Somatosensory Function and Pain Management

This custom essay focuses on Somatosensory Function and Pain Management. Pain can be debilitating and frustrating as it interferes with work, quality time with the family, and sleep. Different management strategies are available to manage both acute and chronic pain including the use of medications and non-pharmacological therapies.

Non-pharmacological therapies aim at decreasing fear, distress, anxiety, and to reduce pain providing patients with a sense of control (El Geziry et al., 2018). These include the use of physical therapies like heat or cold packs, psychological therapies like the use of relaxation techniques and occupational therapies. This discussion focuses on heat and cold pain management therapies together with the use of NSAIDS to identify the mechanisms surrounding pain management.

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Effect of Heat

Pain is a somatic sensation that involves a complex constellation of unpleasant sensory, emotional, and cognitive experiences provoked by tissue damage. Nociceptors are peripheral neurons that sense the presence of noxious chemical stimuli as a result of injury or pain infliction (Malanga et al., 2015). These neurons sense extremes in temperature and pressure and transduce these stimuli into long-ranging electrical signals that are relayed to the brain to bring about pain sensation (Dubin & Patapoutian, 2010). The effect of heat on pain sensation is mediated by sensitive calcium channels whereby heat increases the level of intracellular calcium. The increase in calcium channels generates action potentials that cause the feeling of heat in the brain. When using heat therapy, sensory receptors such as TRPV1, TRPV2, and TRPV4 which are sensitive to normal heat are activated (Dubin & Patapoutian, 2010). Once activated, these channels occupy multiple binding sites leading to decreased pain perception. Additionally, activation of these receptors inhibits the activity of P2X2 and P2Y2 purine pain receptors thus directly inhibiting peripheral pain.

Effect on Endogenous Chemicals

Endogenous opioids represent a class of opioids that are produced in the brain and circulate widely in the body. These chemicals are called opioids because they are confirmed to bind in the sites of opioid receptors in the brain. Endogenous opioids are neuropeptides derived from either proenkephalin A or pro-opiomelanocortin and due to their neural related functions, they are mostly referred to as neuromodulators (Winters et al., 2017). The common endogenous chemicals are enkephalins and endorphins which function to regulate fear, pain, decision making, drug dependence, and memory. Enkephalins and endorphins are opioid receptor agonists that bind to the mu, delta, and kappa receptors in the brain.

The roles of endogenous opioids are dependent on the agonistic or antagonistic nature of the chemicals. For instance, beta-endorphins bind to multiple opioid receptors to diminish pain, mediate cardiovascular regulation, and equilibrate food metabolism. These chemicals are also observed to drive euphoria through their effect on higher-order emotional and neurological systems (Winters et al., 2017). Enkephalins are observed to have classical effects on pain regulation and neurotransmission. These chemicals alter calcium influx causing direct hyperpolarization of neurons. Their effect is best observed in the regions of the spinal cord whereby the enkephalins in the periaqueductal gray region resolve analgesia and inhibit the release of excitatory neurotransmitters.

Endogenous opioids have distinctive roles in the endocrine system. Studies indicate that a high concentration of enkephalins in the hypothalamus contributes to endocrine modulation (Winters et al., 2017). One such role is the contribution of enkephalin in the modulation of growth factors. It is speculated that enkephalins regulate the growth of normal and abnormal cells and tissues. Because of its action of growth regulation, enkephalins are also called opioid growth factor (OGF) and they are physiologically paracrine and exocrine produced, quickly degraded, and obedient to the circadian rhythm (Winters et al., 2017). Endogenous opioids are also observed to have a critical effect in the regulation of fear and emotional responses through their effect on the amygdala. Studies demonstrate that deleting one family of endogenous opioids such as the enkephalins increases behavioral measures of fear and anxiety. The effects of endogenous opioids are also evident in motor activity, intestinal tract motility, peristalsis, and limbic system regulation.

NSAID Analgesics on Somatosensory Function and Pain Management

Nonsteroidal anti-inflammatory drugs are the most common pain relief drugs available over the counter in the world. These drugs which include aspirin, ibuprofen, and naproxen work on a chemical level to regulate pain in the body. The drugs inhibit the production of prostaglandins by exerting their effect on cyclo-oxygenase enzyme (COX) (Osafo et al., 2017). Cyclo-oxygenase enzyme 1 (COX-1) is a constitutive member of the normal cells and cyclo-oxygenase 2 (COX-2) is induced in inflammatory cells. Studies demonstrate that the inhibition of COX-2 presents the most likely mechanism of achieving analgesia (Osafo et al., 2017). The inhibition of COX-1 and COX-2 enzymes leads to diminished production of prostaglandins which are mediators of inflammation. This means the inflammatory activity is inhibited in the body leading to less swelling and less pain. Additionally, some NSAIDs inhibit the lipoxygenase pathway which results in the production of algogenic metabolites. These metabolites interfere with some proteins that mediate signals in the body leading to analgesia. Emerging evidence suggests that NSAIDs have a central mechanism of action that augments the peripheral inhibition of prostaglandin release (Osafo et al., 2017). Together with the release of endogenous opioids, NSAIDS have an effect on the formation and production of prostaglandins through CNS activity.

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References

Dubin, A. E., & Patapoutian, A. (2010). Nociceptors: The sensors of the pain pathway. The Journal of Clinical Investigation, 120(11), 3760-3772. doi: 10.1172/JCI42843

El Geziry, A., Toble, Y., Al Kadhi, F., Pervaiz, M., & Al Nobani, M. (2018). Non-pharmacological pain management. Pain Management in Special Circumstances, 1-14. DOI: 10.5772/intechopen.79689

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

Osafo, N., Agyare, C., Obiri, D. D., & Antwi, A. O. (2017). Mechanism of action of nonsteroidal anti-inflammatory drugs. Nonsteroidal Anti-Inflammatory Drugs, 1-15. DOI: 10.5772/68090

Winters, B. L., Gregoriou, G. C., Kissiwaa, S. A., Wells, O. A., Medagoda, D. I., Hermes, S. M., … & Bagley, E. E. (2017). Endogenous opioids regulate moment-to-moment neuronal communication and excitability. Nature Communications, 8(1), 1-15. https://doi.org/10.1038/ncomms14611

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