Tag Archives: complex regional pain syndrome physiotherapy

21Jan/12

Central sensitisation is more common than you may think

Clifford Woolf recently said this about central sensitisation:

Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.

And Latremolier

Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. PERSPECTIVE: In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.

In essence we are talking about changes within the central nervous system that underpin the widespread, unpredictable and varied nature of persisting pain.

When I am listening to a patient, observing their movements and performing a ‘multi-system’ examination, I am in part looking for the pain mechanisms at play, including central sensitisation. Several of my questions are: ‘what is going on here to create this experience for the person in front of me?’, ‘why are the nervous and other systems responding in such a way?’ and ‘what is influencing the behaviour of those systems?’. I really need to know what it is that is prolonging this protection and is it really worthwhile for the individual.

Suspecting that there is a component of central sensitisation at play in many cases of chronic pain that I see, it is pleasing to see a group looking at this closely and finding evidence to support this thinking:

J Bone Joint Surg Br. 2011 Apr;93(4):498-502.

Evidence that central sensitisation is present in patients with shoulder impingement syndrome and influences the outcome after surgery.

Gwilym SE, Oag HC, Tracey I, Carr AJ.

Source

Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK. [email protected]

Abstract

Impingement syndrome in the shoulder has generally been considered to be a clinical condition of mechanical origin. However, anomalies exist between the pathology in the subacromial space and the degree of pain experienced. These may be explained by variations in the processing of nociceptive inputs between different patients. We investigated the evidence for augmented pain transmission (central sensitisation) in patients with impingement, and the relationship between pre-operative central sensitisation and the outcomes following arthroscopic subacromial decompression. We recruited 17 patients with unilateral impingement of the shoulder and 17 age- and gender-matched controls, all of whom underwent quantitative sensory testing to detect thresholds for mechanical stimuli, distinctions between sharp and blunt punctate stimuli, and heat pain. Additionally Oxford shoulder scores to assess pain and function, and PainDETECT questionnaires to identify ‘neuropathic’ and referred symptoms were completed. Patients completed these questionnaires pre-operatively and three months post-operatively. A significant proportion of patients awaiting subacromial decompression had referred pain radiating down the arm and had significant hyperalgesia to punctate stimulus of the skin compared with controls (unpaired t-test, p < 0.0001). These are felt to represent peripheral manifestations of augmented central pain processing (central sensitisation). The presence of either hyperalgesia or referred pain pre-operatively resulted in a significantly worse outcome from decompression three months after surgery (unpaired t-test, p = 0.04 and p = 0.005, respectively). These observations confirm the presence of central sensitisation in a proportion of patients with shoulder pain associated with impingement. Also, if patients had relatively high levels of central sensitisation pre-operatively, as indicated by higher levels of punctate hyperalgesia and/or referred pain, the outcome three months after subacromial decompression was significantly worse.

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Treat the brain, treat the pain

Arthritis Rheum. 2009 Sep 15;61(9):1226-34.

Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients.

Gwilym SE, Keltner JR, Warnaby CE, Carr AJ, Chizh B, Chessell I, Tracey I.

Source

University of Oxford, Oxford, UK. [email protected]

Abstract

OBJECTIVE:

The groin pain experienced by patients with hip osteoarthritis (OA) is often accompanied by areas of referred pain and changes in skin sensitivity. We aimed to identify the supraspinal influences that underlie these clinical manifestations that we consider indicative of possible central sensitization.

METHODS:

Twenty patients with hip OA awaiting joint replacement and displaying signs of referred pain were recruited into the study, together with age-matched controls. All subjects completed pain psychology questionnaires and underwent quantitative sensory testing (QST) in their area of referred pain. Twelve of 20 patients and their age- and sex-matched controls underwent functional magnetic resonance imaging (MRI) while the areas of referred pain were stimulated using cold stimuli (12 degrees C) and punctate stimuli (256 mN). The remaining 8 of 20 patients underwent punctate stimulation only.

RESULTS:

Patients were found to have significantly lower threshold perception to punctate stimuli and were hyperalgesic to the noxious punctate stimulus in their areas of referred pain. Functional brain imaging illustrated significantly greater activation in the brainstem of OA patients in response to punctate stimulation of their referred pain areas compared with healthy controls, and the magnitude of this activation positively correlated with the extent of neuropathic-like elements to the patient’s pain, as indicated by the PainDETECT score.

DISCUSSION:

Using psychophysical (QST) and brain imaging methods (functional MRI), we have identified increased activity with the periaqueductal grey matter associated with stimulation of the skin in referred pain areas of patients with hip OA. This offers a central target for analgesia aimed at improving the treatment of this largely peripheral disease.

29Sep/11

Mastering your rehabilitation – Part 1: why exercise & train?

When we sustain an injury or experience a painful condition, our movement changes. In the early stages this can be obvious, for example we would limp having sprained an ankle. Sometimes the limp, medically termed an ‘antalgic gait’, persists without the individual being aware. This is the same for other forms of guarding that is part of the body’s way of protecting itself. By tightening the affected area or posturing in a manner that withdraws, the body is changing the way that we work so that healing can proceed. Clearly this is very intelligent and useful. The problem lies with persisting guarding or protection that continues to operate.

Physiotherapy London

We know that when the brain is co-ordinating a response to a threat, a number of systems are active. This includes the nervous system, the motor system, the immune system and the endocrine system (hormones). This is all part of a defence in and around the location that is perceived to be under threat. It is important to be able to move away from danger and then to limit movement, firstly to escape from the threat (e.g. withdraw your hand from a hot plate) and then to facilitate the natural process of healing by keeping the area relatively immobilised. Interestingly, at this point our beliefs about the pain and injury will determine how we behave and what action we take. If we are concerned that there is a great deal of damage and that movement will cause further injury, we will tend to keep the area very still, looking out for anything or anyone who may harm us. Over-vigilance can lead to over-protection and potentially lengthen the recovery process. This is one reason why seeking early advice and understanding your pain and injury is important, so that you can optimise your potential for recovery.

We have established that we move differently when we are injured and in pain. In more chronic cases, the changes in movement and control of movement can be quite subtle. An experienced physiotherapist will be able to detect these and other protective measures that are being taken. These must be dealt with, because if we are not moving properly, this is a reason for the body to keep on protecting itself through feedback and feed-forward mechanisms. Re-training movement normalises the flow of information to and from the tissues to the brain. Often this process needs enhancement or enrichment as the sensory flow and position sense (proprioception) is not efficient. Movement is vital for tissue and brain health, nourishing the tissues with oxygen and chemicals that stimulate health and growth.

To train normal movement is to learn. The body is learning to move effectively and this process is the same as learning a golf shot, a tennis stroke, a language or a musical instrument. Mastery. You are asking yourself to master normal movement. What does this take? Consistency, discipline, practice (and then some more practice), time, dedication, awareness and more. The second part of this blog will look at mastery as a concept that can help you understand the way in which you can achieve success with your rehabilitation.

19Apr/11
Hands of God & Adam

Complex Regional Pain Syndrome (CRPS/RSD)

Complex regional pain syndrome (CRPS), also known as reflex sympathetic dystrophy (RSD), is undoubtedly a nasty condition in many cases. It can be hugely disruptive in the desire to lead a normal and fulfilling life due the experience of sheer pain and the difficulty in doing day to day activities.

I hear a huge range of stories of how the problem began and how it has been treated. Sometimes there is a significant injury, but often it is the type of event that one would associate with recovery such as an ankle sprain, a knocked elbow or a fracture. Unfortunately in a number of cases this simply does not happen. The injury is sustained, the area usually hurts as you would expect but then it continues to hurt and gets worse. There are associated signs and symptoms such as colour change, temperature change, altered sensation (pins and needles, numbness), an altered sense of position, a feeling of ‘largeness’, ‘thickened’ skin, huge sensitivity to light touch (allodynia), changes in skin, hair and nails. Fortunately we understand much more about the underlying mechanisms and can explain what and why this is happening, giving the problem a meaning which is so important in a condition that is troubling and causing great suffering.

CRPS in the foot and leg causes great difficulty in walking and standing in many cases. If the tissues are stiffened and the control of movement is poor, the ability to walk normally can be severely limited. Add the pain to this scenario and it becomes incredibly disabling at times as the sufferer simply cannot undertake normal activities. In CRPS in the upper limb it is writing, computer use, dressing, holding tools and self-care that are challenged.

Similar to any painful state, determining the pain mechanism(s) is important in deciding where to focus the treatment. Often there can be co-existing mechanisms such as inflammatory pain and neuropathic pain underpinned by different processes and manifesting in different ways. Neuropathic pain is often sharp, lancing, shooting and accompanied by a loss of sensation in the same area that can be confounding until you understand how it works. Inflammatory pain can be provoked by movement and touch with the mechanism being excited sensory nerves (nociceptors) as a result of the release of inflammatory molecules. Nerves themselves can release such chemicals into the tissues (neurogenic inflammation) and thereby keep the process going. There are many other aspects to the pain and the drivers and influences.

As well as elucidating the pain mechanisms, identifying the influences is also very important. This can include stress, fatigue, emotional state, past experience, culture, beliefs in addition to lifestyle factors and general health. Personally I look for risk factors for chronicity with all new assessments so that these can be fealty with swiftly. When a condition has been in existence for a longer period, adapting this to understand behaviours, choices and other factors that could be prolonging the problem is important.

Modern treatment of pain including CRPS should be within a biopsychosocial framework. That means looking at the biological mechanisms, psychology and social factors that are all part of the pain experience and mould the individual perception. In many cases the sufferer needs input from physiotherapy, pain medicine and psychology. Initially educating the patient to develop understanding, reduce fear of the pain and movement and enable effective coping and self-care is key. Desensitising the body with a range of techniques that blend the physical with the cognitive through the application of various stimuli is useful. This could be a paint brush or cotton wool for example. Tactile discrimination and two point discrimination are normal sensory functions that can be altered and according to recent studies are likely to need training. The graded motor imagery programme is part of the treatment, targeting brain changes that can occur. The three stages are laterality, imagined movement and mirror therapy. This is a newer intervention and is demonstrating good results in CRPS and with other nasty pains. The self-care aspects are fundamental. Teaching the patient to manage their activities and to develop consistency through their day is key. Sometimes activities are overdone and there is a trade off. For example standing at a party, but you really want to go and afterwards you know it will hurt but accept that this will be the case. Good flare-up management skills can play a huge role during these times. A further group of interventions I call perceptual exercises. Due to the plastic changes in the sensory and motor cortices, the sense of self, body and movement can feel different in many ways. Working with this through the use of imagery, mindfulness, awareness and other strategies can really help to get back in touch with the body alongside the other techniques. Finally, motor control exercise to normalise movement is very important but to be done at the right time in the right way.

The context of the treatment can affect the success of the strategy. Timing, environment, understanding and belief must all be considered when designing a programme. Newer ideas and research about neuroimmune responses to exercise, movement and thoughts suggest that we need to be mindful of these factors. This is the modern way of looking at the individual, their pain and circumstances to offer practical and effective strategies in improving outcomes and quality of life.

Subsequent blogs will look at the other symptoms, why and how they manifest and the effects of stress upon the body.