Getting back to basics on chronic pain

Pain is complex. With this new monthly articles series, I aim to get practitioners on the same page regarding the basics—and then I’ll dive into real patient cases. So, let’s get started with some core terminology on pain neurophysiology: Chronic pain: Chronic pain is a huge issue across all countries and populations. In the United States, more than one in five people suffer from chronic pain with costs estimated as US$560 billion annually (direct medical costs, lost productivity, and disability programs). In Canada, preliminary projections by Health Canada indicate as many as 8.3 million Canadians might live with chronic pain by 2025. Estimated costs in 2030 are expected to reach $52 to $55 billion. Chronic pain is more prevalent in certain types of patients and socioeconomic groups (eg. older adults, females, veterans, unemployed or living in poverty, LGBT+ adults, indigenous, and racial and ethnic groups with historical trauma). This introduction gives an idea of the magnitude of chronic pain. However, epidemiologic studies cannot tell us much about the origin of chronic pain conditions.One question I am asked frequently is “what exactly is chronic pain?” Despite the fact that pain is a universally encountered experience, there are many definitions. When we experience pain, for example from an acute back strain or a broken leg, people will become free of the pain once the cause of pain goes away. Yet a small, but not insignificant, number of people develop long-lasting chronic pain. In the first place, there is no clear relationship between the amount of tissue damage and the degree of pain one experiences or the impairment of function one has. To get anywhere close to understanding how chronic pain develops and is maintained, we must first explore how acute pain is created and perceived—what happens when a hammer strikes a thumb and the person at the end of that thumb shouts “Ouch!” Knowing how acute pain is generated can help with understanding how it is transformed into chronic, unrelenting pain.Pain has much in common with the sensory experiences of hearing and seeing, but it also differs in significant ways. Sensory stimuli in general, are detected by peripheral receptors, which are organs or cells designed to respond to external stimulation. Small amounts of stimulation from different sources, such as from vibration, indentation, stretching, and light, will trigger a response in “low threshold” receptor types. On the other hand, greater amounts of stimulation are required (such as intense mechanical pressure, hot, cold, and/or chemical stimuli —potentially harmful) to trigger activity in pain receptors (called nociceptors). Signals that are generated pass to another set of nerve tissues within the spinal cord dorsal horns. Dorsal horn neurons modulate the nociceptive electrical impulses from the periphery as they are able to turn their intensity up or down. After the dorsal horns, nociceptive impulses are carried primarily via the anterior spinothalamic tract (on the contralateral side of the spinal cord) all the way to several areas of the brain and brain stem, including the thalamus, amygdala, somatosensory cortex etc. A phenomenon that has received great attention recently is Central Sensitization. If nociceptive stimulation persists, certain neurons in the dorsal horn become “sensitized” (in the sense they lower their firing thresholds thus increasing the intensity of nociceptive impulses). The concept of Central Sensitization has been expanded in clinic and is considered to underlie numerous refractory to treatment pain conditions. Once established, simple touch of the skin, as well as other stimuli (e.g., light, sound, smell, heat, cold) feel intensified and uncomfortable.Besides Central Sensitization occurring at the dorsal horn, another process from higher brain and brain stem centres (called descending modulation) can also change electrical impulses arriving at the dorsal horns. This process can be either inhibitory (descending inhibition or anti-nociception) or facilitatory (descending facilitation or pro-nociception). Descending modulation can exert powerful effects. For example, wounded soldiers may experience no pain until they are safely off the battlefield (descending inhibition). Or, a simple papercut during a stressful workday can be very painful (descending facilitation). Tipping the balance on the side of descending facilitation is one of the many mechanisms of chronic pain. Many of the neurophysiological changes described above are adaptive, for example, allowing someone to cope with pain until healing occurs. However, multiple maladaptive changes in the structure and function of the central nervous system can also occur, maintaining and exaggerating pain even after an injury has healed. In subsequent articles, I’ll discuss maladaptive changes in patient cases I’ve seen.Both structural brain changes and “functional” alterations in brain circuits (without actual structural brain changes) are seen in different forms of brain imaging in humans and animals with pain conditions. Indeed, research has confirmed functional and/or structural changes in many clinical syndromes such as back pain, fibromyalgia, irritable bowel syndrome, Complex Regional Pain Syndrome (CRPS), knee osteoarthritis, headaches, and chronic vulvar pain as well as in animal models of chronic pain. The majority of this information is based on the following reference: Mailis A., Assimakopoulos D., Lakha S.F., Hapidou E. An integrated medical and psychological approach to understanding and assessing chronic pain. In: Young, G., Bailey, T., Giromini, L., Soble, J., Rogers, R., & Levitt, B. (2023). Handbook of Psychological Injury and Law. Cham, Switzerland: Springer Nature.

Getting back to basics on chronic pain

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Angela Mailis

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