Category Archives: Neuropathic pain

CRPS in children: the literature

Posted on by under Children and CRPS, Complex Regional Pain Syndrome, CRPS, Neuropathic pain

CRPS affects both adults and children. There is no reason as best the science tells us, that the pathophysiology should be different, involving both central and peripheral mechanisms. This includes inflammation, central nervous system adaptation, immune system activity and the wide range of possible psychosocial influences.

In any persisting condition it is important to be patient-centred and to involve significant others, family and friends. The influence of others’ behaviours should not be underestimated. With children in pain, the primary caregivers are intricately involved in offering loving support, making treatment choices and motivating the young patient to follow the treatment programme.

We learn how to respond to pain early in life, frequently mirroring the behaviours of those around us and looking to them for feedback. It is not uncommon for a child to fall and then look to the parent for their facial and physical response before deciding what to do next.

For these reasons, any treatment programme must involve the parents and other significant people (e.g./ grandparent, teachers).

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Schmerz. 2012 Aug;26(4):389-95.

Please don’t hurt me!: a plea against invasive procedures in children and adolescents with complex regional pain syndrome (CRPS).

[Article in German]

Zernikow B, Dobe M, Hirschfeld G, Blankenburg M, Reuther M, Maier C.

Abstract

BACKGROUND:

Complex regional pain syndrome (CRPS; formerly known as Morbus Sudeck/reflex dystrophy) is diagnosed in children and adolescents, but the clinical presentation is often atypical. Unfortunately, potentially harmful, invasive treatments are used in pediatric patients.

PATIENTS AND METHODS:

A retrospective chart study of pediatric chronic pain patients with CRPS was performed.

RESULTS:

Over the course of 6 years, 37 (35 girls) children and adolescents took part in a multidisciplinary chronic pain inpatient program. At admission, patients took on average 4.4 (range 1-10) different medications and 29 different pharmaceuticals were used overall. Prior to admission, invasive pain treatments were performed without success in 16 of the children (43%). At least 13 children received two or more invasive treatments. Although sympathetic blocks were most prevalent, operations and regional anesthesia were also used.

CONCLUSION:

Despite a lack of evidence for invasive procedures, these continue to be used in children and adolescents with CRPS, who later respond positively to conventional treatment. The English full-text version of this article is available at SpringerLink (under “Supplemental”)

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Acta Paediatr. 2008 Jul;97(7):875-9. Epub 2008 Apr 9.

Complex regional pain syndrome type I in children.

Tan EC, Zijlstra B, Essink ML, Goris RJ, Severijnen RS.

Abstract

BACKGROUND:

Complex Regional Pain Syndrome type I (CRPS I) is a potentially incapacitating syndrome which can occur after a minor injury or operation to a limb. It is a disorder characterized by pain, sensory and motor disturbances. CRPS I is well known in adults, but a relatively new diagnostic entity in children. The clinical presentation of CRPS I in children is, to some extent, different from adults and therefore sometimes not recognized early. The aim of this study was to search for differences in patient characteristics between children and adults with CRPS I.

METHODS:

We have performed a retrospective chart review of 78 children (age </=16 year) with CRPS I and compared the data with those of 951 adults with CRPS I.

RESULTS:

The child population consisted predominantly of girls and older children (median age 13 years). The child population differed from adults in that the skin temperature of the involved extremity at onset was more often cooler, the lower extremity was involved more frequently and neurological and sympathetic symptoms were less pronounced.

CONCLUSIONS:

In several aspects, CRPS I in children has a different presentation than in adults

Click here

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Pain Med. 2010 Aug;11(8):1216-23.

Plasticity of complex regional pain syndrome (CRPS) in children.

Stanton-Hicks M.

Source

Pain Management Department, Center for Neurological Restoration, Consulting Staff, Children’s Hospital CCF Shaker Campus, Pediatric Pain Rehabilitation Program, Cleveland Clinic, Cleveland, Ohio 44195, USA. stantom@ccf.org

Abstract

Complex regional pain syndrome I (CRPS I) is defined by the International Association for the Study of Pain (IASP) criteria to include pain that is disproportionate to the inciting event, sensory disturbances such as allodynia/ hyperalgesia, autonomic dysfunction, and motor dysfunction that usually occurs after trauma that is frequently trivial and generally expressed in an extremity. These symptoms are well described in the adult population, but there are relatively few data or reports of its prevalence in the pediatric population. Recent studies have demonstrated that unlike the adult population, about 90% of the cases reported are females in a range of 8 to 16 years, the youngest being 3 years old. There tends to be delay in recognizing the diagnosis, which may be as long as 4 months. In contrast to adults, the response to treatment, particularly exercise therapy with behavioral management will achieve almost 97% remission. While the pathophysiology is poorly understood, many features, particularly the neurologic abnormalities, suggest both peripheral and central nervous system involvement. Peripheral small fiber neuropathy as an etiology and inflammation involving small nerve fibers (neurogenic inflammatory pain) has been suggested. A tissue inflammatory etiology has been investigated over the past 25 years. However, these inflammatory aspects differ from those seen in other conditions involving tissue inflammation. The suggestion that CRPS in children is a different clinical entity than that seen in the adult, is probably incorrect, as recent evidence would suggest that the pathophysiology is most likely identical involving endocrine, behavioral, developmental, and environmental factors that distinguish clinical presentation in children from the adult. Behavioral management is a mandatory accompaniment of any program of exercise therapy and the sometimes extreme sensory disturbances and parental enmeshment do distinguish the clinical presentation from that in the adult. Interventional procedures may be required in the face of extreme allodynia preventing exercise therapy, and in occasional cases interruption of the sympathetic nerves may reverse this symptom in a few children. Occasionally, continuous analgesia techniques such as that which can be delivered by tunneled epidural catheter or an externalized neurostimulator (spinal cord stimulation) for short periods of time are effective.

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J Am Podiatr Med Assoc. 2012 Mar-Apr;102(2):99-104.

Complex regional pain syndrome of the pediatric lower extremity: a retrospective review.

Harris EJ, Schimka KE, Carlson RM.

Source

Section of Podiatry, Department of Orthopedic Surgery, Loyola University Medical Center, Maywood, IL, USA.

Abstract

BACKGROUND:

Complex regional pain syndrome (CRPS) type 1 is a disorder of the extremities characterized by pain, edema, limited range of motion, integument changes, and vasomotor instability often after an inciting event. In the pediatric population, CRPS may be misdiagnosed, or missed entirely, as CRPS literature for this patient population is lacking.

METHODS:

Twenty-seven pediatric patient medical records with the diagnosis of CRPS type 1 from the institutional and private practices of the principal investigator (E.J.H.) were reviewed for demographics, inciting event, lower-extremity clinical examination, ancillary testing, previous treatments, time to diagnosis, treatment after diagnosis, and time to resolution of symptoms.

RESULTS:

Females composed 85.2% of the patient population (n = 23) (mean age of females, 11.11 years). An inciting event preceded pain in 74.1% of patients (n = 20). On physical examination, more than 50% of patients were identified as having changes in skin color and temperature, edema to the affected lower extremity, painful or decreased range of motion in affected joints, and intact lower-extremity motor function. The average time to resolution of symptoms was 6.8 weeks for the entire population.

CONCLUSIONS:

Diagnosis of CRPS type 1 should be considered in a preadolescent female complaining of pain out of proportion after an inciting event with a physical examination demonstrating change in skin color, decrease in skin temperature, edema, and painful or diminished range of motion in affected joints. Prompt diagnosis can decrease the time to resolution of symptoms.

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Mayo Clin Proc. 2010 Mar;85(3 Suppl):S33-41.

Neuropathic pain in children: Special considerations.

Walco GA, Dworkin RH, Krane EJ, LeBel AA, Treede RD.

Source

Department of Anesthesiology & Pain Medicine, Seattle Children’s Hospital, WA 98105, USA. gawalco@u.washington.edu

Abstract

Neuropathic pain is relatively uncommon in children. Although some syndromes closely resemble those found in adults, the incidence and course of the condition can vary substantially in children, depending on developmental status and contextual factors. There are some neuropathic pain syndromes that are rare and relatively unique to the pediatric population. This article discusses the array of neuropathic pain conditions in children and available treatment strategies. Data are limited by small numbers and few randomized controlled trials. Research and clinical implications are discussed.

Full article here

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CRPS Research Update 29/5/12

Posted on by under Brain and pain, Chronic pain, Complex Regional Pain Syndrome, CRPS, Neuropathic pain, Pain, Research, RSD
Pain Physician. 2012 May;15(3):255-66.

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

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).

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.

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?

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.

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

CRPS-like presentations & neuropathic pain

Posted on by under Chronic pain, Complex Regional Pain Syndrome, CRPS, Neuropathic pain, Pain, Pain assessment, Pain Education

I see a number of cases that feature some of the signs and symptoms of CRPS but would not be actually diagnosed as CRPS according to the Budapest criteria. For example, tendinopathy, neuropathies, post-surgery and following a nerve injury. The latter you may say could underpin CRPS II. There has always been difficulty suggesting that CRPS I is devoid of a nerve injury as of course nerves are ‘soft tissue’ and can easily be damaged during an injury. Of course when a nerve is injured neuropathic pain can be a consequence concurrent with the nociceptive pain.

Immobilisation can lead to similar symptoms including pain, altered movement, atrophy and vasomotor changes. One must consider the fact that for tissues to be healthy they require movement. Change in use of a body part will have a number of consequences including actual tissue change alongside issues of movement. Movement-based problems will be as a result of the altered tissue properties, cortical change and also a willingness to move. Fear avoidance, catastrophising and a belief that movement that hurts is a sign that damage is being done. This scenario can be played out in a number of conditions such as Achilles tendinopathy, tennis elbow, RSI and others.

Neuropathic pain is ‘pain arising as a direct consequence of a lesion or disease affecting the somatosensory system’ NeuPSIG

Neuropathic pain measures are a useful way of determining whether there is a neuropathic component. Commonly used are the s-LANSS and painDETECT – shown below – alongside a thorough assessment. A recent paper discusses the NeuPSIG assessment guidelines.

painDETECT Questionaire

s-LANSS

When neuropathic pain is found to be part of the presentation, this can guide treatment including medication and therapy. The former needs to be attended to with a plan that is fully understood by the patient: how the medication works, how to use it and how to gradually reduce the dosage. The latter includes techniques such as graded motor imagery, 2-point discrimination and desensitisation techniques at a peripheral and central level.

RS www.specialistpainphysio.com

Pain mechanisms (2)

Posted on by under Chronic pain, Explain Pain, Neuropathic pain, Pain, Pain Education, Pain mechanisms, Physiotherapy, Research

Keith Smart has been looking at a mechanisms-based approach to pain. As you may recall from the first piece on pain mechanisms and previous writings, I am a proponent of the view that we should be thinking about pain mechanisms. There are significant advantages to elucidating the underpinning physiological and pathology including understanding the patient’s description of their experience and to be able to focus treatment upon the mechanism(s) for more successful outcomes. Below are the papers by Keith Smart and others who have looked at pain mechanisms.

RS www.specialistpainphysio.com

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Clin J Pain. 2011 Oct;27(8):655-63. doi: 10.1097/AJP.0b013e318215f16a.

The Discriminative validity of “nociceptive,” “peripheral neuropathic,” and “central sensitization” as mechanisms-based classifications of musculoskeletal pain.

Source

St Vincent’s University Hospital, Elm Park, Dublin, Ireland. k.smart@ucd.ie

Abstract

OBJECTIVES:

Empirical evidence of discriminative validity is required to justify the use of mechanisms-based classifications of musculoskeletal pain in clinical practice. The purpose of this study was to evaluate the discriminative validity of mechanisms-based classifications of pain by identifying discriminatory clusters of clinical criteria predictive of “nociceptive,” “peripheral neuropathic,” and “central sensitization” pain in patients with low back (± leg) pain disorders.

METHODS:

This study was a cross-sectional, between-patients design using the extreme-groups method. Four hundred sixty-four patients with low back (± leg) pain were assessed using a standardized assessment protocol. After each assessment, patients’ pain was assigned a mechanisms-based classification. Clinicians then completed a clinical criteria checklist indicating the presence/absence of various clinical criteria.

RESULTS:

Multivariate analyses using binary logistic regression with Bayesian model averaging identified a discriminative cluster of 7, 3, and 4 symptoms and signs predictive of a dominance of “nociceptive,” “peripheral neuropathic,” and “central sensitization” pain, respectively. Each cluster was found to have high levels of classification accuracy (sensitivity, specificity, positive/negative predictive values, positive/negative likelihood ratios).

DISCUSSION:

By identifying a discriminatory cluster of symptoms and signs predictive of “nociceptive,” “peripheral neuropathic,” and “central” pain, this study provides some preliminary discriminative validity evidence for mechanisms-based classifications of musculoskeletal pain. Classification system validation requires the accumulation of validity evidence before their use in clinical practice can be recommended. Further studies are required to evaluate the construct and criterion validity of mechanisms-based classifications of musculoskeletal pain.

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J Man Manip Ther. 2010 Jun;18(2):102-10.

The reliability of clinical judgments and criteria associated with mechanisms-based classifications of pain in patients with low back pain disorders: a preliminary reliability study.

Source

UCD School of Public Health, Physiotherapy and Population Science, University College Dublin, Ireland.

Abstract

Mechanisms-based classifications of pain have been advocated for their potential to aid understanding of clinical presentations of pain and improve clinical outcomes. However, the reliability of mechanisms-based classifications of pain and the clinical criteria upon which such classifications are based are not known. The purpose of this investigation was to assess the inter- and intra-examiner reliability of clinical judgments associated with: (i) mechanisms-based classifications of pain; and (ii) the identification and interpretation of individual symptoms and signs from a Delphi-derived expert consensus list of clinical criteria associated with mechanisms-based classifications of pain in patients with low back (±leg) pain disorders. The inter- and intra-examiner reliability of an examination protocol performed by two physiotherapists on two separate cohorts of 40 patients was assessed. Data were analysed using kappa and percentage of agreement values. Inter- and intra-examiner agreement associated with clinicians’ mechanisms-based classifications of low back (±leg) pain was ‘substantial’ (kappa  = 0.77; 95% confidence interval (CI): 0.57-0.96; % agreement  = 87.5) and ‘almost perfect’ (kappa  = 0.96; 95% CI: 0.92-1.00; % agreement = 92.5), respectively. Sixty-eight and 95% of items on the clinical criteria checklist demonstrated clinically acceptable (kappa ⩾ 0.61 or % agreement ⩾ 80%) inter- and intra-examiner reliability, respectively. The results of this study provide preliminary evidence supporting the reliability of clinical judgments associated with mechanisms-based classifications of pain in patients with low back (±leg) pain disorders. The reliability of mechanisms-based classifications of pain should be investigated using larger samples of patients and multiple independent examiners.

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Man Ther. 2011 Nov 8. [Epub ahead of print]

Self-reported pain severity, quality of life, disability, anxiety and depression in patients classified with ‘nociceptive’, ‘peripheral neuropathic’ and ‘central sensitisation’ pain. The discriminant validity of mechanisms-based classifications of low back (±leg) pain.

Source

St Vincent’s University Hospital, Elm Park, Dublin 4, Ireland.

Abstract

Evidence of validity is required to support the use of mechanisms-based classifications of pain clinically. The purpose of this study was to evaluate the discriminant validity of ‘nociceptive’ (NP), ‘peripheral neuropathic’ (PNP) and ‘central sensitisation’ (CSP) as mechanisms-based classifications of pain in patients with low back (±leg) pain by evaluating the extent to which patients classified in this way differ from one another according to health measures associated with various dimensions of pain. This study employed a cross-sectional, between-subjects design. Four hundred and sixty-four patients with low back (±leg) pain were assessed using a standardised assessment protocol. Clinicians classified each patient’s pain using a mechanisms-based classification approach. Patients completed a number of self-report measures associated with pain severity, health-related quality of life, functional disability, anxiety and depression. Discriminant validity was evaluated using a multivariate analysis of variance. There was a statistically significant difference between pain classifications on the combined self-report measures, (p = .001; Pillai’s Trace = .33; partial eta squared = .16). Patients classified with CSP (n = 106) reported significantly more severe pain, poorer general health-related quality of life, and greater levels of back pain-related disability, depression and anxiety compared to those classified with PNP (n = 102) and NP (n = 256). A similar pattern was found in patients with PNP compared to NP. Mechanisms-based pain classifications may reflect meaningful differences in attributes underlying the multidimensionality of pain. Further studies are required to evaluate the construct and criterion validity of mechanisms-based classifications of musculoskeletal pain.

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Pain. 2011 Jul;152(7):1511-6. Epub 2011 Mar 10.

Identifying neuropathic back and leg pain: a cross-sectional study.

Source

School of Rehabilitation Sciences, Faculty of Health and Social Care Sciences, St. George’s University of London/Kingston University, Cranmer Terrace, London SW17 0RE, UK. I.Beith@sgul.kingston.ac.uk

Abstract

Low back pain is a widespread debilitating problem with a lifetime prevalence of 80%, with the underlying pain mechanism unknown in approximately 90% of cases. We used the painDETECT neuropathic pain screening questionnaire to identify likely pain mechanisms in 343 patients with low back pain with or without leg pain in southeastern England referred for physiotherapy. We related the identified possible pain mechanisms nociceptive, unclear, and neuropathic to standardised measures of pain severity (Numeric Rating Scale), disability (Roland Morris Low Back Pain Disability Questionnaire), anxiety and depression (Hospital Anxiety and Depression Scale), and quality of life (Short Form 36 Health Survey Questionnaire Version 2). In addition, we investigated any relationship between these possible pain mechanisms and leg pain, passive straight leg raise, and magnetic resonance imaging evidence confirming or eliminating nerve root compression. A total of 59% of participants (n=204) reported likely nociceptive pain, 25% (n=85) unclear, and 16% (n=54) possible neuropathic pain. The possible neuropathic pain group reported significantly higher pain, disability, anxiety, and depression, reduced quality of life and passive straight leg raise compared to the other pain groups (P<.05). A total of 96% of participants with possible neuropathic pain reported pain radiating to the leg (76% below the knee); however, leg pain was still more common in patients with nociceptive pain, suggesting that leg pain is sensitive to, but not specific to, possible neuropathic pain. No relationship was demonstrated between possible neuropathic pain and evidence for or absence of nerve root compression on magnetic resonance imaging scans. These findings suggest possible neuropathic pain is less common in low back pain patients referred through primary care and clarifies the usefulness of clinical tests for identifying possible neuropathic pain.

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J Pain. 2011 Oct;12(10):1080-7. Epub 2011 Jul 23.

The neuropathic components of chronic low back pain: a prospective multicenter study using the DN4 Questionnaire.

Source

INSERM U 987, Centre d’Evaluation et de Traitement de la Douleur, Hôpital Ambroise Paré, APHP, Boulogne-Billancourt, France. nadine.attal@apr.aphp.fr

Abstract

The present study investigated the neuropathic components of chronic low back pain (LBP) in patients with and without lower limb pain using the DN4 questionnaire and confirmed its psychometric properties. Patients (n = 132) from 11 French multidisciplinary pain or rheumatology centers were classified by a first investigator into 4 groups derived from the Quebec Task Force Classification of Spinal Disorders (QTFSD): group 1 (pain restricted to the lumbar area); group 2 (pain radiating proximally); group 3 (pain radiating below the knee without neurologic signs); and group 4 (pain radiating towards the foot in a dermatomal distribution, with neurological signs, corresponding to typical radiculopathy). A second investigator applied the DN4 questionnaire to the lower limb (groups 2 to 4) and lower back. A comparison of groups 1 and 4 confirmed the psychometric properties of DN4 (sensitivity 80%; specificity 92%, for a cutoff of 4/10, similar to other neuropathic conditions). In the lower limb, the proportion of patients with neuropathic pain (NP) was related to the distality of pain radiation (15, 39, and 80% in groups 2, 3 and 4, respectively; P < .0001). In the lower back, the proportion of patients with NP was higher for patients with typical radicular pain compared with the other groups (P = .006). Thus, typical radiculopathy has similar characteristics as other neuropathic conditions and is confirmed as the commonest neuropathic syndrome in LBP patients. The observation that neuropathic and nociceptive components of LBP vary in the back and lower limb probably accounts for the discrepancies of reported prevalence rates of NP in LBP. As this study was essentially based on a questionnaire, future studies combining standard clinical sensory testing, specific questionnaires, and more objective assessment of the sensory lesion are now required to further investigate the neuropathic component of chronic LBP. PERSPECTIVE: This study confirms the psychometric properties of the DN4 questionnaire to assess neuropathic pain in patients with low back pain. Neuropathic mechanisms largely contribute to pain in the lower limb as compared to the back, but neuropathic pain is not restricted to typical radiculopathy. This may have significant implications for the choice of treatment strategy in these patients.

Pain mechanisms

Posted on by under Brain and pain, Chronic pain, Explain Pain, Neuropathic pain, Pain, Pain Education, Science, Treatment

Understanding pain mechanisms is the key to effective treatment. The mechanisms that have been studied, written about in science journals and discussed with patients include nociceptive pain, inflammatory pain, neuropathic pain and central sensitisation. Elucidating which are playing a role in the patient’s experience allows the doctor to prescribe the right medication and the modern physical therapist to address the issues of pain in a biopsychosocial manner. I will now clarify the latter point.

In taking a detailed history, observing patterns of movement and protection, assessing the state of the nervous system and health of the body systems, understanding behaviours and the beliefs behind them and learning of the influences upon the individual’s pain experience, one can know about the likely pain mechanisms underpinning the experience. From here the treatment strategies can be chosen to target these mechanisms. For example, top-down approaches for central sensitisation focus on the change in the properties of the central nervous system. The interventions themselves are observant of the amplification that occurs in the spinal cord and higher centres and would seek to dampen the responses with input to the brain that is perceived as normal or non-threatening. This could include sensory stimulation or movements outside of the receptive field, education to reduce fear of movement or imagery to name but a few. Inflammatory pain can also be treated with a top-down approach but local tissue based strategies would also be used. Just to note that the separation of the ‘top end’ (brain and spinal cord) from ‘bottom end’ (tissues) is really a false dichotomy as all conscious experiences are from the brain including what we see and what we feel.

Stephen McMahon and David Bennett, both experts in the field of pain science from King’s College London, produced a poster that describes these mechanisms – click here to visit the page in Nature Reviews Neuroscience. This is what they say about it:

Pain is an unpleasant sensation resulting from the intricate interplay between sensory and cognitive mechanisms. Chronic pain, resulting from disease or injury, affects nearly every fifth person in the Western world, constituting an enormous burden for the individual and society. Sensitization of pain signalling systems is a key feature of chronic pain and results in normally non-painful stimuli eliciting pain. Such sensory changes can occur not just at the sites of injury, but in surrounding normal tissues. This and other observations suggest that sensitization occurs within the CNS as well as within nociceptor terminals. Here we consider the consequences of noxious stimulus applied to our unfortunate builder’s hand, from sensory transduction to pain perception. We describe the structural and functional elements present at different levels of the nociceptive system, as well as some of the changes occurring in chronic pain states. Although our poster highlights a flow of information from the periphery to the CNS, it should be noted that higher brain centres exert both inhibitory and facilitatory controls on lower ones. The challenge for the next decade will be to effectively translate this knowledge into the development of novel analgesic agents for better pain relief.

Richmond Stace – Specialist Pain Physio Clinics, London & Surrey

Neuropathic Pain: The pharmacological management of neuropathic pain in adults in non-specialist settings (3/10)

Posted on by under Chronic pain, Complex Regional Pain Syndrome, CRPS, Neuropathic pain, Pain, Pain Education, Treatment

Neuropathic Pain

The Pharmacological Management of Neuropathic Pain in Adults in Non-Specialist Settings

Click here for the NICE Guidelines: Neuropathic Pain 2010

NICE Clinical Guidelines, No. 96

Centre for Clinical Practice at NICE (UK).

Copyright © 2010, National Institute for Health and Clinical Excellence.

Excerpt

This clinical guideline covers the management of neuropathic pain conditions in adults (aged 18 or over) in primary care and secondary care, excluding specialist pain management clinics. The aim of the guideline is to provide clear recommendations to healthcare professionals in non-specialist settings on the treatment and management of neuropathic pain. This includes recommendations on appropriate and timely referral to specialist pain services and/or condition-specific services. In general, regarding neuropathic pain as a ‘blanket condition’, irrespective of the underlying cause, is helpful and practical for both non-specialist healthcare professionals and patients. However, condition-specific recommendations and research recommendations have been made where robust evidence on clinical and cost effectiveness exists for specific conditions, or where the evidence is clearly uncertain. The guideline excludes acute pain arising directly (in the first 3 months) from trauma or orthopaedic surgical procedures.

CRPS, Pain and Brain Research update November Part 1

Posted on by under Brain, Brain and pain, Chronic pain, Complex Regional Pain Syndrome, CRPS, Explain Pain, Immune system, Neuropathic pain, Neuroscience, Pain, Pain Education, Research, Science, Treatment
Welcome to the first November research update.

Specialist Pain Physio Clinics, London

J Pain 2011 Oct 25. [Epub ahead of print]

Pain-Related Fear, Perceived Harmfulness of Activities, and Functional Limitations in Complex Regional Pain Syndrome Type I.

Source

Department of Rehabilitation, University Hospital Maastricht, Maastricht, The Netherlands; Department Clinical Psychological Science, Maastricht University, Maastricht, The Netherlands.

Abstract

Numerous studies have shown that pain-related fear is one of the strongest predictors of pain disability in patients with chronic musculoskeletal pain, and there is evidence that the reduction of pain-related fear through an exposure treatment can be associated with restoration of functional abilities in patients with complex regional pain syndrome type I (CRPS-I). These findings suggest that pain-related fear may be associated with functional limitations in neuropathic pain as well. The aim of the current study was to test whether the debilitating role of pain-related fear generalizes to patients with CRPS-I. The results of 2 studies are presented. Study I includes a sample of patients with early CRPS-I referred to an outpatient pain clinic. In Study II, patients with chronic CRPS who are members of a patients’ association were invited to participate. The results show that in early CRPS-I, pain severity but not fear of movement/(re)injury as measured with the Tampa Scale for Kinesiophobia was related to functional limitations. In patients with chronic CRPS-I, however, perceived harmfulness of activities as measured with the pictorial assessment method significantly predicted functional limitations beyond and above the contribution of pain severity. Not fear of movement/(re)injury in general, but the perceived harmfulness of activities appears a key factor that might be addressed more systematically in the clinical assessment of patients with CRPS-I. These results support the idea that pain-related fear might be a promising concept in the understanding of pain disability in patients with neuropathic pain. PERSPECTIVE: This is the first study showing that perceived harmfulness of activities contribute to the functional limitations in CRPS-I. The current findings may help clinicians customizing cognitive-behavioral treatments for patients with chronic neuropathic pain.

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Clin J Pain. 2011 Oct 13. [Epub ahead of print]

Effect of Immunomodulating Medications in Complex Regional Pain Syndrome: A Systematic Review.

Source

Erasmus MC, Rotterdam, The Netherlands.

Abstract

BACKGROUND:

Different mechanisms are involved in a complex network of interactions resulting in the painful and impairing disorder, complex regional pain syndrome (CRPS). There is convincing evidence that inflammation plays a pivotal role in the pathophysiology of CRPS. Immunomodulating medication reduces the manifestation of inflammation by acting on the mediators of inflammation. Therefore, as inflammation is involved in the pathophysiology of CRPS, immunomodulating medication in CRPS patients may prove beneficial.

OBJECTIVES:

To describe the current empirical evidence for the efficacy of administering the most commonly used immunomodulating medication (ie, glucocorticoids, tumor necrosis factor-α antagonists, thalidomide, bisphosphonates, and immunoglobulins) in CRPS patients.

METHODS:

PubMed was searched for original articles that investigated CRPS and the use of one of the abovementioned immunomodulating agents.

RESULTS:

The search yielded 39 relevant articles: from these, information on study design, sample size, duration of disease, type and route of medication, primary outcome measures, and results was examined.

DISCUSSION:

Theoretically, the use of immunomodulating medication could counteract the ongoing inflammation and might be an important step in improving a disabled hand or foot, leading to further recovery. However, more high-quality intervention studies are needed.

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PLoS One. 2011;6(10):e26010. Epub 2011 Oct 13. Click here for article

Brain morphological signatures for chronic pain.

Source

Department of Physiology, Northwestern University, Chicago, Illinois, United States of America.

Abstract

Chronic pain can be understood not only as an altered functional state, but also as a consequence of neuronal plasticity. Here we use in vivo structural MRI to compare global, local, and architectural changes in gray matter properties in patients suffering from chronic back pain (CBP), complex regional pain syndrome (CRPS) and knee osteoarthritis (OA), relative to healthy controls. We find that different chronic pain types exhibit unique anatomical ‘brain signatures’. Only the CBP group showed altered whole-brain gray matter volume, while regional gray matter density was distinct for each group. Voxel-wise comparison of gray matter density showed that the impact on the extent of chronicity of pain was localized to a common set of regions across all conditions. When gray matter density was examined for large regions approximating Brodmann areas, it exhibited unique large-scale distributed networks for each group. We derived a barcode, summarized by a single index of within-subject co-variation of gray matter density, which enabled classification of individual brains to their conditions with high accuracy. This index also enabled calculating time constants and asymptotic amplitudes for an exponential increase in brain re-organization with pain chronicity, and showed that brain reorganization with pain chronicity was 6 times slower and twice as large in CBP in comparison to CRPS. The results show an exuberance of brain anatomical reorganization peculiar to each condition and as such reflecting the unique maladaptive physiology of different types of chronic pain.

CRPS medication

Posted on by under Brain and pain, Chronic pain, Complex Regional Pain Syndrome, CRPS, Medication, Neuropathic pain, Pain, Pain Education, Physiotherapy, Treatment

When I first meet a new patient who comes with CRPS, I ask about current medication use. The answers to this question vary from over the counter preparations to prescribed drugs for inflammation and neuropathic pain. For example, paracetamol, anti-inflammatories or NSAIDs (neurofen, naproxen, voltarol), opioids (tramadol, oxycodone, codeine), anti-depressants (amitriptyline, nortriptyline) and anti-convulsants (pregabalin, gabapentin). Medication has an important role to play but must be used wisely, appropriately and optimised for the pain type(s), similar to a lock and key. If the key fits the lock the door will open, in other words when the drug attaches itself to the target receptor there will be action but if it does not match there will not be an effect.

Specialist Pain Physio - CRPS London

Gabapentin

There can be different pain mechanisms at the root of the CRPS symptoms. Commonly we see neuropathic pain and inflammatory pain, the latter often due to neurogenic inflammatory mechanisms when the nerves themselves release chemicals–substance P and CGRP–into the tissues that they supply, triggering inflammation. In this case, your doctor could prescribe medication for neuropathic pain such as gabapentin alongside an anti-inflammatory drug.

I believe in a model of care that is inclusive of appropriate physiotherapy, pain medicine and psychology, working together to provide a psychosocial programme of care. Not everyone will require input from all three disciplines, but this model as a start point means that all aspects of the condition and the effects are considered. Further, these disciplines must be providing care that is based upon the latest thinking and science of both pain and CRPS. As a physiotherapist specialising in chronic pain and conditions such as CRPS, I have ensured that those I work with are dedicated to the contemporary provision of treatment. Therefore, returning to the issue of appropriate and effective medication use, when I ask about the drugs and their effect, it is so I can see whether a review is required to optimise the overall programme of treatment. In the case that I feel the medication is not being optimised, I will recommend that you see one of the pain specialists whom I know will be able to advise you on the most appropriate drug for your current state and how best to use it within the programme.

Briefly, I think it is important to point out that I do not prescribe or change patient’s medication. This is the job of your doctor or consultant. If you do not have a nominated doctor or specialist who is looking after your medication use, I will gladly recommend one who can help you.

Neuropathic Pain Update (Sept)

Posted on by under Brain, Brain and pain, Chronic pain, Complex Regional Pain Syndrome, CRPS, Neuropathic pain, Neuroscience, Pain, Pain Education, Research, RSD, Science

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.

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.

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 symptoms–including 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.

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.

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 P–peptides 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.

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?

Section for Physiotherapy Science, Department of Public Health and Primary Health Care, University of Bergen, Kalfarveien, Bergen, Norway. roar.jensen@broadpark.no

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.