Why doesnt my pain go away? Paul Vaucher Osteopath, MSc in - PDF document

NCOR Congress 2017 January 28th 2017 Helping patients to help themselves: Improving the management of persistent pain Why doesn’t my pain go away? Paul Vaucher Osteopath, MSc in clinical trials, PhD in neuroscience University of Applied Sciences and Arts Western Switzerland (HES-SO) paul.vaucher@hefr.ch

Plan • Pain as a mental construct • Nociception • Chronicity • Solutions Slide 2 During the next 30 minutes, we are going to try and understand the basic physiology of pain. 1. I should convince you to recognise pain as a necessary mental construct. 2. We will then distinguish nociceptive stimuli from pain. 3. This will make it possible for us to understand how pain can be present in the absence of nociceptive stimuli. 4. And we will finally see why focusing on other perceptions or thoughts than pain might help in chronic conditions.

Pain as a mental construct Slide 3 Pain seems to be wired in us to be an unpleasant experience and we known it. It is linked to sufferance, tourment, and torture. We seem to be conditioned to avoid it by all means. Than why do we experience pain? What is its use? Slide 4 What if we were not to feel pain? There is a genetical disorder called familial dysautonomia. Those affected do not feel pain, heat, or cold. So is not having pain a true relief ? Pain seems very useful for us to adapt our behaviour. It helps us avoid situations that could harm us. Slide 5 But as always, things are a little more complicated! Pain is not always experienced with injury (Beecher 1946 & Malzach 1982), pain is not essential for withdrawal to occur, and pain does not necessarily lead to avoidance; some even seek it. Think of eating chilli; its painful but we have a form of pleasure overcoming that pain knowing it is not doing us any harm. The way we experience pain is apparently closely linked to previous experiences, the circumstances in which we are experiencing pain, and our own personality (Leknes et Bastian 2014). Think of how painful an unjust pinch from someone can feel compared to pinching yourself for no reason. Slide 6 The grey lines represent the ascending pathways carrying the nociceptive signal up to the brain. As we can see, the nociceptive signal modulates and is modulated on its pathway up. The thalamus plays a central role in regulating the upcoming signal. So the signal can already be down or up regulated at this level before arriving at the primary and secondary somatosensory cortex that localise and gives a sensation to the nociceptive treated signal. At the brain level, there are two distinct descending modulatory systems that modulate the nociceptive signal. In green, we have the emotional modulation pathway. It links the thalamus to the anterior cingulate cortex, the prefrontal cortex, the periaqueductal grey and the rostroventral medulla from which descending fibres can regulate upcoming signals from the spine. In blue, we have the attentional modulation pathway (saliency). The circuitry involves the superior parietal lobe that sends projections to primary and secondary somatosensory regions and to the insula. Slide 7 There is a close link between emotions, cognition and pain. Pain can have a negative effect on emotions. Conversely, a negative emotional state can lead to increased pain, whereas a positive state can reduce pain. Similarly, cognitive states such as attention and memory can either increase or decrease pain. Of course, emotions and cognition can also reciprocally interact. Pain is a phenomenon that is constructed by the brain. It might be felt at a location, but the pain itself is generated by the brain. In other words, pain is a mental construct. This also means that if the brain is unable to process signals that can lead to pain, it will not generate pain. Pain is altered or inexistent during coma (Boly et al 2008 The Lancet Neurology).

Slide 8 So to summarise: • Even if we do not like pain, we need pain to help us avoid or react to situations that could be a threat. • Pain is a personal strong mental experience and can be modulated at a central level through attention and emotional control. Nociception Slide 9 In our tissues, we have special nerve endings with specific threshold that carry signals that lead to a faster acute feeling of pain (Ad fibres) usually followed by a slower dull throbbing pain (C fibres). This threshold is modulated by local chemical reactions including the release of bradykinin, histamines, serotonin, and prostaglandins. These substances are usually released following tissu injury. They will lower the threshold and protect the injured area from movement or physical contact and favour healing. For example, the degradation of arachidonic acid into prostaglandins by COX1 and COX2 enzymes will cause pain even with slight touch, inflammation, and increase body temperature. Once the injury is healed, the chemicals are not released anymore and the receptors come back to their usual state. So why can we still feel pain 20 weeks after a trauma? Slide 10 Within the spinal cord there are two main regulatory mechanism that will modulate the nociceptive input on its way up to the brain. This modulating mechanism is known as the gate control theory. It means that the way the nociceptive signal can be modulated at the spinal cord level. This is done by regulation from incoming non-nociceptive signals (A alpha fibres), and by the down-regulation that occurs from emotional or cognitive control. Slide 11 To summarise, pain is a perception that normally arises from an initial nociceptive stimuli that can be modulated at three different levels: 1. Free ending fibres threshold can be modulated by the presence of local substances 2. The nociceptive signal can be modulated at the spinal cord 3. The signal can be modulated by the brain before been interpreted as pain Chronicity Slide 12 So if pain is a perception, can we create the illusion of pain? This experience shows that most of us are capable of feeling pain in the absence of a nociceptive stimuli. How does this become possible with chronic pain?

Slide 13 If pain is experienced repeatedly, a phenomenon called sensitisation can occur. To prevent pain, the system uses endogenous opioids. However, the system can become deregulated by increasing both endogenous opioid receptors (MOCs) and their antagonist (AC1). It is like maintaining the speed of a car by increasing the throttle and braking harder at the same time. Spinal cord sensitisation facilitates the perception of pain. This also increases ascending nociceptive signals reaching the brain. Slide 14 The increased nociceptive neural activity creates a highway that now treats most spinal signals from this soma as pain. Pain can arise from normal stimuli that usually should not generate a nociceptive reaction; pain occur in the absence of any lesion. Pain becomes omnipresent and efforts to reduce peripheral nociceptive stimulation become useless. The problem is not injury anymore… Slide 15 MRI structural and molecular imaging have shown chronic pain to affect the same brain regions that are solicited during the placebo effect areas. These are the anterior cingulate cortex, the prefrontal cortex and the insula. 1. There is a reduction in connectivity and white matter as indicated by the reduction in fractional anisotropy (FA). 2. There is a reduction in grey matter as indicated by the decrease in concentration of N-acetyl aspartate (NAA). 3. There is increased difficulties using emotional control to reduce pain given the reduction in the number of opioid receptors. 4. Inflammation suggest possible excitotoxcicity. All these indicate important changes within the cortex and is present in many conditions such as chronic low back pain, fibromyalgia, osteoarthritis, and chronic headache. These changes not only maintain pain but also causes problems with our attention, decision-making, learning and memory. It is a bit like we cannot focus our attention off the pain we are feeling. FA = fractional anisotropy indicates a reduction of diversity of substances within the brain; the diffusion becomes more isotopic. NAA = N-acetyl asparate, a metabolite that is an indicator of neural health and vitality. Slide 16 So what have we learnt so far? Chronic pain affects the central nervous system. Neural plasticity and sensitisation favours nociceptive pathways and induce important changes mainly in the circuit responsible for the emotional control of pain. These changes alone are sufficient to explain why patients cannot get rid of their sensation of pain.