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  • Michele Curatolo

Is the distinction between acute and chronic pain meaningful?


The traditional distinction between acute (less than 3 months) and chronic pain (more than 3 months) is challenged.
The distinction between acute and chronic pain, and the concept of transition from acute to chronic pain, are challenged.
 

This blog is based on an article [1} by John Loeser, one of the pioneers of pain medicine, former Chief of the Multidisciplinary Pain Clinic at the University of Washington, and former president of the International Association for the Study of Pain (IASP). It is a brilliant view that deserves dissemination. The purpose of this blog is to summarize some of the concepts in a non-technical language, and provide a personal view.


The 3-months cutoff

The International Association for the Study of Pain (IASP) distinguishes acute from chronic pain based on the duration: the pain lasts less and more than 3 months for acute and chronic pain, respectively. The advantage of this classification is its simplicity. However ...


Let's consider a patient who has had pain for 100 days or more. Is this patient's condition different from the condition of the same patients 10 or 20 days before? There is little, if any, scientific support for different causes and mechanisms of pain in the same individual, at different time-points. Also, there is no evidence that treatment options should be different at different time-points (here, we do not consider the first few days after a major surgery or trauma, which may require and allow different treatments).


Is there a "transition" from acute to chronic pain?

In the last years, much discussion and research has focused on the concept of "transition" from acute to chronic pain. The concept of transition is based on the assumption that acute pain would become chronic due to processes that intervene during the first 90 days. Some of these processes may be of psychosocial nature, such as the development of depression or negative thoughts ("catastrophizing"). Changes in the cells of the central nervous system produce an enhanced activity of pain pathways, contributing to persisting pain (read more here). However, there is little evidence that these factors determine the transition to chronic pain. Rather, most of these processes take place very soon after an injury and, in most cases, resolve. It is possible that there is no transition, and developing chronic pain would depend on factors that are present at the onset of pain, such as the nature of an injury and genetic predisposition.


Thinking differently

John Loeser proposes to replace the classification acute / chronic pain with peripherally-generated / centrally-maintained pain. Pain is peripherally generated if there is a lesion in a tissue that sends painful signals to the brain. An example is osteoarthritis of the hip. Because pain from hip osteoarthritis is primarily peripherally generated, surgery that replaces the joint resolves the pain in most cases.

Centrally maintained pain has its main origin in the brain and/or the spinal cord. John Loeser provides the example of pain after a stroke, which occurs soon after the stroke and persists for years. This type of pain is clearly a centrally-maintained pain from the beginning, as it is due to lesions of brain areas involved in pain perception. Why would we call this pain differently during the first 3 months and thereafter?


Having a predominantly or exclusively centrally-maintained pain implies that there is no significant lesion in a tissue that would primarily explain the pain. Therefore, these patients will unlikely benefit from interventions that aim to remove a putative "pain generator". As discussed in a previous blog, dysfunctions in pain cells and pathways could occur with minimal or even absent tissue damage. This is illustrated in the figure below. Pathway 3, which implies no peripheral focus, likely applies to fibromyalgia, a widespread musculoskeletal pain condition that is not associated with tissue damage, and is therefore not peripherally generated. Importantly, in post-traumatic pain, these changes in pain cells and pathways can occur very soon after the injury, and are therefore not exclusively typical of long-lasting pain. The widespread belief that such dysfunctions are specific to chronic pain does not seem justified by the current knowledge.



A caveat: Our methods to determine whether the pain is primarily peripherally generated or centrally maintained are limited

If we consider low back pain, most patients have some sort of arthritis that could send pain signals to the spinal cord and the brain. However, as discussed in a previous blog, findings of arthritis on x-ray and MRI are poorly related to pain. Many of these findings are present in individuals with no low back pain, and low back pain can be present in individuals with no image findings of arthritis. Would we conclude that low back pain is not peripherally generated? Or are our current diagnostic tools insufficient to detect painful lesions of the back? Hopefully, future studies that make use of advanced methods to study the molecular mechanisms of pain will improve our understanding of the possible peripheral drivers of low back pain (see here).


Can pain occur without any input from peripheral tissues? If no specific finding from a painful area explain the pain, can this pain be entirely centrally maintained? This seems to be contradicted by the observation that anesthetizing the nerves that supply painful areas almost always produces pain relief, although temporarily. It is worth quoting John Loeser's statements:

It has been noted many times that anesthetizing the nerves in a painful area can eliminate such pains for the duration of the anesthetic block; but then the pain returns. This suggests that some input is required to generate the pain: an analogy to a positive feedback system that produces zero output when there is zero input, but dramatically amplifies even the smallest input. This is one of the potential mechanisms of centrally maintained pains: a positive feedback loop has been established that dramatically magnifies the sensory input so that it is perceived as painful.


How to identify centrally maintained pain?

While our diagnostic tools are still unable to look into central mechanisms of pain, we can base our judgment on a working hypothesis. Signs of pain that is primarily centrally mediated are:

  • Enhanced pain sensitivity (such as tenderness) outside the area on primary injury/pain

  • Pain with innocuous stimuli, such as touch, cold, or light pressure

  • Spread of pain to large body areas

  • Pain at multiple body sites

In these cases, it is likely that central components play a major role. However, explaining patients that their pain is primarily centrally-mediated can be difficult, as pain is interpreted as a threaten to a specific body area that hurts. A guidance for patients and clinicians can be found in a previous blog.


Time for a paradigm shift?

With some exceptions, such as the first days after surgery, causes and mechanisms of pain do not seem to depend on the time from the onset of pain. Treatment options should not depend on whether the pain has been present for more or less than three months. Therefore, a classification based on time, using any cutoff to distinguish acute from chronic pain, has no scientific support and is potentially misleading. The classification proposed by John Loeser into peripherally-generated and centrally-maintained pain can be more helpful and better drive medical decisions.



[1] Loeser, John D.. A new way of thinking about pains. PAIN: September 2022 - Volume 163 - Issue 9 - p 1670-1674. doi: 10.1097/j.pain.0000000000002583

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