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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

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.

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.
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.
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.
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.


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.

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).
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.
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.
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.


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.

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.
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.
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).
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.


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.

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.
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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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.

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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.

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.
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.

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.

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.
Ten patients with CRPS and 10 age- and sex-matched controls.
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.
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.
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.


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.

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.


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.

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.


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.

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.


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.

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 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

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




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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

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

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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.


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.


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)


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.


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.


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


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.


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.


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.


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.


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.


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.


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.



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.


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.


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.


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.


Treatment Update

Come and see the updated treatment programme page. We are regularly updating the site so do check back. This is when there is new knowledge or research that adds to our understanding of pain and how we can best treat on-going problems.


Complex Regional Pain Syndrome – ‘it feels weird’

Complex Regional Pain Syndrome (CRPS) often presents with a number of signs and symptoms. The main complaints are usually pain, colour change (minute to minute sometimes), temperature change, swelling, sweating changes, skin/nail/hair changes (trophic) and an altered perception of the affected part. It is this last sense that I am going to focus upon in this blog.

I hear many different descriptions of the symptoms of CRPS and actually encourage the use of a wide range of words. This is so that I can develop a really good picture and insight into the individual’s experience which is exactly that, individual. One aspect that I am particularly interested in is the perception of the affected area. In the vast majority, if not all, cases there is an altered sense of the region. For example, in the case of the hand it can feel bigger (sausage fingers often a good description of the feel), swollen, distorted, out of place, detached, like it belongs to someone else, like it is not there unless looked at (visual input to confirm presence) or denial that it is there at all (denial – similar to those who suffer strokes).

This variety of descriptions paint the picture of a ‘stranger’ aspect of the condition, often claimed to be ‘weird feelings’ as they are so abstract and like nothing before. Clearly this can be worrying and sometimes I hear that when the descriptions are given to others there maybe disbelief. Any aspect of a problem that creates fear or anxiety can affect pain and must be addressed.

So what is going on? When we have an on-going painful problem and we are not moving normally, changes occur within the central nervous system to give us this different experience. In the brain we have maps, virtual maps, that the brain uses to work out where sensory information is coming from and control movement. These maps are well defined under normal circumstances with a genetic blueprint that is moulded by experiences. This precise definition relies on a constant stream of information coming in from the tissues. In the case that this flow is altered or stopped, the map changes. We know this from fMRI studies that demonstrate reorganisation of the brain in certain areas. Certain representations of body parts are found to be in different locations in pain states. In fact, many brain changes have been found in chronic pain, these changes underpinning our different experiences of the body. The good news is that with effective treatment of the pain, these changes are reversed. Effective treatment will be the subject of another blog, but this includes such therapies as graded motor imagery and others that seek to ‘redefine the maps’.

In summary, chronic pain states, including CRPS and back pain, we know that the cortical (brain) maps change and that this is the reason why the affected area can feel ‘weird’, out of place and just not right. The map is ‘smudged’. In a sense this is useful as it draws our attention to something that needs dealing with imminently. The focus of treatment for this is upon ‘redefining’ the maps, the same for a range of conditions. In fact, my view is that this is what modern rehabilitation is really about in essence, via normalisation of sensation, motor control and the congruence of these factors, alongside the traditional strength gains and tissue changes. Our understanding of smudging and cortical reorganisation has triggered a change in thinking for rehabilitation, targeting the brain, training the brain and offering science based solutions for chronic pain.

The pictures are from the book ‘Explain Pain