Tag Archives: complex regional pain syndrome

12Aug/15
Budapest | Moyan Brenn http://bit.ly/1EnHXWp

I’ve been diagnosed with CRPS

Budapest | Moyan Brenn http://bit.ly/1EnHXWp

Budapest | Moyan Brenn http://bit.ly/1EnHXWp

I’ve been diagnosed with CRPS. This is a common way that the conversation begins with people who contact me, often scared witless by what they have found out online or by what they have been told. Others are confused and do not really understand what CRPS means, except they know it hurts like hell and has turned their life upside down.

Before reading any further, have a look at this link that outlines the latest criteria named after the place where it was recently established: The Budapest Criteria 

Complex Regional Pain Syndrome, also known as RSD (the old term — reflex sympathetic dystrophy), like any ‘syndrome’ is a collection of signs and symptoms that are gathered together and given a name. However, CRPS is complex (biologically), it is regional (usually affecting a limb), it is painful (one of the worst), and as I said, a syndrome. There you have it, CRPS.

Many people like to have a diagnosis, a label and a peg on which they can hang their hat. A diagnosis is useful if everyone then understands the implications and the treatment is standardised thereafter with effect. This is not the case with CRPS as few really seem to understand the condition.

Depending on where you go, you will be in receipt of treatment that varies according to the profession you see. Medically you are often offered drugs and interventions that can work to relieve some of the symptoms. As with any pain though, despite relief that everyone hopes for, drugs do not teach you how to restore normal living. For this you need to work with someone who understands the complexity of pain and CRPS and who can guide you to think in the right way so that you focus upon the right actions to move forward.

Here are some tips:

1. Read the classification and ensure that you are indeed suffering CRPS (there is type 1 and 2, which differentiate those with the condition from a non-nerve injury and a nerve injury that trigger the complex and painful responses)

2. Work with someone who genuinely understands CRPS, can educate, guide and motivate you through a comprehensive programme — that person must also know that pain can and does change!

3. Understand that medication has a role but you have a bigger role. There in only one person who can transform pain, and that is you. You just need to know how.

4. Do not nurture fear by reading about other’s difficulties online. We all suffer fear, anger and other negative emotions, but they are not helpful if they persist. You can learn the skill of deciding how to think, perceive and act using the strengths that you already possess in overcoming your pain.

5. You are NOT complex regional pain syndrome. Do not let this or any other conditions define you. You are ________ ________ (fill your name here) who is a son, brother, wife, husband, father, mother, employee, sport lover, art critic….again, fill in yourself and remember it.

6. Focus on what you can do; focus on your strengths and focus on overcoming the pain and CRPS.

The Pain Coach Programme focuses on your strengths that you will use to overcome your pain, including resilience, motivation, empathy, compassion, concentration and many others. Developing and growing your inner drive, you will learn skills and develop your knowledge so that you in effect become your own coach moment-to-moment, choosing to take each opportunity to transform and change pain on your return to a meaningful life.

t. 07518 445493

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!

14Nov/14
CRPS Clinics | London & New Malden

5 facts about complex regional pain syndrome | CRPS

 

CRPS Clinics | London & New MaldenThanks to modern pain science we know a huge amount about complex regional pain syndrome (CRPS). Of course there is much more to know, and the way in which we think and take action to tackle the problem will evolve accordingly.

 

Here are 5 facts that I believe to be important:

1. The pain is not directly related to the extent of the injury or damage — the pain in CRPS can be unimaginably horrendous without any great change in the tissue health. Remember that pain is part of the way that the body protects itself, and not an indicator of tissue damage.

2. The affected limb can feel very different to the way it looks; size and temperature included.It can even feel like it does not belong, being described as detached or ‘not mine’. The loss of sense of ownership is because the brain provides this sense, but can also modulate it.

3. The symptoms can change according to your mood and the way you feel — stress can often make the pain worse. This is due to the perceived threat to the whole person triggering protection.

4. Seeing someone else move their corresponding body part can hurt. The brain starts to plan the same movement and will also protect at this stage, causing actual pain.

5. The limb changes colour because of blood flow changes. The autonomic nervous system (ANS) controls blood flow. This is the system that responds to perceived threat — ‘freeze, flight or fright’. In essence it is a system that responds to how and what we think. When we are embarrassed, we turn red (blood flow). This is because of the way in which we think about the situation:’ I have said something that I now think is silly’, ‘Is he looking at me?’ The ANS can also become sensitive, and is very involved with CRPS — colour change, altered sense of size, sweaty palms etc.

Suffering complex regional pain syndrome? Visit my specialist CRPS clinic in London to start your programme: call 07518 445493

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 

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

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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Explaining Pain & Treating Pain

21Oct/11

Using neuroscience to understand and treat pain

Neuroscience to treat pain and injury

I love neuroscience. It makes my job much easier despite being a hugely complex subject. Neuroscience research has cast light over some of the vast workings of our brains and helped to explain how we experience ourselves and the richness of life. An enormous topic, in this blog I am briefly going to outline the way in which I use contemporary neuroscience to understand pain and how we can use this knowledge to treat pain more effectively. This is not about the management of pain, it is the treatment of pain. Management of pain is old news.

Understanding pain is the first step towards changing the painful experience. Knowing how the brain and nervous system operate allows us to create therapies that target the biological mechanisms that underpin pain. Appreciation of the plastic ability of the nervous system from top to bottom–brain to periphery–provides us with the opportunity to ‘re-wire’, and therefore to alter the function of the system and make things feel better. Knowing the role of the other body systems when the brain is defending us, is equally important. The synergy of inputs from the immune system, endocrine system and autonomic nervous system provides the brain with infomration about our internal physiology that it must scrutinse and act upon in the most appropriate way. We call this action the brain’s ‘output’ which is the responses that it co-ordinates to promote health and survival.

Treat the brain and to reduce pain

Excellent data from contemporary research tells us that understanding pain increases the pain threshold (harder to trigger pain), reduces anxiety in relation to pain and enhances our ability to cope and deal with the pain. We know that movement can also improve after an education session. This is because the perceived threat is reduced by learning and understanding what is going on inside, and knowing what can be done. The vast majority of patients who come to the clinic do not know why their pain has persisted, what pain really is, how it is influenced and what they can do about it themselves. For me this is the start point. Explaining the neuroscience of pain. Facts that we know people can absorb, understand and apply to themselves in such a way that the brain changes and provides a different experience.

It is the brain that gives us our experience of ourselves and the world around us. This includes the sensory and emotional experience of pain. The brain receives information from the body via the peripheral nervous system that suggests there is a threat to the tissues (input). In response, the brain must decide whether this threat is genuine based upon what is happening at the time, the emotional state, past experience, the belief system, gender, genetics, health status, culture and other factors. In the case that the brain perceives a threat, the output will be pain. The Mature Organism Model developed by Louis Gifford describes this beautifully (see below).

Pain is a motivator. It grabs our attention in the area of the body that the brain feels is threatened based upon the danger signals it is receiving from the tissues via the spinal cord. The brain actually ascribes the location of the pain via the map of the body that exist in the sensory cortex. On feeling the pain, we take action. This is the reason for pain. It motivates us to move, seek help or rest. Pain is an incredible device that we have for survival and learning, necessary to navigate life and completely normal. The brain constructs the pain experience and associated symptoms in such a way that we have to take note and do something about it immediately.

When we injure tissue there is a local release of inflammatory chemicals. These chemicals excite local nerves in the tissues called nociceptors. Normally, nociceptors are quiet but when they are stimulated by inflammation, these nerves send danger signals to the spinal cord where they meet secondary neurons. The early bombardment of signals into the spinal cord causes the secondary neurons to become excited. These cells then send danger signals up to the brain where the information is scrutinised. On the basis of this scrutiny, if the brain perceives a threat, pain will be allocated in the area of the body that is deemed to be in danger. The area of pain is allocated via the representation of the body in the brain (see previous blog here) in the sensory cortex, first mapped by Wilder Penfield and published in 1951. Therefore we know that actually there is no ‘muscle pain’ or ‘knee pain’ but rather pain as a brain experience, and not in the mind I hasten to add, that is detected in a body part or region according to the brain’s perception of threat. These are the body maps that the brain uses to know where information is coming from and to control movement.

This information is part of the neuroscience knowledge that can be used to help people understand their pain and to create therapies that treat pain. Future blogs will look at how we can change and nourish the nervous system to promote healthy tissues at one end of the spectrum with the brain end being targeted by deeper education and Graded Motor Imagery (GMI) for example–click here. The brain and the tissues are not separate, they affect each other in many ways, as do other body systems such as the immune and endocrine systems. Looking at healthy movement and functioning in a truly holistic and biopsychosocial manner with neuroscience underpinnings, provides us with an exciting route forwards in dealing with pain problems.
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.

14Sep/11

Neuropathic pain Update

I have looked at recent papers that focus on neuropathic pain, one of the common pain types seen in CRPS. I’m afraid that some of the research is ‘sciency’ but of course it has to be, so do not worry of you don’t fully understand the methods or the physiology. At the end of the more complex abstracts I have put a summary.

Science. 2011 Sep 9;333(6048):1462-6.

HCN2 ion channels play a central role in inflammatory and neuropathic pain.

Emery EC, Young GT, Berrocoso EM, Chen L, McNaughton PA.

Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, UK.

The rate of action potential firing in nociceptors is a major determinant of the intensity of pain. Possible modulators of action potential firing include the HCN ion channels, which generate an inward current, I(h), after hyperpolarization of the membrane. We found that genetic deletion of HCN2 removed the cyclic adenosine monophosphate (cAMP)-sensitive component of I(h) and abolished action potential firing caused by an elevation of cAMP in nociceptors. Mice in which HCN2 was specifically deleted in nociceptors expressing Na(V)1.8 had normal pain thresholds, but inflammation did not cause hyperalgesia to heat stimuli. After a nerve lesion, these mice showed no neuropathic pain in response to thermal or mechanical stimuli. Neuropathic pain is therefore initiated by HCN2-driven action potential firing in Na(V)1.8-expressing nociceptors.

The excitability of a nerve is determined by the activity of receptors that allow ions to flow in and out. The flow of ions alters the threshold of excitability meaning that it is much easier for the nerve to be stimulated and fire a signal. It is the firing of danger signals to the brain via the spinal cord that can lead to pain. When I say that it ‘can’ lead to pain, this is because sometimes the brain receives these danger signals but does not respond by producing pain. The brain must judge the signals to be a sign of danger for pain to be experienced. Neuropathic pain often includes spontaneous pain that is caused by ectopic firing of signals.

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Pain Med. 2011 Sep 7. doi: 10.1111/j.1526-4637.2011.01227.x. [Epub ahead of print]

The Influence of Chinook Winds and Other Weather Patterns upon Neuropathic Pain.

Ngan S, Toth C.

Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada.

Objective.   Although Chinook winds are often viewed positively during a cold prairie winter, patients suffering with neuropathic pain (NeP) anecdotally report exacerbations of NeP during Chinooks and during other weather changes. Our objective was to identify if Chinook winds lead to acute exacerbations in pain severity in a NeP patient population. Design.  Prospective diary-based assessments of patients with at least moderate NeP over 6-month periods during different seasons of the year were performed. Concurrent weather conditions were tracked hourly, with Chinook winds defined using accepted meteorological definition. We also examined other aspects of weather including precipitation, temperature, and humidity. Days with acute exacerbations were defined when a daily visual analog score pain score was ≥2 points above their average NeP score over the entire 6-month period. Results.  Chinooks were not associated with individual acute exacerbations in NeP. Instead, Chinook days were found to be protective against acute exacerbations in NeP (odds ratio 0.52 [0.33-0.71]). Post hoc study associated Chinooks with NeP relief (odds ratio 1.83 [1.17-2.49]). We could not identify relationship between precipitation or humidity with acute NeP exacerbation. However, days with cold temperature ≤ -14°C were associated with greater risk of NeP exacerbation. Conclusion.  Weather-mediated changes occur for patients with NeP, manifesting as relief from Chinook winds while cold temperature conditions can provoke exacerbations in NeP.

Cold commonly affects neuropathic pain–worsening the symptomsincluding ambient temperature or a cold stimulus applied (e.g. alcohol wipe, cold draft, ice)

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Cochrane Database Syst Rev. 2009 Jul 8;(3):CD007076.

Pregabalin for acute and chronic pain in adults.

Moore RA, Straube S, Wiffen PJ, Derry S, McQuay HJ.

Pain Research and Nuffield Department of Anaesthetics, University of Oxford, West Wing (Level 6), John Radcliffe Hospital, Oxford, Oxfordshire, UK, OX3 9DU.

BACKGROUND:

Antiepileptic drugs have been used in pain management since the 1960s. Pregabalin is a recently developed antiepileptic drug also used in management of chronic neuropathic pain conditions.

OBJECTIVES:

To assess analgesic efficacy and associated adverse events of pregabalin in acute and chronic pain.

SEARCH STRATEGY:

We searched MEDLINE, EMBASE, and CENTRAL to May 2009 for randomised controlled trials (RCTs). Additional studies were identified from the reference lists of retrieved papers and on-line clinical trial databases.

SELECTION CRITERIA:

Randomised, double blind trials reporting on the analgesic effect of pregabalin, with subjective pain assessment by the patient as either the primary or a secondary outcome.

DATA COLLECTION AND ANALYSIS:

Two independent review authors extracted data and assessed trial quality. Numbers-needed-to-treat-to-benefit (NNTs) were calculated, where possible, from dichotomous data for effectiveness, adverse events and study withdrawals.

MAIN RESULTS:

There was no clear evidence of beneficial effects of pregabalin in established acute postoperative pain. No studies evaluated pregabalin in chronic nociceptive pain, like arthritis.Pregabalin at doses of 300 mg, 450 mg, and 600 mg daily was effective in patients with postherpetic neuralgia, painful diabetic neuropathy, central neuropathic pain, and fibromyalgia (19 studies, 7003 participants). Pregabalin at 150 mg daily was generally ineffective. Efficacy was demonstrated for dichotomous outcomes equating to moderate or substantial pain relief, alongside lower rates for lack of efficacy discontinuations with increasing dose. The best (lowest) NNT for each condition for at least 50% pain relief over baseline (substantial benefit) for 600 mg pregabalin daily compared with placebo were 3.9 (95% confidence interval 3.1 to 5.1) for postherpetic neuralgia, 5.0 (4.0 to 6.6) for painful diabetic neuropathy, 5.6 (3.5 to 14) for central neuropathic pain, and 11 (7.1 to 21) for fibromyalgia.With 600 mg pregabalin daily somnolence typically occurred in 15% to 25% and dizziness occurred in 27% to 46%. Treatment was discontinued due to adverse events in 18 to 28%. The proportion of participants reporting at least one adverse event was not affected by dose, nor was the number with a serious adverse event, which was not more than with placebo.Higher rates of substantial benefit were found in postherpetic neuralgia and painful diabetic neuropathy than in central neuropathic pain and fibromyalgia. For moderate and substantial benefit on any outcome NNTs for the former were generally six and below for 300 mg and 600 mg daily; for fibromyalgia NNTs were much higher, and generally seven and above.

AUTHORS’ CONCLUSIONS:

Pregabalin has proven efficacy in neuropathic pain conditions and fibromyalgia. A minority of patients will have substantial benefit with pregabalin, and more will have moderate benefit. Many will have no or trivial benefit, or will discontinue because of adverse events. Individualisation of treatment is needed to maximise pain relief and minimise adverse events. There is no evidence to support the use of pregabalin in acute pain scenarios.

This is a Cochrane Review meaning that a number of research papers are analysed before concluding whether a treatment is effective or not.

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Pain. 2011 Aug 27. [Epub ahead of print]

Genotype-selective phenotypic switch in primary afferent neurons contributes to neuropathic pain.

Nitzan-Luques A, Devor M, Tal M.

Department of Medical Neurobiology, Faculties of Medicine and Dentistry, The Hebrew University of Jerusalem, Jerusalem, Israel.

Pain is normally mediated by nociceptive Aδ and C fibers, while Aβ fibers signal touch. However, after nerve injury, Aβ fibers may signal pain–this means that touch now hurts. Using a genetic model, we tested the hypothesis that phenotypic switching in neurotransmitters expressed by Aβ afferents might account for heritable differences in neuropathic pain behavior. The study examined selection-line rats in which one line, high autotomy (HA)rats chewing themselves as  a pain behaviour–, shows higher levels of spontaneous pain in the neuroma neuropathy model, and of tactile allodynia in the spinal nerve ligation (SNL) model, than the companion low autotomy (LA) line. Changes in calcitonin gene-related peptide (CGRP) and Substance Ppeptides released by cells that cause excitability– expression were evaluated immunohistochemically in L4 and L5 dorsal root ganglia 7days after SNL surgery. Expression of CGRP was decreased in axotomized small- and medium-diameter neurons in both rat lines. However, in HA but not in LA rats, there was a tenfold increase in CGRP immunoreactivity (CGRP-IR) in large-diameter neurons. Corresponding changes in CGRP-IR in axon terminals in the nucleus gracilis were also seen. Finally, there were indications of enhanced CGRP neurotransmission in deep laminae of the dorsal horn. Substance P immunoreactivity was also upregulated in large-diameter neurons, but this change was similar in the 2 lines. Our findings suggest that phenotypic switching contributes to the heritable difference in pain behavior in HA vs LA rats. Specifically, we propose that in HA rats, but less so in LA rats, injured, spontaneously active Aβ afferents both directly drive CGRP-sensitive central nervous system pain-signaling neurons and also trigger and maintain central sensitization, hence generating spontaneous pain and tactile allodynia.

Spontaneous pain and pain from light touch is due to genetic changes in the nerve cells of Aß afferent (sensory) nerves.

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A classic paper

Neurology. 2008 Apr 29;70(18):1630-5. Epub 2007 Nov 14.

Neuropathic pain: redefinition and a grading system for clinical and research purposes.

Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW, Hansson P, Hughes R, Nurmikko T, Serra J.

Institute of Physiology and Pathophysiology, Johannes Gutenberg University, Mainz, Germany.

Pain usually results from activation of nociceptive afferents by actually or potentially tissue-damaging stimuli. Pain may also arise by activity generated within the nervous system without adequate stimulation of its peripheral sensory endings. For this type of pain, the International Association for the Study of Pain introduced the term neuropathic pain, defined as “pain initiated or caused by a primary lesion or dysfunction in the nervous system.” While this definition has been useful in distinguishing some characteristics of neuropathic and nociceptive types of pain, it lacks defined boundaries. Since the sensitivity of the nociceptive system is modulated by its adequate activation (e.g., by central sensitization), it has been difficult to distinguish neuropathic dysfunction from physiologic neuroplasticity. We present a more precise definition developed by a group of experts from the neurologic and pain community: pain arising as a direct consequence of a lesion or disease affecting the somatosensory system. This revised definition fits into the nosology of neurologic disorders. The reference to the somatosensory system was derived from a wide range of neuropathic pain conditions ranging from painful neuropathy to central poststroke pain. Because of the lack of a specific diagnostic tool for neuropathic pain, a grading system of definite, probable, and possible neuropathic pain is proposed. The grade possible can only be regarded as a working hypothesis, which does not exclude but does not diagnose neuropathic pain. The grades probable and definite require confirmatory evidence from a neurologic examination. This grading system is proposed for clinical and research purposes.

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Application

In my view there are many cases of neuropathic pain (NP) that are not identified, mainly because the examiner is not looking for this pain type. This paper considers whether NP exists in anterior knee pain–it does in my experience. I see a large number of people with back complaints and is it not uncommon to find NP hiding in there, often obscured by a more mechanical or inflammatory pain mechanism. Using clinical tests and a measure or two, we can convert suspicion to reality and then consider how this pain type needs to be managed. There are different implications when NP is present including the prognosis. It takes longer to settle down and flare-ups are common. Flare-ups need effective management including self-care strategies to move through these difficultly times effectively. RS

Clin J Pain. 2008 Jun;24(5):384-94.

Is pain in patellofemoral pain syndrome neuropathic?

Jensen R, Kvale A, Baerheim A.

Section for Physiotherapy Science, Department of Public Health and Primary Health Care, University of Bergen, Kalfarveien, Bergen, Norway. [email protected]

There is no consensus among experts regarding the etiology or management of patellofemoral pain syndrome (PFPS). Observations indicating dysfunction of the peripheral nervous system around the patellae have been reported. To what extent these sensory abnormalities cause pain has so far not been investigated. The aim of this study was to assess whether a subgroup of patients with unilateral PFPS have neuropathic pain related to the painful knee.

METHOD:

A total of 91 patients with unilateral PFPS, between 18 and 40 years of age, and a comparable group of 23 healthy participants aged 18 to 44 years were included. Level of knee function, pain intensity, and qualities were assessed. Somatosensory assessments were carried out by bedside neurologic tests and quantitative sensory testing, assessing thermal, tactile, and vibration thresholds.

RESULTS:

Ample signs of sensory aberrations with considerable heterogeneity and overlap regarding the degree and type of dysfunction of the nervous system were found in the painful area of the PFPS patients. No clear subgroup of patients with neuropathic pain or clustering of features related to neuropathic pain was identified.

DISCUSSION:

This study hypothesizes that the observed sensory aberrations may cause neuropathic pain in patients with PFPS. There is no validated method for subgrouping patients with possible neuropathic pain and in this study considerable heterogeneity and overlap regarding signs and symptoms of neuropathic pain made subgrouping even more difficult. A mechanism-based understanding of the pain is, however, essential for the selection of adequate treatment strategies in painful musculoskeletal disorders.