Sunday, 20 April 2014

Dangers Of Neuropathy In Rwanda

Today's post from (see link below) shows that developed countries don't have a monopoly on neuropathic problems and especially those caused by diabetes. Neuropathy is a huge problem in many parts of Africa too, especially amongst the HIV population. However, diabetes too is not exclusive to the rich over-eaters in the developed world and is an increasing problem in Africa. This article looks at the situation in Rwanda and gives some good advice and information to potential patients especially regarding the possibility of autonomic neuropathy affecting the involuntary functions of the body.

Rwanda: Know the Dangers of Diabetic Neuropathy
By Dr Rachna Pande, 13 April 2014 
Diabetes is a condition of elevation of blood sugar levels above normal. Over the years diabetes is known to cause damage to the target organs of the body. These are eyes, kidneys, brain, peripheral blood vessels and nervous system. Complications appear early and are more if not controlled.

Affliction of the peripheral nervous system is well known, which is manifested by tingling, numbness and or burning sensation in hands and feet. But involvement of autonomic nervous system (system responsible for involuntary functions like heart beat, intestinal movements, among others) is more subtle and less known.

This may be associated with other diabetic complications or can occur independently. As the intestinal motility is affected, a person may develop chronic diarrhea. Stasis of food in intestines due to constipation leads to overgrowth of bacteria, which results into recurrent infections and diarrhea with or without abdominal pain.

Absorption of food as well as that of anti-diabetic medication is impaired due to reduced intestinal motility. As a result, the body gets deprived of necessary nutrients over a period of time. Blood glucose levels are deranged leading to sudden low or high levels.

A person starts suffering from low blood pressure, because of affliction of autonomic nervous system. The blood pressure falls and becomes very low as one stands up from sitting or lying down position. Because of this, one tends to feel giddy while standing or walking. Heart rate also tends to be disturbed because of disturbance of autonomic nervous system. This is because heart fails to adjust its rate according to the stress. This also contributes to fainting. Urinary system is also affected. There is difficult to pass urine leading to retention in extreme cases, as the nervous control over bladder is damaged.

Stasis of urine even in small quantities becomes a source for germs to grow causing recurrent urinary tract infections. Infection is further aggravated due to high blood glucose levels. Due to infection of the urinary tract, one suffers from increased frequency of urination. Impotence is the most troublesome problem in autonomic neuropathy. Diabetic neuropathy is the most common organic cause for erectile dysfunction in men.

Alcohol intake and smoking further aggravate these complications caused due to diabetic autonomic neuropathy. Many times, diabetes is diagnosed when a person develops any of these complications. A sufferer may develop one or more features of autonomic neuropathy.

A high index of suspicion is needed to diagnose diabetes in face of autonomic neuropathy.

Unfortunately once autonomic nervous system is damaged there is no medicine to revert it. Drugs such as gabba pentin, B Complex, among others, are used but only provide transient relief. Avoiding standing for long time and sitting with legs spread in front can reduce postural hypotension. Use of elastic stockings or crepe bandage while standing or walking also helps in minimising postural hypotension.

To prevent such troublesome complications it is imperative that diabetes should be diagnosed at the earliest. Screening all middle aged persons for diabetes is a good strategy. A good control of diabetes by means of diet restriction and anti diabetic drugs can delay or minimise the development of complications including neuropathy. Avoidance of alcohol and smoking is helpful in reducing the suffering.

Dr Rachna Pande is a specialist in internal medicine at

Ruhengeri Hospital

Saturday, 19 April 2014

Small Foot Wounds A Threat For Neuropathy Sufferers

Today's post from (see link below) again addresses diabetics as being the target audience but as so often, this article applies to everyone with neuropathic foot problems, irrespective of the cause. It looks at a Dutch study showing how dangerous small wounds on the feet can be if neglected. This especially applies to neuropathy patients experiencing numbness on their feet. The likelihood is that wounds may go unnoticed and rapidly become ulcerated and infected. It goes on to advise people to pay special attention to footwear and daily foot care, something which may seem obvious but is easily forgotten in the daily struggle to get by.


Minor foot wounds a major threat for diabetics
By Krystnell Storr NEW YORK Mon Apr 14, 2014  
(Reuters Health) - For people with diabetes, one foot ulcer is very likely to lead to another, according to a new study that finds even minor lesions create a major risk of more severe foot wounds.

The best defense, Dutch researchers say, is to treat even minor sores carefully and to protect feet from pressure and injury with specialized footwear.

"I hope medical specialists, and other health care practitioners will use this knowledge and implement it in clinical practice," said senior author Sicco Bus, staff scientist with the Academic Medical Center at the University of Amsterdam.

People with diabetes often lose feeling in their feet as a result of nerve damage, known as neuropathy. The lack of sensation makes diabetics prone to injure their feet without realizing it, and allows small wounds to grow into serious ulcers that can eventually lead to infection or gangrene.

In the U.S., 26 million Americans have diabetes. Every year, 65,700 of these patients have lower-limb amputations.

Past research has shown that having had a foot ulcer is a significant risk factor for having more of them.

"Ulcer recurrence is a debilitating condition for the patient, risking further complications such as infection and amputation, and influencing loss of patient mobility and quality of life," Bus told Reuters Health.

To find out what factors most strongly predict who will develop foot ulcers, Bus and his colleagues analyzed data from a large trial of specialized footwear for diabetes patients with nerve damage in their feet (see Reuters Health article of January 24, 2013 here:

For the new analysis, the researchers focused on 171 participants, all of whom reported having a foot ulcer at least 18 months before the study began. For a period of 18 months, each person was checked for new ulcers every three months, and interviewed about their daily habits.

The pressure on their feet while walking barefoot and in the special footwear was also measured. During one week, sensors in the shoes reported how often the participants wore their shoes and how many steps they took.

During the study period, 71 people developed ulcers on the soles of their feet, 41 of them as a result of unrecognized "trauma," Bus and his colleagues report in the journal Diabetes Care.

Among those 41, the people who had minor lesions when the study began were nine times more likely than those who didn't to develop an ulcer. Often the wounds were in the same place as a previous ulcer, suggesting there was ongoing pressure or injury happening at that spot, according to the researchers.

Patients who wore shoes customized to the pressure points of their feet, however, had a 57 percent lower risk of developing a new ulcer compared to those who didn't.

Currently, to prevent ulcers, doctors and nurses have to check the feet of diabetic patients every day for wounds or use specialized tools for determining pressure points that might be prone to blisters.

"Some diabetics wear wounds on their feet kind of in the same way that a person might wear a hole in their sock, but for a diabetic, this hole gets infected and often leads to an amputated foot," Dr. David Armstrong, a professor of surgery at the University of Arizona, told Reuters Health.

"(Neuropathy) is a massive problem, it's silent, and it doesn't hurt, even in instances of gangrene. It's no one's fault, but no one pays attention to it. This study opens up avenues for prevention," said Armstrong, who was not involved in the research.

The protective effect of customized footwear seen in the study highlights the benefits of personalized healthcare in high-risk patients, noted Dr. Lawrence Lavery, a professor of surgery at the Texas A&M Health Science Center College of Medicine and the Scott and White Memorial Hospital in Temple, Texas.

Private insurers will have to step up to pay the expense, Lavery said. "This is something that is well worth investing in."

SOURCE: Diabetes Care, online April 4, 2014.

Friday, 18 April 2014

Sport Can Improve Nerve Connections

Apologies to those of you who are heartily sick of articles pushing sport and exercise as being 'good' for neuropathy. I share your concerns but today's post from (see link below) does sort of reinforce the evidence. It doesn't matter what you end up doing, as long as it's more than you do at the moment. It talks about the importance of a protein concentrate (PGC1α) in helping the muscles to respond to physical activity. It does suggest that this can be introduced externally but doesn't state that directly. In this way, muscles can be strengthened until the patient is able to undergo more exercise on his or her own. Whatever the methods, it's clear that diseases that cause muscle wasting (neuropathy included) will be helped by increased endurance activity. Neuropathy patients may need to think creatively on this one.

Sport makes muscles and nerves fit
Date:April 2, 2014 Source: Universität Basel 



Endurance sport does not only change the condition and fitness of muscles but also simultaneously improves the neuronal connections to the muscle fibers based on a muscle-induced feedback. Scientists were also able to induce the same effect through raising the protein concentration of PGC1± in the muscle.

Endurance sport does not only change the condition and fitness of muscles but also simultaneously improves the neuronal connections to the muscle fibers based on a muscle-induced feedback. This link has been discovered by a research group at the Biozentrum of the University of Basel. The group was also able to induce the same effect through raising the protein concentration of PGC1α in the muscle. Their findings, which are also interesting in regard to muscle and nerve disorders such as muscle wasting and ALS, have been published in the current issue of the journal Nature Communications.

It's springtime -- the start signal for all joggers. It is well known that a regular run through the forest makes your muscles fit. Responsible for this effect is the protein PGC1α, which plays a central role in the adaptation of muscles to training. The research team led by Prof. Christoph Handschin has discovered that such endurance training not only affects the condition of the muscles but also the upstream synaptic neuronal connections in a muscle-dependent manner.

PGC1α does not only make muscles fit

How do muscles change during muscle training or in muscle disease? Christoph Handschin and his team have been addressing this question for some years. In the past, they have already shown that the protein PGC1α plays a key role in the adaptation of the muscle by regulating the genes that cause the muscles to change accordingly to meet the more demanding requirements. When muscle is inactive or ill, only a low concentration of PGC1α is present. However, when the muscle is challenged, the PGC1α level increases. Through artificial elevation of the PGC1α concentration, it is possible to stimulate muscle endurance.

… but also the nerve connections

Now, the scientists have been able to demonstrate that the increase in muscle PGC1α concentration also improves the upstream synaptic nerve connections to the result of this feedback from muscle to the motor neuron: The health of the synapse improves and its activation pattern adapts to meet the requirements of the muscle. Until now, the influence of the muscle on the synaptic connection was primarily recognized in embryonic development. "That in adults, where the nerve and muscular systems are fully developed, not only the muscle changes due to an increase in PGC1α concentration but also a muscle-controlled improvement in the entire nerve and muscular system takes place, was completely unexpected and a great surprise to us," says Handschin. "Our current aim is to identify the exact signal that leads to this stabilization of the synaptic connections, in order to apply this for treating muscle disorders."

and helps in the treatment of muscle and nerve disorders

A direct therapeutic application of the research findings in illnesses such as muscle wasting and amyotrophic lateral sclerosis (ALS) is already conceivable for Christoph Handschin. "In patients, whose muscles due to their illness are too weak to move on their own, an increase in PGC1α levels could strengthen muscles and nerves until the patients can move enough to finally do some physical therapy and to further improve their mobility," he explains. After the pharmacological improvement of the health status of the muscles and nerves, the patient could independently continue their treatment through practicing endurance sports.

Story Source:

The above story is based on materials provided by Universität Basel. Note: Materials may be edited for content and length.

Journal Reference:
Anne-Sophie Arnold, Jonathan Gill, Martine Christe, Rocío Ruiz, Shawn McGuirk, Julie St-Pierre, Lucía Tabares, Christoph Handschin. Morphological and functional remodelling of the neuromuscular junction by skeletal muscle PGC-1α. Nature Communications, 2014; 5 DOI: 10.1038/ncomms4569

Thursday, 17 April 2014

How Good Is Carbamazepine For Neuropathic Pain?

Today's post comes from (see link below) and is part of the Cochrane Collaboration: Cochrane Medical Summaries data banks. In this study, they look at Carbamazepine to see how effective it is as a neuropathic pain treatment and the conclusions may alarm some people because in their view, there's very little evidence to support the hype over Carbamazepine (Tegretol, Equetro). It is an anti-convulsant (anti epilepsy) drug that is more and more frequently used to treat severe neuropathic pain but the results are anything but conclusive. This article goes on to explain why the Cochrane people are equally doubtful as to its efficiency in controlling nerve pain.

Carbamazepine for chronic neuropathic pain and fibromyalgia in adults  Wiffen PJ, Derry S, Moore R, Kalso EA
Published Online:10 April 2014

Neuropathic pain is pain coming from damaged nerves. It is different from pain messages carried along healthy nerves from damaged tissue (a fall, or cut, or arthritic knee). Neuropathic pain is treated by different medicines than pain from damaged tissue. Medicines like paracetamol or ibuprofen are not effective in neuropathic pain, while medicines that are sometimes used to treat depression or epilepsy can be very effective in some people. Our understanding of fibromyalgia (a condition of persistent, widespread pain and tenderness, sleep problems, and fatigue) is lacking, but fibromyalgia can respond to the same medicines as neuropathic pain.

Carbamazepine was developed to treat epilepsy, but it is now used to treat various forms of chronic pain. We performed searches (up to February 2014) to look for clinical trials where carbamazepine was used to treat neuropathic pain or fibromyalgia. We found 10 studies involving 418 people involved in testing carbamazepine. Studies were not generally of very good quality. Most were very small, as well as of short duration. Studies lasting only one or two weeks are unhelpful when pain can last for years.

There was not enough good quality evidence to say how well carbamazepine worked in any neuropathic pain condition. Pooling four small studies showed that it was better than placebo, but the result cannot be relied upon. There was not enough information from these studies to make any reliable comment on adverse events or harm.

Carbamazepine is probably helpful for some people with chronic neuropathic pain. It is not possible to know beforehand who will benefit and who will not. 



This is an update of a Cochrane review entitled 'Carbamazepine for acute and chronic pain in adults' published in Issue 1, 2011. Some antiepileptic medicines have a place in the treatment of neuropathic pain (pain due to nerve damage). This updated review considers the treatment of chronic neuropathic pain and fibromyalgia only, and adds no new studies. The update uses higher standards of evidence than the earlier review, which results in the exclusion of five studies that were previously included.


To assess the analgesic efficacy of carbamazepine in the treatment of chronic neuropathic pain and fibromyalgia, and to evaluate adverse events reported in the studies.

Search strategy:

We searched for relevant studies in MEDLINE, EMBASE and CENTRAL up to February 2014. Additional studies were sought from clinical trials databases, and the reference list of retrieved articles and reviews.

Selection criteria:

Randomised, double blind, active or placebo controlled trials (RCTs) investigating the use of carbamazepine (any dose, by any route, and for at least two weeks' duration) for the treatment of chronic neuropathic pain or fibromyalgia, with at least 10 participants per treatment group. Participants were adults aged 18 and over.

Data collection and analysis:

Two study authors independently extracted data on efficacy, adverse events, and withdrawals, and examined issues of study quality. Numbers needed to treat for an additional beneficial effect (NNT) or harmful effect (NNH) with 95% confidence intervals (CIs) were calculated from dichotomous data.

We performed analysis using three tiers of evidence. First tier evidence derived from data meeting current best standards and subject to minimal risk of bias (outcome equivalent to substantial pain intensity reduction, intention-to-treat analysis without imputation for dropouts, at least 200 participants in the comparison, at least 8 weeks' duration, parallel design), second tier from data that failed to meet one or more of these criteria and were considered at some risk of bias but with adequate numbers in the comparison, and third tier from data involving small numbers of participants that was considered very likely to be biased or used outcomes of limited clinical utility, or both.

Main results:

Ten included studies (11 publications) enrolled 480 participants with trigeminal neuralgia, diabetic neuropathy, and post stroke pain. Nine studies used a cross-over design, and one a parallel group design. Most of the studies were of short duration, lasting four weeks or less.

No study provided first or second tier evidence for an efficacy outcome. Using third tier evidence, carbamazepine generally provided better pain relief than placebo in the three conditions studied, with some indication of pain improvement over mainly the short term, but with poorly defined outcomes, incomplete reporting, and in small numbers of participants. There were too few data in studies comparing carbamazepine with active comparators to draw any conclusions.

In four studies 65% (113/173) of participants experienced at least one adverse event with carbamazepine, and 27% (47/173) with placebo; for every five participants treated, two experienced an adverse event who would not have done so with placebo. In eight studies 3% (8/268) of participants withdrew due to adverse events with carbamazepine, and none (0/255) with placebo. Serious adverse events were not reported consistently; rashes were associated with carbamazepine. Four deaths occurred in patients on carbamazepine, with no obvious drug association.

Authors' conclusions:

Carbamazepine is probably effective in some people with chronic neuropathic pain, but with caveats. No trial was longer than four weeks, had good reporting quality, nor used outcomes equivalent to substantial clinical benefit. In these circumstances, caution is needed in interpretation, and meaningful comparison with other interventions is not possible.
This record should be cited as:

Wiffen PJ, Derry S, Moore R, Kalso EA. Carbamazepine for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database of Systematic Reviews 2014, Issue 4. Art. No.: CD005451. DOI: 10.1002/14651858.CD005451.pub3
Assessed as up to date:
7 February 2014 - See more at:

Wednesday, 16 April 2014

Helping Damaged Nerves To Regrow Using Capsaicin

Today's post from (see link below) talks once more about using capsaicin as a means of reducing nerve pain, especially in the feet and follows on nicely from yesterday's post. This article is more specifically aimed at diabetics but as we all know by now, the symptoms of neuropathy are pretty much the same for everyone, irrespective of the cause. For that reason, this article is worth reading for anyone living with neuropathy. What is well explained is why we suffer so frequently with pain and other symptoms in our feet and why it is most often called peripheral neuropathy. Many people just don't understand why their feet and legs suffer so much more than other parts of the body, especially when there's no obvious injury or reason for foot pain. This post helps explain why that happens.

Encouraging Damaged Nerves to Regrow 
By Andrew Curry April 2014 
  Gordon Smith uses the “hot sauce” way of probing how weight loss can ease neuropathy

Gordon Smith, MD
Neurologist, University of Utah
Diabetes Complications/Neuropathy
ADA Research Funding
ADA-Ethicon Endo-Surgery/Covidien Research Award in Bariatric Surgery and Diabetes

Nerves are our connection to the outside world, relaying information about what’s around us to our brain. There might be a thousand or more nerve endings in a square inch of skin, all exposed to daily wear and tear. “The nerves in your skin are constantly being injured and regrowing,” says Gordon Smith, MD, a neurologist at the University of Utah. “They’re the foot soldiers of the nervous system, absorbing a great deal of the physical insult our bodies encounter every day.”

The nerves in the feet are the most vulnerable, because they have the farthest to travel: A single nerve fiber may stretch from your toe to your backbone, plugging into the spinal column not far from your belly button. “It’s like the Alaska oil pipeline—it’s a pretty big deal, and it takes a lot to maintain it. If there’s stress or injury, the part of the pipeline that’s farthest away absorbs the damage,” Smith says.

Under normal circumstances, nerve cells are surprisingly resilient. For people with diabetes, though, this resilience can decline or disappear, making nerve cells more fragile and less able to regrow when they’re damaged.

Accumulated nerve cell injury equals neuropathy, a common condition (about half of people with diabetes will have it at some point in their lives) with symptoms including pain, numbness, and loss of balance. It’s often part of a group of problems, including uncontrolled blood glucose and poor healing and circulation, that can escalate to the point where foot amputation is necessary. Diabetic neuropathy is one of the most common complications of diabetes, and one of the most costly and damaging. Estimates are that health care costs connected with neuropathy add up to well over $10 billion a year in the United States.

What is it about diabetes that makes neuropathy such a problem? Research has shown that hyperglycemia, or high blood sugar, causes nerves to degenerate. But hyperglycemia is not the only risk factor. “In the setting of diabetes, obesity seems to significantly increase one’s risk of neuropathy,” Smith says.

In recent experiments funded in part by the American Diabetes Association (ADA) involving people with type 2 diabetes, Smith has shown that exercise-related weight loss can temporarily slow neuropathy and encourage nerves to regrow, increasing the regeneration rate by 30 percent. “Those who lost weight or whose A1C got better are the ones who improved,” he says.

The cause and effect can be complex. Does obesity cause type 2 diabetes and thus neuropathy? Or does diabetes come first? One condition, after all, might contribute to the other. “If you have very bad foot pain and are unable to exercise, that might make you more likely to be overweight,” Smith points out.

To better understand how weight loss helps nerves stay in good shape, Smith is now working with patients about to undergo gastric bypass surgery. Other studies have shown that the weight-loss operation—which restructures the digestive system to bypass parts of the stomach and small intestine—leads not just to weight loss but to an almost immediate improvement in the body’s ability to produce and respond to insulin. In many cases, surgical patients with type 2 diabetes are able to immediately stop using or greatly reduce blood glucose–lowering medications. “It provides an ideal opportunity to look at the effects of weight loss and the correction of diabetes on nerve regeneration,” Smith says. “Our hope is that between that and looking at blood markers, we can understand the disease mechanism.”

Smith makes use of capsaicin, a compound familiar to any hot-sauce fan. It’s the stuff in chili peppers that “burns” the tongue. When applied to the skin, it damages nerve cells, causing them to retract from the skin surface.

With the help of another ADA grant, Smith is recruiting 50 people without neuropathy symptoms headed for weight-loss surgery—25 with diabetes, 25 without. In the time leading up to the operation, he takes a tiny sample of skin and underlying tissue from each patient’s thigh. Then he applies a capsaicin patch to the area, waits 48 hours, and takes another sample. The capsaicin simulates nerve damage that accompanies neuropathy. The biopsies can be repeated after the first and third months to determine the rate at which nerves regrow.

The patients go on to have gastric bypass surgery, and Smith monitors the impact on nerve function. Six months later, the nerve regeneration rate is measured again. The goal is to compare the progress of the patients with and without diabetes and to see if weight loss and metabolic improvement affect nerve regeneration.

One of Smith’s goals is to show that capsaicin is a tool that may be useful in future neuropathy research. But more important, understanding the relationship among obesity, diabetes, and nerve damage could help Smith and others treat or even prevent neuropathy in the future.

Tuesday, 15 April 2014

Capsaicin For Neuropathic Pain: An Update

Today's post from (see link below) is a short summary of the findings of a German research study into the effectiveness of high-strength capsaicin patches in reducing neuropathic pain (Qutenza is the most commonly used). Capsaicin cream and patches have sort of fallen off the radar in the last two years but remain an alternative treatment for neuropathic pain. Their reduced popularity may well be due to the difficulty of application and the care needed to avoid burning. The base component capsaicin comes from chili peppers and is extremely powerful, especially in the concentration used on the patches. You really do need expert guidance as to how to apply them and what to do if the negative symptoms are too strong. That said, studies consistently show that capsaicin high strength patches do work in reducing nerve pain. If you've not thought about them, it may be worth discussing the option with your doctor.

High concentration capsaicin for treatment of peripheral neuropathic pain:

...effect on somatosensory symptoms and identification of treatment responders
April 2014, Vol. 30, No. 4 , Pages 565-574 (doi:10.1185/03007995.2013.869491)

Johanna Höpera, * Stephanie Helferta, * Marie-Luise S. Heskampb, Christian G. Maihöfnerc, Ralf Barona
aDivision of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein,
Kiel, Germany
bMedical Department, Astellas Pharma GmbH,
Munich, Germany
cDepartment of Neurology, Fürth Hospital,
Fürth, Germany
Address for correspondence:
Prof. Dr. med. Ralf Baron, Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein,
Campus Kiel, Arnold-Heller-Str. 3, Haus 41, 24105 Kiel, Germany. Tel: +49 431 597 8504; Fax: +49 431 597 8530;

*These two authors contributed equally to the paper.


Pain is usually assessed by spontaneous pain ratings. Time-dependent (brief attacks) or evoked (allodynia) phenomena, common in neuropathic pain, are not captured. To evaluate the overall effectiveness of a treatment, improvement of all sensory symptoms should be measured. Since the pattern of sensory abnormalities might hint at the underlying mechanisms of pain, this baseline information may aid in predicting the treatment effect. Data on sensory neuropathic abnormalities (painDETECT questionnaire) were analyzed aiming to (1) evaluate the frequency of neuropathic symptoms in different peripheral neuropathic pain syndromes, (2) assess the effect of capsaicin 8% patch on neuropathic symptoms and (3) identify treatment responders based on baseline values.


Data analysis of a prospective 12 week non-interventional trial in peripheral neuropathic pain treated with capsaicin 8% cutaneous patch. Average pain intensity during the past 24 hours, pain descriptors and qualities of neuropathic pain were assessed to characterize the patients’ sensory symptoms at baseline and to document changes.

(1) Characteristic symptoms of neuropathic pain were present in all peripheral neuropathic pain syndromes, but frequencies varied in the individual syndromes. (2) Topical capsaicin 8% treatment significantly reduced the overall pain intensity and resulted in a reduction of sensory abnormalities. (3) Short disease duration predicted a better treatment effect. High painDETECT scores, the presence of burning and pressure-evoked pain were weakly associated with treatment response.

Topical capsaicin 8% treatment effectively reduced sensory abnormalities in peripheral neuropathic pain. The association of sensory symptoms and treatment response aids in understanding the mechanism of action of high concentration capsaicin. It is, however, not possible to use sensory symptom patterns to predict treatment response to capsaicin on an individual level.


Completion of painDETECT was optional and therefore data was not available for all patients. Further studies for confirmation of these results are needed.

Monday, 14 April 2014

Exercise Helps Neuropathy

Although directed specifically at people with diabetes, today's post from (see link below) contains a message that can help all people living with neuropathy and that is that exercise does help. Very few people with pain in their feet and legs really want to hear that and if you have severe neuropathy, you'll understand why. However, inactivity, however much easier that is, leads to muscle degeneration and stagnation of your nerve problems; these in turn lead to other problems within the body, not least the build up of fat where it's not wanted and the risk of heart problems etc etc. Exercise is essential. That said, you do need expert guidance as to what sort of exercise is appropriate in your case. Asking the doctor may not provide you with the answers you need, so it may be worthwhile researching on the internet to find the best qualified physical therapists in your area. it's a lot of work but you will benefit in the end.

Research shows exercise therapy helps diabetic peripheral neuropathy 
Created on Wednesday, 09 April 2014 01:00 | Written by Colin Hoobler 

To Your Health

I’m 54 years old and have had Type 2 diabetes for 10 years, but now it’s worse because I also have pain, numbness and tingling going down my legs. My doctor says this is common in people with diabetes and prescribed medication along with a series of injections, which have helped, but I don’t like the side effects. Can physical therapy help? — Gwen (Vancouver)

 Get started -- Physical therapy can help with diabetic peripheral neuropathy, but it should be in the form of exercise therapy as opposed to 'traditional' methods such as manual therapy and ultrasound.The answer is yes, but it should be a certain type of physical therapy if you want to address both your leg pain and diabetes, which is the likely cause of your leg pain.

You get Type 2 diabetes from eating a poor diet and inadequate exercise over an extended period. In Type 2 diabetes, your body’s cells aren’t effectively processing insulin, the hormone from your pancreas that controls blood sugar. Consequently, blood sugar is isn’t absorbed from the bloodstream well and remains chronically higher.

The pain, numbness and tingling you’re having is called diabetic peripheral neuropathy, which occurs in about 33 percent of American diabetics over 40 years old and is the result of nerve degeneration. Many people with peripheral neuropathy eventually have problems with walking, maintaining balance and lower leg injury.

Extensive research has shown the importance of regular exercise accompanied by a sound diet in managing diabetes. Peripheral neuropathy, however, is another story. Only recently has research shown the importance of exercise therapy for people with diabetic peripheral neuropathy. Those who followed a 10-week supervised endurance and strengthening program yielded dramatic reductions in pain and nerve symptoms while increasing new nerve growth.

This is a big deal, because it offers a new, cost-effective physical therapy that you can use in addition to medication and/or injections to expedite recovery.

Physical therapy can help, but it should be in the form of exercise therapy as opposed to “traditional” methods (e.g., manual therapy, ultrasound, modalities) so you start to address the cause of your diabetes. Many physician and physical therapy offices are recognizing the need for an exercise therapy emphasis in the medical treatment of diabetes and peripheral neuropathy. Health insurance companies (including Medicare) are also recognizing the importance of this medical model, as they are covering physical therapy services for exercise therapy to treat diabetic peripheral neuropathy, back pain, osteoarthritis and many other costly lifestyle-related conditions.

Specifically, your exercise therapy program should help you learn how to exercise safely and effectively on your own with whatever equipment you have available. A skilled physical therapist can show you how to strengthen, stretch and improve endurance of your muscles.

Note that your muscles are like “blood sugar sponges;” the stronger they are, the more blood sugar they can absorb and therefore control your blood sugar. One of the great things about strengthening exercise is its brevity, as you can complete a full-body routine in only 90 minutes per week.

The use of exercise therapy to help treat peripheral neuropathy is relatively new, so you may have to suggest it to your doctor to get the proper physical therapy referral for insurance coverage. Regardless, you have more control over your recovery than previously thought.

Colin Hoobler is a licensed physical therapist and has written two books on exercise as treatment for disease and injury

Sunday, 13 April 2014

Neuropathic Pain After Surgery

Today's post from (see link below) looks at the strange phenomenum of how neuropathic pain persists even after successful surgery to repair it. Note, this applies to neuropathy caused by injury (often called radiculopathy) and not other forms of neuropathy. Apparently, injury-caused neuropathy has the potential to alter neurons (nerve cells) in such a way that the damage becomes permanent, even after the injury itself has been resolved through surgery. Not good news for many people but it gives scientists further insight into how the nervous system works and how it can self-harm at a molecular level. This may lead to a better understanding of the  processes in neurons and in the future a way to intervene to prevent that happening.

Reasons for pain after 'successful' spinal surgery  American Association of Neurological Surgeons (AANS) April 9, 2014


A new study sheds light on the basis of neuropathic pain that persists after apparently successful surgery. The topic is a question that has long puzzled physicians. In a study that melds the interrelated domains of spinal surgery and pain medicine, researchers have discovered that in the transition from acute inflammatory pain to chronic neuropathic pain, neurons undergo molecular changes.

Understanding why pain persists despite structurally successful spinal surgery is a question that has long puzzled physicians. In a study that melds the interrelated domains of spinal surgery and pain medicine, researchers have discovered that in the transition from acute inflammatory pain to chronic neuropathic pain, neurons undergo molecular changes.

Team leader Mohammed Farid Shamji, MD, PhD, FAANS, presented the study's findings today during the 82nd Annual Scientific Meeting of the American Association of Neurological Surgeons (AANS). Titled "Peripheral Hypersensitivity to Subthreshold Stimuli Persists after Resolution of Acute Experimental Disc-Herniation Neuropathy and Is Mediated by Heightened TRPV1 Receptor Expression and Activity," the study promises to shed light on the basis of neuropathic pain that persists after apparently successful surgery.

Dr. Shamji noted, "It is extremely novel to learn that an autoimmune neuroinflammatory radiculopathy that we clinically manage in most patients as being self-limited has the potential to cause permanent structural changes to neurons and functional sensitivity in the pain experience."

Understanding the molecular changes that occur, said Dr. Shamji, could help researchers develop appropriate treatments. "If we can minimize the disability caused by this pain syndrome, we may be able to prevent it from occurring upon onset of the acute inflammatory pain, potentially even reversing it once established."

Story Source:

The above story is based on materials provided by American Association of Neurological Surgeons (AANS). Note: Materials may be edited for content and length.

Saturday, 12 April 2014

Recognising Alcoholic Neuropathy

Today's post from (see link below) talks about one of the many cause of neuropathy and that is alcoholism. Many people with other forms of neuropathy will read this article and recognise many of the symptoms - they apply to most neuropathy sufferers, irrespective of the cause. However, alcoholic neuropathy could strike us all, if we drink socially, either moderately or heavily and it is certainly worthwhile knowing what could happen if your drinking gets out of control. If you already have neuropathy, it may be wise to pass on this information to friends and/or family who drink - you wouldn't wish the symptoms on anybody would you?

Alcoholic Neuropathy  
Dr. Mark Willenbring on the challenge of alcohol addiction.

Alcoholic neuropathy is damage to the nerves that results from excessive drinking of alcohol.

Dr. Mark Willenbring on the challenge of alcohol addiction.

Also: Recent findings and perspectives on medical research.
Challenging Old Assumptions About Alcoholism


The exact cause of alcoholic neuropathy is unknown. It likely includes both a direct poisoning of the nerve by the alcohol and the effect of poor nutrition associated with alcoholism. Up to half of long-term heavy alcohol users develop this condition.

In severe cases, nerves that regulate internal body functions (autonomic nerves) may be involved.

Risks of alcoholic neuropathy include:
Long-term, heavy alcohol use
Alcoholism that is present for 10 years or more

Back to TopSymptoms
Numbness in the arms and legs
Abnormal sensations, such as"pins and needles"
Painful sensations in the arms and legs
Muscle weakness
Muscle cramps or muscle aches
Heat intolerance, especially after exercise
Impotence (in men)
Problems urinating, incontinence (leaking urine), feeling of incomplete bladder emptying, difficulty beginning to urinate
Nausea, vomiting

Additional symptoms that may occur with this disease:
Swallowing difficulty
Speech impairment
Loss of muscle function or feeling
Muscle contractions or spasm
Muscle atrophy
Movement disorders

Changes in muscle strength or sensation usually occur on both sides of the body and are more common in the legs than in the arms. Symptoms usually develop gradually and become worse over time. 


Once the alcohol problem has been addressed, treatment goals include:
Controlling symptoms
Maximizing ability to function independently
Preventing injury

It is important to supplement the diet with vitamins, including thiamine and folic acid.

Physical therapy and orthopedic appliances (such as splints) may be needed to make sure muscle function and limb position are maintained.

Medicines may be needed to treat pain or uncomfortable sensations. Because persons with alcoholic neuropathy have alcohol dependence problems, they are advised to take the least amount of medicine needed to reduce symptoms to help prevent drug dependence and other side effects of chronic use.

Positioning or the use of a bed frame that keeps the covers off the legs may reduce pain for some people.

Light-headedness or dizziness when standing up (orthostatic hypotension) may require several different treatments before finding one that successfully reduces symptoms. Treatments that may help include:
Wearing compression stockings
Eating extra salt
Sleeping with the head elevated
Using medicines

Bladder problems may be treated with:
Manual expression of urine
Intermittent catheterization (male or female)

Impotence, diarrhea, constipation, or other symptoms are treated when necessary. These symptoms often respond poorly to treatment in people with alcoholic neuropathy.

It is important to protect body parts with reduced sensation from injury. This may include:
Checking the temperature of bath water to prevent burns
Changing footwear
Frequently inspecting the feet and shoes to reduce injury caused by pressure or objects in the shoes
Guarding the extremities to prevent injury from pressure

Alcohol must be stopped to prevent the damage from getting worse. Treatment for alcoholism may include counseling or social support such as Alcoholics Anonymous (AA), or taking medicines. 


The only way to prevent alcoholic neuropathy is not to drink alcohol.


Chopra K, Tiwari V. Alcoholic neuropathy: possible mechanisms and future treatment possibilities. Br J Clin Pharmacol . 2012;73: 348-362.

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

Friday, 11 April 2014

Watch Out For Neuropathic Antibiotic Side Effects!

Today's post from (see link below) is another powerful argument against taking fluoroquinolone antibiotics (Cipro,Levaquin,Avalox etc), especially if you have or are prone to neuropathic problems. It's astonishing that many doctors are still unaware of the dangers and side effects of these drugs and prescribe them routinely without looking to see whether the patient is at risk. The best advice is to look at the pharmaceutical (not the brand name) name of any antibiotics you are given and check the side effects on the internet ( has a reliable and trustworthy reputation in this regard). After that, if you are still worried, discuss it with your doctor with any evidence you might have gathered and ask for an alternative (there are plenty to choose from). Don't just stop taking them or ignore it - rely on your doctor making the right choice in the end.

Fluoroquinolone Antibiotics: Are You At Risk?
August 26, 2013 by Lisa Bloomquist

Fluoroquinolone antibiotics, Cipro, Levaquin, Avelox, etc. are broad-spectrum antibiotics used to treat a variety of infections, from urinary tract infections to anthrax and everything in between. The first quinolone created was Nalidixic Acid which was discovered by George Lesher in 1962. (Nalidixic Acid was added to the OEHHA prop 65 list of carcinogens in 1998.) Cipro (ciprofloxacin) is a second generation fluoroquinolone patented in 1983 by Bayer, Levaquin (levofloxacin) is a third generation fluroquinolone patented in 1987 by Ortho-McNeil-Janssen (a division of Johnson & Johnson), and Avelox (moxifloxacin) is a fourth generation fluoroquinolone patented in 1991 by Bayer.

Fluoroquinolone Antibiotics – Still on the Market

Of the 30 quinolones that have made it to market since the 1980s, all but 6 have either been removed from the US market or have severely restricted use.

The fluoroquinolone antibiotics that are still on the market are some of the most commonly prescribed antibiotics. Per the FDA, “Approximately 23.1 million unique patients received a dispensed prescription for an oral fluoroquinolone product from outpatient retail pharmacies during 2011,” and “Within the hospital setting, there were approximately 3.8 million unique patients billed for an injectable fluoroquinolone product during 2011.”

When used properly, such as in cases of life-threatening hospital acquired pneumonia, fluroquinolone antibiotics can save lives. 

Fluoroquinolone Antibiotic Side-Effects and Adverse Reactions

When used improperly, fluoroquinolone antibiotics can needlessly cause devastating side-effects. Devastating side-effects can also occur when fluoroquinolone antibiotics are used properly, but the devastation can be justified by weighing it against the alternative – death. In 2001, Dr. Jay S. Cohen published an article on the severe and often disabling reactions some people sustained as a result of taking a fluoroquinolone antibiotic. Dr. Cohen says,

It is difficult to describe the severity of these reactions. They are devastating. Many of the people in my study were healthy before their reactions. Some were high intensity athletes. Suddenly they were disabled, in terrible pain, unable to work, walk, or sleep

Dr. Cohen’s study of 45 subjects suffering from Fluoroquinolone Toxicity Syndrome, a name that I’m pushing for, (without an official name, it is difficult get the word out) showed that they had the following symptoms:

Peripheral Nervous System: Tingling, numbness, prickling, burning pain, pins/needles sensation, electrical or shooting pain, skin crawling, sensation, hyperesthesia, hypoesthesia, allodynia (sensitivity to touch) numbness, weakness, twitching, tremors, spasms.

Central Nervous System: Dizziness, malaise, weakness, impaired coordination, nightmares, insomnia, headaches, agitation, anxiety, panic attacks, disorientation, impaired concentration or memory, confusion, depersonalization, hallucinations, psychoses.

Musculoskeletal: Muscle pain, weakness, soreness, joint swelling, pain, tendon pain, ruptures.

Special Senses: Diminished or altered visual, olfactory, auditory functioning, tinnitus (ringing in the ears).

Cardiovascular: Tachycardia, shortness of breath, hypertension, palpitations, chest pain.

Skin: Rash, swelling, hair loss, sweating, intolerance to heat and\or cold.
Gastrointestinal: Nausea, vomiting, diarrhea, abdominal pain.

When a fluoroquinolone antibiotic triggers a toxic reaction in a person, multiple symptoms are often experienced.

Fluoroquinolone Antibiotic Damage – Technical Aspects

Fluoroquinolones are eukaryotic DNA gyrase and topoisomerase inhibitors very similar to many antineoplastic agents (source). What this means in plain English is that these drugs work the same way as chemotherapeutic drugs; they disrupt DNA and lead to destruction of cells. A recent (2013) study conducted by a team of scientists at the Wyss Institute for Biologically Inspired Engineering at Harvard University Studies showed that Ciprofloxacin, along with a couple of other non-fluoroquinolone antibiotics, causes oxidative stress and mitochondrial malfunction. A 2011 study published in the Journal of Young Pharmacists found that, “There is significant and gradual elevation of lipid peroxide levels in patients on ciprofloxacin and levofloxacin.” They also found that “There was substantial depletion in both SOD (superoxide dismutase, “a free radical scavenging enzyme”) and glutathione levels” and that “On the 5th day of treatment, plasma antioxidant status decreased by 77.6%, 50.5% (and) 7.56% for ciprofloxacin, levofloxacin and gatifloxacin respectively.” The study also notes that administration of fluoroquinolones leads to a marked increase in the formation of Reactive Oxygen Species (ROS) and that “reactive free radicals overwhelms the antioxidant defence, lipid peroxidation of the cell membrane occurs. This causes disturbances in cell integrity leading to cell damage/death.” 

How Many People are at Risk?

The exact rate of adverse reactions to fluoroquinolones is difficult to determine. Studies of adverse reactions to fluoroquinolones have noted that, “During clinical trials, the overall frequencies of adverse effects associated with (fluoroquinolones) to vary between 4.4 and 20%.” Just the fact that the spread is so large, a 15.6% spread in frequency of adverse reactions is a HUGE difference, it implies that the actual occurrence of adverse reactions is difficult to establish or unknown.

With the FDA figures above noting that 26.9 million unique patients were given fluoroquinolones in 2011, if you just take the conservative adverse reaction figure of 4.4%, you’ll get a horrifying number of people with adverse reactions in 2011 alone – 1,183,600 people. 20% of 26.9 million is 5,380,000 people adversely effected. That is scary. Those numbers are truly frightening given the severity of the adverse effects described above.
Fluoroquinolone Toxicity Syndrome

I see fluoroquinolone toxicity everywhere, and even I think that those numbers are high for severe, disabling reactions like mine where multiple symptoms develop simultaneously. Not everyone who has an adverse reaction to a fluoroquinolone has a reaction like mine, or even develops Fluoroquinolone Toxicity Syndrome. Many people have milder reactions. Milder symptoms include any one of the symptoms listed above as well as diarrhea, vomiting, mild tendinitis, decreased energy, painless muscle twitches, memory loss, urgency of urination, or any number of reactions that the body may have to a massive depletion of antioxidants and increases in lipid peroxide levels and reactive oxygen species production.

Even though severe adverse reactions to fluoroquinolones antibiotics can be painful and disabling for years, many (possibly most, but certainly not all) people recover from Fluoroquinolone Toxicity Syndrome with time. I anticipate that I will be fully recovered 2 years after my reaction started. Sadly, there are some people who don’t recover. They suffer from chronic pain, disability, impaired cognitive abilities, etc. permanently.

It is absurd, to say the least, that an acute problem, an infection, that can easily be taken care of with administration of an antibiotic that is not a fluoroquinolone, is converted into a chronic problem, a syndrome that can disable a person for years, by a prescription ANTIBIOTIC, used as prescribed. In my case, a urinary tract infection that could have likely been taken care of with macrobid or even cranberry juice and d-mannos, was treated with Cipro which left me unable to do many physical and mental tasks that I had previously been able to do with ease. It’s a crazy, absurd situation. It’s absurd and it’s wrong.

Some Antibiotics are More Dangerous than Others

The bottom line is that these popularly prescribed antibiotics are dangerous drugs that have caused thousands of people to suffer with a myriad of maladies. Undeniably, they have their place, in treating life-threatening infections. Unfortunately, they are not being reserved for use in life-threatening situations and people are being hurt after taking them for simple sinus, urinary tract, bronchial and prostate infections. A strict and rigorous protocol needs to be established to limit the damage that they cause; because it’s not right to maim and disable people to treat their sinus infections.

Sources are highlighted throughout the article.

Thursday, 10 April 2014

Florida Medical Marijuana Debate (Vid)

Today's post from (see link below) is a report on a debate about the efficacy of medical marijuana. It includes a video of the debate at the end. It's a fascinating look at both sides of the legislative argument regarding marijuana as a pain reliever and as many people with neuropathy are interested in the truths behind the matter, it's well worth a read and a view.

Medical marijuana debate at Tiger Bay
By Jeremy Wallace , Herald-Tribune / Wednesday, February 12, 2014

Selective statistics, references to God and highly-charged emotional stories of lost loved ones were lobbed back and forth Wednesday during the first major debate here over medical marijuana since a proposed constitutional amendment was certified for this year's ballot.

Sarasota County Sheriff Tom Knight and John Morgan, of Morgan; Morgan Attorneys, debate a proposed constitutional amendment allowing Medical Marijuana in Florida during a Sarasota Tiger Bay Club event at Michael's On East in Sarasota on Wednesday. (Staff Photo by Elaine Litherland)

But in the end, Orlando attorney John Morgan, who has become the statewide face of the push to legalize medical marijuana, and Sarasota County Sheriff Tom Knight, who opposes the effort, turned a clash in Sarasota over the issue into two simplified choices.

Morgan argued that allowing marijuana to be prescribed for those in pain is preferable to far more dangerous and addictive medications.

"The downside of marijuana pales with the FDA-approved drugs like Oxy, Percocet, Darvocet, Xanax," Morgan told more than 400 people at a Sarasota Tiger Bay luncheon. "It pales, because one is a narcotic poison and one is an organic plant in nature."

But Knight characterized the choice as one between the current quality of life in Florida and that in California and Colorado after marijuana use became legal there. Both have seen marijuana dispensaries proliferate, including some that have been tied to Colombian drug cartels, Knight said.

"One, our children are going to have much easier access to pot" if the proposed medical marijuana amendment passes, Knight said. "Secondly, crime will increase in this community. And thirdly, our quality of life will be negatively affected."

Knight said tourism, beaches and property values would all be affected if Florida followed other states in loosening restrictions on marijuana for medical use.

Debate over the issue is gaining momentum after the Florida Supreme Court ruled last month that an amendment to legalize marijuana for medical use could be on the Nov. 4 general election ballot.

If 60 percent of voters approve the measure, Florida would follow 18 other states and the District of Columbia in allowing medical patients to use marijuana.

Two states, Washington and Colorado, allow legal purchases for non-medical use.

A Quinnipiac University poll conducted in November showed a large majority of Florida voters, 82 percent, backed allowing adults to use marijuana for medical purposes if their doctor prescribes the drug. Just 16 percent of voters said they opposed marijuana for medical use.

Knight said those poll numbers are bound to change as opponents of the effort spread the word on the unintended consequences of the ballot measure.

"Only one side of the argument has been heard on this so far," Knight said at the meeting of Sarasota Tiger Bay, a civic group that meets monthly to talk about community issues and politics.

No one in the state is more responsible for the marijuana amendment getting on the ballot than Morgan, the attorney known statewide for his Morgan and; Morgan law firm's advertising campaign: "For The People."

Morgan has spent millions of dollars to draft the amendment, pay people to gather the signatures required to get the measure on the ballot and advocate for its passage.

The reason for his commitment is simple, he said. His father had cancer and his brother Tim is quadriplegic. He said when both used marijuana they were in far less pain, had improved appetites, and in the case of his brother, fewer spasms.

"It works," Morgan said. "I don't know why it works. I don't know why water quenches thirst. But it works."

Morgan even wove in a divine reason why marijuana should be legal.

"I don't know why God put this plant onto this Earth for us, but He did," Morgan said.

Knight was quick to counter.

"God put this on the Earth for us, but God also put cocoa leaves for crack cocaine and God also put the plants on the Earth for opiates, for heroin," Knight said. "God also put criminals on Earth."

Knight is part of a growing wave of opposition from sheriffs and law enforcement officials against the marijuana initiative.

He and other sheriffs have been writing letters to the editor in newspapers across the state opposing the marijuana initiative.

During Wednesday's meeting Knight also tried to counter Morgan's characterization of marijuana as a better alternative than prescription drugs. He said if marijuana has medical uses, he needs to see something from the U.S. Food and Drug Administration first that says "for sure" that it is medically useful.

"There is no scientific proof to say if legalized marijuana would help cure chronic pain and illness," Knight said.

Morgan nearly scoffed at the idea that the FDA should be the purveyor of what is safe and effective for patients, given the number of lawsuits his firm has filed against drug makers over the years.

"Sixteen thousand people die every year in American from Oxycotin — approved by the FDA," Morgan said, listing other medications that the agency once approved that are no longer available.

Morgan also sought to counter Knight's comparison of Florida to Colorado and California.

He said Florida's amendment is for medical purposes and conditions, not recreational use as in Colorado. Morgan said it would not allow for home growers of marijuana as California does.

"What our focus groups told me before I put the language together was, loud and clear: 'We don't want to be California,'" Morgan said, adding that he is following the lessons from other states as to what not to do.

He said even if Florida passes the amendment, the state Legislature will have the final say on how marijuana is dispensed and who can do it. The governor has to sign it into law and local governments would permit the places that dispense it.

He told the Tiger Bay audience to be wary of people who say marijuana will be pervasive.

"It's a scare tactic by well-meaning people to say we are going to have these things on every corner," Morgan said.

Knight said the issue is not a moral or even a medical one. He said he is not unsympathetic to people dealing with pain, but worries about the effect on law enforcement, crime and the community at large.

If the amendment passes, Knight said, Florida will be "getting more than we bargained for and it will affect our quality of life."


 Jeremy Wallace can be reached at 361-4966 or jeremy.wallace

Wednesday, 9 April 2014

Dr Oz On Neuropathy (Vid)

Today's short video is a cut from a Dr. Mehmet Oz programme in which he explains neuropathy and especially diabetic neuropathy both simply and well. Worth a view over your coffee; it may give you some information you don't already have.

Peripheral neuropathy and hair loss
ABC video 1 April 2014

Dr. Oz answers audience questions regarding pain due to peripheral neuropathy and hair loss.

Tuesday, 8 April 2014

Neuropathy In The Philippines

Today's post from (see link below) talks about the rising incidence of neuropathy in The Philippines. The medical director of Merck Philippines goes on to suggest that vitamin B supplementation may help. It's always interesting to read about approaches to neuropathy in other parts of the world than North America and Europe because it illustrates how neuropathy has become a world wide problem.

Many Pinoys suffering from neuropathy
(The Philippine Star) | Updated April 3, 2014

MANILA, Philippines - Despite its debilitating effects on a person’s life, neuropathy remains an unrecognized and underestimated condition hounding many Filipinos now, according to experts.

Dr. Gio Barangan, medical director of the Merck Inc. Philippines, said many Filipinos continue to suffer from neuropathy although this could be prevented primarily by taking vitamins B1, B6 and B12 and by observing a healthy lifestyle.

“Neuropathy is the disease of the nerves which are like the electrical power lines that bring electricity to the different parts of our body. The main reason for developing neuropathy is vitamin B deficiency,” he said in a press briefing last Monday.

The other causes are diabetes, malnutrition, and renal diseases that stemmed from high intake of alcohol.

Barangan cautioned that vegetarians are prone to developing neuropathy because they do not eat meat that is rich in vitamin B12.

“Basically, vitamin B complex — composed of vitamins B1, B6 and B12 — are water soluble vitamins. We have to replenish them every day and we can do that by eating foods that are rich in these vitamins… and by taking vitamin B,” he added.

To raise awareness about neuropathy, Merck organized a dance concert last Monday at the TriNoma Atrium in Quezon City that reunited dance icons in the 1990s such as Wowie de Guzman and James Salas of the Universal Motion Dancers; Joshua Zamora and Jon Supan of the Manoeuvres; and Jopay Paguia and two other dan-cers from Sex Bomb.

Debbie Go, Merck head of commercial marketing, said they conceptualized the dance concert to encourage the public to give importance to their nerves.

“It is an advocacy where we want to draw attention to the symptoms of neuropathy and how it greatly affects the quality of life of Filipinos… We want to show the importance of movements in our lives,” she added.

Neuropathy is characterized by pain, numbness and tingling sensation in the hand, arms and legs more often felt in the morning.

Barangan said that while people in their 20s could also develop neuropathy, the condition is most common among older persons.

“We have to take the usual vitamins in tablet form. If we don’t do that, sooner or later we will develop neuropathy… The little trauma that we experience every day can cause nerve damage,” he added.

Vitamin B1 or thiamine is responsible for converting sugar into energy and for repairing damaged nerves.

Vitamin B6 or pyridoxine not only converts sugar into energy but protein as well and, at the same time, makes new nerves, while vitamin B12 or cobalamin is important for metabolism and in the formation of red blood cells and maintenance of the central nervous system.

Monday, 7 April 2014

Fluoroquinolone Antibiotic Neuropathy: A Personal Story

Today's post from (see link below) is an alarming personal story of how taking fluoroquinolone antibiotics changed one woman's life for ever. It cannot be over-stressed how important it is to talk over the side effects of certain antibiotics with your doctor. Fluoroquinolones have long been known to possibly bring on nerve damage and if you have neuropathy already, make it considerably worse. This article is a cautionary tale. Always get advice.

Fluoroquinolone Neuropathy Feels Like Acid Burning and Electrocution  
Wednesday, February 5th, 2014 / Janet Murray

My name is Janet Murray, I am 57 years old. I do not even know how to put my health story into words so that the human mind can understand the pain I have lived with. I lived in Canada and had been given many courses of Cipro for various illnesses over the last 30 years. Sometime ago, I began developing a lot of strange problems that no one could diagnose. I had GI difficulties, body pain, migraines every week, severe interstitial cystitis – so severe they wanted to remove my bladder. Thankfully, they did not. I was given many diagnoses too, including Chronic Fatigue Syndrome (CFS) and fibromyalgia. My cognitive abilities became so impaired. I loose words and my memory is shot. I had to leave my job with the Federal Government and work at home, at my own hours. I have been extremely fatigued for the last 25 years, but I never connected the dots between my health issues and the fluoroquinolone antibiotics like Cipro, Levaquin, Avelox and others until I blew out my forearm tendon, a classic post fluoroquinolone adverse reaction. It was only then that I began to learn more about the chronic symptoms that fluoroquinolone antibiotics evoke. I had them all and more. These symptoms didn’t appear all at once, and so it was difficult to identify at first, but over time, my illnesses became readily apparent and progressive to the point that it was no longer a question of if I was poisoned by a fluoroquinolone, but how badly.

Let me back up a little though and give you some more details. For years, I was fatigued and suffering from post fluoroquinolone reactions, but I didn’t know it. During that time, I had a long distance relationship with the love of my life in NJ. He waited and visited me back and forth for 10 years and I visited when I was well enough. When I was finally was well enough to immigrate to the US, I he asked me to marry him and so I stayed and had two wonderful years. We are jewelry designers and did the large shows. I functioned, at very low level and had to rest always, but I was living my dream. Even functioning at such a low level, I was happy after many years of hell.

One year, I kept getting bronchial issues and went to a walk in clinic. I was given Levaquin with Prednisone with NSAIDS and was on small dose of a benzodiazepine. Fluoroquinolones should never be used with steroids and NSAIDS, something I did not know at the time and apparently neither did the doctors. I took this combination again and again and again across that year.

My reaction to these drugs was delayed and so it did not occur to me to link the Levaquin or my past Cipro use to my strange symptoms. I have since learned that delayed adverse reactions are common post fluoroquinolones. After my first script that year I was more tired, could not walk far and something was not right. I didn’t know what though. During the second year I woke up with acid pain in the shoulder and could not lift it. I was told I had frozen shoulder. It was really a tendon rupture, common post fluoroquinolone.

The pain in my forearm and shoulder was horrific. It took 8 months before I could move my arm again. Then I woke up one morning and the same thing was happening on my buttock tendons. I had the same horrific, acid-like pain. Those tendons ruptured. I crawled for 4 months and tried to stand when I could. I could no longer walk, the pain was unbearable.

One morning I woke up and my entire body felt like it was beaten with a baseball bat. I had a shot-like feeling in the base of my neck. I sat up, vomited and shook. The next day my entire body started to shake. I felt like I had been electrocuted. I had sharp pains of electricity though my entire body. My skin felt ripped off of the bones with electric jabs and jolts. I had large jolts of electricity cursing through my body. I sat for 5 months frozen, feeling like I was living in a body of large, angry hornets, stinging me all over 24 hours a day, 7 days a week. The electrocutions were never ending.

My stomach almost shut down almost. Every joint in my body popped and cracked when I moved. My legs would not hold me. I lost the vision in my right eye due to a macular tear. I lost four teeth due severe periodontal damage. Other symptoms include:
Up to 40 mouth sores at a time. The doctors say they look like burns or lesions. I wonder if it’s not a form of Steven-Johnson Syndrome.
Swaying, if walking, dizzy, feeling of being “stoned” in the head.
Sensory chills so severe with stinging that it takes 4 hot water bottles and wearing then down top as well.
Arms and hands go dead and numb
Constant feelings of being electrocuted
Severe bowel constipation
Intolerance to most foods
Body hair stopped growing
My skin has become very thin and transparent with enlarged veins.
Pin prick sores on my legs and what looks like burns all over my body.

On the right, the burn-like lesions all over my body. On the left, the pin-prick sores on my legs.
I experience severe changes in body temperature.
Feelings of terror and anxiety, not related to any surrounding, that come out of the blue
Severe depression

And the strange symptoms go on and on. No one seemed to understand. I was almost dead. I dropped 40 pounds in three months. My heart pounds non-stop. Terrors and jolts surge through me. I was hysterical and crying.

The doctors keep saying I have fibromyalgia. FIBRO, I am being electrocuted..!! It couldn’t have fibro. I sat and thought this is NO normal illness but nothing showed up much on my tests. I have seen 50 doctors and no one can find anything. I feel like I have been poisoned. I soon learned, I was not alone. It was the Levaquin, a fluoroquinolone antibiotic that I have since learned, causes severe peripheral neurophathies, mitochondrial damage, and all of the seemingly unrelated symptoms that I have experienced over the last couple of years.

Right now, I am in so much pain, I cry daily. I wake up with night terrors, heart pounding. My feet feel frozen, as if they are dying due to extreme hypothermia – the kind mountain climbers face when their fingers and toes turn black. That’s what my feet feel like. My tongue burns like a hornet’s nest, day in, day out. It has been a year now, living with all over the body hornet stings and large tree like branch zapping about 40 at a time. I had the EMG and nerve biopsy that shows axonal swelling. I had an MRI showing two white matter lesions in the frontal lobe, the doctors say are consistent with MS or Lyme disease.

I should mention, I also tested positive for the MTHFR mutation that makes methylating vitamin B’s difficult. Even with the axonal damage, no one knows what to do. They tried to give me painkillers but I cannot tolerate them and vomit them back up. I have been on Paxil for years, more because I cannot seem to withdraw from it than anything else. Gabapentin, even at a high dose, does nothing and so I suffer. I cannot take this much longer. I cannot live with the nerve pain. Please help.

A few other clues that might be helpful for understanding this mess. When I tried acupuncture to relieve the nerve pain, it made it worse. The hornet’s nest sting lit up. Ditto for niacin. When I was given niacin, my body reacted very strongly. If there are doctors, researchers, patients, or anyone out there that can help reduce the pain I experience, who can help heal, reverse, or even just slow what seems to be a progression of increasing pain, please leave your comments here.