Thursday, 24 April 2014

Are We Close To Restoring Neuropathy Nerve Damage?

Today's post from (see link below) is a doctor's answer to a patient's query about the possibility of ever repairing damaged nerves. His answer suggests that gene therapy may well be the answer in the future. He also quite rightly says that more research is urgently needed but research needs funding. Well worth a read.

What's on the horizon for restoring nerve function in peripheral neuropathy?
Smith, A. Gordon M.D.
Neurology Now:
April/May 2014 - Volume 10 - Issue 2 - p 34

 Q What's on the horizon for restoring nerve function in peripheral neuropathy? Will there ever be a way to quiet the faulty nerves, as opposed to masking the pain with drugs like gabapentin and oxycodone?


A It is estimated that more than 20 million Americans have peripheral neuropathy, making it one of the most common neurologic conditions. Peripheral neuropathy is caused by damage to the peripheral nervous system, which is responsible for sending information back and forth between the brain and spinal cord to every other part of the body. The condition often causes weakness, numbness, and pain in the hands and feet, but it may also occur in other areas of the body. Because peripheral neuropathy is not a single disease but rather a symptom with many possible causes, it may be difficult to diagnose and to treat.

However, different forms of peripheral neuropathy may also share common mechanisms of nerve injury. This means that discovery of a treatment for one form of peripheral neuropathy might benefit others.

Diabetes is the most frequent cause of peripheral neuropathy. In many cases, the cause of peripheral neuropathy is never known (called idiopathic peripheral neuropathy). Patients, physicians, and researchers are all interested in discovering effective therapies to slow progression, improve pain control, and hopefully reverse nerve injury in peripheral neuropathy.

Recent advances in uncovering the genetics of peripheral neuropathy have been made. Researchers have discovered that some people with painful idiopathic peripheral neuropathy have a mutation in a particular gene. This discovery has led to new studies—including planned human trials—exploring these genetic mutations as potential targets for treatment.

In addition, patients are being actively recruited for a number of exciting clinical trials including studies of growth factors (groups of proteins that stimulate the growth of specific tissues) delivered using gene therapy technology, which allows targeted delivery for peripheral neuropathy caused by diabetes. (Read more on these therapies at

For many neuropathies caused by an immune attack of the nerves, good therapies already exist and others are in development. The outlook for these forms of peripheral neuropathy is even more hopeful. For patients with chronic inflammatory demyelinating polyradiculoneuropathy (a rare and chronic condition characterized by gradually increasing weakness of the legs and, to a lesser extent, the arms), the use of corticosteroids or intravenous immunoglobulin (IVIg)—alone or in combination with immunosuppressant drugs—is effective. However, better treatments are needed for patients who do not respond to currently available approaches.

There is even hope for patients with certain types of genetic neuropathies. Several promising experimental treatments are being studied for familial amyloid polyneuropathy, a rare genetic condition where impaired nerve function is caused by amyloid protein deposits in peripheral nerves.

While the lack of a recognized underlying cause for idiopathic peripheral neuropathy is frustrating, we have learned a great deal about this disorder over the past decade. A number of studies now link obesity and its related metabolic consequences (such as insulin resistance and elevated lipids in the blood) with peripheral neuropathy. In addition, several studies suggest that successful diet and exercise can improve nerve regeneration and improve symptoms including pain. This provides a non-drug treatment approach that would immediately benefit many people with peripheral neuropathy.

Despite all of this good news, more research is urgently needed. Relative to the number of patients who have neuropathy, very few research grants are funded. To help change this, consider joining one of the patient advocacy organizations focused on neuropathy. For example, the Neuropathy Association has many programs to encourage involvement and advocacy:

© 2014 American Academy of Neurology

Wednesday, 23 April 2014

Autonomic Neuropathy: A Full Definition

Today's post from (see link below) gives a simple, general explanation for what autonomic neuropathy is. Sometimes, when presented with a diagnosis, all you want is a simple description of what you're dealing with, that you can read at your leisure after you've left the doctor's office. This give you just that. Please remember, you can have neuropathy (peripheral or otherwise) and still go on to develop autonomic neuropathy at a later date. It's not something that happens overnight but is a gradual accumulation of symptoms over a period of time. It's always worthwhile keeping a medical diary (while realising how easy it is to become obsessed!) then you will have a better overview to present to your doctor when necessary.

Autonomic Neuropathy
The New York Times Health Reference from A.D.A.M. Saturday, April 19, 2014

Autonomic neuropathy is a group of symptoms that occur when there is damage to the nerves that manage every day body functions such as blood pressure, heart rate, sweating, bowel and bladder emptying, and digestion.

Alternative Names

Neuropathy - autonomic; Autonomic nerve disease


Autonomic neuropathy is a group of symptoms, not a specific disease. There are many causes.

Autonomic neuropathy involves damage to the nerves that carry information from the brain and spinal cord to the heart, bladder, intestines, sweat glands, pupils, and blood vessels.

Autonomic neuropathy may be seen with:
Alcohol abuse
Diabetes (diabetic neuropathy)
Disorders involving scarring of tissues around the nerves
Guillain Barre syndrome or other diseases that inflame nerves
Inherited nerve disorders
Multiple sclerosis
Parkinson's disease
Spinal cord injury
Surgery or injury involving the nerves


Symptoms vary depending on the nerves affected. They usually develop gradually over years. Symptoms may include:

Stomach and intestines
Constipation (hard stools)
Diarrhea (loose stools)
Feeling full after only a few bites (early satiety)
Nausea after eating
Problems controlling bowel movements
Swallowing problems
Swollen abdomen
Vomiting of undigested food

Heart and lungs

Abnormal heart rate or rhythm
Blood pressure changes with position and causes dizziness when standing
High blood pressure
Shortness of breath with activity or exercise

Difficulty beginning to urinate
Feeling of incomplete bladder emptying
Leaking urine

Sweating too much or not enough
Heat intolerance brought on with activity and exercise
Sexual problems including erection problems in men and vaginal dryness and orgasm difficulties in women
Small pupil in one eye
Weight loss without trying

Exams and Tests

Signs of autonomic nerve damage are not always seen when yourdoctor or nurse examines you. Your blood pressure or heart rate may change when lying down, sitting, and standing.

Special tests to measure sweating and heart rate may be done. This is called "autonomic testing."

Other tests depend on what type of symptoms you have.


Treatment to reverse nerve damage is most often not possible. As a result, treatment and self-care are focused on managing your symptoms and preventing further problems.

Your doctor or nurse may recommend:
Extra salt in the diet or taking salt tablets to increase fluid volume in blood vessels
Fludrocortisone or similar medications to help your body retain salt and fluid
Medicines to treat irregular heart rhythms
Sleeping with the head raised
Wearing elastic stockings

The following may help your intestines and stomach work better:
Daily bowel care program
Medications that increase gastric motility (such as Reglan)
Sleeping with the head raised
Small, frequent meals

Medicines and self-care programs can help you if you have:

Urinary incontinence
Neurogenic bladder
Erection problems

Outlook (Prognosis)

How well you do depends on the cause of the problem and if it can be treated.

Possible Complications
Fluid or electrolyte imbalance such as low blood potassium (if excessive vomiting or diarrhea)
Injuries from falls (with postural dizziness)
Kidney failure (from urine backup)
Psychological/social effects of impotence

When to Contact a Medical Professional

Call for an appointment with your health care provider if you have symptoms of autonomic neuropathy. Early symptoms might include:
Becoming faint or lightheaded when standing
Changes in bowel, bladder, or sexual function
Unexplained nausea and vomiting when eating

Early diagnosis and treatment increases the likelihood of controlling symptoms.

Autonomic neuropathy may hide the warning signs of a heart attack. They are sudden fatigue, sweating, shortness of breath, nausea, and vomiting.


Preventing or controlling disorders associated with autonomic neuropathy may reduce the risk. For example, people with diabetes should closely control blood sugar levels.


Shy ME. Peripheral neuropathies. In: Goldman L, Ausiello D, eds. Cecil Medicine . 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 446.

Benarroch E, Freeman R, Kaufman H. Autonomic nervous system. In: Goetz CG, eds. Textbook of Clinical Neurology . 3rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 21.

Chelimsky T, Robertson D, Chelimsky G. Disorders of the Autonomic Nervous System. In: Daroff: Bradley's Neurology in Clinical Practice . 6th ed. Philadelphia,Pa; Elsevier; 2012: chap 77.

Tuesday, 22 April 2014

Merkel Cells: Sensory Nerve Endings

Today's post from (see link below) may look somewhat complex and 'scientific' but is actually an interesting look at Merkel cells, which are cells in the skin that detect sensory stimulation (touch). Up to now, scientists had no idea what the function of these cells was but now they know and their understanding has direct relevance to people living with neuropathy. Definitely worth a read and to store up as a piece of trivia to impress your friends.

Research illuminates 'touchy' subject: Sensory nerve endings 
Date:April 15, 2014 Source: University of Cincinnati Academic Health Center


Merkel cells -- which contact many sensory nerve endings in the skin -- are the initial sites for sensing touch, researchers have demonstrated. "Scientists have spent over a century trying to understand the function of this specialized skin cell and now we are the first to know … we've proved the Merkel cell to be a primary point of tactile detection," said the principal investigator.

By solving a long standing scientific mystery, the common saying "you just hit a nerve" might need to be updated to "you just hit a Merkel cell," jokes Jianguo Gu, PhD, a pain researcher at the University of Cincinnati (UC).

That's because Gu and his research colleagues have proved that Merkel cells -- which contact many sensory nerve endings in the skin -- are the initial sites for sensing touch.

"Scientists have spent over a century trying to understand the function of this specialized skin cell and now we are the first to know … we've proved the Merkel cell to be a primary point of tactile detection," Gu, principal investigator and a professor in UC's department of anesthesiology, says of their research study published in the April 15 edition of Cell, a leading scientific journal.

Of all the five senses, touch, Gu says, has been the least understood by science -- especially in relation to the Merkel cell, discovered by Friedrich Sigmund Merkel in 1875.

"It's been a great debate because for over two centuries nobody really knew what function this cell had," Gu says, adding that while some scientists -- including him -- suspected that the Merkel cell was related to touch because of the high abundance of these cells in the ridges of fingertips, the lips and other touch sensitive spots throughout the body; others dismissed the cell as not related to sensing touch at all.

To prove their hypothesis that Merkel cells were indeed the very foundation of touch, Gu's team -- which included UC postgraduate fellow Ryo Ikeda, PhD -- studied Merkel cells in rat whisker hair follicles , because the hair follicles are functionally similar to human fingertips and have high abundance of Merkel cells. What they found was that the cells immediately fired up in response to gentle touch of whiskers.

"There was a marked response in Merkel cells; the recording trace 'spiked'. With non-Merkel cells you don't get anything," says Ikeda.

What they also found, and of equal importance, both say, was that gentle touch makes Merkel cells to fire "action potentials" and this mechano-electrical transduction was through a receptor/ion channel called the Piezo2.

"The implications here are profound," Gu says, pointing to the clinical applications of treating and preventing disease states that affect touch such as diabetes and fibromyalgia and pathological conditions such as peripheral neuropathy. Abnormal touch sensation, he says, can also be a side effect of many medical treatments such as with chemotherapy.

The discovery also has relevance to those who are blind and rely on touch to navigate a sighted world.

"This is a paradigm shift in the entire field," Gu says, pointing to touch as also indispensable for environmental exploration, tactile discrimination and other tasks in life such as modern social interaction.

"Think of the cellphone. You can hardly fit into social life without good touch sensation."

Story Source:

The above story is based on materials provided by University of Cincinnati Academic Health Center. Note: Materials may be edited for content and length.

Journal Reference:
Ryo Ikeda, Myeounghoon Cha, Jennifer Ling, Zhanfeng Jia, Dennis Coyle, Jianguo G. Gu. Merkel Cells Transduce and Encode Tactile Stimuli to Drive Aβ-Afferent Impulses. Cell, 2014; DOI: 10.1016/j.cell.2014.02.026

Monday, 21 April 2014

Mercury Can Cause Nerve Damage (Vid)

Today's post from (see link below) is an interesting one, including a video, about the potential for mercury causing neuropathy. Now you may not immediately think that you're in any danger of absorbing mercury into your system but dental fillings, chemical wastes, pesticides and even vaccines can introduce mercury into your body. Amongst other toxic effects, mercury can attack your nervous system and cause significant nerve damage. There are ways to neutralize any mercury in your system, by eating foods rich in sulfur (see list in the article). An interesting read but remember you have to look at everything you read in perspective and look at your own personal circumstances to see if there's a risk.

Mercury Toxicity – Beware! It can deteriorate your neurons. 

According to the Environmental Protection Agency (EPA), Mercury can destroy your digestive system, cause mood swings, irritability, muscle weakness, skin rashes, memory loss, central nervous system damage, and the list goes on. This list does not list all the damage that Mercury can cause to the body, but it gives you a brief overview and can be viewed here:

Please view this week’s video about Mercury. If you are unable to view the video, the text can be viewed below in its entirety. When you are done, be sure to watch the video from Calgary University by clicking here . This video is the coolest in cutting edge medical technology. 



Hello, I’m Dr. Ian Rainey with your weekly health tip. This week we are going to talk about Mercury, not to be confused with the planet. Mercury is an element. In fact, it is one of the most toxic substances on Earth and it has many negative effects on the body. Because of this, it has become what many call the great mimicker of many health conditions. It can damage the immune system and the reproductive system. It can also inhibit neurological and cardiovascular health. This video will provide information about the sources of mercury exposure, potential health effects, how to eliminate Mercury and ways to reduce your exposure to mercury.

Sources of mercury include: dental amalgam fillings, hazardous waste, vaccines, pesticides, shellfish, and coal burning power plants

Here are some the things you should know about mercury toxicity.

Mercury is known to denervate nerve fibers. This works in a similar fashion to the way the multiple sclerosis. Essentially, it makes it so the nerves cannot do their job.

Mercury can leak into the blood brain barrier. Not many things can. That is what makes it so toxic and difficult to remove. Once this happens the nerves lose their ability to conduct information and create visual responses.

Mercury can cause depression. It does this by binding to the hormones that make you happy, such as serotonin.

Mercury can cause hearing loss.

Mercury can change your emotions. It does this by decreasing norepinephrine and dopamine activity. This will make you lose excitement and joy for life.

Mercury can cause peripheral neuropathy autoimmunity, recurring sinus problems, prostate issues and gum infection.

Mercury is also at the root of many undiagnosed patients who have chronic fatigue and fibromyalgia. One of the most common ways that a patient presents with Mercury toxicity is with a terrible burning sensation and pain that seems to migrate to different areas.

All of these symptoms resemble nerve damage. But the medical community looks for nerve damage with things like EMG’s, nerve conduction tests and MRI’s. You are never going to find any mercury toxicity with these tests.

As a result, out of confusion and an inability to find the solution, health professionals begin diagnosing things like erythromelalgia, fibromyalgia, idiopathic pain syndrome and neurosis.

Out of this confusion came an answer. We now are able to test for mercury toxicity in the body with a simple urine test. I do offer this test for patients who exhibit many of the signs of mercury toxicity.

So now you may be wondering what you can do to reduce the mercury load on your body. You should eat foods that are high in sulfur. This would include things like kale, horseradish, collards, cilantro, watercress, cabbage and broccoli. You should also include foods that have cysteine. This includes oats, chicken and red peppers because they contain metallothionein. Metallothionin is a natural chelator that will help eliminate mercury from the body. Even chlorophyll is a natural chelator! So don’t forget to eat your green veggies.

If you can’t seem to stomach all of these foods, there are special vitamins and supplements that combine the best of all natural chelators to help you eliminate the mercury in your body. Those are available at my office or at the Good Earth.

I want to thank Joe Buishas and and Dr. Ron Grisanti for providing material, as well as the University of Calgary for the video explaining how Mercury causes nerve damage to the brain. Please watch this extra video if you have the time. It is amazing to see how Mercury actually destroys your nervous system.

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.