflammatory activity is suppressed, resulting in decreased swelling and discomfort. In addition, many NSAIDs block the lipoxygenase pathway, leading to the generation of algogenic metabolites. These metabolites interfere with certain proteins that mediate analgesia-causing signals in the body. New research reveals that NSAIDs have a central mode of action that enhances the peripheral suppression of prostaglandin release (Osafo et al., 2017). In conjunction with the release of endogenous opioids, the CNS action of NSAIDs influences the synthesis and production of prostaglandins.
References
A. E. Dubin and A. Patapoutian (2010). Nociceptors are the pain pathway’s receptors. 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). Non-pharmaceutical pain relief. Management of Pain in Unique Circumstances, 1-14. DOI: 10.5772/intechopen.79689
Malanga, G. A., Yan, N., & Stark, J. (2015). Mechanisms and effectiveness of heat and cold treatments in the treatment of 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). The action mechanism of nonsteroidal anti-inflammatory medications. 1-15 of Nonsteroidal Anti-Inflammatory Drugs. DOI: 10.5772/68090
Winters, B. L., G. C. Gregoriou, S. A. Kissiwaa, O. A. Wells, D. I. Medagoda, S. M. Hermes,… & E. E. Bagley (2017). Endogenous opioids influence neuronal transmission and excitability on a moment-to-moment basis. 8(1) Nature Communications, 1-15. https://doi.org/10.1038/ncomms14611
