Tag Archives: CRPS

15Feb/15
Georgie

CRPS | Georgie’s Story

Georgie suffers with complex regional pain syndrome (CRPS), which is a condition that can feature the most severe and extraordinary pain and symptoms. Soon after starting to work together, Georgie told me that she wanted to raise the awareness of CRPS and chronic pain. For some months we played with ideas, culminating in ‘UP’ — Understanding Pain.

UP has a mission. This is to raise awareness that chronic pain is the largest global health burden and that one of the biggest problems is the lack of understanding of pain. This leads to poor communication about chronic pain, low expectations with regards to overcoming pain, and poor treatment of chronic pain. Our aim is to change this thinking by raising the level of understanding so that people can see that there is a way forward. All too often the label of chronic pain is associated with isolation, hopelessness, disbelief and being discarded with regards to recovery. If only healthcare at large, policy makers, private health insurers and sufferers were aware of the facts about chronic pain based on rigorous research and pain science, than we can go about changing this situation.

This is our purpose:

  • Facts about pain so that everyone understands
  • Practical and effective ways of overcoming pain and living a meaningful life.

Here is Georgie’s story:

‘I suffer from CRPS – Complex Regional Pain Syndrome. CRPS is a chronic systemic disease causing severe pain which scores 42 out of 50 on the McGill pain scale. CRPS has many symptoms including skin colour changes and temperature changes from hot to cold, burning pain, stabbing like pains, numbness, pins and needles to name but a few. It can often start in one limb following an injury or surgery, some cases with no known injury and the disease can spread to other limbs and in some cases throughout the whole body. CRPS has a major impact on day to day life, it is debilitating and has a negative impact physiologically for the patient, their family and friends around them.

My story

When I was young, I was always very athletic. I came first in sprinting, loved horse riding and I was very good at gymnastics. I also had an artistic streak, studying piano, singing and gained honors in grade 8 organ. What I didn’t realise then was that I had hypermobility. This is not necessarily a bad thing as for gymnasts/dancers and musicians/ singers this means you are more flexible, which can be an advantage. But it can sometimes trigger other underlying possible conditions. I was not aware of my hypermobility until recently and it now explains so much about my life.

Once I left school, it took me a while to know what I wanted to do, I was an office junior, a travel agent, and then I went to Australia for what was supposed to be 12 months on a working travel visa. I travelled from Perth to Sydney by bus taking plenty of stops until I got to Melbourne. One day I woke up in my hostel room and I was unable to see properly. I got myself to hospital and they just told me I wasn’t eating properly which was common in travellers. I then took a 4 day bus to Sydney during this time my sight deteriorated. I then went to hospital in Melbourne and I was told I had Bilateral Papillitis a swelling of the optic nerve and they were not sure what damage it may do to my sight. I am not sure if this is related to my condition but I am not ruling that out. I spent so many hours listening to music and this saw me through my time there, I made a huge life decision and decided to become a singer…what did I have to lose? I wanted to live life to the full. I quickly returned home after being in the hospital for 2 weeks. The cause was never found after a few MRI scans, CAT Scans, Lumber Punches. However the symptoms reduced over 6 months on their own.

I found a college and became a professional singer. Of course, this is not the easiest path but I loved every minute of it. However from around 2002 I started to fall regularly as my ankle would give way, I would recover from one fall then months later have another fall from the weakness in the joint. In 2005 I had a fall that changed my life forever. I had fractured my metatarsal bone and badly sprained my ankle. I spent 4 weeks on crutches and started to realize something was really not right at all. My foot was freezing cold, it was black and purple in color and was highly sensitive to touch. I had drop foot and could not move my foot at all. The pain was unbearable burning, stabbing, shooting pains, pins and needles, numbness. I went back to the hospital who immediately knew something wasn’t right and after some 12 weeks in physio and after more scans I was informed that I had CRPS – Complex Regional Pain Syndrome. The first thing my physio said was don’t read anything on the internet it will just scare you, it will be a long journey and there is no guarantee of a good outcome. I had some treatment in the Surrey hospital undergoing a 
Guanethidine Block under sedation. Then my treatment was moved to St Mary’s in Paddington under the care of Dr Jenner.

I had many Guanethidine Blocks every 2 weeks nearly, but these were so traumatic for me that after a year I was unable to take any more treatment – my body was too week and after the last procedure the doctors found it too difficult to wake me up. I was on a cocktail of tablets to ease the pain. But I had no life left. I couldn’t work, I was on crutches or wheelchair bound for 3 years and my life felt completely hopeless. Depression started to set in, it felt like the darkest and most lonely place. Many of my friends were unable to understand and completely unable to help me, I lost a few friends along the way. CRPS is completely isolating, its an evil disease and its not called “The Suicide disease” for nothing as many people give up the fight. If pain is all you feel what else is there? But I had so much to live for and I am a fighter. I loved music and in those times of darkness it saw me though.

One day I started to write music again I don’t even know what inspired me, I just picked up my pen and started to write. I thought I had lost all of my passion, but there it was again still inside somewhere and I’m so glad I found it again. I wrote every day and I still do to this day. The music, singing and writing kept me occupied and in some brief moments made me forget the pain as my mind was busy creating. The music gave me hope back, if I could bring back passion, what else could I achieve? So I decided I was going to work at trying to walk to my kitchen and back to the sofa – now in actual fact this is only a few steps these days, but back then it took me a really long time, shuffling and holding on to everything I could find to hold me up, hopping, but I made it there. Now all I had to do was get back to the sofa with a cup of tea, this I hadn’t quite thought through and by the time I made it back to the sofa most of the tea was on the floor. I suffered a flare up after this attempt but I decided not to give up and little by little I found a way to make this small journey. Once I had achieved this, I started to make longer journeys to the bathroom and I even attempted the stairs. Going out without crutches was really scary, after 6 months I thought now is my time to try. Every week my friend Pete would pick me up for a jazz gig. He knocked on the door and I was stood there without my crutches, he asked me “Where’s your crutches” and I said “look…” I walked myself to his car (only a few feet away) with no aids. He started to cry. He said he couldn’t believe it and he was so proud of me. Pete is such a loyal and close friend he was there for me in some of my darkest times. From there I decided I had to try more and I wanted to find more to do in music. I saw an ad for Rock Choir leaders and I went for an audition, I tried to hide my limp and I got the job! (although, now that I know the Rock Choir team, I shouldn’t have been so worried about my limp). It was one of the happiest days of my life and I have never looked back.

When I started Rock Choir 5 years ago I ran 6 choirs. Before I started the job I was never sure how my body would cope – but it did and slowly I got used to my schedule and I loved every second of it, from training to rehearsals and shows. The adrenaline for me was the best part of it as it helped cover the pain I had and the music was so uplifting it always made me happy and lifted my spirits, I had never been happier. I was writing more than ever and started my own original band The Big Bads! Then just over a year ago my CRPS spread up my leg and into my arm and hand. This was devastating as it made it so much harder to play piano and do the one thing I love so much, conducting my choirs and getting to all my rehearsals and writing. I quickly realized that I would have to give up my morning choirs so that my body could recover and so that the CRPS would not spread to other limbs. I found it so hard to adapt and I felt so very low. It felt like all that I had fought so hard to have back could just be taken from me again.
I went back to my consultant who put me in touch with Richmond Stace, a specialist pain physiotherapist, to help me overcome the spread of the condition. He explained the condition so that I understood my role and what I could achieve, and taught me techniques including mindfulness, breathing, motor imagery and specific exercises. We talk about how I will get through some of my conducting, right down to visualizing and practicing the moves before I see my choir. I use nourishing techniques and try to remember to pace myself and move every so often into a different position. We talk though the schedule I have coming up and how best to manage it and every time I start to have a flare up we nip it in the bud before it develops. This year will be the first year in 10 years that I have not had a major flare up that has lasted longer than a couple of weeks!

I can see a future now; a future that means I can deal with the condition I have and co- exist with it. I would like to help others now to regain their lives from pain. I know how hard it is, but if I told you it was possible would you try too? I don’t want people to give up. There has to be a better way and if we can help more people find their path through the pain by understanding their symptoms, using music and techniques that work such as mindfulness, imagery, graded exercise, then that would make me even happier!

28Oct/14
CRPS Clinics | London & New Malden

Intense pain after wrist fracture — predicting CRPS

CRPS Clinics | London & New MaldenA recent study concluded that “… excessive baseline pain in the week after wrist fracture greatly elevates the risk of developing CRPS. Clinicians can consider a rating of greater than 5/10 to the question “What is your average pain over the last 2 days?” to be a “red flag” for CRPS”.

Most of what we need to know as clinicians comes from what the patient says. I have written previously about the importance of the narrative and taking heed. It appears from this study that paying attention to the early levels of pain after a wrist fracture can indicate a risk for developing complex regional pain syndrome.

Pain is poorly understood, especially more complex and persisting pain. Raising the level of pain understanding is fundamental to its treatment and for sufferers to overcome their problems. In knowing that intense pain (more than 5/10) could be a sign that CRPS is developing, the right action can be taken early and thereby prevent the condition evolving uncontrollably.

Of course the intensity of pain is but one dimension and clinicians should observe other characteristics of protection to design a comprehensive rehabilitation programme — e.g. inflammatory signs, posturing, behaviours and language to name but a few; this in the name of tackling the problem of pain more efficiently and successfully.

CRPS clinic in London — call us now to start your comprehensive treatment and training programme 07518 445493

 

 

20Oct/14
CRPS Clinics | London & New Malden

Complex Regional Pain Syndrome Update | #CRPS October 2014

CRPS Clinics | London & New MaldenWelcome to the latest review of complex regional pain syndrome research.

Eur J Pain. 2014 Oct 16
Optokinetic stimulation increases limb pain and forehead hyperalgesia in complex regional pain syndrome.
Knudsen LF, Drummond PD.

Abstract
BACKGROUND:
Ambiguous visual stimuli increase limb pain in patients with complex regional pain syndrome (CRPS), possibly due to afferent sensory feedback conflicts. Conflicting sensory stimuli can also generate unpleasant sensations in healthy people such as during motion sickness. We wanted to investigate the mechanisms underlying the link between sensory conflicts and pain in CRPS using optokinetic stimulation (OKS) – a method known to induce motion sickness.
METHODS:
Twenty-one CRPS patients underwent OKS and rated symptoms of motion sickness. Patients also rated limb pain and pain-related distress before, during and after OKS. In addition, pressure-pain and sharpness sensations were investigated on both sides of the forehead and in the affected and contralateral limb before and after OKS.
RESULTS:
Limb pain and forehead hyperalgesia to pressure increased in parallel in response to OKS. In a subgroup of nauseated patients who withdrew early from OKS, hyperalgesia to pressure in the ipsilateral forehead persisted longer than in the remaining participants. Sharpness sensations remained constant at all sites.
CONCLUSIONS:
Sensory conflicts may facilitate pain in CRPS by activating the mechanisms of general facilitation of nociception and, during more severe sensory conflicts, also a facilitatory mechanism that operates mainly ipsilateral to the affected limb.

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Clin J Pain. 2014 Apr;30(4):301-6.
A disturbance in sensory processing on the affected side of the body increases limb pain in complex regional pain syndrome.
Drummond PD, Finch PM.

Abstract
OBJECTIVES:
The aim of this study was to determine whether a central disturbance in somatosensory processing contributes to limb pain in complex regional pain syndrome (CRPS).
METHODS:
In 37 patients with CRPS, the effect of cooling the ipsilateral forehead on pain in the affected limb was compared with the effect of cooling the contralateral forehead. In addition, symptoms associated with cold-evoked limb pain were explored.
RESULTS:
Limb pain generally increased when the ipsilateral side of the forehead was cooled but did not change when the contralateral side of the forehead was cooled. Increases were greatest in patients with heightened sensitivity to cold, brushing, and pressure-pain in the ipsilateral forehead, in patients with heightened sensitivity to pressure-pain in the limbs, and in patients with chronic symptoms. In contrast, sensitivity to light touch was diminished in the CRPS-affected limb of patients whose limb pain remained unchanged or decreased during ipsilateral forehead cooling.
CONCLUSIONS:
These preliminary findings suggest that a central disturbance in sensory processing and pain modulation, which extends beyond the affected limb to the ipsilateral forehead, contributes to symptoms in a subgroup of patients with CRPS.

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Arch Orthop Trauma Surg. 2014 Oct 14.
Factors associated with complex regional pain syndrome type I in patients with surgically treated distal radius fracture.
Roh YH1, Lee BK, Noh JH, Baek JR, Oh JH, Gong HS, Baek GH.

Abstract
PURPOSE:
Wrist fracture is considered a typical initiating trauma for complex regional pain syndrome type I (CRPS I). However, few studies have comprehensively evaluated factors associated with the occurrence of CRPS I after the surgical treatment of a distal radius fracture (DRF). This study evaluates the factors influencing the occurrence of CRPS I after the surgical treatment of a DRF.
METHODS:
A total of 477 patients with a DRF who had been treated surgically were enrolled in this prospective observational study. Patients were followed for 6 months after surgery, and CRPS I was diagnosed using the Budapest diagnostic criteria for research. The factors assessed for the development of CPRS I were age, gender, the body mass index, the type of fracture, the energy of trauma, the number of trial reductions, the type of surgery, and the duration of immobilization. A multivariate logistic regression analysis was conducted to identify independent predictors of the occurrence of CRPS I.
RESULTS:
Among the 477 patients, 42 (8.8 %) satisfied the Budapest criteria for CRPS I within 6 months of surgery. Female patients developed CRPS I more frequently, and the patients who developed CRPS I were older and more likely to sustain a high energy injury or have a comminuted fracture. According to the multivariate analysis, female patients and those with a high energy trauma or severe fracture type were significantly more likely to develop CRPS I (p = 0.02, 0.01, and 0.01, respectively).
CONCLUSIONS:
High energy injuries, severe fractures, and the female gender contribute to the development of CRPS I after the surgical treatment of DRF. The results have important implications for physicians who wish to identify patients at high risk for CRPS I after operative fixation for DRF and instigate treatment accordingly.

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J Pain. 2014 Jan;15(1):16-23
Intense pain soon after wrist fracture strongly predicts who will develop complex regional pain syndrome: prospective cohort study.
Moseley GL1, Herbert RD2, Parsons T3, Lucas S3, Van Hilten JJ4, Marinus J5.

Abstract
Complex regional pain syndrome (CRPS) is a distressing and difficult-to-treat complication of wrist fracture. Estimates of the incidence of CRPS after wrist fracture vary greatly. It is not currently possible to identify who will go on to develop CRPS after wrist fracture. In this prospective cohort study, a nearly consecutive sample of 1,549 patients presenting with wrist fracture to 1 of 3 hospital-based fracture clinics and managed nonsurgically was assessed within 1 week of fracture and followed up 4 months later. Established criteria were used to diagnose CRPS. The incidence of CRPS in the 4 months after wrist fracture was 3.8% (95% confidence interval = 2.9-4.8%). A prediction model based on 4 clinical assessments (pain, reaction time, dysynchiria, and swelling) discriminated well between patients who would and would not subsequently develop CRPS (c index .99). A simple assessment of pain intensity (0-10 numerical rating scale) provided nearly the same level of discrimination (c index .98). One in 26 patients develops CRPS within 4 months of nonsurgically managed wrist fracture. A pain score of ≥5 in the first week after fracture should be considered a “red flag” for CRPS.
PERSPECTIVE:
This study shows that excessive baseline pain in the week after wrist fracture greatly elevates the risk of developing CRPS. Clinicians can consider a rating of greater than 5/10 to the question “What is your average pain over the last 2 days?” to be a “red flag” for CRPS.

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Suffering with Complex Regional Pain Syndrome (CRPS aka RSD)? Have a patient with CRPS?

Call now to begin a comprehensive treatment, training and mentoring programme designed specifically for CRPS: 07518 445493 

02Oct/14
Pain is a whole person experience

CRPS Research Update | October 2014 #CRPS

Physiotherapy LondonWelcome to the Complex Regional Pain Syndrome Research Update for October, a summary of the latest studies. 

If you are suffering with CRPS, I am here to show you how you can move forward — come and visit the CRPS clinic page here.

Spinal cord stimulation for complex regional pain syndrome type 1 with dystonia: a case report and discussion of the literature.
Voet C1, le Polain de Waroux B2, Forget P2, Deumens R3, Masquelier E4.

Abstract
BACKGROUND:
Complex Regional Pain Syndrome type 1 (CRPS-1) is a debilitating chronic pain disorder, the physiopathology of which can lead to dystonia associated with changes in the autonomic, central and peripheral nervous system. An interdisciplinary approach (pharmacological, interventional and psychological therapies in conjunction with a rehabilitation pathway) is central to progress towards pain reduction and restoration of function.
AIM:
This case report aims to stimulate reflection and development of mechanism-based therapeutic strategies concerning CRPS associated with dystonia.
CASE DESCRIPTION:
A 31 year old female CRPS-1 patient presented with dystonia of the right foot following ligamentoplasty for chronic ankle instability. She did not have a satisfactory response to the usual therapies. Multiple anesthetic blocks (popliteal, epidural and intrathecal) were not associated with significant anesthesia and analgesia. Mobilization of the foot by a physiotherapist was not possible. A multidisciplinary approach with psychological support, physiotherapy and spinal cord stimulation (SCS) brought pain relief, rehabilitation and improvement in the quality of life.
CONCLUSION:
The present case report demonstrates the occurrence of multilevel (peripheral and central) pathological modifications in the nervous system of a CRPS-1 patient with dystonia. This conclusion is based on the patient’s pain being resistant to anesthetic blocks at different levels and the favourable, at least initially, response to SCS. The importance of the bio-psycho-social model is also suggested, permitting behavioural change

RS: With CRPS we absolutely need to consider ‘multilevel’ modifications and adaptations within the nervous system but also how all the other systems that have a role in protecting us are functioning. This often manifests as habitual thinking and activities that maintain protection. Realising these habits, automatic by the nature of being a habit, and making changes with specific training creates new patterns of activity that head towards health.

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Longstanding Complex Regional Pain Syndrome is associated with activating autoantibodies against α-1a adrenoceptors.
Dubuis E1, Thompson V2, Leite MI3, Blaes F4, Maihöfner C5, Greensmith D6, Vincent A7, Shenker N8, Kuttikat A9, Leuwer M10, Goebel A11.

Abstract
Complex Regional Pain Syndrome (CRPS) is a limb-confined post-traumatic pain syndrome with sympathetic features. The cause is unknown, but the results of a randomized crossover trial on low-dose IVIG treatment point to a possible autoimmune mechanism. We tested purified serum immunoglobulin G (IgG) from patients with longstanding CRPS for evidence of antibodies interacting with autonomic receptors on adult primary cardiomyocytes, comparing with control IgG from healthy and disease controls, and related the results to the clinical response to treatment with low-dose intravenous immunoglobulins (IvIG). We simultaneously recorded both single cell contractions and intracellular calcium handling in an electrical field. Ten of 18 CRPS preparations and only 1/57 control preparations (p<0.0001) increased the sensitivity of the myocytes to the electric field and this effect was abrogated by pre-incubation with alpha1a receptor blockers. By contrast, effects on baseline calcium were blocked by pre-incubation with atropine. Interestingly, serum-IgG preparations from all four CRPS patients who had responded to low-dose IVIG with meaningful pain relief were effective in these assays, although 4/8 of the non-responders were also active. To see if there were antibodies to the alpha1a receptor, CRPS-IgG was applied to alpha 1a receptor transfected rat1-fibroblast cells. The CRPS serum IgG induced calcium flux, and FACS showed that there was serum IgG binding to the cells. The results suggest that patients with longstanding CRPS have serum antibodies to alpha 1a receptors, and that measurement of these antibodies may be useful in the diagnosis and management of the patients.

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A CRPS-IgG-transfer-trauma model reproducing inflammatory and positive sensory signs associated with complex regional pain syndrome.
Tékus V1, Hajna Z1, Borbély É1, Markovics A1, Bagoly T1, Szolcsányi J2, Thompson V3, Kemény Á1, Helyes Z2, Goebel A4.

Abstract
The aetiology of complex regional pain syndrome (CRPS), a highly painful, usually post-traumatic condition affecting the limbs, is unknown, but recent results have suggested an autoimmune contribution. To confirm a role for pathogenic autoantibodies, we established a passive-transfer trauma model. Prior to undergoing incision of hind limb plantar skin and muscle, mice were injected either with serum IgG obtained from chronic CRPS patients or matched healthy volunteers, or with saline. Unilateral hind limb plantar skin and muscle incision was performed to induce typical, mild tissue injury. Mechanical hyperalgesia, paw swelling, heat and cold sensitivity, weight-bearing ability, locomotor activity, motor coordination, paw temperature, and body weight were investigated for 8days. After sacrifice, proinflammatory sensory neuropeptides and cytokines were measured in paw tissues. CRPS patient IgG treatment significantly increased hind limb mechanical hyperalgesia and oedema in the incised paw compared with IgG from healthy subjects or saline. Plantar incision induced a remarkable elevation of substance P immunoreactivity on day 8, which was significantly increased by CRPS-IgG. In this IgG-transfer-trauma model for CRPS, serum IgG from chronic CRPS patients induced clinical and laboratory features resembling the human disease. These results support the hypothesis that autoantibodies may contribute to the pathophysiology of CRPS, and that autoantibody-removing therapies may be effective treatments for long-standing CRPS.

RS – as ever we must consider the role of the immune system but in the light of other systems as no system works in isolation to the others. There is vast interaction between the immune system, nervous system, endocrine system and autonomic nervous system to the point where I believe we are a single system interpreting and responding. One response maybe pain as part of protection and our systems become very good at protecting us — this is not to suggest that our systems and ‘me’ are separate entities. Whole person is the only way we can sensibly think about this.

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Local Anesthetic Sympathectomy Restores fMRI Cortical Maps in CRPS I after Upper Extremity Stellate Blockade: A Prospective Case Study.
Stude P, Enax-Krumova EK1, Lenz M, Lissek S, Nicolas V, Peters S, Westermann A, Tegenthoff M, Maier C.

Abstract
BACKGROUND:
Patients with complex regional pain syndrome type I (CRPS I) show a cortical reorganization with contralateral shrinkage of cortical maps in S1. The relevance of pain and disuse for the development and the maintenance of this shrinkage is unclear.
OBJECTIVE:
Aim of the study was to assess whether short-term pain relief induces changes in the cortical representation of the affected hand in patients with CRPS type I.
STUDY DESIGN:
Case series analysis of prospectively collected data.
METHODS:
We enrolled a case series of 5 consecutive patients with CRPS type I (disease duration 3 – 36 months) of the non-dominant upper-limb and previously diagnosed sympathetically maintained pain (SMP) by reduction of the pain intensity of more than > 30% after prior diagnostic sympathetic block. We performed fMRI for analysis of the cortical representation of the affected hand immediately before as well as one hour after isolated sympathetic block of the stellate ganglion on the affected side.
STATISTICS:
Wilcoxon-Test, paired t-test, P < 0.05.
RESULTS:
Pain decrease after isolated sympathetic block (pain intensity on the numerical rating scale (0 – 10) before block: 6.8 ± 1.9, afterwards: 3.8 ± 1.3) was accompanied by an increase in the blood oxygenation level dependent (BOLD) response of cortical representational maps only of the affected hand which had been reduced before the block, despite the fact that clinical and neurophysiological assessment revealed no changes in the sensorimotor function.
LIMITATIONS:
The interpretation of the present results is partly limited due to the small number of included patients and the missing control group with placebo injection.
CONCLUSIONS:
The association between recovery of the cortical representation and pain relief supports the hypothesis that pain could be a relevant factor for changes of somatosensory cortical maps in CRPS, and that these are rapidly reversible

RS – we are either in pain or not in pain. If our focus is elsewhere and we are not experiencing pain, then we are not in pain. Whilst this may sound obvious, many people tell me that they are in pain all of the time. When I ask about times that they feel no pain, an oft given answer is that the pain is hidden at times when they do not feel it. Pain cannot hide. It is on-off, binary. At any given moment, we are either in pain or not in pain. Every moment changes and hence pain can change in a moment — referring to the rapidly reversible change in maps in this article; and why wouldn’t we have the ability to rapidly adapt? I believe we can change and it happens in a moment — our thinking, actions and experiences. Consider how we can be happy in a moment, and sad in a moment. Happiness is a feeling, pain is a feeling. Both have a purpose, to motivate us to do something or think in a particular way. There is a desperate need to change the globe’s thinking on pain, this being my main purpose. In doing so, we can alleviate a vast amount of suffering from pain, narrowing it down the pain that we need for survival and eliminating the pain that persists for no good reason.

28Sep/14
CRPS Clinics | London & New Malden

CRPS – the narrative holds the clues |#CRPS

CRPS Clinics | London & New MaldenThe story told by the patient with CRPS provides insight into their suffering, characterised and brought to life by their chosen language, body posturing, body language, and changing facial expressions. The priming for a condition frequently arises months or years before from an illness, a stressful event, a previous injury or painful event. The way in which the body systems respond to the prior challenge creates a learning experience so that when the body is faced with another similar threat, the responses swiftly kick in. In CRPS this can be with absolute gusto as the level of protection reaches the stratosphere in many cases.

One of the common problems in CRPS is an altered sense of the body, particularly where the condition manifests but this can extend to that whole side of the body. Careful testing of movement precision and sensation identifies these changes as does questioning about clumsiness and the feel of the body. The feel of the body has a substrate in at least the sensory cortex — neurons + immune cells and their neurotransmitters and cytokines.

On questioning, people will volunteer that the limb feels detached, as if it does not belong to them, the sense of size changes and that it does not do what they demand. This is vital information as this identifies a key feature of CRPS (and other pain problems) that must be addressed with understanding and specific training. It is highly unlikely that pain will improve until body sense and precision improves.

So, as a patient you should always explain this feeling, strange (and scary) as it may appear, and as a clinician you should always ask.

London CRPS clinic with Richmond Stace — call now to book your first appointment 07932 689081

28Jul/14
CRPS Specialist Clinics in London

CRPS Bugle | July 2014 | #CRPS

Dear Readers,

Welcome to the July 2014 CRPS Bugle, your research update for complex regional pain syndrome.

Immobilization contributes to exaggerated neuropeptide signaling, inflammatory changes, and nociceptive sensitization after fracture in rats — Guo TZ1, Wei T1, Li WW2, Li XQ3, Clark JD3, Kingery WS4.

J Pain. 2014 Jul 22. pii: S1526-5900(14)00817-7.

Abstract
A tibia fracture cast immobilized for 4 weeks can induce exaggerated substance P (SP) and CGRP signaling and neuropeptide-dependent nociceptive and inflammatory changes in the hindlimbs of rats similar to those seen in complex regional pain syndrome (CRPS). Four weeks of hindlimb cast immobilization can also induce nociceptive and vascular changes resembling CRPS. To test our hypothesis that immobilization alone could cause exaggerated neuropeptide signaling and inflammatory changes we tested 5 cohorts of rats; 1) controls, 2) tibia fracture and hindlimb casted, 3) hindlimb casted, no fracture, 4) tibia fracture with intrameduallary pinning, no cast, and 5) tibia fracture with intrameduallary pinning and hindlimb casting. After 4 weeks the casts were removed and hindlimb allodynia, unweighting, warmth, edema, sciatic nerve neuropeptide content, cutaneous and spinal cord inflammatory mediator levels, and spinal c-Fos activation were measured. After fracture with casting there was allodynia, unweighting, warmth, edema, increased sciatic nerve SP and CGRP, increased skin NK1 receptors and keratinocyte proliferation, increased in inflammatory mediator expression in the hindpaw skin (TNF-α, IL-1β, IL-6, NGF) and cord (IL-1β, NGF), and increased spinal c-Fos activation. These same changes were observed after cast immobilization alone, except spinal IL-1β levels were not increased. Treating cast only rats with an NK1 receptor antagonist inhibited development of nociceptive and inflammatory changes. Four weeks after fracture with pinning all nociceptive and vascular changes had resolved and there were no increases in neuropeptide signaling or inflammatory mediator expression.
PERSPECTIVE:
Collectively, these data indicate that immobilization alone increased neuropeptide signaling and caused nociceptive and inflammatory changes similar to those observed after tibia fracture and casting, and that early mobilization after fracture with pinning inhibited these changes. Early limb mobilization after fracture may prevent the development of CRPS.

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Heart Rate Autonomic Regulation System at Rest and During Paced Breathing among Patients with CRPS as Compared to Age-Matched Healthy Controls — Bartur G1, Vatine JJ, Raphaely-Beer N, Peleg S, Katz-Leurer M.

Pain Med. 2014 Jul 24. doi: 10.1111/pme.12449.

Abstract
OBJECTIVE:
The objective of this study is to assess the autonomic nerve heart rate regulation system at rest and its immediate response to paced breathing among patients with complex regional pain syndrome (CRPS) as compared with age-matched healthy controls.
SUBJECTS:
Ten patients with CRPS and 10 age- and sex-matched controls.
METHODS:
Participants underwent Holter ECG (NorthEast Monitoring, Inc., Maynard, MA, USA) recording during rest and biofeedback-paced breathing session. Heart rate variability (HRV), time, and frequency measures were assessed.
RESULTS:
HRV and time domain values were significantly lower at rest among patients with CRPS as compared with controls. A significant association was noted between pain rank and HRV frequency measures at rest and during paced breathing; although both groups reduced breathing rate significantly during paced breathing, HRV time domain parameters increased only among the control group.
CONCLUSIONS:
The increased heart rate and decreased HRV at rest in patients with CRPS suggest a general autonomic imbalance. The inability of the patients to increase HRV time domain values during paced breathing may suggest that these patients have sustained stress response with minimal changeability in response to slow-paced breathing stimuli.

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Pathological mechanism of musculoskeletal manifestations associated with CRPS type II. An animal study — Ota H1, Arai T2, Iwatsuki K2, Urano H2, Kurahashi T2, Kato S2, Yamamoto M2, Hirata H2.

Pain. 2014 Jul 9. pii: S0304-3959(14)00305-4. doi: 10.1016/j.pain.2014.06.016.

Abstract
Patients with complex regional pain syndrome (CRPS) often complain of abnormal sensations beyond the affected body part, but causes of this spread of musculoskeletal manifestations into contiguous areas remain unclear. In addition, immobilization can predispose to the development of CRPS. We examined functional, biochemical, and histological alterations in affected parts, including contiguous zones, using an animal model. Ten-week-old male Wistar rats were assigned to 5 groups: a normal group receiving no treatment; a sham operation group with surgical exploration; an immobilization group with surgical exploration plus internal knee joint immobilization; a surgical neuropathy group prepared by spinal nerve ligation (SNL) of the left L5 nerve root; and a surgical neuropathy + immobilization group with simultaneous SNL and knee joint immobilization. Mechanical allodynia and knee contracture were compared between groups, and tissues were harvested for histological assessments and gene and protein expression analyses. Neither surgical procedures nor immobilization induced detectable mechanical sensitivity. However, the addition of nerve injury resulted in detectable mechanical allodynia and immobilization not only accelerated hyperalgesia, but also resulted in muscle fibrosis. Nerve growth factor (NGF) and other mediators of neurogenic inflammation were highly expressed not only in denervated muscles, but also in innervated muscles in contiguous areas, suggesting the spread of NGF production beyond the myotome of the injured nerve. Transforming growth factor β was involved in the development of contracture in CRPS. These findings imply that neuroinflammatory components play major roles in the progression and dispersion of both sensory and pathologies and that are exacerbated by immobilization.

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Med Sci Monit. 2014 Jun 25;20:1067-77. doi: 10.12659/MSM.890702.

Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part I) — Wang F1, Stefano GB2, Kream RM2.

Abstract
DRG is of importance in relaying painful stimulation to the higher pain centers and therefore could be a crucial target for early intervention aimed at suppressing primary afferent stimulation. Complex regional pain syndrome (CRPS) is a common pain condition with an unknown etiology. Recently added new information enriches our understanding of CRPS pathophysiology. Researches on genetics, biogenic amines, neurotransmitters, and mechanisms of pain modulation, central sensitization, and autonomic functions in CRPS revealed various abnormalities indicating that multiple factors and mechanisms are involved in the pathogenesis of CRPS. Epigenetics refers to mitotically and meiotically heritable changes in gene expression that do not affect the DNA sequence. As epigenetic modifications potentially play an important role in inflammatory cytokine metabolism, neurotransmitter responsiveness, and analgesic sensitivity, they are likely key factors in the development of chronic pain. In this dyad review series, we systematically examine the nerve injury-related changes in the neurological system and their contribution to CRPS. In this part, we first reviewed and summarized the role of neural sensitization in DRG neurons in performing function in the context of pain processing. Particular emphasis is placed on the cellular and molecular changes after nerve injury as well as different models of inflammatory and neuropathic pain. These were considered as the potential molecular bases that underlie nerve injury-associated pathogenesis of CRPS.

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Cyberpsychol Behav Soc Netw. 2014 Jun;17(6):366-70. doi: 10.1089/cyber.2014.0046.

Application of virtual body swapping to patients with complex regional pain syndrome: a pilot study — Jeon B1, Cho S, Lee JH.

Abstract
This study aimed to apply virtual body swapping through mental rehearsal for patients with complex regional pain syndrome (CRPS) and to investigate whether it is applicable to them. Ten patients who met the diagnostic criterion for CRPS type 1 were randomly assigned to either the treatment or control group. All participants were asked to watch the virtual body swapping training video clip with a head mounted display. The treatment group was additionally asked to assume a posture similar to the body on the screen and rehearse the movements mentally, as if the body presented on the screen was their body. No difference between the groups was found for pain intensity, however, the treatment group showed significantly more improvement in body perception disturbance (BPD) after the treatment than the control group. Even if the presented study is a preliminary one, the above results suggest that virtual body swapping through mental rehearsal is applicable for patients with CRPS and may be useful for improving BPD. The limitations of the study and the future investigations needed to provide clearer clinical suggestions are presented and discussed.

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Pain. 2014 Aug;155(8):1527-39. doi: 10.1016/j.pain.2014.04.029. Epub 2014 Apr 30.

Functional significance of macrophage-derived exosomes in inflammation and pain — McDonald MK1, Tian Y1, Qureshi RA2, Gormley M3, Ertel A4, Gao R1, Aradillas Lopez E5, Alexander GM5, Sacan A2, Fortina P6, Ajit SK7.

Abstract
Exosomes, secreted microvesicles transporting microRNAs (miRNAs), mRNAs, and proteins through bodily fluids, facilitate intercellular communication and elicit immune responses. Exosomal contents vary, depending on the source and the physiological conditions of cells, and can provide insights into how cells and systems cope with physiological perturbations. Previous analysis of circulating miRNAs in patients with complex regional pain syndrome (CRPS), a debilitating chronic pain disorder, revealed a subset of miRNAs in whole blood that are altered in the disease. To determine functional consequences of alterations in exosomal biomolecules in inflammation and pain, we investigated exosome-mediated information transfer in vitro, in a rodent model of inflammatory pain, and in exosomes from patients with CRPS. Mouse macrophage cells stimulated with lipopolysaccharides secrete exosomes containing elevated levels of cytokines and miRNAs that mediate inflammation. Transcriptome sequencing of exosomal RNA revealed global alterations in both innate and adaptive immune pathways. Exosomes from lipopolysaccharide-stimulated cells were sufficient to cause nuclear factor-κB activation in naive cells, indicating functionality in recipient cells. A single injection of exosomes attenuated thermal hyperalgesia in a murine model of inflammatory pain, suggesting an immunoprotective role for macrophage-derived exosomes. Macrophage-derived exosomes carry a protective signature that is altered when secreting cells are exposed to an inflammatory stimulus. We also show that circulating miRNAs altered in patients with complex regional pain syndrome are trafficked by exosomes. With their systemic signaling capabilities, exosomes can induce pleiotropic effects potentially mediating the multifactorial pathology underlying chronic pain, and should be explored for their therapeutic utility.

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CRPS sufferer? Come and see us at our specialist clinics in London in Harley Street and Chelsea — 07932 689081

Specialist Pain Physio Clinics in London for chronic pain, complex regional pain syndrome, back pain, sports injuries (persisting and recurring), repetitive strain injury, IBS, migraine, and other persisting pain problems.

27Jan/14
Pain is a whole person experience

Where do we tackle pain?

Where does pain come from?

Where does pain come from?

When someone tells you that they have a painful knee, it makes sense to have a look at the joint to see what has gone wrong. Perhaps an x-ray or a scan would help to determine the state of the cartilage, bone and surrounding soft tissue. An assessment of the range of motion, motor control and the responses to sensory testing reveal any functional limitations and adaptations. Is this enough to truly understand where pain really sits? Is it enough to decide where to intervene? In some cases yes is the answer, but not always!

Important that this kind of evaluation maybe, we must consider the significant pile of literature that points out pain is not an accurate indicator of tissue damage, as so eloquently concluded by Lorimer Moseley. One has only to think about phantom limb pain to realise that there is no need to have an arm, or a leg, or indeed any body part, for there to be pain in that location.

Phantom limb painPhantom limb pain is the condition that illustrates the concept that pain is allocated a space. This space could be the knee as in our example above, any other body region or regions, or even outside of the body. A study by Lorimer Moseley also suggested that pain is felt in a space and not within the tissues. Subjects were asked to cross their arms, placing the affected hand into the space usually occupied by the unaffected hand. The effect? Pain relief. This is of course one study, however there was an impact that needs to be further investigated. Assuming that pain is allocated a space, this would explain why, when you position the hand in that of the non-painful side, both the pain and movement quality improve.

This is easily tested in the clinic with both hands and feet. The demonstration is a potent one for the individual as their limb experience can change. Seemingly there is an ease of the tension and guarding as well as the sensitivity. It can be profound, especially when someone has been suffering with a nasty pain such as in complex regional pain syndrome (CRPS) or neuropathic pain. The caveat is that this is not a cure, and it does not work every time, however in those that the effect is apparent, the ability to move more normally promotes healthy tissue and perception by the brain, especially if you are looking at the movement — extra sensory feedback via the visual system.

In summary, as best we know, pain is allocated a space. This can be a space that is occupied by a body region that why we feel pain in the tissues, the place where the pain emerges. The actual location of the pain is determined by the brain as it decides where we need to attend for protection. Recall that pain is a protective device involving a widespread network of neurons within the brain. There is no higher pain centre, but rather a network that monitors the sensory situation and responds as needed. On the basis that the sensory feedback suggests something dangerous is happening, the network will create an output that we experience in the body via a space that is deemed to need protection. Unfortunately, this output can occur without sensory input in some cases of persisting pain as the neuroimmune system becomes very sensitised and responsive to a range of stimuli including those that are not actually dangerous, hence why normal activities can hurt.

On this basis, when considering where to treat pain, we have to consider the space where the brain feels we need protecting. With the emergent property that is pain, the sensation is at the end of a process and it is therefore wise to target the entire biology from top to bottom and bottom to top. This means we need to address the higher centres, for example developing the individual’s understanding of their pain, reducing fears and using strategies for the brain maps of the body concurrent with using techniques within the space, i.e. the body area where the pain is felt.

For more about our comprehensive treatment and training programmes for persisting pain and injury, call us on 07932 689081 to make an appointment. Clinics in London & Surrey.

 

01Jul/13
CRPS Bugle

Complex Regional Pain Syndrome | Diagnosis using the Budapest Criteria

The Budapest Criteria should now be used to diagnose Complex Regional Pain Syndrome (CRPS):

A: The patient has continuing pain which is disproportionate to the inciting event

B: The patient has at least one sign in two or more of the categories

C: The patient reports at least one symptom in three or more of the categories

D: No other diagnosis can better explain the signs and symptoms

Sensory: Allodynia (to light touch and/or temperature sensation and/or deep somatic pressure and/or joint movement) and/or hyperalgesia (to pinprick)

Vasomotor: Temperature asymmetry (more than 1 deg.) and/or skin colour changes and/or skin colour asymmetry

Sudomotor/oedema: Oedema and/or sweating changes and/or sweating asymmetry

Motor/trophic: Decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair/nail/skin)

Signs – see or feel a problem

Symptoms – patient reports a problem

Click here for The CRPS Concise Guide on the Royal College of Physicians website

If you have been diagnosed or think that you may have CRPS, contact us for information or to book an appointment to start your specialist treatment and training programme; call 07932 689081

CRPS UK Blog for the latest research and thinking in Complex Regional Pain Syndrome

 

 

21Jun/13

Come and see our CRPS blog

Complex Regional Pain Syndrome (CRPS) is a condition that we commonly see – click here for the clinic page

In support of the treatment, training and coaching programme we have a blog dedicated to the latest science and thinking in CRPS

CRPS UK Visit the blog here

See here on our CRPS UK blog the latest diagnostic criteria for CRPS

For further information about the treatment programmes for CRPS, please contact us on 07932 689081

31May/12

Complex Regional Pain Syndrome | CRPS Research Update 31/5/12

Welcome to the May research update – see more at www.crpsuk.com

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Pain Physician. 2012 May;15(3):255-66.

Skin biopsy in complex regional pain syndrome: case series and literature review.

Kharkar S, Venkatesh YS, Grothusen JR, Rojas L, Schwartzman RJ.

BACKGROUND:

Accumulating experimental and clinical evidence supports the hypothesis that complex regional pain syndrome type I (CRPS-I) may be a small fiber neuropathy.

OBJECTIVES:

To evaluate the use of commercially available standard biopsy methods to detect intradermal axon pathology in CRPS-I, and to ascertain if these structural changes can explain quantitative sensory testing (QST) findings in CRPS-I.

STUDY DESIGN:

Retrospective review of charts and laboratory data.

SETTING:

Outpatient clinic

METHODS:

Skin biopsies from 43 patients with CRPS-I were stained with PGP 9.5, and epidermal nerve fiber density, sweat gland nerve fiber density and morphological abnormalities were evaluated. Thirty-five patients had quantitative sensory testing.

RESULTS:

Alterations in skin innervation were seen in approximately 20% of CRPS-I patients with commercial processing. There were no patient characteristics, including duration of disease, that predicted a decreased epidermal nerve fiber density (ENFD). There was no consistent relationship between QST changes and ENFD measured by standard commercial skin biopsy evaluation procedures.

LIMITATIONS:

Commercial processing of tissue does not utilize stereologic quantitative analysis of nerve fiber density. Biopsy material is utilized from a proximal and distal source only, and differences in denervation of a partial nerve territory may be missed. The functional attributes of small fibers cannot be assessed.

CONCLUSIONS:

The negative results indicate that CRPS-I may be associated with changes in the ultramicroscopic small fiber structure that cannot be visualized with commercially available techniques. Alternatively, functional rather than structural alterations of small fibers or pathological changes at a more proximal site such as the spinal cord or brain may be responsible for the syndrome.

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Curr Pharm Des. 2012 May 16. [Epub ahead of print]

Immunological Aspects of the Complex Regional Pain Syndrome (CRPS).

Krämer HH.

Abstract

Limb trauma can lead to the development of a complex regional pain syndrome (CRPS). CRPS is a descriptive term of a variety of different symptoms. According to the current IASP-approved criteria, human CRPS can be diagnosed if a combination of signs is present: continuing pain and hyperalgesia, disproportionate to the initial trauma, skin temperature and colour asymmetry, sweating asymmetry, edema, decreased range of motion, and trophic changes. The diagnosis and treatment of human CRPS can be demanding and the pathophysiology underlying the disease is still under investigation. Immunological aspects are considered to play an important role in the development of CRPS. The impact of elevated pro-inflammatory cytokines systemically as well as locally, increased neurogenic inflammation and auto-antibodies in the pathophysiological development of CRPS are discussed in this review.

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Curr Med Res Opin. 2012 May 2. [Epub ahead of print]

Topical pain management with the 5% lidocaine medicated plaster – a review.

Mick G, Correa-Illanes G.

Abstract

Abstract Background: The topical 5% lidocaine medicated plaster is recommended as first-line treatment for localized peripheral neuropathic pain. Scope: In order to provide an overview of the efficacy and safety of the lidocaine plaster in the treatment of different neuropathic pain conditions, all efficacy and safety studies (randomized, controlled, or open-label with well described methodology), case reports, and pharmacological studies on the lidocaine plaster retrieved from a PubMed literature research (1960 – March 2012) plus additional references identified from retrieved articles were included. Findings: The lidocaine plaster is efficacious in the treatment of neuropathic pain symptoms associated with previous herpes zoster infection. Results from a large open-label controlled study suggest that the lidocaine plaster could be at least as effective as systemic pregabalin in the treatment of postherpetic neuralgia and painful diabetic polyneuropathy. Open-label studies indicate efficacy in the treatment of other localized neuropathic pain conditions, such as painful idiopathic sensory polyneuropathy, complex regional pain syndrome, carpal tunnel syndrome sequelae, postsurgical and posttraumatic pain. Quality of life markedly improved in a variety of neuropathic pain conditions and long-term treatment provided sustained relief in patients with neuropathic pain who are responsive to lidocaine plaster. The lidocaine plaster is usually well tolerated. The risk of systemic adverse events and pharmacokinetic interactions with concomitant medication is minimal owing to low systemic exposure. Conclusions: Treatment of several, primarily neuropathic and mixed-pain conditions with the 5% lidocaine medicated plaster was found efficacious and safe. Further controlled studies, in particular where only small open-label studies or case reports are available, should be considered.

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B-ENT. 2012;8(1):37-42.

A possible case of complex regional pain syndrome of the nose?

Faraj-Hakim S, Bleys RL, Buwalda J, de Ru JA.

Abstract

OBJECTIVE:

We present a case report of a patient with a putative diagnosis of complex regional pain syndrome of the nose. We would like to bring this disorder to the attention of rhinologists.

CASE REPORT:

A 53-year-old man presented with a history of extreme, constant, debilitating pain in his nose that started after he underwent several extensive nasal surgeries. Examination revealed atrophic nasal mucous membranes at the nasal septum. No other abnormalities were found. The pain did not diminish despite administration of analgesics and neuropathic pain medications. We propose a diagnosis of complex regional pain syndrome of the nose.

CONCLUSION:

The large number of nasal surgeries performed worldwide and the far reaching consequences of this debilitating syndrome indicate that it merits further investigation to determine whether it is a distinct disorder that should be recognized as such.

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J Neurosci. 2012 Apr 25;32(17):5747-56.

Abnormalities in hippocampal functioning with persistent pain.

Mutso AA, Radzicki D, Baliki MN, Huang L, Banisadr G, Centeno MV, Radulovic J, Martina M, Miller RJ, Apkarian AV.

Abstract

Chronic pain patients exhibit increased anxiety, depression, and deficits in learning and memory. Yet how persistent pain affects the key brain area regulating these behaviors, the hippocampus, has remained minimally explored. In this study we investigated the impact of spared nerve injury (SNI) neuropathic pain in mice on hippocampal-dependent behavior and underlying cellular and molecular changes. In parallel, we measured the hippocampal volume of three groups of chronic pain patients. We found that SNI animals were unable to extinguish contextual fear and showed increased anxiety-like behavior. Additionally, SNI mice compared with Sham animals exhibited hippocampal (1) reduced extracellular signal-regulated kinase expression and phosphorylation, (2) decreased neurogenesis, and (3) altered short-term synaptic plasticity. To relate the observed hippocampal abnormalities with human chronic pain, we measured the volume of human hippocampus in chronic back pain (CBP), complex regional pain syndrome (CRPS), and osteoarthritis patients (OA). Compared with controls, CBP and CRPS, but not OA, had significantly less bilateral hippocampal volume. These results indicate that hippocampus-mediated behavior, synaptic plasticity, and neurogenesis are abnormal in neuropathic rodents. The changes may be related to the reduction in hippocampal volume we see in chronic pain patients, and these abnormalities may underlie learning and emotional deficits commonly observed in such patients.

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