Mechanism of Referred Pain

Referred pain results in discomfort in a location not at the actual source of injury or irritation [1]. This intriguing aspect of the sensation of pain has long fascinated medical professionals and researchers, spurring research into how it works. While more research is needed, several key concepts of the mechanism of referred pain are now known.

At its core, referred pain arises from the convergence of sensory nerve fibers within the nervous system. The body’s intricate network of nerves conveys signals from various tissues to the brain, allowing for the perception of pain and other sensations. When injury or irritation occurs in one part of the body, these signals can sometimes be misinterpreted or shared with neighboring nerves, leading to the perception of pain in a different location [1].

One prominent theory on the mechanism of referred pain is the convergence-projection theory [2]. According to this model, sensory neurons from different regions of the body converge onto the same neurons within the spinal cord or brainstem. This convergence allows for the integration of sensory information from multiple sources, but it also creates the potential for confusion when interpreting the origin of pain signals. As a result, sensations from one area may be perceived in another, thereby giving rise to referred pain.

In addition, referred pain is closely linked to the phenomenon of dermatomes and myotomes [2]. Dermatomes refer to specific regions of the skin that are innervated by sensory nerves originating from a particular spinal nerve root. Similarly, myotomes correspond to groups of muscles that are supplied by motor nerves from the same spinal nerve root. Disruptions in these neural pathways can result in aberrant sensory or motor responses, as such contributing to the manifestation of referred pain.

Furthermore, the role of viscero-somatic and viscero-visceral reflexes cannot be overlooked in the mechanism of referred pain [3,4]. Viscero-somatic reflexes involve the transmission of sensory signals from internal organs to the spinal cord, where they are integrated with somatic sensory information. This integration can result in the perception of pain in somatic structures, even though the source of the sensation originates internally. Similarly, viscero-visceral reflexes involve the transmission of signals between different internal organs, potentially leading to the referral of pain between visceral structures.

Moreover, the central sensitization of nociceptive pathways may contribute to the amplification and spread of pain signals, further complicating the perception of pain [5]. Chronic pain conditions and persistent inflammation can induce changes in the central nervous system, resulting in heightened sensitivity to pain stimuli and alterations in pain processing. These neuroplastic changes may exacerbate or lead to referred pain, making it challenging to distinguish between primary and secondary sources of discomfort.

The mechanism of referred pain is an interplay of neural pathways, sensory integration, and central nervous system processing [6,7]. While our understanding of this phenomenon has advanced significantly in recent years, many aspects remain incompletely understood. Continued research, alongside the ongoing development of the therapeutic avenues to address it, is necessary [8].

References
1) Referred Pain: What It Is, Causes, Treatment & Common Areas. Available at: https://my.clevelandclinic.org/health/symptoms/25238-referred-pain. (Accessed: 6th March 2024)
2) Jin, Q., Chang, Y., Lu, C., Chen, L. & Wang, Y. Referred pain: characteristics, possible mechanisms, and clinical management. Front. Neurol. 14, (2023). doi: 10.3389/fneur.2023.1104817
3) Arendt-Nielsen, L. et al. Viscero-somatic reflexes in referred pain areas evoked by capsaicin stimulation of the human gut. Eur. J. Pain (2008). doi:10.1016/j.ejpain.2007.08.010
4) Physiology, Viscerosomatic Reflexes – StatPearls – NCBI Bookshelf. Available at: https://www.ncbi.nlm.nih.gov/books/NBK559218/. (Accessed: 6th March 2024)
5) Latremoliere, A. & Woolf, C. J. Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity. Journal of Pain (2009). doi:10.1016/j.jpain.2009.06.012
6) Jinkins, J. R. THE ANATOMIC AND PHYSIOLOGIC BASIS OF LOCAL, REFERRED AND RADIATING LUMBOSACRAL PAIN SYNDROMES RELATED TO DISEASE OF THE SPINE. J. Neuroradiol 31, 163–80 (2004). doi: 10.1016/s0150-9861(04)96988-x.
7) The Anatomy and Physiology of Pain – Pain and Disability – NCBI Bookshelf. Available at: https://www.ncbi.nlm.nih.gov/books/NBK219252/. (Accessed: 6th March 2024)
8) Referred Pain – Physiopedia. Available at: https://www.physio-pedia.com/Referred_Pain. (Accessed: 6th March 2024)