Neuropathic pain: an evidence-based update.
Neuropathic pain (NeP) is defined by the International Association for the Study of Pain (IASP) as pain arising as a direct consequence of a lesion or disease affecting the somatosensory system (Loeser and Treede, 2008). Symptoms of NeP often include a reported lack of sensation in the area and pain, with the pain being described as electric-like or lancinating. Common conditions such as diabetes, stroke, multiple sclerosis and cancer can cause NeP (Table 1). The World Health Organisation indicates that chronic or long term conditions including diabetes, cardiovascular disease and cancer, are the leading cause of preventable morbidity and mortality in New Zealand (WHO, 2008). The New Zealand Health Strategy (2000) prioritizes the reduction, impact and incidence of these conditions, and has targeted primary care as a service delivery area. It is however, anticipated that NeP may become more prevalent in years to come due to: an aging population, increased survival rates of conditions such as diabetes and cancer, and use of treatment strategies (for example medical and surgical management of cancer) which can cause NeP (Dworkin, 2002). This clinical commentary provides a critique of recent literature in response to key questions health care consumers and providers, such as physiotherapists, may have as regards NeP.
How many people have neuropathic pain?
Prevalence may be defined as the total number of cases (of the condition) in the population at a given time (Collins, 2009). A systematic review of the prevalence of NeP, and for NeP associated with specific conditions (Table 1) according to world regions, settings and populations (Gagnon et al, 2007). Seventy-nine studies were included in the systematic review however only three were conducted in the general population: one in the USA (reporting prevalence of 0.021% for complex region pain syndrome (CRPS) I and 0.009% for CRPS II), one in the UK (reporting prevalence of probable NeP of 8.2%) and one in India (reporting prevalence of peripheral neuropathies) (Gagnon et al, 2007). Both USA and Indian data are based NeP caused by one or two conditions whereas UK data is based on probable NeP in the general population. The authors concluded that prevalence of NeP in the general population was higher than previously thought, although this needs to be confirmed in general populations of countries other than the UK. Therefore although the exact prevalence of NeP in New Zealand is unknown, extrapolating the UK general population figure of 8.2% to New Zealand suggests there may be nearly 340 000 people with NeP (based on general population of 4,143,279 people from 2006 Census (Statistics New Zealand, 2006)).
What is the impact of neuropathic pain?
The impact of NeP on health-related quality of life (HRQOL) was recently systematically reviewed by Jensen and colleagues (2007). Fifty two studies were identified which examined the association between a wide variety of HRQOL domains and NeP. One of these studies is presented in Figure 1 to illustrate the percentage of people with moderate to severe pain and the association with HRQOL variables. These studies commonly use HRQOL measures such as the SF-36 and the Brief Pain Inventory. The SF-36 is a generic measure with 8 dimensions covering physical function, physical role, bodily pain, general health, mental health, emotional role, social function and vitality (Ware, 2009). The Brief Pain Inventory is a 17 item self-rated scale which includes demographic data, medication use and the sensory and reactive components of pain (Keller et al, 2004). It comprises numeric rating scales (0-10), with moderate pain severity as 4-6, and severe pain as 7-10. Results from the systematic review indicated that pain presence and severity was significantly associated with impairments in physical functioning and had a negative impact on emotional functioning (Jensen et al, 2007). Pain presence was also significantly associated with sleep interference and a negative impact on role and social functioning. Peripheral and central NeP conditions (for example painful diabetic neuropathy and post-stroke pain, respectively) showed similar associations between pain severity and HRQOL. The authors conclude that the negative effects of NeP on physical, social, and emotional HRQOL domains indicates the needs for a psychosocial approach to the assessment and management of NeP. As associations were generally stronger with pain-specific measures of HRQOL such as the Brief Pain Inventory compared to the SF-36 physical function subscale, the authors suggest the brief pain inventory maybe a useful tool in clinical practice and clinical trials. Limitations of the reviewed research were that almost all studies were descriptive or correlational designs therefore causal relationships could not be established.
It is unclear whether HRQOL can predict treatment outcome. One study investigated whether HRQOL could predict analgesic effect of treatment in patients with painful polyneuropathy (Otto et al, 2007). Data from 93 patients were included in the analysis and were obtained from three randomized, placebo-controlled studies testing the effect of different drugs on pain. Patients completed the SF-36 at baseline (no treatment period) and at the end of each treatment. At baseline all SF-36 scores were lower than the normal population and regression analysis indicated that baseline scores predicted response to treatment. The authors reported that they could not identify any other studies on HRQOL predicting treatment outcome in chronic pain conditions.
What are patient experiences of neuropathic pain?
Qualitative research focuses on answering the 'why' and 'how' questions (Kuper et al, 2008a). Qualitative research aims to generate in-depth accounts from individuals or groups, with data usually being gathered via interviews (semistructured or unstructured); focus groups, or observations (Kuper et al, 2008b). Data analysis is usually inductive (reasoning by drawing general rules from individual cases) allowing meaning to emerge from the data as opposed to deductive 'hypothesis driven' quantitative approaches (Kuper et al, 2008b). Qualitative research surrounding patient experiences of NeP includes impact on relationships (Closs et al, 2009), social consequences (Sofaer-Bennett et al, 2007) and managing symptoms (Closs et al, 2007).
Themes which emerged from the data concerning the social impact of NeP include: the loss of ability to maintain established roles leading to feelings of guilt, inadequacy and frustration (Closs et al, 2009), social isolation (Closs et al, 2009, Sofaer-Bennett et al, 2007) and the invisibility of pain causing issues with communication and the resultant fear of being labeled mentally ill (Closs et al, 2009). Themes which emerged from the data concerning symptomatic management included: self management using alternative strategies, conventional medications, and trying to accept pain adjusting to the situation (Closs et al, 2007). Repeated cycles of seeking help to manage pain were also described with each unsuccessful attempt followed by new attempts (Closs et al, 2007).'.... I was four years trying all different medications to try and control the pain.... they weren't any good really...." (Closs et al 2007, p426). Patients reported little or no psychological, social, emotional or practical support to help them try to accept their pain (Closs et al, 2007).The researchers may be commended for the credibility of their research in establishing the experiences of patients with NeP, their criticality of investigating alternative theories that included a critical examination of deviant cases, and integrity of the number of repetitive checks of by different authors of the data to explore alternative meanings. The authors of these qualitative studies all suggested that there is a need to validate the theoretical findings that they proposed in larger studies. These studies were conducted in the UK therefore it is unclear whether all the findings might be applicable or transferable to the health care context of New Zealand.
How is neuropathic pain diagnosed?
There is no 'gold standard' test used for the diagnosis of NeP (Treede et al, 2008). NeP results from disease or injury to the nervous system therefore positive and negative sensory symptoms and signs are typical (Dworkin et al, 2003). In patients with suspected NeP, clinicians and physicians use information gained from the subjective history to inform further assessment such as the neurological examination. The European Federation of Neurological Sciences guidelines of NeP assessment recommend that in the clinical setting a neurological exam, which includes an accurate sensory exam, is often sufficient to reach a diagnosis (Cruccu et al, 2004); the abnormal sensory signs being neuroanatomically compatible with a definite lesion site (Cruccu et al, 2004). Guidelines of the management of NeP also highlight the importance of an accurate history and examination with characteristics of NeP being defined within: spontaneous (stimulus independent; e.g. burning sensation, intermittent shooting, electric shock-like pain) and stimulus evoked pains (evoked by mechanical, thermal or chemical stimulus; e.g. static pressure evoked, dynamic brush evoked and cold allodynia (pain evoked by cold)) (CREST, 2008). They also recommend the use of diagnostic screening tools (such as the DN4 or the LANSS; see Table 2) to differentiate NeP and nociceptive (NP) (CREST, 2008).
Screening tools based primarily on pain description/pain symptoms have been developed to identify NeP. It is important to recognize that these tools do not include questions concerning the patient's medical history, and only some of the tools include limited sensory testing (Table 2). In addition, some of these tools have been validated for administration by a clinician whilst others are self-rated by the patient. A previous critical review of such screening tools provided an overview of their diagnostic accuracy by referring to primary diagnostic studies (Bennett et al, 2007). The authors concluded that these questionnaires offered guidance regarding diagnosis as they could not correctly identify 10--20% of patients with clinically diagnosed NeP. However, this critical review did not explore potential clinical and methodological sources of variation (heterogeneity) of the studies which might explain this level of diagnostic accuracy. For example, clinical diagnosis of NeP is usually based on diagnosis by a physician where it is often not stated which tests are used to make the diagnosis. It has been suggested that the main clinical role of these screening tools is that they may aid diagnosis of NeP particularly by non-specialists (Bennett et al, 2007). Specifically, such questionnaires may serve as a triage to inform subsequent assessment and decision making.
Experts (neurologists and pain specialists) have reached consensus concerning a grading system regarding the likelihood of the certainty of the presence of NeP in an individual patient (Treede et al, 2008). The grading system is as follows:
* Possible neuropathic pain: If the patients' history suggests a relevant lesion or disease and a temporal link between the lesion or disease causing the pain, and pain distribution is in a neuroanatomically plausible area (e.g. use of a body drawing)
* Probable neuropathic pain: The possible criteria and either, (1) a diagnostic test confirming a lesion or disease, or (2) negative or positive sensory signs confined to the neuroanatomical area
* Definite neuropathic pain: The possible criteria and both of the probable criteria.
The medical history, pain distribution on a body drawing, and sensory testing are pivotal to these diagnostic criteria. Studies to provide evidence (or not) for these criteria are required as currently there is level C evidence (retrospective study evaluated by a blinded assessor) for bed side sensory testing and quantitative sensory testing has never been used to make a differential diagnosis between NeP and NP pains (Cruccu et al, 2004). An important question to ask is "where do screening tools 'fit' in this grading system?" Treede (et al, 2008 p1634) state that "future studies are required to determine the utility of this grading system and possible necessity for revision, for example by including symptoms in the grading." The authors should be commended for this classification system as opposed to the alternative situation whereby the neuropathic pain syndrome is stated and it is assumed that pain is NeP. The main screening tools to differentiate NP and NeP are listed in table two, along with an indication of the classification criteria they may satisfy.
What are current management strategies for neuropathic pain?
CREST guidelines recommend that the evaluation of NeP (in addition to diagnosis, cause of NeP and history) should include 1) location, quality, intensity, and duration of pain; 2) functional impact include activities and sleep pattern; 3) psychological factors including effect on mood; and 4) response to previous treatment (CREST, 2008). NeP can be managed in primary or secondary care. Initial treatment options for NeP include: (1) non-pharmacological options, as these have the lowest risk of side affects and must be offered early, with possible referral to physiotherapy, occupational therapy, psychology (if predominantly psychological issues) or a pain management programme (if significant physical, social, and functional issues), and (2) pharmacological interventions such as unconventional and conventional analgesics (CREST, 2008).
What is the evidence-base for these strategies?
For strategies other than physiotherapy, key guidelines or the most recent systematic reviews are used for evidence. For physiotherapy searches were conducted for systematic reviews in this area. Few studies were indexed under the heading 'neuropathic pain' therefore Mesh (medical subject word headings) headings of NeP conditions were used (e.g. Complex regional pain syndrome, neuropathy) and physiotherapy using the search strategy identified by Montori (2005) in MEDLINE via Pubmed.
Evidence-based pharmacological strategies for the management of NeP suggest that first line treatments may be: antidepressants (tricyclics or dual re-uptake inhibitors of serotonin or noradrenaline), calcium channel [alpha]2-[delta] ligands (gabapentin and pregabalin), local anaesthetic type drugs (lidocaine), and opioids (Dworkin et al, 2007). These recommendations are based on randomized controlled trial data. However, it should be noted that only 30-40% of patients will receive >50% pain relief. Recommendations for trials investigating combinations of pharmacological treatments and/ or pharmacological and non-pharmacological treatments have therefore been made (Dworkin et al, 2007).
This section primarily focuses on physiotherapy, spinal cord stimulation, and pain management programmes as recommended in the CREST guidelines for the management of NeP (2008).
Neuropathic pain and physiotherapy
A systematic review of complementary therapies for NeP and neuralgia pain included randomized controlled trials (RCTs) and systematic reviews for acupuncture and electrostimulation (including transcutaneous electrical nerve stimulation (TENS)) (Pittler and Ernst, 2008). Three RCTs were identified which investigated acupuncture. No analgesic benefit of acupuncture compared to mock TENS was reported (Hempenstall et al, 2005), or acupuncture compared to placebo (Shlay et al, 1998) for post-herpetic neuralgia and HIV induced peripheral neuropathy, respectively. The third RCT compared two forms of needling and found deep needling to increase the therapeutic effect in trigeminal neuralgia (Zhang, 2005). This review indicates there is little evidence for the use of acupuncture in NeP conditions. Future trials should use an appropriate sham needle (rather than mock TENS) and dosage of acupuncture before the efficacy of this modality is known (White et al 2008). Four RCTs were identified which investigated electrostimulation (TENS with electrodes or PENS with needles) (Pittler and Ernst, 2008). They found that pain scores improved compared to baseline (Forst et al, 2004; Hamza et al, 2000) or placebo (Kumar et al, 1997; Cheing and Luk, 2005) in diabetic neuropathy or hypersensitivity of the hand. Although these results are encouraging, it is also not reported which stimulation parameters were used. A review of systematic reviews on TENS and chronic pain (osteoarthritis, rheumatoid arthritis, low-back pain) found that two out of six reviews reported that high intensity (strong but tolerable) intensities of TENS were more effective compared to placebo than low intensity (strong but comfortable) applications (Claydon and Chesterton, 2008). These results were based on a total of eight high quality (adequate randomization and blinding) trials which used validated pain intensity or relief visual analogue (VAS) or numeric rating scales (NRS) as the outcome measure. The systematic review by Pittler and Ernst (2008) did not rate the studies for quality and did not report the search strategy (inclusion criteria and sources searched). It appears that systematic reviews for TENS and chronic pain may have not extensively searched for various neuropathic as opposed to nociceptive conditions.
Complex regional pain syndrome and physiotherapy
A systematic review recently reported on the effectiveness of physiotherapy management for adult complex regional pain syndrome (CRPS) type I (Daly and Bialocerkowski, 2009). The authors found that a six week graded motor imagery programme is effective in reducing pain by a clinically relevant amount, and this effect is maintained for 6 months. This evidence was graded as good to very good (scored 11-14/16 on quality tool) level II (properly designed RCT(s)) based on the work by Moseley (Moseley, 2004; Moseley, 2005; Moseley, 2006). The authors also reported that there is no evidence to support frequently recommended treatments in guidelines such as stress loading.
Neuropathy and physiotherapy
Systematic reviews of interventional RCTS for neuropathy include: Charcot-Marie-Tooth disease (Young et al, 2008), chemotherapy-induced neuropathy (Visovsky et al, 2007), and exercise for peripheral neuropathy (White et al, 2004). Charcot-MarieTooth disease covers a lot of different forms of sensory and motor neuropathies (Young et al, 2008) and the authors of this Cochrane review systematically looked for RCTs or quasiRCTs on any treatment for this disease. They found that small trials of exercise have been performed; however, none showed a significant benefit. The chemotherapy-induced peripheral neuropathy systematic review included evidence for pharmacological and non-pharmacological strategies; the non-pharmacological evidence is considered here (Visovsky et al, 2007). The authors reported that there are no RCTS concerning acupuncture, assistive devices, physical activity and exercise, or TENS for this type of neuropathy. The authors made treatment recommendations based on literature reviewed previously and on the following Cochrane systematic review on exercise for peripheral neuropathy. The role of exercise for individuals with peripheral neuropathy (sensory, motor or combined) found that there was inadequate (quality) evidence to evaluate the effect of exercise in this population (White et al, 2004). Only one trial was randomized or quasi-randomised comparing the effects of exercise to drugs or non-pharmacological management on outcomes at least 8 weeks after randomization. The authors also stated that pain was infrequently reported in the primary studies.
Neuralgia and physiotherapy
A systematic review recently reported on interventional RCTs concerning conservative treatments (including physiotherapy) for lumbrosacral radicular syndrome (Luijsterburg et al, 2007). They found that: (1) at long-term there is no evidence in favour of corticosteroid injections compared to placebo, (2) at short term there is no evidence in favour of traction compared to placebo or other treatments, (3) at short term there is no evidence in favour of physiotherapy, bed rest, manipulation or medication compared to other treatments or surgery, and (4) no evidence was found regarding acupuncture. The authors stated that they could not conclude whether clinicians should prescribe physiotherapy, bed rest, or manipulation as there was no evidence of treatment superiority (Luijsterburg et al, 2007). This parallels the evidence reviewed in Cochrane reviews concerning bed rest in back pain and sciatica (Hagen et al, 2004) and traction in back pain with and without sciatica (Clarke et al, 2007).
Central pain (Stroke, Multiple Sclerosis, Parkinson's Disease) and physiotherapy
Systematic reviews on stroke pain and physiotherapy included: supportive devices for preventing and treating subluxation of the shoulder (Ada et al, 2005) and electrical stimulation for preventing and treating post-stroke shoulder pain (Price and Pandyan, 2000). Ada (et al 2005) found that strapping the hemi-shoulder could prevent the onset of pain but not decrease pain severity. Price and Pandyan (2000) found that electrical stimulation improved pain free lateral rotation but did not decrease pain incidence or intensity. However it is unclear whether the pain was NeP or due to tissue injury (NP). A search for Parkinson's disease and pain and physiotherapy, only resulted in a review for the treatment options for nonmotor symptoms in late-stage Parkinson's (where treatments for dementia, psychosis, fractures and pain are considered) (Coelho et al, 2008). As regards Multiple Sclerosis, one systematic review reported an overview of RCTs concerning physiotherapy (Wiles, 2008). Generally the RCTs reported benefits for people with MS. However, it was not reported which patients had pain apart from two trials of TENS for back pain in Multiple Sclerosis, the effects of which were negative (Warke et al, 2006; Al-Samadi et al, 2003).
An indication of the RCT evidence for physiotherapy in various NeP conditions has been outlined. Applying the classification of NeP considered earlier, most RCTs stated diagnosis of the NeP condition rather than indicating pain distribution and sensation testing making it unclear whether NeP was present. There appears to be an absence of quality research for physiotherapy management of various neurological conditions which cause NeP, apart from the physiotherapy management of CRPS type I.
Spinal cord stimulation
A recent health technology assessment was commissioned to evaluate the effects of spinal cord stimulation in patients with NeP or ischaemic pain (Simpson et al, 2009). Spinal cord stimulation is a device implanted in the epidural space which stimulates the dorsal columns of the spinal cord, the implantation costing around $30,000 (10,000 [pounds sterling]). The authors found three RCTs concerning spinal cord stimulation and NeP and concluded that it is effective for NeP associated with failed back surgery syndrome (persistent pain after anatomically correct surgery) and CRPS type I (Simpson et al, 2009).
Pain management programmes
Recommended guidelines for pain management programmes in adults have been published by the British Pain Society (BPS, 2007). The authors of this guideline state the programmes are based on cognitive behavioural principles and are the treatment of choice for people with persistent pain which adversely affects their HRQOL. The programmes consist of education on pain physiology, psychology, healthy function, self management, goal setting, relaxation, changing habits which are contributing to disability, and changing unhelpful beliefs. The references regarding evidence of effectiveness for these programmes are largely based on musculoskeletal pain, and/or any NeP component is unspecified. The authors of this guideline state that the 'majority of the patients which attend these programmes have musculoskeletal pain (NP) although a minority have NeP or central pain p13.'
Conclusion--what does the future hold?
Evidence has been reviewed concerning the prevalence of NeP, impact of NeP on HRQOL, patient experiences of NeP, and diagnostic and management strategies. Key points of this review are summarized below. With consideration for the New Zealand scene, the following areas of research have been highlighted,
* What are New Zealanders experiences of NeP? What research would they like to be conducted in this area? What outcomes are important to them?
* How do physiotherapists identify possible NeP? How useful do they find the assessment and management guidelines?
* What are possible sources of variation in the screening tools for NeP? Which tool has the highest quality (best)?
* How valid is the classification system for NeP? Does it need to include screening tools?
* Is TENS effective for NeP?
* Is exercise effective for NeP?
Studies concerning these key questions are currently underway.
* Neuropathic pain (NeP) may affect 340,000 New Zealanders.
* NeP affects multiple domains of life (physical, social, and emotional function and sleep).
* Patients experience social isolation and lose the ability to maintain established roles.
* Patients seek management for symptoms via conventional and unconventional treatments and attempt to accept the pain.
* A diagnostic classification system for NeP has been proposed, the utility of which needs investigating.
* Management strategies for NeP includes pharmacological and non-pharmacological treatments.
* RCTs usually state the neurological condition making it unclear whether NeP is present.
* RCT data supports the use of motor imagery for CRPS type I; high quality RCTs appear to be lacking in other neurological conditions which can cause NeP.
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Leica Sarah Claydon
Lecturer, REAL Neurology Research Group, Centre for Physiotherapy Research, University of Otago, Dunedin, New Zealand
ADDRESS FOR CORRESPONDENCE:
Dr Leica Claydon, Centre for Physiotherapy Research, University of Otago, PO Box 56, Dunedin, New Zealand, 9054.
Table 1: Common causes of NeP (adapted from Dworkin 2002) Chemotherapy-induced neuropathy Complex regional pain syndrome HIV sensory neuropathy Neuropathy secondary to tumor infiltration Painful diabetic neuropathy Phantom limb pain Post-herpetic neuralgia Central post-stroke pain Multiple sclerosis pain Parkinson's disease pain Spinal cord injury pain Table 2: Some screening tools of NeP and their characteristics (see text for further details) Space for Medical Body Tool and reference Population History map Leeds Assessment of Chronic pain No No Neuropathic Symptoms of any origin questions about and Signs (LANSS) pain and sensation. (Bennett, 2001) No temporal questions with history. S-LANSS Chronic pain No Yes (Bennett et al, 2005) of any origin questions about pain and sensation. No temporal questions with history. DN4 Chronic pain No No (Bouhassira et al, of any origin questions about 2005) pain and sensation. No temporal questions with history. Neuropathic Pain Chronic pain No No Questionnaire (NPQ) of any origin questions about (Krause and pain and sensation. Backonja, 2003) No temporal questions with history. Clinician or patient Tool and reference Sensory testing completes Leeds Assessment of Yes. Painful area compared Clinician Neuropathic Symptoms to non-painful area (not and Signs (LANSS) neuroanatomical) (Bennett, 2001) * Stroke with cotton wool * Pin-prick S-LANSS Yes. Painful area compared Patient (Bennett et al, 2005) to an non-painful area (not neuroanatomical) * Patient rubs area * Patient presses DN4 Yes. Not in a neuroanatomical Clinician (Bouhassira et al, area 2005) * Pain with touch * Pain with pin-prick * Pain with brushing Neuropathic Pain No Patient Questionnaire (NPQ) (Krause and Backonja, 2003) Figure 1: Study by McDermott et al: 2006 Burden of NeP: results from a cross-sectional survey * A cross-sectional survey of 602 patients with NeP (from six countries) was conducted * Patients reported functional health, well-being, pain experience, and health care utilization using the brief pain inventory (see text), and completed a score regarding HRQOL (EuroQol) * The mean age of patients was 62.9 years. * Most patients reported moderate (54%) or severe pain (25%) on the BPI. * Pain severity was associated with poorer EuroQol scores * 93% of patients took medications, 76% visited the physician at least once a month, and 9.8% missed an average of 5.5 days of employment.
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|Title Annotation:||Invited Clinical Commentary|
|Author:||Claydon, Leica Sarah|
|Publication:||New Zealand Journal of Physiotherapy|
|Date:||Jul 1, 2009|
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