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    Continued the process of making this section into a more substantive exploration of the idea of specific back pain, and added a new example, a case study of back pain caused by a tumour on a nerve root.

    Merged content from the back and neck pain tutorials, resulting in major upgrades to two important sections in both books. The role of true nerve problems in low back pain.

    The nerve pinch myth. Discussed potential harms of strength training in a little more detail. Core strengthening has failed to live up to the hopes and dreams of therapists and patients.

    A new standard chapter for most PainScience. Some important things to keep in mind about placebos. Added an important new sub-section about anticonvulsants. New key new citations and thorough analysis. Do you really need to lose some weight?

    Added much more detail about the basics of neuropathy and revised everything else quite thoroughly. Expanded the discussion of implications of Jayson as promised last month. A science update … with quarter century old science about blood supply and radiculopathy see Jayson. Just a new section. Phase 1 of a reboot of this part of the book. An introduction to your care options. Well, new to the book anyway. It has been available as a free article for quite a while, and it will remain so indefinitely.

    Although this content is not exclusive to the book, it definitely does belong here. Kill it with fire! Treatment by nerve destruction. Needles for back pain: The section has been re-written and expanded significantly, with a key change in position.

    After reviewing the same scientific papers previously cited more carefully, I decided that they were much less promising than I originally thought. Diagnostic numbing of facet joints. Added a substantive footnote explaining the relationship between ulcers, stress, and H. Low back pain is the new ulcer. Although the topic is not covered in detail here, much study went into making this summary possible. The evidence for massaging back pain. The bottom line is now that the science is inconclusive and discouraging instead of optimistic.

    Added an excellent recent example of awful back pain information. Added discussion of orthotics to treat leg length differences for back pain. An important and interesting acknowledgement that mechanical causes of back pain do exist.

    Some light editing of everything else in the chapter. Added a small but key new point and citation about genetic factors in degeneration; and an important new citation about the disconnect between imaging results and pain. Your low back is not fragile! Discussed important new review of SMT for acute low back pain.

    Significant revision of the section. Spinal manipulative therapy SMT: Adjustment, manipulation, and cracking of the spinal joints. Even serious structural problems in the low back are often painless. Newer, better, evidence-based good news about disc herniation resorption. Updated references for debunking of TENS for back pain. Added ultrasound to the section. A few more snack-sized reality checks: Sitting, chairs, and ergonomics.

    Added discussion of a remarkable example of poor MRI reliability. An evidence-based reversal of position and advice about sitting and back pain, correcting a long-standing error: The fascinating case of acupuncture, formerly a contender in low back pain therapy, but which has now miserably failed well-designed scientific tests.

    Thorough revision and modernization. Although I revised this section just five years ago, it needed it again! A trigger point checklist: There is now a good scientific concensus on the subject of spinal fusion, thanks to papers like Mannion and Hedlund Putting a spotlight on this called for some serious revision and editing. The whole section is greatly improved. The back surgery placebo problem, and how it limits our knowledge of the effectiveness of back surgeries.

    Greatly improved information about opioids and linking to much more information. Added much more information. Removed overconfident statements about the clinical significance of the effects of psychoactive drugs, plus related minor updates. Some editing and new caveats. Some fresh citations that strongly reinforce the main point of the section, and a few entertaining new examples of weird placebo effects.

    Updated opioid summary for consistency with new CDC guidelines. Added new intro to section about distorted body image. Clarification of the significance of some previously cited science, Ferreira et al. New citations and more information about spontaneously resolving herniations. Beefed up the evidence that vertebroplasty is an ineffective surgical fix for an allegedly structural problem.

    Added a note about the odds of back pain having a serious cause. Added some general explanation of cognititive-behavioural therapy, with a key reference. Added discussion of a popular acupuncture-for-back-pain paper, Cherkin Which is not fit to line a birdcage, in my opinion.

    Modernization of trigger point summary, more science, and more acknowledgement of controversies. Modernization of trigger point summary, more science, acknowledgement of controversies.

    The missing muscle piece. Added surprisingly good news about methylene blue injections. Facet joint and intradiscal steroid injections are not recommended for most patients. And still not enough!

    Antibiotics for back pain: Added a reference for reassuring data about recovery rates. Who is this low back pain tutorial for? The first complete professional editing of this book has now been completed. Although the difference will not be obvious to most readers, several hundred improvements and corrections were made, and it is definitely a smoother read.

    Added Digital Motion X-ray. Plugged a good quality microbreaking reminder app [Section: Is it core weakness? Back bracing and stabilization contraptions especially inflatable ones. Cleaned up and modernized, more information, especially a more useful and evidence-based self-treatment tip. Morning pain and sleep posture. Joint popping, muscle dominance, and the mind game. Added some great backup from a terrific surgeon blogger — who advocates for the necessity of testing placebo surgeries, exactly as I have in this section for many years.

    Added a fascinating footnote about the myth of anaesthetic paralysis. Added subsection on electroacupuncture. Reporting on the greatest hits of back pain science Machado , a source of several important points here and in other sections. Interpretation of a little junky new science about Pilates. Pain and fear, together at last: Added a quote that beautifully expresses the reason for treating chronic pain with … maturity.

    This way pain and fear power each other is now explained much more clearly and thoroughly than before. Important new chapter about a hype-hot news item.

    Interesting, useful new reference. Upgraded risk and safety information about Voltaren Gel. All major professional treatment options now summarized.

    All major self-treatment options now summarized. How to save yourself from low back pain, or at least avoid getting hurt or ripped off trying. Added more evidence showing the role of smoking in chronic back pain. An action-oriented summary of recommendations. New reference strongly supporting a key, controversial point. Added an intriguing quote about evolution and the lack of back pain in hunter gatherers. Is it all in your feet?

    Foot-o-centric low back pain theories. Added evidence that the stakes are high with chronic pain: A tragic low back pain myth. Added a new suggestion for safe, pleasant self-tractioning. Back pain and sneezing. Interesting evidence that massage therapists cannot reliably find the side of pain by feel.

    Structural problems in the low back are hard to diagnose accurately. Added a fine example of taking yoga very, very seriously as an option. See first footnote in section. Stress relief and the tyranny of meditation and yoga. Editing, and several new paragraphs about safety issues. Yoga and meditation are still an option, of course. Some simple revision for clarity and quality, and a bit more content.

    More science, and a few substantial new footnotes fielding common concerns and questions. Clarified information about pelvic tilt, and beefed it up with some more science. Important new, skeptical footnote about the dangers of the powerful narcotic drugs. More evidence of the exercise effects are limited and non-specific.

    Minor, but fun — a great quote about models of slipped discs, and a good new image to help it along. Those scary spine models. Detailed reporting on some new yoga science. Significant re-writing of the section ensued. Sometimes new science does not back up my preconceptions: I stumbled across a fantastic scientific paper about the prevalence of nerve pinches hint: A key concept covered in the trigger points tutorial long ago, but so relevant to low back pain that I decided it needed to be here as well.

    Could it be a vicious cycle of pain-spasm-pain? From the frying pan of injury pain to the fire of trigger point pain. A few new paragraphs summarizing an important new study of massage for low back pain with disappointing results. Added a reference about the poor overall quality of online information about common injuries. More information about an important characteristic of muscle-dominated back pain.

    A few new checklist items were added, most were expanded, and all were clarified. Major improvements to the table of contents, and the display of information about updates like this one. Sections now have numbers for easier reference and bookmarking. The structure of the document has really been cleaned up in general, making it significantly easier for me to update the tutorial — which will translate into more good content for readers.

    Care for more detail? Added evidence that spinal fusion surgeries are not just ineffective but often harmful Nguyen. Added a fascinating science item about the effect of anti-inflammatory gels on back pain Huang. Long overdue, I finally added some science to this section, showing that the connection between low back pain and obesity is weaker than it seems Wright.

    New artwork from PainScience. Added a fun and informative quote from the TV show House. Added some new evidence about back pain and aging, and a nice new graph.

    Just added a link, but a really great link! The CBC show Marketplace did an amazing job last year reporting on spinal decompression machines. Well worth a look — the show and their show page is probably now the single best source of information on this topic. Some editorial cleanup on core strengthening, and I a link to a good summary of recent research. Re-written and significantly expanded. Rest minimally and strategically, while maintaining as much normal activity as you can. Could low back pain be an overuse injury?

    Rewriting and expansion of the Special Supplement on spinal manipulative therapy. Added a very beefy footnote about some new research showing that muscle imbalance does not result in higher rates of injury. Section now includes discussion of that bizarre and already infamous paper in the New England Journal of Medicine see Berman.

    I also make an important new point: Updated with a summary of a bizarre experiment with muscle relaxants that had quite surprising results. Added a scientific thumbs down for transcutaneous electric nerve stimulation TENS. A surprising scientific thumbs up for comfrey ointment was worth a whole new small section. Comfrey makes backs comfy, study claims.

    Rewritten and significantly expanded information about medications. Less than a cure, but better than nothing: Having debunked expensive spinal traction using expensive decompression machines, here are some ideas for cheaper and safer methods of tractioning. It all evolved from writing about an important bit of research, showing that manual therapists cannot reliably diagnose trigger points.

    Limitations of trigger point therapy, and how to take advantage of them. Nikolai Bogduk has authored dozens of scientific papers about low back pain.

    He also questions and challenges many common beliefs about low back pain, and is one of the expert sources this tutorial relies upon. Cartoon by Loren Fishman, HumoresqueCartoons. This situation has not improved over time. This paper presents some unusually optimistic old data about low back pain recovery: This study of changes in spinal characteristics in Swiss adults since the late 19th century found … well, basically nothing. Spines are pretty much the same now as they were then.

    At least in Switzerland. There are more footnotes in the full version of this book. P a i nScience. Save Yourself from Low Back Pain! There are footnotes in this document. A study in the United States US revealed that the prevalence rates for NP determined by either clinical examination or self-reporting were 9.

    It is difficult to obtain a true estimate, due to epidemiological studies using different methods of assessment and different definitions of NP [8]. A recent systematic review of epidemiological NP studies across the world by van Hecke et al.

    Patients suffering from chronic NP have higher degrees of anxiety and depression scores, as well as sleep disturbances, compared with patients with non-neuropathic chronic pain, and patients without chronic pain [10] , [14]. A study by Smith et al. Information about the common types of peripheral NP and their pharmacological treatments is presented. In addition, the recommendations from different organisations are highlighted and compared in order to provide healthcare professionals with a global perspective on the treatment of NP.

    Information for this narrative review was collected based on a search of the literature in the following areas: The following databases were also searched for relevant information: References of retrieved articles were scanned for additional relevant studies. Peripheral NP is the result of injury to nerve fibres due to various aetiologies including toxic, traumatic, ischaemic, metabolic, infectious or compressive damage [3].

    Positive symptoms are typically altered or painful sensations such as tingling, prickling, or pain described as shooting, stabbing, burning, or having an electric shock sensation [16]. Negative symptoms are described as diminished sensations due to loss of sensory function [16]. Patients may also experience allodynia pain caused by a stimulus that usually does not cause pain , hyperalgesia increased pain from a stimulus that normally provokes pain , and anaesthesia dolorosa pain in an area that is anaesthetic or numb [17] , [18].

    The diagnosis of NP is primarily based on patient history and physical examination. The Special Interest Group on Neuropathic Pain NeuPSIG recently updated a grading system to assist with determining the level of certainty that the pain is neuropathic in nature and not related to other causes [19].

    For patients to be classified at the possible level, pain distribution must be consistent with suspected lesion or disease, and patient history must be assessed and associated with NP using validated screening tools Table 1 [20] , [21] , [22] , [23] , [24] , [25] , [26].

    The next level of probable NP is obtained through clinical examination, particularly focusing on negative sensory signs [19]. If a patient is classified with probable or definite NP, consideration should be given to pharmacologic treatment using clinical guidelines [19]. NP has multiple aetiologies. Some of the more common underlying conditions that are associated with NP include diabetic peripheral neuropathy, HIV-associated neuropathy, chemotherapy-induced peripheral neuropathy CIPN , postherpetic neuralgia PHN and trigeminal neuralgia [16].

    Although the aetiologies may vary, the signs and symptoms of NP that patients experience can be similar [8]. Diabetic peripheral neuropathy is a condition that affects many patients with diabetes. In the UK, the annual incident rate per 10, population for painful diabetic neuropathy was 3.

    Diabetic neuropathy is recognised in patients with diabetes by the presence of peripheral nerve dysfunction symptoms after other causes have been excluded [28].

    Although the exact mechanism is unknown, this type of NP is thought to be the result of oxidative and inflammatory stress caused by metabolic dysfunction, which ultimately damages the nerve cells [28]. Diabetic neuropathy plays a major role in foot ulcerations, the development of Charcot neuroarthropathy, falls and fractures [28]. This type of neuropathy presents as a distal polyneuropathy in a symmetrical pattern that occurs in patients with both treated and untreated HIV infections.

    HIV-SN can be the result of injury to the nerve by the HIV virus itself, or it could be caused by medication-induced mitochondrial dysfunction of the nerve cells [30].

    Risk factors associated with the development of HIV-SN include exposure to neurotoxic antiretroviral drugs, increasing age, malnutrition, ethnicity, increasing height, certain genetic factors and comorbid conditions such as diabetes [31]. CIPN is the most common neurological cancer treatment complication [30]. It is a dose-dependent, adverse effect associated with chemotherapy agents such as platinum drugs, vinca alkaloids, bortezomib and taxanes [32].

    These agents cause sensory nerve damage in the dorsal root ganglion [30]. The symptoms may become progressively worse as chemotherapy is continued [30] , [33]. In many cases, CIPN improves once the therapy is discontinued; however, with cisplatin and oxaliplatin, it may continue even after the drugs have been discontinued [34].

    PHN is type of NP that develops when the herpes zoster virus is reactivated. The virus can affect the nerves through sensitisation hyperexcitability and deafferentation sensory nerve death or damage [30]. Pain is typically distributed unilaterally along spinal dermatomes or the ophthalmic branch of the trigeminal nerve [2].

    The annual incidence rate per 10, population for post-herpetic neuralgia was 3. Trigeminal neuralgia is the most frequent cranial neuralgia [36]. In the UK, the incidence of trigeminal neuralgia is reported as 28 per , person years observation [35]. Patients with trigeminal neuralgia experience facial pain limited to areas associated with one or more branches of the trigeminal nerve [2] , [36]. The symptoms that patients experience are the result of compression of this nerve by vasculature or tumours.

    This type of pain can also be caused by demyelination in patients with multiple sclerosis. Pain attacks begin suddenly and last from several seconds to a couple of minutes. The pain is usually unilateral in nature and is described as sharp, shooting, shock-like, burning and excruciating [36]. These attacks are usually accompanied by involuntary spasms or contractions of the facial muscles [36]. Trigeminal neuralgia is usually triggered by non-painful physical stimulation of a specific area that is located close to the pain [36].

    Patients with NP typically do not respond to traditional analgesics paracetamol, NSAIDs or weak opioids because these do not focus on treating the types of symptoms associated with NP [2]. Many patients do not achieve satisfactory pain relief even with evidence-based treatment, or do not tolerate effective doses because of adverse effects [16] , [37]. In this article, a brief description of the mechanism of action MOA for each drug class is provided, along with UK dosing information.

    Detailed descriptions of the MOA have been reported in other studies [2] , [16]. Caution in elderly patients who are cardiovascular compromised. Post-marketing reports of congestive heart failure. CNS depression caution with activities requiring mental alertness and elderly at risk for falls. Adverse effects may be more severe in older patients, lower starting doses and more gradual titration recommended. Day 3 — mg three times daily [39]. Dose can be increased 10—25mg every three to seven days as tolerated [40].

    Doses above mg should be used with caution [40]. Contraindicated in patients with recent myocardial infarction or cardiac rhythm disorders or severe liver disease. Botulinum toxin type A [47]. May repeat every three months [47].

    Tramadol [48] , [88]. Extended release 50mg, twice daily [49]. The onset of action is more rapid in pregabalin and, because of a narrower dosing range, it requires less titration [28]. An adequate trial duration, in order to assess efficacy, is four weeks [16]. Gabapentin is started at a dose of mg on day one and titrated up to a total daily dose of 1,—3,mg. Equivalent doses given three times a day is optimal, but a higher dose may be given at bedtime to limit daytime sedation [16].

    An adequate trial of gabapentin is between 5 and 10 weeks with at least 2 weeks of therapy at the maximum tolerated dose [16]. An extended-release form of gabapentin, gabapentin enacarbil, has also been used for NP treatment; however, it is not available to prescribe on the NHS in the UK. A systematic review and meta-analysis by Finnerup et al.

    Both come with a risk of increased suicidal thoughts or behaviours and both should be dose adjusted for patients will renal impairment [16]. Older patients may be more susceptible to adverse effects from either medication, therefore, lower starting doses and a slower titration is recommended [28].

    Tricyclic antidepressants TCAs , such as amitriptyline, nortriptyline and desipramine, achieve their effects by inhibiting norepinephrine reuptake in the spinal dorsal synapses and have secondary activity at sodium channels [16]. Adverse effects are the main limitations of this class of medications and include somnolence and anticholinergic effects. There is also concern about TCAs causing possible cardiotoxicity, therefore, caution should be used in patients with known or suspected cardiac disease [28] , [40].

    Patients will usually see the analgesic effect after two to four weeks of therapy [40]. The review and meta-analysis by Finnerup et al. The NNT for amitriptyline was reported as 3.

    A Cochrane review in by Moore et al. The review did not find any lack of efficacy, but the concern was that there may be an overestimation of treatment effect. It was emphasised that amitriptyline should continue to be used as part of the treatment for NP, but only a minority of people will experience good pain relief [51]. Serotonin norepinephrine reuptake inhibitors SNRIs work to block the presynaptic serotonin and norepinephrine transporter proteins, which inhibits the reuptake of these neurotransmitters.

    Both medications are associated with increasing blood pressure and cardiac conduction abnormalities so should be used cautiously in patients with cardiac disease [43] , [44]. Older patients may experience more severe adverse effects so it is recommended to start at a low dose and titrate slowly [28]. In painful diabetic neuropathy, duloxetine had a higher level of evidence of pain reduction compared with venlafaxine [28]. An adequate trial of venlafaxine is four to six weeks [16].

    When discontinuing either duloxetine or venlafaxine, doses should be tapered down gradually to prevent withdrawal symptoms [28]. Overall, these medications are not recommended as first-line therapy because of concerns about diversion, misuse, opioid-associated overdose, morbidity and death [2] , [16] , [50] , [52]. These medications should be avoided in those with a history of substance abuse [50].

    Tramadol, a centrally acting analgesic, has weak mu-opioid receptor agonist activity and inhibits norepinephrine and serotonin reuptake [2] , [16] , [28]. Tramadol was found to be effective NNT: Tramadol is limited by its potential for abuse as mentioned above, even though the risk is lower compared with other opioids [28].

    Tapentadol is another centrally acting opioid analgesic that is a mu-opioid agonist, but also inhibits noradrenaline reuptake [50]. The abuse potential of tapentadol may be similar to other opioids, although because of its low use compared with other opioids, the risk for addiction is currently unknown.

    At this time, tapentadol is not a recommended treatment for NP in the UK. Cochrane reviews have reported low or very low-quality evidence related to the use of strong opioids in the treatment of NP. These reviews do not provide much evidence because of the limited number of studies that focus on these medications as treatment for NP, limited participants in the studies, bias and the potential mishandling of dropout information [58]. For peripheral NP, the meta-analysis by Finnerup et al. These include capsaicin, lidocaine and botulinum toxin type A.

    Topical therapies are recommended in patients with local NP e. Advantages of topical or local therapies include lower systemic drug levels, fewer adverse effects and fewer drug interactions [60] , [61] , [62]. Unlike systemic therapies, titration is unnecessary with targeted topical therapies [62]. Capsaicin is derived from hot chili peppers and desensitises TRPV-1 sensory axons over several days to decrease depolarisation, initiation of an action potential and pain signal transmission [16].

    The long-term safety of repeated applications of these patches has not been established [50]. Creams are of limited use because they must be applied multiple times per day and can cause pain for the first few weeks of therapy [16].

    Lidocaine plasters or patches are licensed in the UK, Europe and US for the treatment of post-herpetic neuralgia only [64]. Patches can be cut if needed and should be applied to painful sites.

    Minimal absorption occurs if hepatic function is normal, but if patients take a Class I arrhythmic medication, systemic absorption should be considered [16]. Titration is not necessary but patients should allow two to four weeks for an adequate trial [16]. Skin reactions at the site of application can be seen. Evidence for the efficacy in the treatment of postherpetic neuralgia is limited [66]. Subcutaneous injections of botulinum toxin type A has shown efficacy for the treatment of peripheral NP [2] , [67].

    The NNT found with a single administration of this therapy compared with placebo was 1. Botulinum toxin type A is a neurotoxin that treats focal muscle hyperactivity with repeated administration locally over six months [2].

    There are other medications e. Cannabinoid use for NP has been recommended as a third-line agent in a few select guidelines, but the use of this product is not recommended in the UK for the treatment of NP pain.

    It is associated with dizziness, sedation, dry mouth, oral discomfort and gastrointestinal adverse effects [16]. Additionally, cannabinoids should not be used in patients with a history of heart disease or psychiatric disorders [52].

    There is concern and controversy about their long-term use [16]. Interventional therapies may be considered in select patients with refractory NP if medications fail to provide relief.

    Spinal cord stimulation is recommended by the National Institute for Health and Care Excellence NICE guidelines as a therapy for patients who experience chronic NP for greater than six months despite standard treatments and have had successful trials with spinal cord stimulation by a specialist [77].

    Other interventional therapies include transcutaneous electrical nerve stimulation, sympathetic nerve blocks and steroid injections [2]. Nonpharmacological treatments have also been suggested to help patients suffering from NP. In general, nonpharmacologial treatments are considered safe and may decrease pain, decrease the use of medications and help increase function [16]. A Cochrane review did not find sufficient evidence to evaluate the effectiveness of exercise in NP.

    However, it did state that there were several small trials that have shown exercise may help patients with muscle strength, functional ability and fatigue [78]. Recommendations for exercise in patients with NP include both aerobic and strengthening exercises [78]. Psychotherapy is another nonpharmacological treatment that has received attention for helping patients with NP. Cognitive behavioural therapy is a type of psychotherapy that uses methods to assess biases associated with pain and avoiding unpleasant thoughts [79].

    A Cochrane review focused on psychotherapy as a treatment for NP found insufficient evidence on the efficacy or safety of psychotherapy [79]. Other nonpharmacological treatments include physical therapy and occupational therapy. Combination therapies are often used in patients with NP who have either failed to have a response, or only had a partial response to monotherapy [16].

    In theory, utilising lower doses of different classes of drugs may help alleviate or prevent adverse drug effects that are seen with higher doses of monotherapy. Studies have focused on the use of combination therapies and have found mixed results [50]. A meta-analysis of two studies did find that a combination of gabapentin with an opioid were superior to monotherapy or placebo , but the combination of the two medications were associated with higher drop-out rates due to adverse effects [80].

    A large study that focused on comparing duloxetine and pregabalin at high doses as monotherapy to lower doses in combination did not show any difference in efficacy or side effects [81]. Owing to the limited number of studies, there is not much available evidence that supports specific combinations of medications for NP [80]. Researchers continue to seek new treatments for NP. There are new voltage-gated sodium channel blockers that are receptor specific and may have less risk of cardiac, motor and central nervous system adverse effects [2] , [82].

    A new selective angiotensin type 2-receptor antagonist, EMA, has been used in trials including one that focused on treating patients with postherpetic neuralgia [83]. Additional medications that are being evaluated include acetyl-L-carnitine and alpha-lipoic-acid [82]. A review of stem cell therapy focused on preclinical data suggested that adult stem cell therapy in patients with NP showed positive effects, with peripheral appearing to be more responsive than central NP [84].

    Personalised pain therapy is another approach that can provide patients with the most effective treatment for NP. The phenotype-based classification system focuses on categorising patients by mechanisms responsible for NP rather than aetiology [2] , [37]. Several phenotypes have been identified and are associated with a positive response to various treatments [2]. Studies that focus on genetics and subgrouping patients based on their phenotypes may play an important role in the future of personalised pain management for NP [2].

    Guidelines and recommendations presented by key organisations around the world focus on NP in general or on specific types of NP. The following recommendations from each organisation are designed to help healthcare practitioners select appropriate pharmacologic treatment for patients with NP.

    In addition to the recommendations listed in this article, there are also local guidelines available to help guide therapy for NP. NICE provided recommendations for treating patients with NP in non-specialist settings in , which were updated in February [18]. In September , it was decided that these guidelines did not require updating futher at this time.

    First-line treatments for NP include a choice of monotherapy with amitriptyline, duloxetine, gabapentin or pregabalin see Table 3 [18]. If a patient does not experience effective results, or if the medications cannot be tolerated, then it is recommended to choose one of the three remaining first-line therapies. If a patient does not respond, then trials with the other first-line agents should be initiated. Tramadol may be considered for short-term, acute rescue therapy, but long-term use is not recommended unless advised by a pain specialist [18].

    For patients with painful diabetic neuropathy, the first-line choice is duloxetine, unless contraindicated see Table 4 [18]. Capsaicin cream may be used for localised NP if a patient cannot tolerate the oral first-line agents. NICE also recommends carbamazepine for the first-line treatment of trigeminal neuralgia [18]. These recommendations are based on high- or moderate-quality RCTs and cost-effectiveness.

    As for other therapies, the guideline development group also states that treatment with cannabis sativa extract, capsaicin patch, lacosamide, lamotrigine, levetiracetam, oxcarbazepine, topiramate, venlafaxine and opioids e. The group states that although combination therapy is commonly prescribed, there is a lack of evidence showing tolerability and cost-effectiveness with various drug combinations [18].

    Duloxetine has been studied more, and is the preferred choice of SNRIs [50]. NeuPSIG also recommends that TCAs not be used in doses greater than 75mg in patients aged 65 years and older because of the adverse effect profile and the potential risk for falls in this patient population [50]. Strong opioids are now recommended as a third-line agent because of the potential risk for abuse, overdose, mortality, diversion and misuse [50].

    It provided a weak recommendation against the use of cannabinoids in NP because of negative results, potential misuse, diversion and long-term mental health risk in susceptible individuals [50]. NeuPSIG also provided a weak recommendation against the use of valproate and a strong recommendation against the use of levetiracetam and mexiletine [50]. In , the Canadian Pain Society CPS updated guidelines that provided healthcare providers with an evidence-based approach to managing patients suffering from NP.

    The organisation presented NP management in a stepwise approach. The CPS also states that if a first-line agent only provides partial relief, it is reasonable to add another first-line agent for combination therapy [87].

    Although the CPS does not have any recommendations regarding specific drug combination pharmacotherapy for NP, it does emphasise that this practice may be beneficial [87]. Second-line agents for NP include tramadol and opioid analgesics [87]. When prescribing these medications, caution should be used because of their extensive side-effect profiles and risk of addiction, misuse and abuse. Patients on these medications should also be monitored strong recommendation [87] and providers should consult the Canadian Guidelines for the Safe and Effective Use of Opioids for Chronic Noncancer Pain [88].

    The CPS also states that cannabinoids are considered a third-line agent for NP, but require judicious prescribing practices and close monitoring [87]. Fourth-line agents for NP include topical lidocaine, methadone, tapentadol, lacosamide, lamotrigine and topiramate [87]. Carbamazepine is considered first-line therapy for this condition and topical lidocaine is a second-line agent [87]. The American Academy of Neurology AAN published an evidence-based guideline that focused on the efficacy of treatment to reduce pain and improve quality of life in patients with painful diabetic neuropathy in [76].

    In , the guideline developers reaffirmed the findings. Pregabalin was found by the AAN to have the strongest evidence in support of efficacy to treat painful diabetic neuropathy see Table 4 [76] as it lessened the pain, caused less sleep interference and improved quality of life. Additional medications from various classes also showed probable efficacy and could be considered for the treatment of diabetes-related NP Table 4 [76].

    AAN recommends against the use of sodium valproate and opioids in NP. The use of capsaicin may be limited because many patients experience side effects such as burning [76]. The American Diabetes Association ADA reports that neither glycemic control nor lifestyle management provide effective relief from NP and that pharmacotherapy is necessary to control symptoms [28].

    In the most recent position statement, the ADA supports the use of pregabalin and duloxetine to treat NP in patients with diabetes see Table 4 [28]. Gabapentin received a Level B recommendation as an initial approach to NP treatment with cautions concerning comorbidities and potential drug interactions [28].

    The ADA does not recommend the use of opioids, including tramadol or tapentadol as first- or second-line therapies for NP in patients with diabetes because of the high risk of addiction and complications Level E [28].

    The American Society of Clinical Oncology has provided evidence-based recommendations to assist healthcare professionals with the prevention and treatment of CIPN in adult patients. The data were associated with patients who were experiencing neuropathy related to oxaliplatin or paclitaxel therapy [33].

    A side-by-side comparison of the recommendations reveal that there is little variation on first- and second-line therapies to treat NP. Most recommendations for first- and second-line treatments are based on antidepressants and antiepileptic medications [18 ] , [28] , [33] , [50] , [54] , [76].

    Opioid use remains controversial and is generally not recommended as first-line treatment [18] , [28] , [33] , [50] , [76]. The evidence to support the use of opioids is lacking, and many organisations state concerns about long-term safety. Adverse effects related to many of these medications can also be very limiting in certain patient populations e. TCAs in elderly patients. Even with these evidence-based recommendations, pain control in patients with NP continues to be a challenge.

    The goal for most cases of NP is to make the pain tolerable, not necessarily eliminate the pain [87]. In patients who are receiving a first-line agent for NP, the pain control may be weak or modest [50] , [52].

    Epidemiological studies have shown that many times, patients do not receive the treatment that they need to control NP [14] , [86] , [90]. There are many factors that may contribute to the under-treatment of this type of pain, including not recognising NP or not using first-line medications to treat the pain [91]. Finally, there is a lack of well-designed clinical trials identifying new therapeutic approaches with improved efficacy and tolerability to treat NP.

    One issue that limits the progress of studies is the risk of high placebo effect [81]. Placebo response in studies can contribute to the underestimation of the treatments effects [92]. While placebo responses increase and drug responses remain the same, the therapeutic advantage is diminished [92]. Studies have shown a correlation between higher placebo response rates and certain types of NP. HIV-related NP has high placebo response [93].

    Patients with peripheral NP were found to have higher levels of placebo response compared with patients with central NP [93] , [94]. Patients with diabetic neuropathy compared with postherpetic neuralgia also demonstrated higher placebo response [68], [69]. Factors that were found to have lower placebo responses included male patients, increased age, higher baseline pain intensity and longer durations of NP [94].

    Since the effectiveness of pain management for patients with NP is limited, future studies are needed to support new treatment approaches. Furthermore, as pain management should be multi-modal, trials focusing on combination pharmacotherapy treatments to provide strong evidence for efficacy and tolerability are also required.

    Advances have been made to help identify patients suffering from true NP, with the use of validated screening tools and staging to help reduce diagnostic heterogeneity [37] , [50].

    Emphasis should also be placed on mechanism-based treatment strategies by identifying responders through phenotyping [16] , [19] , [50] , [52]. These suggestions may be considered during the design and implementations of future trials in NP. NP is a condition that affects the quality of life of many patients.

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