Anti Epileptics For Neuropathy An Australian View

Today's post from nps.org.au (see link below) is a very interesting look at the workings of anti-epileptic drugs in the treatment of neuropathy. It's always interesting to look at how different countries approach the treatment of chronic pain and/or neuropathy. In Australia, it's generally recommended that neuropathy patients are treated with a progressive scale of treatments, beginning with non-drug options and moving on, if necessary, via anti-depressants and anti-epilepsy drugs to opiates. This ties into a general world-wide approach to the disease but the article agrees that neuropathy is hard to treat, whatever you use to control the symptoms. Regarding anti-epileptic drugs, it concludes that the only two that are effective (however limited) are gabapentin and pregabalin. However, once again, this ignores Pfizer's own advice that pregabalin (Lyrica) is not suitable for particular groups of neuropathy sufferers (HIV- and diabetic neuropathy patients for instance) and it does seem strange that that advice from the makers is being overlooked across the world. This may partly be due to that fact that doctors see some successes with neuropathy patients being treated with Pregabalin but that doesn't take into account whether the drug is actually good for you or not. Whatever the issues around pregabalin, this is an interesting article for those already on anti-epileptics, or about to begin using them.

Treating neuropathic pain with anticonvulsants — which ones work?
Published in Health News and Evidence Date published: 10 January 2014

Summary
 
Neuropathic pain is a common form of chronic pain, with an array of drugs available for its treatment, including anticonvulsants.

A recent Cochrane review assessed the evidence around efficacy and safety for 10 anticonvulsant drugs used to treat neuropathic pain and found evidence of efficacy for only 2 — gabapentin and pregabalin.
The study provides support for the use of pregabalin and gabapentin in treatment of neuropathic pain, but was not able to distinguish between the 2 drugs in terms of efficacy for the treatment of painful diabetic neuropathy or postherpetic neuralgia. Nor was the study able to identify patients most likely to benefit from treatment with either drug.
Gabapentin and pregabalin are TGA-approved in Australia for the treatment of neuropathic pain. Currently, pregabalin is PBS subsidised when prescribed for neuropathic pain, and gabapentin is subsidised for this indication only under the RPBS. 

Practice points
Use a comprehensive clinical assessment to determine the cause of pain, its nature and severity, and the effect of the pain on the patient.1
Provide each patient with an individual management plan based on this assessment.1
Use a multidisciplinary approach to management that includes patients in decision making, and consider non-drug treatments first.1,2
Consider the TCA amitriptyline as first line if drug treatment is required.3
Consider next an anticonvulsant such as pregabalin or gabapentin if first line is unsuccessful.3
Conduct early and regular clinical reviews of patients on drug treatment.4
Refer patients whose pain relief is inadequate to a pain specialist, a multidisciplinary pain clinic or a palliative care service.3,5
Chronic pain in Australia

Chronic pain affects 1 in 5 Australian adults,6,7 with incidence increasing with age. Much of the burden of patient management falls on general practitioners.1

Chronic pain is Australia's third most costly health condition after cardiovascular diseases and musculoskeletal conditions.8 The total cost of chronic pain to the Australian economy was reported to be $34 billion in 2007, including $7 billion in health system costs.8

Neuropathic pain

Neuropathic pain is a form of chronic pain, and is difficult to treat effectively.3

Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory system9 and is usually described as burning, painful, cold or electric shocks. These symptoms may occur alongside tingling, pins and needles, numbness or itching.3,10

Causes include nerve damage, which can be followed by changes to the central nervous system.11 This condition can present for months or years, causing significant, disabling, moderate to severe pain.11
Neuropathic pain: Australian guidelines

Australian guidelines recommend that patients with chronic pain, such as neuropathic pain, have an individualised management plan. This plan should be linked to a comprehensive patient assessment to determine the cause of pain, its nature and severity as well as the effect of the pain on the patient.1

There is no generally accepted 'stepwise' approach to treatment of neuropathic pain. Australian guidelines recommend non-drug approaches first.1,5 Many drugs are available for the treatment of neuropathic pain, with TCAs and anticonvulsants the drugs of choice.3,5 However, comparative studies are limited, there is no evidence for differences in the relative efficacies of individual drugs5,11 and these treatments are often associated with adverse events.

Guidelines recommend starting drug therapy for neuropathic pain with a TCA (such as amitriptyline) or an anticonvulsant.3,5 The anticonvulsants gabapentin and pregabalin are recommended by Therapeutic Guidelines as a second-line treatment of neuropathic pain after the TCA amitriptyline.3 The dose of the drugs can be escalated at weekly intervals if tolerated, but it may take several weeks to achieve clinical efficacy.

*TCAs are an established treatment for neuropathic pain but are not approved by the TGA for this indication.
Efficacy and safety of anticonvulsant drugs for neuropathic pain: Cochrane review

The Cochrane Collaboration recently reviewed the efficacy and safety of 10 anticonvulsant drugs for the treatment of neuropathic pain and fibromyalgia.11 This was not a new systematic review of individual studies,11 but compiled data from the 10 previous Cochrane reviews published between 2009 and 201312-21 and comprising 17,955 participants (with at least moderate pain) from 91 studies.11-21

These studies were placebo controlled, double blind, randomised controlled trials. Results were presented for each different drug for 3 different neuropathic pain conditions — painful diabetic neuropathy, postherpetic neuralgia and central neuropathic pain — and for fibromyalgia. This article will focus on the findings related to neuropathic pain.

Evidence of pain reduction for gabapentin and pregabalin only

This Cochrane review reported on efficacy as well as patient impression of improvement, and investigated outcomes including patient-reported pain relief of 50% or more and Patient Global Impression of Change (PGIC).11 Results were reported in terms of whether patients were more likely to achieve the benefit with the treatment than by taking placebo.11

A reduction in pain intensity of 50% or more is considered to be a clinically relevant benefit.3

The Patient Global Impression of Change (PGIC) is a measure of global improvement with treatment where participants rate their improvement from 'very much improved' to 'very much worse' with 'no change' as the mid-point.22

Among the 10 anticonvulsants studied, evidence of pain reduction was only found for gabapentin and pregabalin.11 People taking either of these drugs were more likely to report pain relief of 50% or more for painful diabetic neuropathy and postherpetic neuralgia than those taking placebo†.11 People taking pregabalin for the treatment of central neuropathic pain were also more likely (compared to placebo) to report pain relief of 50% or more†.11

The number of patients who would need to be treated with pregabalin or gabapentin for one patient to see this improvement was estimated to range from 4 to 10 for >=50% reduction in pain.11 Therapeutic Guidelines advises that for pain treatment to be considered to be effective, the number needed to treat for one person to achieve an outcome should be between 2 and 5.3
Further findings

The Cochrane review also found that people taking gabapentin for painful diabetic neuropathy or postherpetic neuralgia were more likely to rate their improvement as 'excellent' or 'very good or excellent' than those people taking placebo*.11

People taking lacosamide or pregabalin for painful diabetic neuropathy were more likely to rate their improvement as 'very good or excellent' than those people taking placebo*.11 The data suggest that the benefit with pregabalin may be dose dependent, as a benefit was seen with the 600mg/day dose but not the 300mg/day dose. Data for other drugs was not presented.11
*These results were statistically significant. The rating of improvement by patients was determined using the PGIC.

Carbamazepine: an accepted treatment for neuropathic pain but insufficient evidence of effect

Carbamazepine is an accepted treatment in Australia for neuropathic pain but is not TGA-approved for this indication.5

This Cochrane review found that evidence of efficacy for carbamazepine was of low quality and consequently likely to be subject to a number of biases that would overestimate efficacy.11 Most studies with carbamazepine were less than 4 weeks' duration, in contrast to studies with other drugs that were of 10-12 weeks or longer.11
Safety

The risk of adverse events in people taking anticonvulsant drugs is high, with CNS adverse events relatively common and often dose dependent, particularly for pregabalin and lacosamide.11 In this Cochrane review, available data showed that only oxcarbazepine statistically significantly increased the risk of a serious adverse event in people taking anticonvulsants for either neuropathic pain or fibromyalgia compared to those taking placebo.11

Limitations of the study

This Cochrane review benefits from, and is also limited by, the fact that the data are taken solely from previous Cochrane reviews. While this ensures that each study included is of a comparative and high standard, it also means that some trials would have been omitted.11 For example, levetiracetam does not feature in a Cochrane review and therefore was not assessed in this study, although it has been tested in other randomised controlled trials.11
Conclusions: pregabalin and gabapentin are the preferred anticonvulsants

While all evidence considered in this Cochrane review was described as 'second tier' or lower due to the potential for biases to overestimate efficacy, the results provide support for current Australian guidelines.3
Treatment best practice and implications for patients
Assess the nature of the pain experience and inform people of realistic outcomes with treatment.23,24
Provide each patient with an individualised management plan based on a comprehensive clinical assessment of their pain.1
The primary treatment goal in most cases is to make the pain tolerable — not usually to eliminate the pain.23
Aim for medium-term drug therapy with a drug holiday after 6 months. Patients who relapse during a drug holiday can resume treatment.
Conduct early and regular clinical reviews.

This Cochrane review supports the use of pregabalin and gabapentin as part of a management plan for neuropathic pain, but is not able to distinguish between their efficacies for treatment of painful diabetic neuropathy or postherpetic neuralgia. Drug therapy is best used as part of a multifaceted, multidisciplinary, active self-management approach to the physical, psychological, social and vocational impacts of neuropathic pain.2

Analgesic failure is common in the treatment of neuropathic pain and there is currently no evidence to inform which patients are most likely to benefit from what drugs and indeed the order in which drugs should be taken to optimise outcomes.11 However, patients who do not respond to one drug may respond to another, even within the same drug class.5 Combination drug therapy may be needed by many patients.24,25 A specific combination of treatments cannot be recommended due to the limited number of studies for any combination therapy, as well as other study factors, such as the limited trial size and duration.25

More information is available from NSW Health.

Refractory, severe neuropathic pain

Assistance from a pain specialist and a multidisciplinary pain service may be required for refractory, severe neuropathic pain, as treatment options are complex.2
Further information
Pregabalin (Lyrica) for neuropathic pain (NPS Medicinewise RADAR: April 2013).26
Information for patients

Patient information leaflet: Key points for patients about chronic pain (Therapeutic Guidelines).

References

1. eTG complete [Internet]. Therapeutic Guidelines: Analgesic. Melbourne: 2012. [Online] (accessed 19 December 2013).
2. Australian Pain Society. Evidence-based recommendations for the pharmacological management of neuropathic pain. Position Statement, June 2008. [Online] (accessed 20 October 2012)
3. eTG complete [Internet]. Therapeutic Guidelines: Neurology. Melbourne: 2011. [Online] (accessed 19 December 2013).
4. National Institute for Clinical Excellence (Nice). Neuropathic Pain: The pharmacological management of neuropathic pain in adults in non-specialist settings. NICE Clinical Guideline 173. Manchester: National Institute for Clinical Excellence, 2013. [Full text]
5. Rossi S e. Australian Medicines Handbook, 2013. Adelaide.
6. Hogg MN, Gibson S, Helou A, et al. Waiting in pain: a systematic investigation into the provision of persistent pain services in Australia. Med J Aust 2012;196:386-90. [PubMed]
7. Blyth FM, March LM, Brnabic AJ, et al. Chronic pain in Australia: a prevalence study. Pain 2001;89:127-34. [PubMed]
8. Access Economics Pty  Ltd. The high price of pain: the economic  impact of persistent pain in Australia. Sydney Deloite Access Economics, 2007 [Full text]
9. Jensen TS, Baron R, Haanpaa M, et al. A new definition of neuropathic pain. Pain 2011;152:2204-5. [PubMed]
10. Votrubec M, Thong I. Neuropathic pain — a management update. Aust Fam Physician 2013;42:92-7. [PubMed]
11. Wiffen PJ, Derry S, Moore RA, et al. Antiepileptic drugs for neuropathic pain and fibromyalgia — an overview of Cochrane reviews. Cochrane Database Syst Rev 2013;11:CD010567. [PubMed]
12. Birse F, Derry S, Moore RA. Phenytoin for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2012;5:CD009485. [PubMed]
13. Corrigan R, Derry S, Wiffen PJ, et al. Clonazepam for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2012;5:CD009486. [PubMed]
14. Gill D, Derry S, Wiffen PJ, et al. Valproic acid and sodium valproate for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2011:CD009183. [PubMed]
15. Hearn L, Derry S, Moore RA. Lacosamide for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2012;2:CD009318. [PubMed]
16. Moore RA, Straube S, Wiffen PJ, et al. Pregabalin for acute and chronic pain in adults. Cochrane Database Syst Rev 2009:CD007076. [PubMed]
17. Moore RA, Wiffen PJ, Derry S, et al. Gabapentin for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2011:CD007938. [PubMed]
18. Wiffen PJ, Derry S, Lunn MP, et al. Topiramate for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2013;8:CD008314. [PubMed]
19. Wiffen PJ, Derry S, Moore RA. Lamotrigine for acute and chronic pain. Cochrane Database Syst Rev 2011:CD006044. [PubMed]
20. Wiffen PJ, Derry S, Moore RA, et al. Carbamazepine for acute and chronic pain in adults. Cochrane Database Syst Rev 2011:CD005451. [PubMed]
21. Zhou M, Chen N, He L, et al. Oxcarbazepine for neuropathic pain. Cochrane Database Syst Rev 2013;3:CD007963. [PubMed]
22. Dworkin RH, Turk DC, Farrar JT, et al. Core outcome measures for chronic pain clinical trials: IMMPACT recommendations. Pain 2005;113:9-19. [PubMed]
23. Moulin DE, Clark AJ, Gilron I, et al. Pharmacological management of chronic neuropathic pain - consensus statement and guidelines from the Canadian Pain Society. Pain Res Manag 2007;12:13-21. [PubMed]
24. Dworkin RH, O'Connor AB, Audette J, et al. Recommendations for the pharmacological management of neuropathic pain: an overview and literature update. Mayo Clin Proc 2010;85:S3-14. [PubMed]
25. Chaparro LE, Wiffen PJ, Moore RA, et al. Combination pharmacotherapy for the treatment of neuropathic pain in adults. Cochrane Database Syst Rev 2012;7:CD008943. [PubMed]
26. National Prescribing Service. Pregabalin (Lyrica) for neuropathic pain. RADAR; April 2013. [Full text]

http://www.nps.org.au/health-professionals/health-news-evidence/latest-issue/treating-neuropathic-pain

Fluoroquinolone Antibiotics And Neuropathy A Report

Today's important post from the Journal of Investigative Medicine at hic.sagepub.com (see link below) is another piece of the jigsaw showing how dangerous fluoroquinolone antibiotics can be for people whether living with, or prone to, nerve damage (neuropathy). It's quite long but worth reading because it's very important to check what sort of antibiotics your doctor is prescribing. Permanent neuropathy from an antibiotic is no joke and is so easily avoided - it's in your own interests to check the label on the box and question your doctor's choice afterwards.
 

Permanent Peripheral Neuropathy
A Case Report on a Rare but Serious Debilitating Side-Effect of Fluoroquinolone Administration
Published July 27, 2014, doi: 10.1177/2324709614545225 Journal of Investigative Medicine High Impact Case Reports April-June 2014 vol. 2 no. 2 2324709614545225

Jacquelyn K. Francis, BA1
Elizabeth Higgins, MD1
1Albany Medical College, Albany, NY, USA
Jacquelyn K. Francis, Albany Medical College, 47 New Scotland AvenueAlbany, NY 12208, USA. Email: francij@mail.amc.edu

Abstract

The health risks and side effects of fluoroquinolone use include the risk of tendon rupture and myasthenia gravis exacerbation, and on August 15, 2013, the Food and Drug Administration updated its warning to include the risk of permanent peripheral neuropathy. We present a case of fluoroquinolone-induced peripheral neuropathy in a patient treated for clinically diagnosed urinary tract infection with ciprofloxacin antibiotic.

Introduction

While there has been success in recent years in decreasing the numbers of unnecessary antibiotic administrations,1 still rampant in medical practice is the inappropriate use of antibiotics. Fluoroquinolones administration is no different. These bactericidal agents are capable of central nervous system (CNS) penetration,2 with an impressive treatment profile that includes an enhanced spectrum of activity, high oral bioavailability, high serum drug concentration that parallels that of intravenous drug administration, and rapid mechanism of action. It is for this reason that physicians favor these drugs for treatment of simple infections, which range from uncomplicated urinary tract infections (UTIs) and gastrointestinal infections to lower respiratory infections and pneumonias. According to established guidelines, however, these antibiotics are recommended as drugs of last resort and for treatment of cases refractory to other safer antibiotic alternatives. Reports in recent years of the adverse drug events of these drugs are on the rise, with not only an overrepresentation of common antibiotic complaints, including diarrhea, nausea, and headache that occur at rates higher than most other antimicrobials on the market,3 but there is also mounting evidence suggesting the potential for long-term adverse peripheral nervous system (PNS) effects from fluoroquinolone usage. The need for physicians to be judicious when prescribing these drugs is therefore paramount.

Case Presentation

A 57-year-old Caucasian female presented to outpatient clinic with complaints of dysuria, polyuria, and urinary urgency. Urinalysis showed 2+ leukocytes and trace blood. Based on her clinical presentation, she was treated for UTI with a ciprofloxacin regimen of 250 mg twice a day for 5 days. Subsequent urine culture showed no evidence of organism, and against advice for reevaluation, she was lost to follow-up. She presented 2 months later reporting whole body burning and alopecia. The burning, she claimed, started 2 or 3 days after completion of the prescribed course of ciprofloxacin. The burning lasted 3 weeks and resolved only to recur, unrelentingly, 3 weeks later. She had been unable to adorn clothing during this time, for she said this triggered whole body burning. At the point wherein she was finally able to wear clothing, she presented to the clinic. Hydration and Epsom salt soaks provided no relief. She reported pain of 10/10. Her past medical history is significant for trigeminal neuralgia, in remission for 12 years. The patient was on no medications at the time of her visit. She has no specific medication allergies, but does get gastrointestinal symptoms with opioids, namely, fentanyl. Physical examination was unremarkable. Vitals at the time that she was seen included the following: blood pressure 132/78 mm Hg, temperature of 97°F, heart rate of 60 beats per minute, respirations of 18. Her body mass index was 17.94, down from 20.3 two months earlier. On detailed neurologic examination, cranial nerves II through XII were intact bilaterally. There was no pronator drift of outstretched arms. There was some muscle wasting in biceps; however, overall tone was normal. Strength was full bilaterally. Reflexes were 2+ and symmetric at the biceps, triceps, knees, and ankles. Plantar responses were flexor. Light touch and pinprick produced pain and paresthesias diffusely in the upper and lower extremities; however, position sense and vibration sense were intact in fingers and toes. Rapid alternating movements and fine finger movements were intact. There was no dysmetria on finger-to-nose and heel-knee-shin. There were no abnormal or extraneous movements. Romberg was absent. The patient’s posture was normal. Gait was steady with normal, though tentative, steps, base, arm swing, and turning. Heel and toe walking were normal. Tandem gait was normal. She had no discernable rash or skin lesions.

Subsequent complete blood work analysis to check for an electrolyte abnormality basis of her complaints was unremarkable. Her complete blood count was normal with a hematocrit of 41%. Her vitamin B12 level was 258 pg/mL, with a normal range of 200 to 900 pg/mL. Her thyroid stimulating hormone level was 2.05, with a normal range of 0.4 to 6.0. Her immunoglobulin levels were normal. Her vitamin D level was 13 nmol/L (optimal >30 nmol/L). Copper level was 98 mg (normal 50-80 mg). Vitamin E was normal at 12.7 µg/mL (normal range = 5.5-17 µg/mL). Vitamin B1 was normal at 5.4 µg/dL (normal range = 2.5-7.5 µg/dL).

Her blood work and further questioning could provide no new medical etiology for her symptoms, and so the patient was subsequently sent for complete neurological workup. Workup included heavy metal toxicity screening to assess for possible heavy metal exposure to lead, mercury, cadmium, and zinc. Electrophysiological studies were also done to assess neuromuscular nerve action potential transmission, a test that could discern a neuromuscular disorder etiology. Three-millimeter skin punch biopsy to assess for small fiber density and possible neurologic process were also done. These tests were all negative. Neurological workup could not determine a unique cause of her symptoms. It was concluded that if her symptoms were neurologic-based, it was, in fact, a multifocal process.

Two years after the initial onset of symptoms, the patient continues to suffer from polyneuropathies chronologically related to ciprofloxacin use. At her most recent visit, she describes constant pain of 7/10 and is unable, she states, to ambulate for more than 2 minutes, without intense shooting pains up and down her lower extremities. She describes “pins and needles” up and down her legs and thighs radiating to her buttocks and feet. She claims that her upper body and abdomen have now been spared of such feelings. She describes severe alopecia and ambulates now with a broad-based gait. She describes being on permanent disability because of her condition. The rest of her physical examination remains unchanged. There are no gross neurological deficits discernible on neurologic examination. The patient remains on amitriptyline 20 mg daily for control of her pain symptoms.

Discussion

Fluoroquinolones are fluorinated quinolones, the only bactericidal agent in the antibiotic class capable of directly inhibiting DNA synthesis. They do this by promoting cleavage of bacterial DNA in the DNA–enzyme complexes of DNA gyrase and topoisomerase IV.2 Generally, gram-negative antibacterial activity correlates with inhibition of DNA gyrase, and gram-positive antibacterial activity corresponds with inhibition of DNA type IV topoisomerase.2,4 With the introduction of these drugs in the 1960s, physicians were able, for the first time, to treat severe gram-negative infections orally.3 The first successful fluorination of part of the quinolone drug in 1986, in the form of norfloxacin, brought with it the capability of crossing the blood–brain barrier and achieving CNS penetration.5 This and the already great treatment profile in the form of enhanced spectrum of activity, high oral bioavailability, high serum drug concentration comparable to intravenous infusion, and rapid mechanism of action added to the popularity of these drugs ultimately resultingin the indiscriminate use of these drugs. The enhanced treatment profile of these drugs came at a price however, with adverse effects so severe that use of many fluoroquinolones since then being restricted or the drugs withdrawn from the market entirely.6,7

One of the challenges of diagnosing a patient with fluoroquinolone-associated peripheral neuropathy is the diffuse, confusing, and delayed array of symptoms that can occur. A 1996 study first brought these adverse effects to light.7 While patients on the fluorinated drugs exhibited less side effects than those associated with first-generation quinolone predecessors, such as nausea and gastrointestinal disturbances, 0.9% to 1.6% experienced adverse reactions relating to the peripheral and central nervous system, including headache, dizziness, drowsiness, agitation, psychosis, and convulsions, as well as peripheral sensory disturbances, symptoms that had never been complained of prior, at least not on any significant scale. Of these patients, 81% had symptoms occurring within 1 week of drug administration, with paresthesia being the mainly reported symptom. Five years later, a 2001 study found that contrary to previous reports suggesting that fluoroquinolone-associated PNS events are mild and short term, 80% of study participants reported severe events that typically involved multiple organ systems, especially the PNS, with symptom onset as early as 24 hours within initiation of treatment. 58% of these cases had symptoms lasting greater than 1 year.8

Another 2001 formal study that sought to assess the prevalence of fluoroquinolone-induced PNS adverse side effects highlighted the severity of these effects. The study concluded that there was a high association between fluoroquinolone antibiotics and severe, long-term adverse PNS and multiple organ system effects that included PNS sensory symptoms (91%), peripheral neuropathy motor symptoms (55%), and CNS effects (75%). Over 80% of the patients surveyed had sequalae stemming from fluoroquinolone use that lasted for greater than 1 year.9 A subset of these patients and their adverse drug events are included in Table 1.


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Table 1.

15 of the 45 Total Reported Cases of Fluoroquinolone-Associated Events in the Literature6.

Despite these seemingly significant numbers and overwhelming reports from patients, physicians continue to prescribe fluoroquinolone antibiotics unsystematically, against US Food and Drug Administration recommendations. The pressures of health care facilities and patients alike to increase patient turnaround and quickly alleviate symptoms may compound this problem 10.

As highlighted in the aforementioned case, the peripheral neuropathy reported with fluoroquinolone administration can be severe, debilitating, and permanent. It is for this reason that physicians need to practice due diligence when prescribing not only antibiotics, but any drug. Physicians also need to practice vigilance in the event of an adverse reaction. They can do this with careful follow-up of patients and ensure that patients are aware of all the side effects that may be associated with their prescribed drug. Patients need to know what to look for and where to go in the event that one of these symptoms become manifest. It is our hope that the updated FDA warning and presentation of this case will encourage physicians to be more conscientious of their treatment selections.

Take Home Points

The FDA recommends that fluoroquinolones be used as a drug of last resort and for treatment of cases refractory to other safer antibiotic alternatives.

The FDA updated their black box warnings on all fluoroquinolones to stress the rapidity of onset and permanence of peripheral neuropathy associated with their use.

Physicians should be aware of the risks and side effects associated with the drugs that are prescribed and be able to inform patients of the risks associated with the use of these drugs.

Physicians should always aim to administer the least broad spectrum antibiotic possible based on known sensitivities and regional resistance patterns.

Article Notes

Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm).

References
1.↵
US Food and Drug Administration. FDA drug safety communication: FDA requires label changes to warn of risk for possibly permanent nerve damage from antibacterial fluoroquinolone drugs taken by mouth or by injection. http://www.fda.gov/Drugs/DrugSafety/ucm365050.htm. Accessed August 15, 2013.
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Scheld M. Quinolone therapy for infections of the central nervous system. Rev Infect Dis. 1989;11(suppl 5):S1194-S1202.
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Turnidge J. Pharmacokinetics and pharmacodynamics of fluoroquinolones. Drugs. 1999;58(suppl 2):29-36.
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Wolfson JS. Mechanisms of Quinolone Action and Bacterial Killing. Quinolone Antimicrobial Agents. 2nd ed. Washington, DC: American Society for Microbiology; 1993:53-57.
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Spigset O. Peripheral sensory disturbances related to treatment with fluoroquinolones. J Antimicrob Chemother. 1996;37:831-837.
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Gold L,
Igra H. Levofloxacin-induced tendon rupture: a case report and review of the literature. J Am Board Fam Pract. 2003;16:458-460.
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Mandell L,
Tillotson G. Safety of fluoroquinolones: an update. Can J Infect Dis. 2002;13:54-61.
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Linder JA,
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Weight Bearing Exercise Can Be Dangerous For Neuropathy Patients

Today's post from huffingtonpost.com (see link below) looks at the problems that certain forms of exercise may bring the neuropathy patient who has lost most of the feeling in their feet. These problems are not to be underestimated but it's important to say here that the vast majority of neuropathy patients have some feeling in their feet, despite the numbness that can affect the toes and pads of the foot. These patients are unlikely to step on a nail and not feel something. That said, many people living with neuropathy feel very little and this can certainly lead to serious accidents. When this is the case, load-bearing exercises can be more dangerous than helpful. Nevertheless the article recommends exercise as being essential, as long as this is controlled and the feet are carefully and regularly monitored. The article is aimed at diabetic neuropathy patients but applies to all people living with neuropathy and foot problems.

Type 2 Diabetes and Peripheral Neuropathy: To Walk or Not to Walk?
 
Milt Bedingfield Posted: 05/11/2015 

It is now well known that engaging in light to moderate physical activity on a regular basis is of significant value for most people that have either Type 1 or Type 2 diabetes. In fact the American Diabetes Association recommends that people with diabetes should get a minimum of 150 minutes of light to moderate exercise per week including aerobic and resistance training.

What the ADA says...

It has also been recommended that people with peripheral diabetic neuropathy that have reduced or absent feeling in their feet should not engage in any form of weight bearing exercise activity. The American Diabetes Association recommends that people with diabetes-related peripheral neuropathy should limit the amount of weight-bearing physical activity they perform due to their increased risk of foot ulcers and amputation (1, 2). This is based on the fact that with peripheral neuropathy there is either a decreased ability or total inability in the feet to feel pain or discomfort.

As an example, standing barefoot on hot asphalt maybe in a parking lot in the middle of the summer would be very uncomfortable for someone with normal sensation in their feet, however go unnoticed for someone with peripheral neuropathy. Similarly, the person with peripheral neuropathy may develop a painful nickel-sized blister after walking too far or when wearing new shoes and not even feel it. Without daily inspection of the ankles and feet (which a lot of people do not do) this blister could go unnoticed for days resulting in a potentially infected, slow to heal, or non-healing wound. In the worst case this could lead to an amputation. All of this is the result of losing what is called the protective sensation in the feet.

In the absence of peripheral neuropathy whenever there is insult to the foot or feet such as a blister, a cut or scrape or stepping on a small piece of glass or nail, there would be pain which would cause you to notice the injury and hopefully treat the wound accordingly.

There are also painful stages of neuropathy that can precede lack of sensation which are characterized by frequent but intermittent pain in the feet throughout the day, having pain only in the evening while in bed to constant pain. This stage of neuropathy can result in changing the way you walk, that is your stride length, which part of your feet you strike the ground with first and ultimately what part of your feet support your body weight.

Because of everything I have just mentioned above this leads to the unfortunately recommendation that discourages walking for a great many people with diabetes.

To Walk or Not to Walk?

So where does that leave us? Exercise is arguably the best treatment there is, particularly in controlling Type 2 diabetes, and preventing diabetes related complications, such as peripheral neuropathy, however once you have peripheral neuropathy in your feet you should avoid doing any weight bearing exercise.

I have wrestled with the dilemma for years about how to guide my patients that would benefit immensely from starting to exercise or increasing their exercise however have various stages of neuropathy.

According to the Centers for Disease Control and Prevention, from 2000-2002, approximately 60 percent of lower-extremity amputations in the United States were diabetes-related, with the majority of those amputations being preceded by a foot ulcer (3). Almost all diabetic foot ulcers occur in those people that have lost feeling in their feet due to diabetic peripheral neuropathy (4, 5).

On the other hand poorly controlled blood glucose control contributes greatly to peripheral neuropathy.

Eight-year cardiovascular mortality is 34 percent lower among people with diabetes who walk two hours per week compared with non-walkers (6).

Feet First Randomized Controlled Trial

The Feet First Randomized Controlled Trial was designed to look at the effect of weight-bearing activity on foot ulcer incidence in people with diabetic peripheral neuropathy. The study, conducted over a 12-month period by Lemaster and colleagues, showed that participants in the Feet First intervention group achieved a modest increase in activity, with no increase in foot lesions, compared with those in the control group. The group also recommended additional research be conducted in this area to investigate the current guidelines and close supervision for patients with diabetes and peripheral neuropathy (7).

Tuttle and colleagues found that people with Type 2 diabetes and peripheral neuropathy experienced no negative consequences when performing moderate-intensity, weight-bearing exercise in their study (2).

Dr. Sheri Colberg reports in her article "Exercising with Peripheral Neuropathy" that recent descriptive studies suggest that patients with a lack of feeling in their feet who participate in daily weight-bearing activity are at decreased risk of foot ulceration compared with those who are less active (8, 9), especially if their daily routine is very similar with little variation from day to day regarding their physical activity (9, 10).

As a result of the above information, I am going to continue evaluating each of my class participants on a case by case basis, however, for those patients with peripheral neuropathy that I believe will be prudent in checking their feet and following the recommended foot care guidelines and stand to gain significant benefit from performing some weight bearing exercise, I will be more likely to recommend it to them.

References:

1. Singh, N., D. G. Armstrong, and B. A. Lipsky: Preventing foot ulcers in patients with diabetes. JAMA 293 (2):217-228, 2005

2. Tuttle, L. J., M. K. Hastings, and M. J. Mueller: A moderate-intensity weight-bearing exercise program for a person with Type 2 diabetes and peripheral neuropathy. Phys Ther 92 (1):133-141, 2012

3. Centers for Disease Control and Prevention. History of foot ulcer among persons with diabetes -- United States, 2000-2002. MMWR. 2003;52:1098-1102. Medline

4. Pham H, Armstrong DG, Harvey C, et al. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care. 2000;23:606-611.

5. Reiber GE, Smith DG, Wallace C, et al. Effect of therapeutic footwear on foot reulceration in patients with diabetes: a randomized controlled trial. JAMA. 2002;287:2552-2558. CrossRefMedline

6. Gregg EW, Gerzoff RB, Caspersen CJ, et al. Relationship of walking to mortality among US adults with diabetes. Arch Intern Med. 2003;163:1440-1447. CrossRefMedline

7. Lemaster, J. W., M. J. Mueller, G. E. Reiber, D. R. Mehr, R. W. Madsen, and V. S. Conn: Effect of weight-bearing activity on foot ulcer incidence in people with diabetic peripheral neuropathy: feet first randomized controlled trial. Phys Ther 88 (11):1385-1398, 2008

8. Richerson, S., and K. Rosendale: Does tai chi improve plantar sensory ability? A pilot study. Diabetes Tech Ther 9(3):276-286, 2007

9. Ko, S. U., S. Stenholm, C. W. Chia, E. M. Simonsick, and L. Ferrucci: Gait pattern alterations in older adults associated with type 2 diabetes in the absence of peripheral neuropathy--results from the Baltimore Longitudinal Study of Aging. Gait Posture 34 (4):548-552, 2011

10. Kanade, R. V., R. W. van Deursen, K. Harding, and P. Price: Walking performance in people with diabetic neuropathy: benefits and threats. Diabetologia 49 (8):1747-1754, 2006

http://www.huffingtonpost.com/milt-bedingfield/post_9394_b_7188266.html

Duloxetine Cymbalta Reviews For Neuropathy

Today's post from the always reliable Drugs.com (see link below) talks about user reviews of Duloxetine (Cymbalta, Ariclaim, Xeristar, Yentreve, Duzela), which is an antidepressant drug used to treat neuropathy. It's a somewhat controversial drug due to the potential side effects which many people just can't take.The reviews are not extensive and not really up to date, which is why this post asks for your input. Drugs.com is always a trustworthy source for information about any drugs you may take and is worth adding to your favourites, especially when you are taking multiple drugs for different conditions.
If you are taking Duloxetine/Cymbalta, or have taken it in the past, please share your experiences for the benefit of others, especially in comparison with other anticonvulsant or antidepressant drugs prescribed for neuropathy.

User Reviews for Duloxetine
Also known as: Cymbalta

The following information is NOT intended to endorse drugs or recommend therapy. While these reviews might be helpful, they are not a substitute for the expertise, skill, knowledge and judgement of healthcare practitioners in patient care.
Learn more about Duloxetine.

Compare all 38 medications used in the treatment of Diabetic Peripheral Neuropathy.

Reviews for Duloxetine to treat Diabetic Peripheral Neuropathy


Review by Anonymous (taken for less than 1 month):January 25, 2013 11:21 AM User Rating: 8.0

Cymbalta (duloxetine): I’m a Type 1 Diabetic for 39 years. Had VERY painful muscle spasms/seizing and twitching. I tried various supplements which "should" have helped but no improvement. I started Neurontin at 1,800mg/day and I had terrible swelling plus gained 18 lbs in 6 months (and my eating habits actually got better while on it). The 1,800mg of Neurontin no longer controlled the muscle spasms. I started Cymbalta, 30 mg before bed, and had significant reduction in pain the first morning. I did notice a very strong headache that first day. I had only 3-4 muscle spasms that first day as well....Wow!! Second day...almost NO pain in the morning and only a dull headache with much weaker muscle spasms. Side effects: Crazy dreams, difficulty sleeping, headache.

Review by Anonymous (taken for 1 to 2 years): September 14, 2012 

User Rating: 9.0

Cymbalta (duloxetine): I was not sure how well it worked at first. Then I was unable to get it for awhile, and was in a lot of pain, trouble getting through the day. I just wanted to sleep. Once back in my system I noticed the difference. This helps my depression, back pain, and the neuropathy.

Review by Anonymous:August 12, 2012 10:37 AMUser Rating: 1.0

Cymbalta (duloxetine): Did not work for me. I had nausea, abdominal & stomach pain, loss of appetite. I lost 5 lbs. in less than a week.


Review by Tonywwk1:March 23, 2012 4:51 PMUser Rating: 8.0

duloxetine: I have severe Diabetic Neuropathy to both feet, and Neurotin seemed rather ineffective. The pain was a combination of burning, needles and pins sensation, and severe knife stabbing sensations intermittently to both feet. I started taking Cymbalta over a year ago, and it has significantly reduced the sensations and pain, making them tolerable. I initially noticed a loss of appetite, which was a blessing in disguise for me, and I lost 25 pounds before the anorexia disappeared. I have several severe disorders which require close monitoring of my blood, but overall, Cymbalta has been a God send to me.

Review by Sewanhaka100: February 18, 2012 1:23 AM

Cymbalta (duloxetine): I started on 30mg Cymbalta daily with a little foot pain improvement - as this was still not enough my doctor put me on 60mg daily. I am so happy and relieved to be able to actually "walk" again and function like a normal person. I was crawling to the bathroom at night before for 8 months I was in pure agony. I have been on Cymbalta for 5 weeks and so far great results! Thank you Eli Lilly and my doctor.

Review by Anonymous: September 6, 2010 7:28 PMUser Rating: 8.0

Cymbalta (duloxetine): Cymbalta lessens the burning pain in my feet that used to wake me up and keep me awake at night. It often relieves burning pain almost completely.

Review by kathygirl: August 6, 2010 10:50 AM 

User Rating: 3.0

Cymbalta (duloxetine): I was very unsteady on my feet, at first some of the pain was resolved, but it didn't work. Even though my feet were NOT swollen they felt that way, very tight feeling. It felt like I was walking on balloons, terrible feeling and I was afraid to walk with that unsteadiness. Didn't work for me, since then, I have been on many different medications. Neurontin, didn't help, amitriptiline, didn't help, Lyrica, didn't help. I am on nortriptyline now with a pain patch. The fentanyl patch really helps, but I don't want to stay on this forever, so trying different medications. I am only supposed to leave the pain patch on 3 days, and found with the new medication, nortriptyline, I can go 5 days. So I am hopeful here.

Review by Anonymous: February 1, 2010 1:25 PM
User Rating: 8.0

Cymbalta (duloxetine): I have peripheral neuropathy and very bad pain in my back. Cymbalta made a huge improvement in my pain level. The doctor started me gradually to lessen the nausea. I have worked up to 30 mg. twice a day for a total of 60 mg. I have been taking it for 3 months and still find the pain level, and my frame of mind, much improved. I do have slight nausea occasionally, and dry mouth. The excessive sweating has gone away.

Review by Jo.Nigle: October 27, 2009 5:22 AM 

User Rating: 9.0

Cymbalta (duloxetine): Cymbalta was the first drug that actually improved the diabetic neuropathy pain I was experiencing in my legs, feet, arms and hands. For the first time, I was able to sleep through the night without waking in tears from the pain. I was so happy my doctor put me on this drug in conjunction with Neurontin. The pain almost disappeared! Approximately 6-8 weeks later, I noticed that the neuropathy pain started back up again despite continuing on the medicines. I too, had insomnia making it difficult, at best, to be alert, focused or have any energy the following day. To this day, I still have some insomnia and an increase in the neuropathy symptoms; BUT Cymbalta 60mg & Neurontin 600mg are the BEST drugs so far in lessening the pain.

Review by TerryinAlaska: October 20, 2009 6:45 PM 

User Rating: 3.0

Cymbalta (duloxetine): It was like a wonder drug at first. Then, even though I went up to the maximum dose of 60 mg, I can no longer tell I am even taking it. I stop it - then start it back up - still no help. It's just no good anymore.

Review by Tomasue: September 4, 2009 5:38 PM 

Cymbalta (duloxetine): I was only able to take this for about 3 days. It made me so unsteady on my feet that falling was a great threat. I also spoke, looked and felt like a "drunken sailor". Totally uncoordinated and 'out of it'. It did nothing for my neuropathy.

Review by KimberDawn38: July 25, 2009 5:09 AM 

User Rating: 10

Cymbalta (duloxetine): I've tried many, many different medicines for my nerve pain. Finally after being put on Cymbalta for my depression, I noticed that my nerve pain was not near as bad as it was before. I'm overwhelmed with my results. Almost to tears, of joy, instead of tears of pain! Thank you!

Review by HAPPYKAT: June 26, 2009 11:24 PMUser Rating: 10

Cymbalta (duloxetine): Works great on my nerve pains, due to diabetes.

Review by Anonymous: June 11, 2009 4:10 PM

Cymbalta (duloxetine): Cymbalta worked for my neuropathy for about 6 weeks then suddenly stopped working. I was very sad that is stopped. I did experience very bad insomnia but other than that I didn't have any major side effects.

Review by Anonymous: June 9, 2009 3:43 PMUser Rating: 1.0

Cymbalta (duloxetine): Debilitating side effects after only 2 hours with only one 60mg pill. Extreme sweating, fatigue, difficulty swallowing and walking. Next came the nausea and intense insomnia. Had to call in sick to work the next day due to lack of sleep and weakness. Didn't get out of bed until 3 pm.

Review by hemaro: April 6, 2009 7:01 PM

User Rating: 9.0

Cymbalta (duloxetine): Cymbalta has been a lifesaver for my Diabetic Neuropathy. In just a few days the pain and discomfort went away. The only problem I am facing with Cymbalta is insomnia even in combination with Xanax 4mg and Vistaril 150mg.

Review by Anonymous: February 25, 2009 9:25 PM
User Rating: 9.0

Cymbalta (duloxetine): Caused me to have serotonin syndrome.
..................................................................................................................................

http://www.drugs.com/comments/duloxetine/for-diabetic-neuropathy.html

Neuropathy Warnings About Hivid Zalcitabine

Today's post from the very reliable drugs.com (see link below) talks about the dangers of getting neuropathy from taking Hivid (Zalcitabine) as part of your HIV medication combination. Fortunately Hivid is one of the older HIV drugs these days but is still widely taken across the world, especially in countries where budgets are tight and drug companies cynically sell their older products at reduced prices. The possibilities of suffering nerve damage are significant with Hivid (amongst other possible nasty side effects) so it may be worth your while discussing this with your HIV specialist and arguing the case that an alternative would be a better choice. Whether those alternatives are available is the question.

Hivid Dosage Generic name: zalcitabine
Dosage form: Tablets
Overview Side Effects Dosage Interactions For Professionals More...

This dosage information does not include all the information needed to use Hivid safely and effectively. See full prescribing information for Hivid.

The information at Drugs.com is not a substitute for medical advice. ALWAYS consult your doctor or pharmacist.

Patients should be advised that HIVID is recommended for use in combination with active antiretroviral therapy. Greater activity has been observed when new antiretroviral therapies are begun at the same time as HIVID. Concomitant therapy should be based on a patient's prior drug exposure. The recommended regimen is one 0.750 mg tablet of HIVID orally every 8 hours (2.25 mg HIVID total daily dose) in combination with other antiretroviral agents. Please refer to the complete product information for each of the other antiretroviral agents for the recommended doses of these agents. Based on preliminary data, the recommended HIVID dosage reduction for patients with impaired renal function is: creatinine clearance 10 to 40 mL/min: 0.750 mg of HIVID every 12 hours; creatinine clearance less than 10 mL/min: 0.750 mg of HIVID every 24 hours.

Monitoring of Patients

Complete blood counts and clinical chemistry tests should be performed prior to initiating HIVID therapy and at appropriate intervals thereafter. For comprehensive patient monitoring recommendations for other antiretroviral therapies, physicians should refer to the complete product information for these drugs. Serum amylase levels should be monitored in those individuals who have a history of elevated amylase, pancreatitis, ethanol abuse, who are on parenteral nutrition or who are otherwise at high risk of pancreatitis. Careful monitoring for signs or symptoms suggestive of peripheral neuropathy is recommended, particularly in individuals with a low CD4 cell count or who are at a greater risk of developing peripheral neuropathy while on therapy (see WARNINGS).

Dose Adjustment for HIVID

For toxicities that are likely to be associated with HIVID (eg, peripheral neuropathy, severe oral ulcers, pancreatitis, elevated liver function tests especially in patients with chronic Hepatitis B), HIVID should be interrupted or dose reduced. FOR SEVERE TOXICITIES OR THOSE PERSISTING AFTER DOSE REDUCTION, HIVID SHOULD BE INTERRUPTED. For recipients of combination therapy with HIVID and other antiretroviral agents, dose adjustments or interruption for each drug should be based on the known toxicity profile of the individual drugs. SEE INFORMATION FOR EACH DRUG USED IN COMBINATION FOR A DESCRIPTION OF KNOWN DRUG-ASSOCIATED ADVERSE REACTIONS.

Patients developing moderate discomfort with signs or symptoms of peripheral neuropathy should stop HIVID. HIVID-associated peripheral neuropathy may continue to worsen despite interruption of HIVID. HIVID should be reintroduced at 50% dose — 0.375 mg every 8 hours only if all findings related to peripheral neuropathy have improved to mild symptoms. HIVID should be permanently discontinued if patients experience severe discomfort related to peripheral neuropathy or moderate discomfort that progresses. If other moderate to severe clinical adverse reactions or laboratory abnormalities (such as increased liver function tests) occur, then HIVID and/or the other potential causative agent(s) should be interrupted until the adverse reaction abates. HIVID and/or the other potential causative agent(s) should then be carefully reintroduced at lower doses if appropriate. If adverse reactions recur at the reduced dose, therapy should be discontinued. The minimum effective dose of HIVID in combination with zidovudine for the treatment of adult patients with advanced HIV infection has not been established.

In patients with poor bone marrow reserve, particularly those patients with advanced symptomatic HIV disease, frequent monitoring of hematologic indices is recommended to detect serious anemia or granulocytopenia. Significant toxicities, such as anemia (hemoglobin of less than 7.5 gm/dL or reduction of more than 25% of baseline) and/or granulocytopenia (granulocyte count of less than 750 cells/mm3 or reduction of more than 50% from baseline), may require a treatment interruption of HIVID and zidovudine until evidence of marrow recovery is observed. For less severe anemia or granulocytopenia, a reduction in daily dose of zidovudine in those patients receiving combination therapy may be adequate. In patients who experience hematologic toxicity, reduction in hemoglobin may occur as early as 2 to 4 weeks after initiation of therapy, and granulocytopenia usually occurs after 6 to 8 weeks of therapy. In patients who develop significant anemia, dose modification does not necessarily eliminate the need for transfusion. If marrow recovery occurs following dose modification, gradual increases in dose may be appropriate depending on hematologic indices and patient tolerance. For more details, refer to the complete product information for zidovudine.

http://www.drugs.com/dosage/hivid.html

Food Allergies and Neuropathy

It is mostly overlooked in articles about neuropathy but if a lack of Vitamin B12 for instance, is thought to be one of the causes of neuropathy, then why not certain food allergies too? Today's article from myiho.com, which is a Florida based neuropathy blog, (see link below) looks at the theory that certain food allergies may be primary causes of nerve damage. Aspartame, for instance, as one of the commonest ingredients of sweeteners, may surprise you.

Nutrition’s Role in Neuropathy
Posted on March 7, 2012

Neuropathy has wide variety of causes, and nutritional causes are a major subset of it. Neuropathy secondary to deficiency of Vitamin B (especially B12 and Folic Acid) is well known and one of the first suspicion in otherwise normal patients presenting with symptoms of neuropathy like numbness, pin-and-needle sensation, burning sensations, pain or loss of sensations. When it affects the nerves supplying the muscles, it may result in weakness of muscle, muscle atrophy, lack of fine muscle control which may result in many symptoms depending on which muscles are affected.

But one cause of peripheral neuropathy that is not readily thought to be associated with neuropathy is food allergy. The association between food allergy and neuropathy is often overlooked because only recently conclusive evidence from research has become available establishing a certain link between neuropathy and allergic response to certain food items. The culprits so far found to be most commonly occurring are derivatives of glutamic acid and aspartic acid, gluten, pesticides on fruits and vegetables, food coloring dyes. One very common artificial sweetener, Aspartame, is used in fruit juices, diabetic food and numerous other products. It is one of the most commonly recognized allergen triggering symptoms of neuropathy like tingling, numbness, burning sensation etc. and also affecting auditory nerve causing tinnitus. Consumption of large quantities greatly increases the chances of having the neuropathy. Often, stopping the consumption of aspartame cures the symptoms almost entirely.

Many more agents commonly found in food may cause allergic response which may present as neuropathy. The ones that are currently believed to be responsible for most of the cases are Azino-moto (Mono Sodium Glutamate) which is commonly used in Chinese foods, gluten found in wheat containing edible items, some coloring dyes used in foods. Not only these, but normal fully natural food items like fruits, eggs, and milk may be the cause of food allergy induced neuropathy. Often it may happen, that the tracking of the allergy causing food item may not be very simple and straightforward.

So what if your neuropathy is suspected to be due to food allergy. Main diagnostic test used is a Radioallergosorbent Test (RAST Test) which detects antibodies against “common” food allergens. Since not all antigens could be detected in 100% of cases, sometimes the treatment may involve just hit and trial in which suspected food items are stopped for few week and observed whether it alleviates the neuropathy. Also it would be advisable to stop common known allergens like aspartame, MSG, food dyes, and gluten and observe if the symptoms are alleviated by this. Also thoroughly wash fruits and vegetables before consuming, as pesticides present on them could be the cause.

If you are one of the many thousands of sufferers of Neuropathy, you know all to well that numbness and tingling is still a pain to deal with. Peripheral Neuropathy is a condition that is characterized by altered sensation or a change in motor control of a body part. The nerve becomes irritated or damaged and it no longer conducts the messages it should. If your neuropathy is left untreated, it will begin to affect your quality of life.

http://myiho.com/orlandoneuropathyblog/?m=201203

Accepting The Pain Of Neuropathy And Moving Forward

Today's post from instituteforchronicpain.org (see link below) is a self-help article with a difference - it makes sense! Most self-help articles are well-meaning but stuffed with clichés and so-called new age philosophy and go over most people's heads. What we need is to know why we need to become proactive in our health problem and why that will do us good. This article sets out to explain how not fighting our pain (as we're expected to do) is the first step towards learning to live with it and improve it. Worth a read...even for cynics.

Finding Hope in Acceptance  
Author: Murray J. McAllister, PsyDPosted on August 26, 2013

At first thought, it might seem crazy to accept that your pain is chronic. When I bring it up with patients, many of them tell me, not without some irritation in their voice, “I’ll never give up hope of finding someone who can fix me!” Indeed, it’s common to think that accepting the chronicity of your pain is the same thing as giving up hope that you’ll ever get better. So, why in the world would you ever want to accept that your pain is chronic?

Contrary to what you might think, accepting that your pain is chronic is the first step in actually getting better. It opens up a whole new way of getting better, a way that takes into account the realities of your pain condition. As such, it’s a new and more realistic way to have hope.

To understand the point more clearly, let’s briefly review two different models of healthcare – two different ways that we get better when having an illness or injury. These two models are what we might call the ‘acute medical model’ and the ‘rehabilitation model.’ The latter is sometimes called the ‘self-management model.’ (For a more thorough review of these models of healthcare, click on this post here.) 


Acute Medical Model

The acute medical model of healthcare is what most of us think of when we go to see a healthcare provider. When sick or injured, we go to a provider who determines what’s wrong and provides a treatment that cures us. The healthcare provider is an expert who usually knows more about the condition and the treatments than we do. The treatments themselves are usually medications or procedures that act on us. We don’t typically get better by doing things ourselves. Rather, it’s the treatments that get us better and we rely on healthcare providers to provide us with those treatments. Lastly, getting better in the acute medical model is usually thought of as getting cured. We return to our usual state of health — how we were before we became ill or injured.

Hope of getting better within the acute medical model lies in finding the right healthcare provider who knows what’s wrong and knows how to cure you. In this model, hope lies external to you. You find it in the expertise and treatments of a healthcare provider.

Now there’s nothing wrong with the acute medical model. It’s all well and good when we have a condition for which there actually is a cure. Indeed, it’s likely the best thing to do. But, what do you do when you have a condition for which there is no cure?

Rehabilitation Model

The answer to the question, of course, isn’t to give up hope and do nothing. There’s actually a different way of getting better. It’s the rehabilitation model of care. It requires, however, redefining how to get better and even redefining what it means to get better.

In the rehabilitation model of care, the emphasis is on what you, the patient, do to get better — not on what the healthcare provider does to get you better. Specifically, the focus is on the patient acquiring the abilities to make healthy changes, which, when done over time, have a positive impact on the chronic health condition that you have. These changes fall into two categories: a) changes in health behaviors, or what’s often referred to as lifestyle change, and b) changes in coping, or what’s often referred to as stress management. The goal of learning and engaging in these health behaviors over time is two-fold: you reduce the symptoms of the condition and you reduce the impact that the chronic health condition has on you. In other words, you get so good at self-managing the condition that it no longer is as problematic as it once was. As a consequence, you can move on with the rest of your life, engaging in the meaningful activities of life – such as work, family activities, social and recreational activities.

Notice that the rehabilitation model doesn’t promise a cure. The reason is that the conditions for which the rehabilitation model is best suited are those conditions that are chronic. They have no cure. Nonetheless, the patient does get better in very real and meaningful ways.

Notice too that hope gets redefined. It allows for having hope even when there is no cure. Finding a cure is not the only way to get better. Therefore there’s still hope. It’s just a different way to have hope, a hope that realistically takes into account the chronic nature of the condition you have, but nonetheless points to how to how you still can get better.

The conditions for which the rehabilitation model is best suited are chronic conditions, where there is no cure, such as chronic pain syndromes, diabetes, heart disease, and spinal cord injuries, among others.

Finding Hope in Acceptance

Acceptance that your pain is chronic is the first step in pursuing the rehabilitation model of care. Rehabilitation is hard work. It also takes time. You don’t do it if you think that a cure is just around the corner. Once you recognize, though, that your chronic pain really is chronic, it becomes your life-saver – or life-retriever. You start to get your life back. You learn how to self-manage your pain and you practice it to the point that you move on with the rest of your life. Your life doesn’t have to be about chronic pain.

Patients can keep their life on hold when they insist on finding hope only in a cure. They seek out appointment after appointment, attempting to find the right specialist who will know what to do to make their pain go away. Oftentimes, they seek out surgeries or interventional procedures that seem as if they might be a cure, but aren’t. Each time they seek out a new specialist, there is hope. Each time, though, it gets dashed because there really is no cure for chronic pain. Chronic pain really is chronic.

The point, here, is not a criticism of such patients. What we are describing makes sense if you think of healthcare as only the acute medical model. If we think of healthcare providers as specialists who fix us when sick or injured, it makes all the sense in the world to look for the right one who can do the job – even if you have to try one after another. It’s a hard lesson to learn when realizing that it’s only sometimes that healthcare providers act like a mechanic. A lot of the time, we have no fixes. So, again, I’m not judging when I describe patients who fail to accept that their pain is chronic. We can all understand how it happens. They are trying to find hope in a cure.

What if, though, at the end of the day, the hope is really a false hope? It can become a vicious cycle that leads to depression and oftentimes more pain. Hope is found with each new procedure, but each procedure fails to cure the pain and so hope is dashed. If hope is defined by finding a cure, and if there really is no cure, then you are left helpless – and hopeless.

Maybe it’s best to find a new way to have hope.

You find it by accepting that chronic pain really is chronic. You accept that you are not going to get better by finding a cure. Rather, you accept that you are going to get better by learning to self-manage it. You learn how to make healthy changes in your life that, when done over time, reduce your symptoms and reduce the impact that chronic pain has on your life. You get so good at managing chronic pain that it is no longer the preoccupying problem that it once was. Your life consists of the stuff of life and chronic pain comes along for the ride, but remains in the side car.

It’s okay if you don’t know how to do it yet. Most patients have to learn how to do it. Oftentimes, I remind patients that you’re not born with the knowledge of how to self-manage pain successfully. People have to learn it. And it’s okay if you don’t know how and have to learn it.

What matters, though, is that you learn how. It’s possible to learn how to self-manage pain and do it successfully. People learn how to do it everyday in chronic pain rehabilitation programs. And you can too.

You just have to first accept that your chronic pain is really chronic.

(For more information, please see: “What is chronic pain?” or “Why the healthcare system refuses to accept the chronicity of chronic pain.”)

http://www.instituteforchronicpain.org/blog/finding-hope-acceptance/

Medication Related Neuropathy

Today's post from nytimes.com (see link below) is a general look at how neuropathy can be caused by certain drugs you are taking. We all underestimate the toxicity of drugs over the long term but some of the ones listed here may surprise you. That said, by no means all people who take these drugs as prescribed, get neuropathy - it's mostly the exception rather than the rule but if you and your doctor are searching for reasons why you have neuropathic problems, it may be worth while looking at your medications to see if there's a possible link there.

Neuropathy Secondary to Drugs Reference from A.D.A.M. New York Times Health

Neuropathy secondary to drugs is a loss of sensation or movement in a part of the body due to nerve damage from a certain medicine.

Causes

The damage is caused by the toxic effects of certain medications on the peripheral nerves (nerves that are not in the brain or spinal cord). There may be damage to the axon part of the nerve cell, which interferes with nerve signals.

Most commonly, many nerves are involved (polyneuropathy). This usually causes sensation changes that begin in the outside parts of the body (distal) and move toward the center of the body (proximal). There may also be changes in movement, such as weakness.

Many medications may affect the development of neuropathy, including:
 
Heart or blood pressure medications
Amiodarone
Hydralazine
Perhexiline
Drugs used to fight cancer
Cisplatin
Docetaxel
Paclitaxel
Suramin
Vincristine
Drugs used to fight infections
Chloroquine
Isoniazid (INH) -- used against tuberculosis
Metronidazole (Flagyl)
Nitrofurantoin
Thalidomide (used to fight leprosy)
Drugs used to treat autoimmune disease
Etanercept
Infliximab
Leflunomide
Drugs used to treat skin conditions (Dapsone)
Anticonvulsants (phenytoin)
Anti-alcohol drugs (disulfiram)
Drugs to fight HIV
Didanosine (Videx)
Stavudine (Zerit)
Zalcitabine (Hivid)
Arsenic
Colchicine
Gold

Symptoms
Numbness, loss of sensation
Tingling, abnormal sensations
Weakness

Sensation changes usually begin in the feet or hands and move inward.

Exams and Tests

A brain and nervous system examination will be done.

Other tests include:
Blood tests to check levels of the medication (even normal blood levels of certain drugs may be toxic in elderly or certain other persons)
EMG and nerve conduction test of the electrical activity of nerves and muscles

Treatment

Treatment is based on the symptoms and how severe they are. The medication causing the neuropathy may be stopped, reduced in dose, or changed to another medication. (Never change any medication without first talking to your health care provider).

The following medications may be used to control pain:
Over-the-counter pain relievers may be helpful for mild pain (neuralgia).
Phenytoin, carbamazepine, gabapentin, pregabalin, duloxetine, or tricyclic antidepressants such as nortriptyline may reduce the stabbing pains some people experience.
Opiate pain relievers, such as morphine or fentanyl, may be needed to control severe pain.

Whenever possible, avoid or reduce medication use to lessen the risk of side effects.

If you have lost sensation, you may need to take safety measures to avoid injury.

Outlook (Prognosis)

Many people can partially or fully return to their normal function. The disorder does not usually cause life-threatening complications, but it can be uncomfortable or disabling.

Possible Complications
Inability to function at work or home because of permanent loss of sensation
Pain with tingling in the area of the nerve injury
Permanent loss of sensation (or rarely, movement) in an area
When to Contact a Medical Professional

Call your health care provider if you have a loss of sensation or movement of any area of the body while taking any medication.
Prevention

Your health care provider will closely monitor your treatment with any medication that may cause neuropathy. The goal is to keep the proper blood level of medication needed to control the disease and its symptoms while preventing the medication from reaching toxic levels.

References
Katirji B, Koontz D. Disorders of peripheral nerves. In: Daroff RB, Fenichel GM, Jankovic J, Mazziotta JC. Bradley’s Neurology in Clinical Practice. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 76.

Weimer LH, Sachdev N. Update on medication-induced peripheral neuropathy. Curr Neurol Neurosci Rep. 2009;9(1):69-75.

http://www.nytimes.com/health/guides/disease/neuropathy-secondary-to-drugs/overview.html

Calcium For Neuropathy Vid

Today's video from the ever informative beatingneuropathy.tv (see link below) produced by Dr John Hayes Jr, talks about the value of calcium in relation to neuropathy. These videos are short and always worth watching whatever your views on supplements are.



Episode 31 – Calcium
Posted by John Hayes Jr Thursday, October 24th, 2013

Dr. Hayes discusses calcium, possible issues with supplementation, and how neuropathy and chronic pain patients can make sure they’re getting enough. This is one nutrient that the truth is often not what it seems with powerful media driven economics behind it. Watch and learn More!




http://beatingneuropathy.tv/2013/10/episode-31-calcium-neuropathy/

Psychosocial Considerations and Quality of Life Issues in Peripheral Neuropathy

It's something your doctor may not have time to address but unless you have help from elsewhere, the psychological effects of neuropathy are easily underestimated, whilst contributing to making your life a misery. This article from Medifocus Health (see link below) shows what happens to many neuropathy patients, sometimes without them realising it themselves. It's very important to be aware of how quickly your mental state can change when you're continually under stress from ill health. If you're also HIV positive, these problems can become exaggerated and friends and family become more important than ever!

Psychosocial Considerations and Quality of Life Issues in Peripheral Neuropathy

"Quality of life" is a measure of how well patients adjust to their condition. It measures many factors related to living with a medical condition, including:
•Physical and material well-being
•Social relationships with other people (e.g., spouse, siblings, or friends)
•Social activities (e.g., helping others, getting together with other individuals or groups, community/religious involvement)
•Personal fulfillment (e.g., career, creativity, pursuit of intellectual interests)
•Recreational activities (e.g., sports or relaxation)
•Health status (perceived and actual)

A significant aspect of quality of life and ability to function daily is related to how individuals with peripheral neuropathy perceive themselves and regard their situation. Physical well-being has the greatest influence on a person's perceived health status and on most other measures evaluated in quality of life test scales.

Chronic neuropathic pain can be very debilitating and can affect several dimension of daily life as reflected in lower scores of quality of life scales including:
•Psychological health (e.g., depression, anxiety)
•Work-related problems (e.g., reduced levels of productivity, absenteeism)
•Sleep disturbances
•Feelings of isolation
•Sense of disappointment that expectations of recovery are not being met

Peripheral neuropathy affects a wide range of people and its impact on quality of life is closely related to the severity of this interference in daily life. In some people it is very debilitating and chronic, while others may be affected only intermittently with varying degrees of discomfort ranging from mild to severe. Pain management programs play an important role in teaching individuals how to live with their condition. These programs focus on pain control, as well as social and physical functioning, and emotional health. Another benefit of pain management programs is that they usually consist of several types of professionals, including psychologists or psychiatrists who can help monitor emotional status and try to prevent secondary conditions such as depression and withdrawal from society in individuals with peripheral neuropathy.

Depression is not uncommon in persons with peripheral neuropathy due to the chronic aspect of the pain, loss of function, emotional burden, and reduced quality of life. Some of the medications used to treat peripheral neuropathy are actually antidepressants and may help to control depression as well. However, it is very important that patients share feelings of depression with their health care providers so that they can be addressed appropriately. Support groups are helpful for many persons in coping with the pain and discomfort and its impact on daily life.

Response to medications is extremely variable and many patients try numerous types and doses of medications before finding one that brings some measure of relief. Some doctors and patients find that keeping a daily pain diary is a useful tool to monitor responses to medications and therapies so that changes or adjustments to patients' pain management programs can be implemented as needed. Response to monotherapy (one drug) is estimated to bring a 30-50% reduction in pain, at best. Multi-drug therapies that target different parts of the nerve pathways may be more effective. Although there are no clinical trials to date regarding multi-drug treatment of peripheral neuropathy, this strategy is often practiced by physicians.

http://www.medifocushealth.com/NR021/Understanding-Peripheral-Neuropathy_Psychosocial-Considerations-and-Quality-of-Life-Issues-in-Peripheral-Neuropathy.php

Lung Cancer Patients Who Also Have Neuropathy

Today's post from cancergrace.org (see link below) is very useful if you have lung cancer or lung problems in general and have contracted neuropathy as a result of the cancer drugs you're taking. It explains the issue simply and highlights the chemotherapy drugs most likely to cause neuropathic symptoms. Whatever your medical history, there is always a possibility that  you may end up with a form of cancer and neuropathy is a fairly common side effects of cancer treatment drugs. It's important that you discuss the options with your doctor or specialist.
 

What about treating patients who have medical problems? Treating lung cancer in patients with kidney issues or neuropathy.
Published March 2, 2014 | By Dr West 
Download PDF

One of the challenges of cancer care is that we guide our treatments by what clinical trial evidence tells us is best for particular patient populations. However, trials exclude patients who have significant medical issues other than cancer. So what do you do for patients who have lung cancer but also have common medical problems like compromised kidney function or pre-existing numbness and tingling (neuropathy) from diabetes or vascular disease? A purist in evidence-based medicine would say that patients who don’t have good kidney function or who have other medical problems that would exclude them from the trials of our standard treatments can’t get treated, but fortunately most oncologists are more flexible than that. What’s the right way to proceed? The answer is that it falls to best medical judgment. But can we be more specific than that?

In the setting of renal insufficiency, which is common as patients get older, as well as being a result of years of high blood pressure or diabetes, we need to substitute out the treatments that are most threatening to kidney function worsening. Specifically, this means avoiding the particularly kidney-threatening cisplatin, considering avoiding carboplatin (or perhaps giving it and carefully monitoring kidney function and dropping if it kidney function worsens, and then substituting non-kidney damaging agents instead). If kidney function is only minimally impaired, it may be very acceptable to give carboplatin plus a taxane: Taxol (paclitaxel), Abraxane (nab-paclitaxel), or Taxotere (docetaxel)), Gemzar (gemcitabine), Navelbine (vinorelbine), or Alimta (pemetrexed). An alternative, and the leading one if kidney function is quite compromised or gets worse on carboplatin-based chemo, is to give a nonplatinum doublet, which basically means pairing two drugs for lung cancer that are more commonly partners for cisplatin or carboplatin. Common nonplatinum doublets include Gemzar/Navelbine or Gemzar with one of the taxanes. About 15 years ago, there was a significant hope that these agents might turn out to be an improvement from platinum-based doublets, with comparable or slightly superior efficacy and improved tolerability. That didn’t turn out to be the case: the nonplatinum doublets were typically of the same or very slightly lower efficacy, and the same or slightly better tolerability. Overall, they were a lateral move and never took hold as a leading choice, but they are certainly a fine choice and arguably the ideal one for people with limited kidney function.

Then there’s the case of patients with peripheral neuropathy. The taxanes and especially Taxol are the worst offenders here, as is cisplatin, and Navelbine can also worsen neuropathy. Here, we commonly favor carboplatin with a less neuropathy-inducing partner drug, so Gemzar is often a leading choice, or Alimta for a non-squamous lung cancer.

It’s also reasonable to consider single agent chemotherapy, though several recent trials have shown that carboplatin doublet chemotherapy is associated with better outcomes as first line treatment than single agent chemo, even in patients with a marginal performance status. But it’s certainly reasonable to consider single agent chemo in individual patients with significant organ compromise, or simply in patients who are particularly wary about significant side effects.

Though there are certainly other problems that merit individual treatment recommendations, these are among the most common ones. In the end, it still comes down to individualized judgments and considerations of the circumstances of the particular patient.

http://cancergrace.org/lung/2014/03/02/treating-patients-with-other-med-problems/#more-14241

Is Massage Really Wise For Neuropathy

Today's post from painscience.com (see link below) warns about the possible disadvantages of massage therapy. Many people with neuropathy symptoms somehow assume that massage will help them feel better and in many cases they do but you need to go to a massage therapist who knows what he or she is doing. The idea that you may come away with symptoms that are worse than before should be enough to make you think about whether a good pummelling is really good for your nerves or not. Gentle massage may well be very effective in calming down painful nerve areas, or generally making you relax but the minute the masseur goes for deep tissue and joint massage may be the moment you ask how much experience he or she has with neuropathy. You probably know yourself, if you've tried massaging your neuropathic feet. Half the time you can't feel anything due to the numbness but the moment you push just that little bit too hard to relieve the burning or tingling, you can be suffering for days. Always best to go to a qualified masseur with relevant experience, or else the happy ending may not be as happy as you thought (goes for all kinds of massage!!)
 

What Could Possibly Go Wrong With Massage?
Rare but real adverse effects of massage therapy, especially “deep tissue” massage
updated July 16 2014 by Paul Ingraham, Vancouver, Canada bio

People think of massage therapy as a “safe” therapy, and of course it mostly is. But things can go wrong, or at least a bit sour. While serious side effects in massage therapy are extremely rare, minor side effects are downright common. A 2007 survey of 100 massage patients1 found that 10% of 100 patients receiving massage therapy reported “some minor discomfort” in the day following treatment. This would mainly be a familiar slight soreness that is common after a massage, known as “post-massage soreness and malaise” (PMSM) — and I’m surprised only 10% reported it. The massages they were getting must have been quite gentle.2

Interestingly, 23% reported unexpected benefits that had nothing to do with aches or pains. (Benefits for musculoskeletal problems were not documented.)

This study is underpowered. It cannot and does not rule out rare and/or serious side effects of massage therapy, which do exist. You could probably do several studies of 100 patients without encountering a single nasty situation. But what if you surveyed 1,000 patients? Or 10,0000? Massage is not completely safe — what is? — and other adverse effects would almost certainly turn up in a big enough survey. Nevertheless, according to one of alternative medicine’s most vigorous critics, Dr. Edzard Ernst, “Serious adverse events are probably true rarities.”3 And yet, reviewing the literature again in 2013, Ernst and Posadzki found at least 18 reported examples of “moderately severe” reactions to normal massage, especially of the neck.4
When massage goes bad

So what could possibly go wrong? Massage can…
directly cause new injuries (mostly quite minor, but not all)
aggravate existing injuries and chronic pain problems
distract patients from more appropriate care
mildly stress the body And don’t forget, of course, that that pointlessly draining your wallet is another kind of pain. If someone spends $5,000 on massage therapy that has only a minor therapeutic effect, or none at all, is that an “injury”? It’s an insult, at the least!

In my decade (2000–2010) as a massage therapist, I met many patients who had been harmed by massage therapy to some degree — fortunately, mostly just expensive disappointments and minor backfires, but quite a few more serious cases too.5 

Sensory injury

A painful, alarming sensory experience can actually dial up pain sensitivity — even long term.6 Furthermore, vulnerability to this awful phenomenon is much more common and significant in desperate patients who already have chronic pain — so they seek and tolerate intense therapy. People experiencing pain system dysfunction can have minor & major setbacks in response to excessively painful massage.

The experience of pain is affected by many factors, including emotional and psychological ones. People in chronic pain usually experience some degree of pain neurology dysfunction, and a breakdown of the relationship between how bad things feel and how much is really wrong. That breakdown can be seriously worsened by threatening sensations. Thus, people experiencing pain system dysfunction can have minor and major setbacks in response to excessively painful massage.

One of my readers suffered this kind of disaster. She was injured by “fascial release” therapy, a style which is often too intense and may focus on treating connective tissues to the exclusion of considering the patient’s comfort and nervous system.

I may have been too aggressive with a few patients over the years. I never did serious harm this way as far as I know, but I’m sure that I occasionally did more harm than good. This failure was due entirely to my ignorance of pain science: despite being an unusually well educated massage therapist, I simply did not know that an intense massage could change pain sensitivity itself. Does your therapist?
Pain is Weird Pain science reveals a volatile, misleading sensation that is often more than just a symptom, and sometimes worse than whatever started it ~ 9,000 words
The Pressure Question in Massage Therapy What’s the right amount of pressure to apply to muscles in massage therapy and self-massage? ~ 4,500 words
Poisoned by massage

Excessive pressure probably has another predictable outcome: a light poisoning. Seriously.

For example: an 88-year old man collapsed the day after an unusually strong 2-hour session of massage therapy.7 He had too much myoglobin in his blood, and it was poisoning his kidneys and generally making him feel rotten. It’s not a sure thing that his condition was cause by the massage — but it is quite likely. It is almost certainly a perfect example of one of those rare but serious complications of massage. Another case study comes up below.

Ironically, many people believe that massage is a detoxification treatment, but in fact it’s probably the opposite. Ironically, many people believe that massage is a detoxification treatment, but in fact it’s probably the opposite. Post-massage soreness and malaise is probably caused by mild rhabdomyolysis (“rhabdo”): poisoning by the waste products of injured muscle.

True rhabdo is a medical emergency in which the kidneys are poisoned by myoglobin from muscle crush injuries. But many physical and metabolic stresses cause milder rhabdo-like states — even just intense exercise, and probably massage as well. There are many well-documented cases of exertional or “white collar” rhabdo, and there is a strong similarity between PMSM and ordinary exercise soreness. A rhabdo cocktail of waste metabolites and by-products of tissue damage is probably why we feel a bit cruddy after all biological stresses and traumas — including massage, sometimes.

PMSM is just an unavoidable mild side effect of strong massage. And for a few more vulnerable patients, it could actually be a little dangerous.
Poisoned by Massage Rather than being “detoxifying,” massage may cause a modestly toxic situation in the body ~ 4,500 words 

Other examples of massage wounds

The neck is not generally a fragile structure, but it is in some people. Another serious example of an adverse effect of massage is what happened to my barber — either a brain stem injury or mini-stroke caused by careless massage of a vulnerable neck. One of my own patients was injured the same way by another therapist, vomiting and retching for hours afterwards (a nasty symptom of brain stem impingement, or ripping of an artery going to the brain). I came close to doing this to another patient — that’s three examples of such patients in my career — but I’m proud to say that I spotted the warning signs and avoided disaster.

A weird case of brain artery damage (extracranial internal cartoid artery dissection, specifically) was reported in 2004 by the Southern Medical Journal: a 38-year-old woman gave herself a stroke by using a vibrating massage tool for long and too hard on her neck.8 Obviously such an incident has little to do with professional massage. Nevertheless, it demonstrates that the arteries of the neck are a little bit fragile — and I have no doubt that there are poorly trained or incompetent therapists out there would might get carelessly exuberant in this region, while trying to treat the scalenes: see Massage Therapy for Neck Pain, Chest Pain, Arm Pain, and Upper Back Pain.

Another weird, extreme case study paper tells the horror story of one person’s awful experience with a severe reaction to (apparently) infrared heat and massage therapy.9 The trouble started after several treatments. His neck and arms were swollen, the pain became “unbearable,” and his “serum muscle enzymes were increased” — which means some degree of rhabdo, which implicates the massage itself as a significant mechanism of injury. Massage is not likely to “blame” for the incident, though — it was probably interacting with some unidentified vulnerability in the patient, such a muscle disease or a complication caused by a medication. Clearly massage and heat alone do not normally cause such severe side effects! Nevertheless, the potential for very unpleasant interactions exists.

“Alternative therapies may have serious complications, and patients usually do not report them unless asked specifically,” the authors point out.

I am one-degree of separation from a patient whose femur (the big leg bone!) was fractured by a massage — it was a weak and injured femur already … but wow!

Nerves aren’t nearly as vulnerable to pressure as people generally think — most of them can actually take quite a licking and keep on ticking without a single symptom — but they aren’t invulnerable. And I once caused a nerve injury myself: it was a minor injury, but it did — augh — result in weeks of aggravating discomfort for my client. The Archives of Physical Medicine & Rehabilitation reported a similar spinal accesory nerve injury: “a rare and illustrative case of spinal accesory neuropathy associated with deep tissue massage leading to scapular winging [the shoulder blade sticking out] and droopy shoulder as a result of weakness of the trapezius muscle.”10
What Happened To My Barber? Either atlantoaxial instability or vertebrobasilar insufficiency causes severe dizziness and vomiting after massage therapy, with lessons for health care consumers ~ 2,750 words 

Lessons for professionals and patients

These are rare but real incidents. Healthy people are unlikely to be injured by massage. Most of dangers are related to undetected vulnerabilities, and they emphasize the importance of alternative health professionals being trained to spot the scary stuff. The measure of a health professional’s competence is not what they do with relatively healthy patients, but whether they have the training and humility to realize when they are on thin ice.

Manual therapists need to know that the most important part of their job is the smart management high-risk situations that they may see only a handful of times in their entire career. It’s like being on guard duty: 99.9% of the time, nothing bad happens. But how do you handle a curve ball when it finally comes?

Consumers need to know that cocky, overconfident therapists who trash-talk “mainstream” health care are all-too-likely to be ignorant of critical warning signs, or dismissive of them. The skeptical salamander thinks these therapists shouldn’t be allowed to touch anyone. See Missing Serious Symptoms.

About Paul Ingraham

I am a science writer, former massage therapist, and assistant editor of ScienceBasedMedicine.org. I have had my share of injuries and pain challenges as a runner and ultimate player. My wife and I live in downtown Vancouver, Canada. See my full bio and qualifications, or my blog, Writerly. You might run into me on Facebook and Google, but mostly Twitter.




Notes
Cambron JA, Dexheimer J, Coe P, Swenson R. Side-effects of massage therapy: a cross-sectional study of 100 clients. J Altern Complement Med. 2007 Oct;13(8):793–6. PubMed #17983334. BACK TO TEXT
 
Indeed, that seems very likely given the context. I doubt they would test painfully strong massage on 100 people without mentioning the intensity. However, painfully strong massage is quite common “in the wild.” Certainly intense massage is unusually common here in Vancouver, where there’s a regrettable professional predeliction for it. BACK TO TEXT
Ernst E. The Safety of Massage Therapy. Rheumatology. 2003;42 (9):1101–1106. PubMed #12777645. PainSci #54834.

Is massage safe? Researchers attempted to answer that question. Four databases were reviewed; all articles which reported adverse effects of any type of massage therapy were looked at. In the end, 20 reports were looked at. “The majority of adverse effects were associated with exotic types of manual massage or massage delivered by laymen, while massage therapists were rarely implicated.”

The conclusion was that, while not entirely risk free, “serious adverse events are probably true rarities.” BACK TO TEXT
Posadzki P, Ernst E. The safety of massage therapy: an update of a systematic review. Focus on Alternative and Complementary Therapies. 2013;18(1):27–32. PainSci #53974.


OBJECTIVE: To update a systematic review evaluating the safety of massage therapy.

METHODS: A literature search was carried out using four electronic databases for the period December 2001 to May 2012. All articles reporting adverse effects of massage therapy were retrieved. Adverse effects relating to atypical massage, aromatherapeutic massage oil or ice were excluded. No language restrictions were applied. Data were extracted and evaluated according to predefined criteria.

RESULTS: Seventeen case reports and one case series were published since our previous review. The reported adverse effects comprised acute paraplegia and abdominal distension, bladder rupture, bilateral cerebellar infarction, cervical lymphocele, cervical cord injury, cervical internal carotid and vertebral dissection, chylothorax, haematuria, interosseous nerve palsy, myopathy, perinephric haemorrhage, rhabdomyolysis, severe headache, blurred vision, paraesthesia and focal motor seizures. In the majority of the reports, a cause–effect relationship was certain or almost certain. Serious adverse effects were most commonly associated with massage techniques applied to the neck area.

CONCLUSION: Evidence suggests that massage may occasionally lead to moderately severe adverse effects. BACK TO TEXT
 
Several dozen at least who experienced minor negative effects and a lighter wallet. I recall only about dozen or so having really poor experiences, mostly aggravated chronic pain. Only a handful of those were obviously significantly injured by massage. But those were sad cases. BACK TO TEXT
 
Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain. Pain. 2010 Oct;152(2 Suppl):S2–15. PubMed #20961685. PainSci #54851.

Pain itself often modifies the way the central nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation. That sensitization is called “central sensitization” because it involves changes in the central nervous system (CNS) in particular — the brain and the spinal cord. Victims are not only more sensitive to things that should hurt, but also to ordinary touch and pressure as well. Their pain also “echoes,” fading more slowly than in other people.

For a much more detailed summary of this paper, see Central Sensitization in Chronic Pain. BACK TO TEXT
 
Lai MY, Yang SP, Chao Y, Lee PC, Lee SD. Fever with acute renal failure due to body massage-induced rhabdomyolysis. Journal of Nephrology, Dialysis and Transplantation. 2006 Jan;21(1):233–4. PubMed #16204282. PainSci #54301. BACK TO TEXT
 
Grant AC, Wang N. Carotid dissection associated with a handheld electric massager. South Med J. 2004 Dec;97(12):1262–3. PubMed #15646768. BACK TO TEXT
 
Tanriover MD, Guven GS, Topeli A. An unusual complication: prolonged myopathy due to an alternative medical therapy with heat and massage. South Med J. 2009 Sep;102(9):966–8. PubMed #19668045. BACK TO TEXT
 
Aksoy IA, Schrader SL, Ali MS, Borovansky JA, Ross MA. Spinal accessory neuropathy associated with deep tissue massage: a case report. Arch Phys Med Rehabil. 2009 Nov;90(11):1969–72. PubMed #19887226. BACK TO TEXT

https://www.painscience.com/articles/whats-the-harm.php