Arthritis and pain – beyond the joints | #arthritis #pain October 11, 2013 By richmondstace “…osteoarthritis is so common, it would make us think that we would be very good at treating it, but we aren’t”. Why is this the case? OAAs with many painful conditions that persist, most of the therapies used to treat osteoarthritis (OA) primarily target the tissues. In some cases this provides relief and improves the function of the affected joint. However, there are many individuals who receive such treatments and do not experience any significant change in their pain or ability to move. So, what is happening in these folk? The first point to understand is that we need a brain to feel pain – see Lorimer Moseley talking about this here. Of course the pain is experienced in the body tissues as this is where the sensation emerges, however, neuronal networks in the brain play a significant role in creating the feeling. Usually something happens in the body to begin the process of sensitisation such as an inflammatory process when we injure tissue or it degenerates as in arthritis when the joint structures change-worth noting is the fact that all of our tissues change as we age and this is entirely normal yet of course can be a painful process. The brain wants to know about inflammation and does so via the danger signals sent by nociceptors from the tissues to the spinal cord before reaching the higher centres. On scrutininsing these signals, the brain has to conclude that there is a threat to the integrity of the body based on the current status, prior experiences and a prediction of what this could mean, for pain to emerge in the area deemed to be in danger. The question that the brain asks is, “how dangerous is this?”. The answer to this question will determine the response. Perceived danger triggers pain but as part of an overall protective set of measures that include changes in movement, e.g. guarding and limping, autonomic activation in ‘fright or flight’, hormonal responses and immune system activity. All of these responses are normal, adaptive and desirable albeit accompanied by unpleasant conscious experiences such as pain and spasm. Pain is meant to be unpleasant as it drives behavioural change to promote survival. Typically, if we injure ourselves we expect the body to hurt although the intensity of the pain can vary enormously depending upon the context of the situation. There are many reports of people in casualty with significant trauma yet they describe a lack of pain. This is because pain is not an accurate indicator of tissue damage. One only has to consider phantom limb pain to see how we can experience pain in a body part that is no longer present. The representation of the limb still exists in the sensory cortex creating a conundrum for the brain as it seeks confirmative data from the periphery that does not show up. Maybe 80% of people who lose limbs will describe pain in the space once occupied. Something similar can happen following a joint replacement. Some patients report feeling on-going pain in the joint as if it is still present rather than the shiny new titanium joint surfaces actually in situ. Therefore, it has become apparent that to feel pain, the brain does not even need to receive danger signals but rather determines a threat value for a particular situation or context. Many people experience relief once they have a joint replacement but some do not. Prior to a replacement, the sensitivity that arises can cause changes throughout the nervous system similar to other persisting pain states. This is called central sensitisation, the term defined by plastic remodelling of neurons in the central nervous system that underpin widespread pain, amplified responses to normal stimuli and a reduced ability to inhibit the process of nociception. There are clinical ways in which we can test for this mechanism alongside listening to the clues from the patient’s narrative that is usually very revealing. On detecting this form of sensitivity, a different approach is required to tackle the pain and influencing factors. So, we need the brain to feel pain that emerges from the body. What does this mean for OA? In particular, those who continue to suffer with joint pain and stiffness despite treatment or surgery need to be considered as having a more centralised aspect although all pain patients should be thought about in terms of the brain’s perception of threat. The bottom line: reduce the threat, reduce the pain; and conversely, increased threat, increased pain. Therapies and strategies must bear this in mind in order to change the pain experience and improve the functioning of the joint. All too often patients are told that a joint is degenerate and that there is nothing that they can do. Of course we have acknowledged that some people will need surgery, but either way, there is plenty that they can do to proactively seek to gain control and change their experience. The fact that we have identified the role of the brain in pain, that the brain is plastic and designed to change (neuroplasticity) and that we have techniques that target the known changes (e.g. cortical reorganisation) and mechanisms provides great optimism. Below, Dr Tasha Stanton talking about osteoarthritis and the brain, describing the mechanisms and highlighting the altered sense of the affected area that is so common. The change in body schema, that is how the brain constructs the sense of self, is often part of a persisting pain state yet many patients do not volunteer the experince for fear of disbelief. Knowing that the area feels bigger, smaller, missing or detached is a vital clue that reveals features of the conidion that must be targeted with therapy and hence patients should be encouraged to fully express their story using their own language and metaphors. With the knowledge of these mechanisms we are making headway in treating conditions such as arthritis. We are all going to experience joint and tissue changes in our bodies as we age, so it is vital that we improve the way in which we tackle the issues.
Posted on: Mon, 11 Nov 2013 01:24:19 +0000
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