Sunday, 1 February 2015

End Of A Neuropathy Era

Today's post from (see link below) marks the end of an era in that it announces the end of which is the site of the American Neuropathy Association. The Neuropathy Association has long been a bulwark of information for neuropathy patients throughout North America and the world and it's somewhat surprising that they are ending their operations. In fact, they are passing the torch on to the Foundation for Peripheral Neuropathy, who will continue their work; so there will continue to be a US organisation representing neuropathy patients.
Tina M. Tockarshewsky President and CEO December 2014 – Final Edition

Dear reader,

When The Neuropathy Association started 20 years ago, our main purpose was to bring awareness and legitimacy to peripheral neuropathy, as well as to offer support and outreach to millions suffering alone in the darkness of their unrecognized disease.

Over the years, the community’s needs grew exponentially alongside our growing understanding of the complexities...and pervasiveness...of the global neuropathy epidemic. We expanded beyond the patients who founded the organization during their IVIG infusion time to include patients with all types of neuropathy, as well as the family members, caregivers, healthcare professionals and researchers dedicated to helping them. We reached out to media and policy makers nationally and locally to make sure they understood the extreme challenges our community faced due to lack of proper care, therapies, and cures. From the halls of Congress to Today show viewers’ TV screens and up into the night skies over famous landmarks, we gave neuropathy the exposure it had never had before. The ultimate goal has been and continues to be that, through research, education, and greater awareness, we would learn the causes and how to treat, prevent and/or cure the over 100 different types of neuropathy.

The Neuropathy Association and its supporters and volunteers over the years can take great pride in what we have accomplished together in two decades. And despite the fact that the search for cures continues, the milestones reached to date have been significant. Our innovative educational and social media programs have received high praise and inspired others to follow our lead. Our advocacy work resulted in appointments on high-level and influential federal government advisory councils. Our research grants program yielded significant findings, including discovering key genes for hereditary neuropathies. Our support groups comforted and counseled thousands every year. Thanks to partnerships with our community and our corporate partners, there is an ever-increasing rate of clinical trials in development...and keep in mind that ALL of the FDA-indicated therapies available today only came to market within the past 10 years!

At the end of 2007, no one anticipated the national economic downturn. At the time, the Association had just completed a major re-organization and new strategic directions, but like all other nonprofit and for profit organizations we, too, were not prepared for the national financial crisis, reduced foundation funding, or the impact of new restrictions and tighter regulations put on companies that had helped to financially support us in the past. Then followed the drastic Medicare cuts suffered by healthcare professionals specializing in neuropathies that have severely compromised their business and forced many professionals out of business...that, in turn, has hurt you as well as us.

With so many in the neuropathy community struggling...and with new times needing new approaches to getting the job done, it became mission critical for the Association to find a new way to do business...and find a new battleplan to bring our community the cures and treatments we so desperately need...

When 2015 starts this week, the new year will begin a new chapter for our neuropathy community. Recently, you received communication from us by email and mail sharing that The Neuropathy Association has decided to dissolve and close its doors, passing the torch of our mission to the Foundation for Peripheral Neuropathy. It is a bittersweet and difficult decision for us but a necessary one to move our mission forward in the new way that is necessary. Please know that our decision was a thoughtful one that was based on our commitment to high-level service for you and took into account our options according to New York law. In doing so, we have chosen a strategic partner that we fully support and trust will achieve our mutual goals in the future. The decision to close our doors is difficult, but the decision to select the Foundation for Peripheral Neuropathy to continue to work on behalf of The Neuropathy Association’s donors is the right choice. We believe the result will be a single and powerful charitable 501(c)(3) organization that will capitalize on the strengths of both organizations to better serve the neuropathy community. (See lead article below)

We encourage you to join us in supporting the Foundation for Peripheral Neuropathy as they move forward with our collective mission and continue to cultivate and grow the programs we started for you. The future is exciting and the possibilities are within our grasp...let’s seize the day and make it happen!

On behalf of the Association, I want to thank everyone who has worked with us over the years as community volunteers, support group leaders, national and chapter board members, and advisory council members...your leadership kept our mission strong for two decades. I also thank everyone who generously donated monies, time, and talents to support our helped to make us the trusted community resource millions could turn to for help. And, finally, I want to express my great thanks and deep appreciation to the staff team working tirelessly with me for so many years: Natacha Pires, director of medical and public affairs, and Paul Guidos, director of operations. 24/7/365 the staff team committed themselves to the mission of this organization and to helping as many of the 20 million Americans as they could…their work and their legacy lives on in the improvements in neuropathy patient education, the greater national awareness, and significant care improvements big and small that many of us today benefit from that were not available just a few short years ago.

In saying goodbye and closing our doors, we should all know that great work has been accomplished to move the mission forward...and we should all feel hopeful about the opportunities ahead of us. May our greatest hope for cures be realized soon, and may you continue to fight for the care and quality of life improvements you deserve. It has been my honor to fight for you over past 10 years, and thank you for the privilege of working on your behalf as your national advocate. The experiences have enriched my life, and I am grateful for every wonderful person I have met over the years, every candid conversation, and every wisdom you have taught me.

I wish each and every one of you good health and every happiness in the New Year.


Tina M. Tockarshewsky
President and CEO

Saturday, 31 January 2015

Corydalis Yanhusuo - Herbal Remedy For Neuropathic Pain

Today's post from (see link below) talks about a compound derived from the Corydalis plant that is both effective against neuropathic pain and non-addictive. Everybody is looking for alternatives to opioids as nerve pain analgesics and as such, there has been more investigation into Chinese medicine, where herbal drugs such as Corydalis have been used for a great deal of time. As far as the West is concerned, they are accepting the analgesic qualities but looking for a more 'refined' and scientifically acceptable way of presenting the compound. In the meantime, the herb is available in health shops. However, many health shop preparations are not fully tested and the customer takes a risk if they use them. Maybe it's a question of doing as much research as possible and trying it out for yourself, for a reasonable but relatively short period of time but again...let the buyer beware.
Chinese herbal compound relieves inflammatory and neuropathic pain
 Irvine, Calif., Jan. 2, 2014 
UCI study also shows novel analgesic to be nonaddictive

— A compound derived from a traditional Chinese herbal medicine has been found effective at alleviating pain, pointing the way to a new nonaddictive analgesic for acute inflammatory and nerve pain, according to UC Irvine pharmacology researchers.

Working with Chinese scientists, Olivier Civelli and his UC Irvine colleagues isolated a compound called dehydrocorybulbine (DHCB) from the roots of the Corydalis yanhusuo plant. In tests on rodents, DHCB proved to diminish both inflammatory pain, which is associated with tissue damage and the infiltration of immune cells, and injury-induced neuropathic pain, which is caused by damage to the nervous system. This is important because there are no current adequate treatments for neuropathic pain.

Moreover, the researchers found that DHCB did not generate the tolerance seen with continued use of most conventional pain relievers, such as morphine.

“Today the pharmaceutical industry struggles to find new drugs. Yet for centuries people have used herbal remedies to address myriad health conditions, including pain. Our objective was to identify compounds in these herbal remedies that may help us discover new ways to treat health problems,” said Civelli, the Eric L. ; Lila D. Nelson Chair in Neuropharmacology. “We’re excited that this one shows promise as an effective pharmaceutical. It also shows a different way to understand the pain mechanism.”

Study results appear in the Jan. 20 issue of Current Biology.

They are the product of a collaboration between two teams separated by the Pacific Ocean. As traditional Chinese medicine gains greater acceptance in Western medical practice, Xinmiao Liang at the Dalian Institute of Chemical Physics in China and his group have been working to create an “herbalome” of all the compounds in plant extracts that display pharmacological properties. The UC Irvine team suggested applying “reverse pharmacology” – a novel drug discovery approach that Civelli devised about 25 years ago – to the herbalome project.

Together they screened 10 traditional Chinese medicines known as analgesics, testing nearly 500 compounds for their pain-relief abilities. Only DHCB in corydalis induced a reproducible effect.

Corydalis is a flowering herbal plant that grows in Siberia, Northern China and Japan. People utilize its root extract to alleviate menstrual cramps, chest pain and abdominal pain. It’s been previously studied for its analgesic properties, but this is the first time DHCB has been identified, extracted and tested.

Chronic neuropathic pain affects more than 50 million Americans, yet management of this pain remains a major clinical challenge due to the poor results and severe side effects of conventional analgesics. Civelli said that drawing upon traditional Chinese medical-herbal products could lead to a breakthrough treatment for these patients.

DHCB needs to be evaluated for any toxicity before it can be developed as a drug. It’s also possible that if the compound is chemically modified, a more potent pharmaceutical may be found. While DHCB is not currently available, it is part of the Corydalis yanhusuo root or extracts that can be purchased in health stores or online.

Yan Zhang, Lien Wang, Gregory Scott Parks, Kang-Wu Li, Mi Kyeong Kim, Benjamin Vo, Emiliana Borrelli, Zhiwei Wang, M. Julia Garcia-Fuster and Z. David Luo of UC Irvine;

Chaoran Wang, Xiuli Zhang, Zhimou Guo, Guangbo Ge and Ling Yang of the Dalian Institute of Chemical Physics in China; and Yanxiong Ke of the East China University of Science & Technology also contributed to the study, which was supported by the National Institutes of Health (grants MH60231 and DA024746), the National Alliance for Research on Schizophrenia & Depression (now the Brain & Behavior Research Foundation), the Tourette Syndrome Association, the National Natural Science Foundation of China, and the National High-Tech Research & Development Program of China.

About the University of California, Irvine: Located in coastal Orange County, near a thriving employment hub in one of the nation’s safest cities, UC Irvine was founded in 1965. One of only 62 members of the Association of American Universities, it’s ranked first among U.S. universities under 50 years old by the London-based Times Higher Education. The campus has produced three Nobel laureates and is known for its academic achievement, premier research, innovation and anteater mascot. Led by Chancellor Michael Drake since 2005, UC Irvine has more than 28,000 students and offers 192 degree programs. It’s Orange County’s second-largest employer, contributing $4.3 billion annually to the local economy.

Media access:
UC Irvine maintains an online directory of faculty available as experts to the media at Radio programs/stations may, for a fee, use an on-campus ISDN line to interview UC Irvine faculty and experts, subject to availability and university approval. For more UC Irvine news, visit Additional resources for journalists may be found at

Friday, 30 January 2015

Problems With Legalising Marijuana For Neuropathy Pain

Today's post from (see link below) is really a local news story but is symptomatic of the arguments surrounding marijuana as a medical drug. Rational argument and scientific evidence seems to strongly suggest that marijuana is one of the most effective pain medications for people living with severe neuropathy, yet outdated laws both local and national stand firmly in the way. Sometimes the punishments for possession are so severe that people are discouraged from using something that will relieve their pain. Slowly but surely, official attitudes are changing but it's a slow and painful process as this story from North Dakota illustrates.

Backers fire up attempt to get medical marijuana legalized in ND
By Helmut Schmidt on Jan 21, 2015 .

FARGO – If you ask Rilie Morgan, it’s time for North Dakota to make medical marijuana legal.

The affable silver-haired financial planner, who goes by his middle name, Ray, has neuropathy.

The neurological affliction has for the past two years given the 64-year-old Fargo man constant tingling in his feet and calves, sometimes punctuated by sharp shooting pains.

“It’s like when your hand or foot falls asleep and you get a tingling sensation. It’s constant. It’s 24/7,” Morgan said.

“If your mind is busy, then it’s not too bad. But once in a while there is some pain, a shooting pain that’s like, ‘Wow! Where did that come from?’ ” he said. “You always know it’s there.”

Morgan, a partner in a Fargo financial firm, said a painkiller he uses can cause liver damage. He used morphine for several months after a back surgery. That’s a route he doesn’t want to take again.

He said medical cannabis may make the pain “a little more tolerable. I’d like to explore the possibility anyway.”

State Rep. Pamela Anderson, a Fargo Democrat, has taken up Morgan’s cause, and introduced House Bill 1430 on Monday.

The bill would allow patients and caregivers to possess up to 2½ ounces of cannabis – or products such as cannabis oils, beverages, vapors, extracts, ointments or pills – for medical use.

It also has a provision that allows people who have obtained a prescription for medical marijuana to cultivate up to six marijuana plants.

The bill lists a number of ills eligible for treatment: cancer, glaucoma, HIV, hepatitis C, amyotrophic lateral sclerosis (Lou Gehrig’s disease), Crohn’s disease, ulcerative colitis, agitation due to Alzheimer’s disease and post-traumatic stress disorder.

Conditions that lead to wasting, severe debilitating pain or nausea, seizures, or severe and persistent muscle spasms, including those characteristic of multiple sclerosis are also listed, with an option for more to be added.

HB 1430 was crafted from information on what other states have done to regulate medical marijuana that was provided by the Council for State Governments, Anderson said.

She said she’s heard from people suffering from glaucoma, multiple sclerosis or seizures who would support legalizing medical cannabis in North Dakota.

To date, 23 states and the District of Columbia allow the use of medical cannabis, including neighboring Minnesota and Montana.

Rep. Kathy Hawken, R-Fargo, a co-sponsor of the bill, has her own connection to the issue – a son who suffers from seizures.

“More than one neurologist has said that if he could, he would prescribe medical marijuana,” Hawken said. “They think it does work.”

She said the bill contains controls on medical marijuana products from farm to pharmacy.

But she’s unsure of its fate – at least this year.

“I think it is something that will eventually pass. This session? Well, stranger things have happened,” Hawken said. “Realistically, at least the discussion will start.”

The 29-page bill provides for:
Exemptions from prosecution for the possession, manufacture or sale of medical marijuana for those licensed, and for people certified as in need of medical marijuana by a physician.
Creating a system to license manufacturing and distribution of medical marijuana products.
Criminal penalties for violating provisions of the medical marijuana law.
Protections from discrimination in schooling and housing for medical cannabis users, unless allowing the use would violate federal law or regulations.

Rep. Eliot Glassheim, D-Grand Forks, another bill sponsor, said he used to smoke a joint now and then 30 years ago.

“It seems to me the whole hysteria was misplaced,” Glassheim said.

Now, he’s being treated for cancer.

“It’s not in remission, but it’s not spreading. I feel OK,” he said. He understands that others dealing with the side effects of cancer treatments could benefit from having medical marijuana available as an option.

“I certainly could imagine a situation where you’re nauseous or where you’re in unbearable pain,” Glassheim said.

Supporting the bill, “just seemed to me to be a rational thing to do,” he said.

Glassheim expects some resistance.

“It may have to wait until next session. I expect it will pass one of these days,” he said. “It’s one of these bills people have to get their minds around.”

Morgan, meanwhile, is plan a trip to Arizona to test-drive the idea of becoming a snowbird as he nears retirement. Arizona also allows medical cannabis to treat a number of ailments, he said.

But he will hop on a plane to Bismarck to testify for HB 1430, he said.

“I think medical marijuana has been understudied” for its efficacy, Morgan said. “I think it’s time to explore the options and let pharmaceutical companies see what they can come up with. It’s time.”

Other sponsors of HB 1430 are Andrew Maragos, R-Minot; Marvin Nelson, D-Rolla; Mary Schneider, D-Fargo; and Marie Strinden, D-Grand Forks.

Lower pot penalties?

Another House bill aims to lower penalties for college students caught with small amounts of marijuana on campus.

HB 1394, sponsored by Reps. Lois Delmore, D-Grand Forks, Thomas Beadle, R-Fargo, Kim Koppelman, R-West Fargo, and Hawken, would make the possession of one-half ounce to a full ounce of marijuana a Class B misdemeanor, down from its current designation as a Class B felony.

Possession of less than a half-ounce of marijuana would be charged as an infraction, rather than as a Class B misdemeanor.

If someone is found guilty of possession of an ounce or less of marijuana, the bill also calls for the conviction to be sealed by the court after two years if there are no further drug possession convictions.

Delmore said the bill is designed to make sure that the mistake of smoking pot in a dorm or elsewhere on campus isn’t one that haunts a student the rest of their lives.

“If you have something like that on your record, you have a hard time getting a job” or housing, she said.

Thursday, 29 January 2015

The Fluoroquinolone Argument Just Won't Go Away

It just isn't going away! This article about the dangers of fluoroquinolone antibiotics from (see link below) is part personal account and part analysis of the problem. There is no doubt that fluoroquinolones have the potential to cause nerve damage; the US FDA admits this and warns that the risks should be clearly shown on packaging. So why should we take the risk? The problem is that fluoroquinolones are so widely prescribed and doctors are so widely convinced of their value, that new evidence is having real problems getting through. In that case, we need to take responsibility for our own health and seriously discuss the dangers to ourselves with our health professionals. They need to prove that the risk of nerve damage is minimal and if they can't do that then there are alternatives available. Forewarned is forearmed.

Fluoroquinolones, FDA Memo Highlights Damning Evidence 
David/Admin December 27, 2014 | 

Enough already! I have heard the arguments about the necessity of having Fluoroquinolones (FQ) (Levaquin, Cipro, Avelox, Floxin etc…) in our antibiotic arsenal for over eight years now. These worn out arguments are paraded out, each time someone gets any type of attention calling out the serious health risks associated with taking these drugs.

Assuming we are all able engage in rational thought; let us reason it out for a brief moment. If it is true that these drugs are, in fact, needed in our arsenal for life threatening infections (as I am so often told by medical personnel), then why are they still being handed out pervasively for routine infections? Why are these being used for sinusitis, pharyngitis, urinary tract infections, and, God forbid, being used in children? Let me ask you, when is enough, enough?

Many years ago, the discussion about the truth that these drugs create the perfect storm for permanent and long term chronic health problems, was relegated to darkened back rooms and internet discussion forums and only populated by those unlucky enough to have fallen prey to their hideous and, many times, permanent adverse effects. Patients who complained about permanent or long last adverse effects of these drugs were marginalize, ridiculed, scoffed at, and dismissed by health care providers.

Those who publicly attempted to point out that the pervasive use of FQ’s (one of the most prescribed class of antibiotics worldwide) was also the reason for the worldwide rise in mystery illnesses such as chronic fatigue, fibromyalgia, and possibly other ill-defined neurological disorders that doctors dismiss as being caused ‘de-novo’ or due to unknown environmental factors were often called conspiratorial or delusional.

Recently an internal memo dated April 17, 2013, issued by the Food and Drug Administration’s Center for Drug Evaluation and Research, Office of Surveillance and Epidemiology, was obtained through the freedom of information act shows the FQs in a damning light. The pharmacovigilance review shows that the FDA is fully aware of permanent disabling peripheral neuropathy in otherwise healthy individuals and that the likely method of action (or damage) for the peripheral neuropathy is mitochondrial toxicity.

They go on to note that the method of damage, mitochondrial toxicity, is also the underlying mechanisms in neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and ALS. Allow me to editorialize that mitochondrial issues can set a patient up for health problems that appear long after cessation of medication.

So, let’s take a quick look at some of the highlights of this memo (my comments added after each in italics).
Overall, this review did not identify any predictable risk factors for peripheral neuropathy.”In other words everyone could be at equal risk in getting peripheral neuropathy.“
Symptom onset seemed to be unrelated to the duration of therapy.”In other words you could get peripheral neuropathy from one pill or 20 pills, it didn’t matter. “
Patients were relatively young, healthy, and had no conditions predisposing them to peripheral neuropathy.”In other words, your health status was not a factor. Most people that I know who were hit the hardest were in good shape, not sickly. “
Some of these patients were told (by their doctors) that this class of drugs could not cause peripheral neuropathy.”In other words many doctors are still clueless about the adverse reactions these drugs can cause.“
None of the cases from a 2003 review reported a complete recovery…. suggesting potential irreversibility of the condition. “Irreversibility…..need I say more.”
Implies method of action as the same that causes ALS, Parkinson’s and other neurodegenerative diseases.“Again, this should frighten most sane adults. “

It was concluded that “The current fluoroquinolone labels are inconsistent in the details regarding the risk of peripheral neuropathy and do not describe the possible permanence of peripheral neuropathy, rapid onset, nor the need to consider discontinuation of drug with first symptoms.”

This memo recommended changes to the current label as the current wording downplays the seriousness of the risk; A risk that is not taken seriously by doctors or completely unknown to patients. In the meantime the frivolous prescription usage of FQ’s continues unabated.

Human beings are funny creatures. We do not believe that certain tragedies will befall us. We usually believe that bad things only happen to the ‘other guy’, and if they do happen to us, we usually respond with shock or disbelief. We bring false presuppositions into our medical assumptions and allow ourselves to get lulled into a sense of security that does not really exist. We put unconditional trust the medical establishment and at the same time abrogate our own personal responsibility. I know, at one time, I was guilty of the same assumptions and blind trust.

If you are reading this article and you are new to FQ antibiotics, please, let me take a moment and dispel a few myths regarding these drugs.
FQ antibiotics are not like any other class of antibiotics.
FQ antibiotics are very powerful and have a high collateral damage capability.
Stopping an FQ antibiotic may not stop an adverse reaction (not to be confused with a side effect).
Adverse reactions to FQ antibiotics can start ‘after’ stopping, sometimes long after.
FQ antibiotics are suspected in the causation of many of today’s mystery health problems.

Do you know of a loved one, a friend, a co-worker, or someone else who suffers from a diagnosis of mysterious origin, such as peripheral neuropathy with an unidentified cause? If so ask them to do some detective work to find out if they have had FQ usage in their past, and not necessarily their immediate past.

If you are faced with potential antibiotic use, for yourself or a loved one, please become informed as to the choices that you have available. If antibiotic use is necessary there are generally safer alternatives than the Fluoroquinolones. Discuss all potential avenues of treatment with your doctor and choose the safest method.

Wednesday, 28 January 2015

Stomach Weight-Loss Surgery And Neuropathy

Today's post from (see link below) addresses a problem that arises out of one of the largest cultural health problems of our age (obesity) and that is neuropathy caused by gastric bypass surgery. Ironically, without the surgery, many seriously obese people will go on to develop neuropathy anyway thanks to diabetes but again for many, surgery is the last option and almost always necessary at that point. Smoking and drinking have always been the habits most associated with health problems and once again, ironically, both can cause nerve damage but obesity is rapidly catching them up. In the best of all possible worlds, people would change their lifestyles and diets and obesity-related problems would disappear but for some, the obesity is so serious that surgery is the only option left to save their lives. Read this article to see how they may be confronted with lifelong nerve damage and its symptoms as a result of the surgery.

June 2003 - Volume 3 - Issue 6 - pp 1,13–14

Honolulu, HI — At a time when obesity has reached epidemic proportions in the US, physicians should be aware that neurological complications are common following bariatric surgery to shed potentially deadly excess pounds, according to speakers at a plenary session here at the AAN Annual Meeting.

“Physicians unfamiliar with the complications of the surgery may not recognize these neurological disorders for what they are and therefore may attribute them to something else,” said Joseph R. Berger, MD, Professor and Chair of the Department of Neurology at the University of Kentucky in Lexington.

“This is particularly unfortunate because some of the complications are associated with long-term, even life-long, morbidity, and in some cases, death,” he said. “Yet many respond to simple measures such as thiamine, if administered as quickly as possible.”


At the plenary session, Dr. Berger's points were driven home by a new Mayo Clinic study, which found that a constellation of factors – rapid weight loss, postoperative complications, protracted gastrointestinal problems, and poor nutritional support – appear to place morbidly obese patients who undergo gastric bypass surgery at heightened risk of developing neurological ailments, chiefly peripheral neuropathy.

“The most important factor that emerged was probably rapid weight loss, which occurs in most patients who develop peripheral neuropathy following surgery,” said Pariwat Thaisetthawtkul, MD, a neurology fellow at the Mayo Clinic in Rochester, MN. “Rapid weight loss, in turn, may be associated with a high incidence of nausea and vomiting, which would prevent patients from taking nutritional supplements,” he said. “There may be cause and effect.”

Adding to the problem is the fact that fewer than 1 in 5 patients who developed neurological complications even attended a nutritional clinic, compared with 9 in 10 who did not develop neuropathies, Dr. Thaisetthawtkul said.

“The best treatment is probably prevention,” he said. “Gastric bypass surgery patients should attend a nutritional clinic and receive nutritional support.”


Dr. Thaisetthawtkul drew his conclusions from a retrospective study of 356 morbidly obese adults who underwent gastric bypass surgery for morbid obesity from 1985 to 2001. Sixty-three patients, or 17.7 percent, developed clinically defined symptomatic peripheral neuropathy, he said.

Almost three-fourths of the 63 patients, whose average age was 49, were women. The patients lost an average of 44 kilos, with a mean change in BMI of 16 points.

The median time to reach maximum weight loss was 7.5 months, he said. The median time to the development of peripheral neuropathy after surgery was 24 months.


The neurological disorders ranged from mononeuropathy to sensory neuropathy, sensory motor neuropathy, and plexopathies, the study showed. Thirty-one of the 63 patients developed a mononeuropathy, with a diagnosis of carpal tunnel syndrome leading the list.

“The clinical pattern was similar to that seen in other patients who develop a median neuropathy at the wrist,” Dr. Thaisetthawtkul said.

Eight patients developed sensory motor neuropathies, with sensory symptoms developing in a symmetrical pattern. “This tended to involve more large fibers, and sensory ataxia was very common,” he said. EMG showed a typical pattern of length-dependent, axonal sensory neuropathy.

Nineteen of the 63 patients developed sensory neuropathy, accompanied by abdominal and thoracic pain, Dr. Thaisetthawtkul said. In contrast to the sensory motor neuropathy, this tended to involve large and small fibers, and sensory ataxia was not common. The EMG showed mild sensory changes.

The other five patients were diagnosed with plexopathy that usually started in a subacute assymetrical pattern in the arms or legs, he said. The onset was usually near the time of surgery and started with pain, followed shortly by weakness. The EMG showed a typical pattern.


When the patients who developed peripheral neuropathy were compared with those who had no neurological complications, the study showed that the type of operation and the number of procedures had no association with the development of peripheral neuropathy, Dr. Thaisetthawtkul reported.

But when the researchers looked at the rate of weight loss or time to reach maximum weight loss, there was an important link, he said. All the patients who developed peripheral neuropathy reached their lowest weight within one year, with an average time of seven months. In contrast, patients who did not develop peripheral neuropathy did not hit their nadir until up to six years, with a mean time of 18 months.


Also, 30 percent of patients who developed peripheral neuropathy had prolonged vomiting and 25 percent had diarrhea for at least three months postoperatively, compared with 6 percent (who had vomiting) and 5 percent (with diarrhea) who did not develop neurological complications.

Nutritional support also emerged as an important predictor of complications, Dr. Thaisetthawtkul said. Only 17 percent of patients with neurological complications attended a nutritional clinic, compared with 90 percent of those who did not.

More patients in the peripheral neuropathy group had a mild nutritional disorder after surgery as defined by an albumin level of less than 3.5: 39 percent versus 12 percent in the group without neuropathy, he said.

Also, significantly more patients in the no-neuropathy group than in the peripheral neuropathy group received B-12 injections (88 percent versus 43 percent), multivitamins (83 percent versus 31 percent), and calcium supplementation (78 percent versus 25 percent), he said.

The peripheral neuropathy group also tended to have more complications that required readmission to surgically correct: 18 percent versus 3 percent in the group with no neurological complications, he said.

Next, the researchers compared the clinical pattern of peripheral neuropathy that developed after gastric bypass surgery to the clinical pattern of peripheral neuropathy after open cholecystectomy in a control group of obese patients, matched by age and gender.

“Polyneuropathy was not seen at all in the cholecystectomy group, and even mononeuropathy was much less frequent than in the gastric bypass patients,” he said.

“Only about 3 percent of patients who underwent open cholecystectomy developed peripheral neuropathy, all of which were mononeuropathies, compared with 17 percent in the gastric bypass arm,” Dr. Thaisetthawtkul said.


“We as physicians must bear in mind the risk of neurological complications following bariatric surgery, which is increasingly performed in the US and other countries,” Dr. Berger said. “Between 1 in 20 and 1 in 10 of these individuals develop neurological complications, many of which require rapid diagnosis and intervention.”

While bariatric surgery can result in lasting weight loss of 50 percent of body weight, the complications exceed those of all other abdominal surgery, Dr. Berger said. The mortality rate is 0.4 percent, with pulmonary embolisms responsible for the majority of deaths. The complication rate is 10 percent, with reoperation not uncommon due to bleeding, abscesses, and wound problems.

Delayed complications are frequently the result of nutritional deficiencies, Dr. Berger said. “Iron, calcium, and potassium are often depleted. It's estimated up to 6 percent of patients develop hypocalcemia unless repleted, 10 to 12 percent develop vitamin B-12 deficiencies, and up to 6 percent develop fat-soluble vitamin deficiencies – each with their attendant neurological complications.”


Many of the neurological complications associated with bariatric surgery can be ascribed to metabolic abnormalities, which, in turn, can often be traced to poor nutritional status, particularly vitamin B1 and vitamin B12 deficiencies, Dr. Berger said.

“But studies show that peripheral neuropathies related to vitamin deficiencies develop even in patients who are given oral vitamin supplementation,” he said. “It is insufficient to simply give oral vitamins to these patients,” Dr. Berger stressed. “Repletion should never be by the oral route alone.”


Neurologists will probably be seeing more cases of bariatric surgery-associated neuropathies as the number of obese persons around the world continues to skyrocket, said Joseph R. Berger, MD, Professor and Chair of the Department of Neurology at the University of Kentucky in Lexington.

According to Centers for Disease Control and Prevention data, the prevalence of obesity, defined as a Body Mass Index (BMI) of over 30, doubled from 1976 to 2000.

The numbers are sobering: 33 percent of American adults are obese, 25 percent of children are overweight, and 60 percent of adults are overweight, with the numbers rapidly rising. Overweight is defined as a BMI of over 25.

In one state, 1 in 4 adults is obese, while in 29 states, 20 to 24 percent of adults are, he said. The other 20 states have prevalence rates of 15 to 19 percent.

Groups at highest risk are women, the elderly, those of lower socioeconomic status, and African Americans and Hispanics, Dr. Berger said.

Obesity is responsible for 300,000 deaths annually in the US, he said, and carries a price tag of $100 billion a year.

It is not a problem unique to the US, Dr. Berger added. In the last 10 years, the prevalence of obesity has risen 10 to 40 percent in European nations and among urban populations in undeveloped countries.

From 1990 to 1997, the number of bariatric surgeries performed in the US more than doubled. The operation is typically reserved for those patients with a BMI of over 40 or a BMI of over 35 and two comorbidities related to obesity, he said, with gastric bypass being the most common procedure.

©2003 American Academy of Neurology

Tuesday, 27 January 2015

An Attractive New Zealand View Of Neuropathic Pain

We're always looking for eye-catching material that helps explain neuropathy better to the reader and today's post from (see link below) does exactly that. It is an advertisement for a physio and pain-management clinic (which this blog doesn't normally do) but the information is attractive to all neuropathy patients Take a read - it certainly makes a change from dry as dust PDFs which will turn off the casual reader after the first paragraph. This blog could learn some presentation lessons from this. Worth a look.

Neuropathic pain and pharmacological management in particular 
January 2015

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Dworkin RH et al, Pharmacologic management of neuropathic pain, Evidence-based recommendations. Pain. 2007;132: 237-251.
Woolf CJ. Pain: Moving from symptom control toward mechanism-specific pharmacologic management. Annals of Internal Medicine. 2004;140:441-451
Smith BH el at, Neuropathic pain: a pathway for care developed by the British Pain Society. British Journal of Anaesthesia. 2013; 111(1):73-9
Vargas-Schaffer G, Is the WHO analgesia ladder still valid?. Canadian Family Physician 2010; 56:514-7-0 5.
Okubo M et al, Transition to persistent orofacial pain after nerve injury involves supraspinal serotonin mechanisms. The Journal of Neuroscience, 2013;33(12):5152-5161
Jensen TS et al, A new definition of neuropathic pain. Pain. 2011;152:2204-2205
Dworkin RH et al, Advances in neuropathic pain. Archives of Neurology. 2003;60:1523-1534
Jensen IB et al, 3-year follow up of a multidisciplinary rehabilitation programme for back and neck pain. Pain. 2005;115:273-283
Neuropathic pain (2014 Dec 30th). Retreived from

Monday, 26 January 2015

How To Recognise Autonomic Neuropathy

Today's post from (see link below) the site of Medline Plus, gives an overview of a form of neuropathy that is troubling more and more people; either because it is becoming more common, or because it is being better diagnosed. It's the nightmare for all living with nerve damage, when the functions you take for granted also begin to go awry and the psychological ramifications are often underestimated, both by patient and doctor. Basically autonomic neuropathy is a collective term for the symptoms caused when the involuntary functions of the body you take for granted your whole lives, start letting you down. Reading this article will give you a good idea of what I mean. It's very important that if you notice this sort of thing happening, you contact your doctor and possibly get referred to a neurologist because each symptom/problem may need to be dealt with apart from the others. Unfortunately, at the moment, there's little that can be done to address the neuropathy itself but the symptoms may be relieved by medications and adapting your lifestyle and daily habits.

Autonomic neuropathy
Medline Plus (last updated Jan 2015)

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.

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.
Alternative Names

Neuropathy - autonomic; Autonomic nerve disease


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.
Update Date: 10/3/2012

Updated by: Luc Jasmin, MD, PhD, Department of Neurosurgery at Cedars-Sinai Medical Center, Los Angeles, and Department of Anatomy at UCSF, San Francisco, CA. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M. Health Solutions, Ebix, Inc.

Sunday, 25 January 2015

Peripheral Neuropathy: A Doctor's Analysis

Ever wondered how the doctors or neurologists assess you and come to their conclusions? Today's post from (see link below) is a doctor's summary of a patient's condition after examination. His conclusion is neuropathy, probably caused by diabetes. It's interesting to look at this particular case study and see the bigger picture and maybe see similarities with our own general health. There may be a few warning pointers to look out for!

Diabetic Peripheral Neuropathy Personal history

Tuesday, November 4, 2014

 A known diabetic patient male patient, 46 years old, from ……….…., ………..……, married and has 3 off spring, the youngest is 16 years old, heavy smoker with no other special habits of medical importance, he is Rt. handed.

4 c/o

Loss of sensation in both hands and feet of 15 years duration.

The condition started 15 years ago by nocturnal burning painassociated with tingling, numbness started in both feet then progressed, one year later , to involve both hands then the patient developed gradual loss of sensation in both hands and feet, and he felt as if he walkedon cotton.
4 years later, the patient experienced weakness associated with flaccidity, falling of hair, brittle nails with no wasting or twitches. This weakness started in L.Ls then progressed, one year later, to involve both ULs. It's more in distal than proximal muscles, in extensor more than flexor muscles, in adductor more than abductor muscles. The patient also suffers from unsteadiness during eye closure with no involuntary movements.

The condition was associated with diminutionof vision, visual field defects, disturbance of color vision, ptosis in both eyes for which the patient was investigated and treated by laser photocoagulation more than once. The patient can't close his eyes firmly, with accumulation of the food behind both cheeks, no symptoms of other cranial nerve affection.
The patient has organic impotence with lost morning erection with no history of drugs known to cause erectile dysfunction.

The patient developed unsteadiness during standing with palpitation, nocturnal diarrhea, gustatory sweating and dyspepsia.

No symptoms of increased I.C.T.
No speech disturbance.
No symptoms suggesting other system affection.

4 Past history
- There is past history of D.M started 20 years ago manifested by polyuria, polydypsia, polyphagia. The patient is on insulin treatment and his blood sugar is out of control.

- There is past history of HPN started 15 years ago manifested by headache, blurred vision. The patient is on capoten and his hypertension is not controlled.
- Appendectomy operation was done at the age of 20 years.
- No history of other drug intake.
4 Family history
- No similar condition in family.
- No consanguinity.
- No common disease in family.

4 General exam
- Temperature: 37.2o c.
- Bl. Pressure: 140/80 (Recumbent position), 100/60 (standing position).
- Pulse: regular, 110 beat/minute, average volume, no special character, vessel wall not felt, equal in both sides with absent dorsalis pedis, anterior and posterior tibial and popliteal pulsation with intact femoral, radial, brachial and axillary pulsation.
- Mentality: The patient is fully conscious, well oriented for time, place and person. Average mood and memory. The patient is co-operative with average intelligence.
- Head: Examine for Retinopathy, teeth (Artificial teeth).
- L.L: Trophic ulcer, diabetic dermopathy.

4 Sensory:
- Superficial sensations: above knee and elbow level stock and glove anesthesia. Circumferential comparison must be done to exclude diabetic radiculopathy.
- Deep sensation:
§ Joint sense lost on both sides.
§ Vibration sense lost at level of peripheral nerve (medial malleolus, radial styloid process) with intact vibration sense at the level of posterior column (ASIS, clavicle).
§ Muscle sense lost (Calf muscles).
§ Lost nerve sense (Ulnar and lateral popliteal nerves).
§ +Ve Romberg's test.
- Cortical sensation : can't be examined due to loss of superficial sensation.

4 Examination of Speech: Normal.

4 Examination of Cranial Nerves:
- Optic Nerve is affected in the form of: diminution of visual acuity (Rt. eye : can count fingers at one meter, Lt. eye :blind), Tubular visual field defect .
- Ocular nerves
§ Inspection: bilateral ptosis (thumb test >> can't elevate his eye lids),pupils are dilated and irreactive to light or accommodation with no squint.
§ Power: loss of eyeball movements in all direction denoting paralysis of recti and oblique muscles of the eye.
N.B: nystagmus and conjugate eye movements can't be examined b because of loss of eye movements on examining each eye separately .
§ Reflexes: absent light and accommodation reflexes.
- Facial nerve
§ Inspection: symmetrical forehead, obliterated nasolabial folds on both sides with no tearing, no drippling of salive, no mouth deviation
§ Power: patient can't close his eyes firmly, can't elevate his eye brows , can't whistle, can't show his teeth, can't blow his cheeks
§ Reflexes: absent glabellar reflex à (bilateral LMNL).

4 Examination of Motor System :
- There is wrist and ankle drop, trophic ulcer in L.L, loss of hair and brittle nail in U.L,L.L.
- No muscle wasting, no skeletal deformities, no involuntary movement.

4 Examination of Tone__
- Bilateral symmetrical hypotonia in both upper and lower limbs.

4 Percussion__
No fasciculation or myotonia.

4 Examination of Muscle Power

- Bilateral symmetrical Weakness in both upper and lower limbs. It is distal more than proximal, abductors more than abductors, extensors more than flexors.
- Abdominal muscles: weakness may be attributed to trunkal neuropathy or related to myopathy as the patient gives history of thyrotoxicosis.

4 Coordination
Coordination cannot be examined on both upper and lower limbs because of weakness.

4 Reflexes

- Deep reflexes: Areflexia in both upper and lower limbs.
- Superficial reflexes: lost plantar reflex in both L.L., lost abdominal reflex (trunkal neuropathy).
N.B: lost planter reflex may be due to loss on sensation on the sole of the foot, LMNL at S1, weakness in muscles of the big toe or skeletal deformities in big toe).

4 Back: No deformity, no swelling, no scars .
4 Gait: stamping (may be high steppage).
4 other system examination (search for autonomic neuropathy):

1- Cardiovascular system:

- Absent respiratory sinus arrhythmias.
- Persistent sinus tachycardia (already examined with pulse, and ask for palpitation).
- Painless myocardial infarction.
- Postural hypotension (already examined with pulse).

2- Genitourinary:

- Bladder disturbances (incontinence à ask for it)
- Impotence (psychic and organic à ask for it)

3- Marked sweating specially with meals (gustatory sweating à ask for it )

4- Gastrointestinal:
- Gastroparesis diabeticorum (ask for dyspepsia).
- Diabetic enteropathy (ask for nocturnal watery diarrhea and constipation).

4 pathogenesis
Sorbitol pathway.

- For diabetes: Bl. Sugar level with HBA1C, ECG, RFTs, blood lipid profile (cholesterol, HDL, LDL, TG)
- For P.N: Nerve Conduction velocity.

4 Treatment
- For diabetes: tight control.
- For the P.N.: Tegretol, gabapentin, vitamins, aldose reductase inhibitor
(disappointing results).

4 Diagnosis :
Diabetic Peripheral Neuropathy

4 N.B.

Lost abdominal reflex in this case may be due to trunkal neuropathy.
Abdominal muscles power can't be examined by resistance because of proximal myopathy à the patient has history of Thyrotoxicosis.
Lost knee reflex à not related to high stock level as lost superficial sensation has nothing to do with deep reflexes but is related to lost deep sensation at the level of the knee (evidenced by lost vibration sense at the knee and may be due to amyotrophy due to femoral neuropathy).
No muscle wasting à mainly sensory.

Saturday, 24 January 2015

Peripheral Neuropathy Reappears - Personal Story

Today's post from (see link below) is a personal story of someone who has more than one neuropathic problem and it highlights the difficulty we often have, of differentiating between neurological problems and their causes. In this case, the original cause was the aftermath of surgery but just as you think you can pinpoint where the symptoms are coming from and why that has happened, other symptoms appear or reappear, showing that the nerve problems have expanded, leading to new difficulties and new medication choices. Many readers will identify with the frustrations felt here. Follow the link to see more of her story.

Peripheral Neuropathy -- Again 
Posted by Julia Oleinik Thursday, January 22, 2015 
Guys. I feel like a walking zombie lately.

I've definitely chalked some of my zoned-out spaciness to recovering from our trip; but I think that this particular fogginess has a different quality than my usual post-vacation crash. It's hard to explain but after this many years of autoimmune fatigue and brain fog, I know what THAT feels like. And this isn't it.

I also suspect that I know what's causing it all. It's complicated. Ready for a long story?

Over the past six months or so all sorts of things have happened to this old body of mine, the biggest being the symptoms from spinal stenosis and the laminectomy that followed. As I healed from the surgery and the compression was relieved on those nerves, I realized that the radiculopathy from the stenosis was masking other neurological problems.

Gee. What a treat.

Make no mistake -- I'm thrilled with the results of my laminectomy. I can walk for any length of time without that terrible radiating pain and numbness in my butt and leg and foot. But the neurological problems that I'm having now have nothing to do with those large nerves that exited my T4 and S1 vertebrae.

When the major pain and numbness went away after my surgery, it unmasked other pain that was not caused by the stenosis: peripheral neuropathy manifested by generalized burning and pain in my feet along with the bizarre sensation that the skin of my lower legs is vibrating. Buzzing. Strange. Worse at night just when I'm trying to sleep.

I have been dealing with PN for quite some time, although to a lesser degree than lately. You can read my earlier post addressing this issue written back in January of 2013 here.

The result is that I have added Neurontin (gabapentin) to my medications, and I have to say that it has indeed reduced my symptoms. But unfortunately along with the good, came my dopey sensations. I have let my doctor know about it's effects, and hopefully after continued use the side effects will decrease.

In the meantime, well....don't be expecting many posts that are coherent.

Do you take gabapentin? How has it affected you?

Friday, 23 January 2015

What Is Peripheral Neuropathy?

Today's post from (see link below) is another general article describing peripheral neuropathy, its causes and its treatments. It's very useful as a starting point for people new to the condition; or family members and friends, trying to understand what's happening to the patient. It's compiled by a hospital group in the UK and can be trusted although there just isn't room in this sort of article for 100% coverage of the disease (people love to point out the smallest details that are missing from this sort of piece). Worth a read for everybody coming into contact with neuropathy.

Painful Peripheral Neuropathy
Pain Service Website, Gloucestershire Hospitals NHS Foundation Trust
Webmaster Dr J G de Courcy, Consultant in Pain Medicine and Anaesthesia
What is it?

Peripheral neuropathy, a result of nerve damage, is a common cause of numbness and pain in the hands and feet. In some cases this can also be associated with pain which can be very distressing. People typically describe the pain of peripheral neuropathy as tingling or burning, while they may compare the loss of sensation to the feeling of wearing a thin stocking or glove. Because the nerve fibres affected include those involved in telling us where our joints are in space (proprioception) people with peripheral neuropathy often describe problems with balance and may have a tendency to fall.

One of the most common causes is diabetes. Peripheral neuropathy can also sometimes result from problems such as traumatic injuries, infections, metabolic problems such as vitamin deficiencies and exposure to toxins including some drugs: however, in non-diabetic patients it is most common that no other cause can be identified and it can best be described as an ageing process of the nerves. The longest nerve fibres are most readily affected, which is why the feet and hands are most commonly affected.

In many cases, peripheral neuropathy symptoms improve with time — especially if the condition is caused by an underlying condition that can be treated. A number of medications often are used to reduce the painful symptoms of peripheral neuropathy.

What symptoms can it cause?

The nerves of your peripheral nervous system carry information from your brain and spinal cord (central nervous system) to and from all other parts of your body. Several groups of nerves may be affected by peripheral neuropathy:
Sensory nerves that carry sensations back to your Central Nervous System such as heat, pain or touch
Motor nerves that carry impulses to make your muscles contract
Autonomic nerves that control functions such as blood pressure, heart rate, digestion and bladder function

Most commonly, peripheral neuropathy starts in the longest nerve fibres — the ones that reach to your toes. Symptoms vary, depending on which types of nerves are affected. Signs and symptoms may include:
Gradual onset of numbness and tingling in your feet or hands, which may spread upward into your legs and arms. This may be insidious in its onset so that many patients may not be aware of it.
Burning pain
Sharp, jabbing or electric shock-like pain
Extreme sensitivity to touch, even light touch (termed allodynia)
Lack of coordination and balance
Muscle weakness or paralysis if motor nerves are affected
Bowel or bladder problems if autonomic nerves are affected

Peripheral neuropathy may affect one nerve (mononeuropathy), two or more nerves in different areas (multiple mononeuropathy) or many nerves (polyneuropathy).


Apart from Diabetes, in many patients it is not possible to identify a cause for cause of peripheral neuropathy. Despite this, a number of factors that can cause neuropathies should be considered:
Alcoholism. This may relate both to the alcohol and because many alcoholics also have vitamin deficiencies.
Autoimmune diseases. These include lupus, rheumatoid arthritis and Guillain-Barre syndrome.
Diabetes. When damage occurs to several nerves, the cause frequently is diabetes. At least half of all people with diabetes develop some type of neuropathy.
Exposure to poisons. These may include some toxic substances, such as heavy metals, and certain medications — particularly those used in cancer chemotherapy.
Infections. Certain viral or bacterial infections can cause peripheral neuropathy, including Lyme disease, shingles (varicella-zoster), Epstein-Barr, hepatitis C and HIV/AIDS, and the leprosy bacillus.
Inherited disorders.
Trauma or pressure on the nerve. Traumas and injuries (including surgery) can injure peripheral nerves. Nerve pressure can result from using a cast or crutches..
Tumours. Growths can form directly on the nerves themselves, or tumours can exert pressure on surrounding nerves. Both cancerous (malignant) and noncancerous (benign) tumours can contribute to peripheral neuropathy.
Vitamin deficiencies. B vitamins — B-1, B-6 and B-12 — are particularly important to nerve health. Vitamin E and niacin also are crucial to nerve health.
Other diseases. Kidney disease, liver disease and an underactive thyroid (hypothyroidism) also can cause peripheral neuropathy.
Drugs. A number of drugs, notably some of those used in cancer chemotherapy, can cause peripheral neuropathy.


Complications of peripheral neuropathy may include:
Risk of injury. Because parts of your body may be numb, you may be less likely to feel temperature changes or pain. This can make you more susceptible to burns or skin injury.
Infection. Make sure to check your feet, as well as any other areas lacking usual sensation, regularly so that you can treat minor injuries before they become infected. This is especially important for people with diabetes, who tend to heal more slowly.

Potential treatments

One goal of treatment is to manage the condition causing your neuropathy. If the underlying cause is corrected, the neuropathy often improves on its own. Another goal of treatment is to relieve the painful symptoms.


Many types of medications can be used to relieve the pain of peripheral neuropathy, including:
Simple analgesics. Mild symptoms may be relieved by over-the-counter pain medications. We would normally be cautious about using strong opioid type pain medications because of potential side-effects, though sometimes these may be tried. Opioid drugs may have some benefit but this has to be considered against the potential adverse effects of these drugs.
Anti-epileptic medications. Drugs such as gabapentin, pregabalin and carbamazepine were originally developed to treat epilepsy. However, doctors often also prescribe them for nerve pain. Side effects may include drowsiness and dizziness.
Capsaicin. A cream containing this naturally occurring substance found in chilli peppers can cause modest improvements in peripheral neuropathy symptoms. This is further discussed at the linked page.
Lidocaine patch. More details are given on a linked page on our site.
Antidepressants. Tricyclic antidepressant medications, such as amitriptyline and nortriptyline, were originally developed to treat depression. However, they have been found to help relieve pain by interfering with chemical processes in your brain and spinal cord that cause you to feel pain. The serotonin and norepinephrine reuptake inhibitor (SNRI) duloxetine also has proved effective for peripheral neuropathy caused by diabetes. Side effects may include nausea, drowsiness, dizziness, decreased appetite and constipation.


Transcutaneous electrical nerve stimulation (TENS) may help to relieve symptoms. TES is discussed further at the linked page.

The following suggestions can help you manage peripheral neuropathy:
Take care of your feet, especially if you have diabetes. Check your feet daily for signs of blisters, cuts or calluses. Tight shoes and socks can worsen pain and tingling and may lead to sores that won't heal. Wear soft, loose cotton socks and padded shoes. You can use a semicircular hoop, which is available in medical supply stores, to keep bedcovers off hot or sensitive feet.
Exercise. Ask your doctor about an exercise routine that's right for you. Regular exercise may reduce neuropathy pain and can help control blood sugar levels.
Stop smoking. Cigarette smoking can affect circulation, increasing the risk of foot problems and possibly amputation.
Eat healthy meals. If you're at high risk of neuropathy or have a chronic medical condition, healthy eating is especially important to ensure that you get essential vitamins and minerals. Emphasize low-fat meats and dairy products and include lots of fruits, vegetables and whole grains in your diet. Drink alcohol in moderation, if at all.
Avoid prolonged pressure. Don't keep your knees crossed or lean on your elbows for long periods of time. Doing so may cause new nerve damage.


a good summary page on different aspects of peripheral neuropathy is given at the National Institute of Neurological Disorders and Stroke website.

You may also find the page on diabetic neuropathy helpful, as well as the page on the NHS Chices site on this topic.

The Foundation for Peripheral Neuropathy website.

For professionals, the American Academy of Neurologists have published guidelines on the Treeatment of Painful Diabetic Neuropathy. A detailed BMJ review of Painful Diabetic Neuropathy is a useful resource.

Thursday, 22 January 2015

How Do Anti-Convulsants Work For Neuropathy?

Today's post from (see link below) looks at a common treatment for neuropathic pain and that is anti-convulsants or anti-epilepsy drugs. Many people living with neuropathy are prescribed these drugs after anti-depressants have failed and they are generally a pre-cursor to opiates (if they don't work for you). It is wise to consult carefully with your doctor (especially with Lyrica)depending on which anti-convulsant is prescribed and what the cause of your neuropathy is, as the side effects can be significant and for certain groups these drugs haven't been proven to work at all. It is a useful article in that it explains what they are and how they work and very often patients are not given this information by their doctors because it's assumed the patient will have difficulty understanding the science behind the drug's working process.

No author or date available

What are Anticonvulsants?

Anticonvulsants are a group of drugs that were designed to help manage seizures, but have since been used in the treatment and management of neuropathic pain. It is a fairly large and diverse family of drugs, sometimes referred to as ‘anti-seizure medications’ or ‘antiepileptics’. These drugs are thought to work through a number of different mechanisms: some may block different neurotransmitters; others may affect nerve signalling and ‘firing’ through binding to different receptors; altering ion channels in the brain; or ‘stabilizing’ some of the nerve cell membranes to ‘quiet’ pain signalling. On balance, it is thought that through these various mechanisms anticonvulsants affect pain communication pathways for patients with neuropathic pain.

How do they work?

Anticonvulsants were first used in pain management because it was thought that the nature of pain was somewhat similar to that of epileptic seizures – too much nerve cell firing. A number of these drugs have been shown to block the signals from damaged neurons which would normally communicate pain within the body.

What kinds are there? 

Gabapentin (Neurontin): Gabapentin works by binding to the calcium channels in neurons. These calcium channels help communicate pain within the body and, when blocked, help to dull the signal. Gabapentin is one of the only drugs used to treat neuropathic pain that is solely metabolized through the kidney (most are metabolized through the liver). It is considered one of the ‘first line’ medication treatments for most neuropathic pain syndromes. It is often used for treating post-herpetic neuralgia and diabetic neuropathy. 

Pregabalin (Lyrica)
: Developed as a more potent follow-up to Gabapentin, Pregabalin has been prescribed for postherpetic neuralgia, diabetic peripheral neuropathy and central neuropathic pain. Pregabalin is also associated with a lower risk for dependency and potential abuse. 

Carbamazepine (Tegretol)
/ Oxcarbazepine (Trileptal): Carbamazepine works by binding to sodium channels in neurons and limiting pain signals. Used It is frequently used to treat trigeminal neuralgia, but also diabetic neuropathy and potentially other forms of neuropathic pain (though more research is necessary). 

Valproate (Sodium valproate, valproic acid)
: Valproate helps block calcium channels and increases the levels of GABA in the brain. The calcium channels help to communicate pain while GABA helps to black dull pain signals in the brain by blocking communication channels and affecting nerve transmission. More evidence is needed to determine the use of Valproate in the treatment of neuropathic pain. 

Lamotrigine (Lamictal): Lamotrigine helps to block sodium channels and helps to regulate signals between neurons. Used it is sometimes used in the treatment of trigeminal neuralgia, diabetic neuropathy and central neuropathic pain. There are increased risks of side effects in woman using Lamotrigine, which also poses certain risks for pregnancies. 

Topiramate (Topamax): Topiramate has a number of mechanisms of action including sodium channels, calcium channels, GABA receptors, AMPA receptors and carbonic anhydrases. More evidence is needed to determine the use of Topiramate in the treatment of neuropathic pain.

Levetiracetam (Keppra): Levetiracetam works by binding to calcium channels in neurons, though it’s mechanisms aren’t fully understood. It can be used in the treatment of peripheral neuropathic pain. 

Lacosamide (Vimpat): Lacosamide works by binding to sodium channels in neurons, which prevents them from firing. Lacosamide also targets the cell which have been active for a longer period of time; in other words, damaged, over-active nerve cells that are sending pain signals (versus healthy cells). Lacosamide is used in the treatment of diabetic peripheral neuropathy.

What kind of Anticonvulsant is most effective for you?

Gabapentin (0)

Pregabalin (0)

Carbamazepine (0)

Valproate (0)

Lamotrigine (0)

Lacosamide (0)

Levetiracetam (0)

Topiramate (0)

Related evidence

Hearn L, Derry S, Moore RA. Lacosamide for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev. 2012 Feb 15;2:CD009318. doi: 10.1002/14651858.CD009318.pub2.
Moore RA, Straube S, Wiffen PJ, Derry S, McQuay HJ. Pregabalin for acute and chronic pain in adults. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.: CD007076. DOI: 10.1002/14651858.CD007076.pub2
Moore R, Wiffen PJ, Derry S, Toelle T, Rice AS C. Gabapentin for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database of Systematic Reviews 2014, Issue 4. Art. No.: CD007938. DOI: 10.1002/14651858.CD007938.pub3

Price MJ. Levetiracetam in the treatment of neuropathic pain: three case studies. Clin J Pain. 2004 Jan-Feb;20(1):33-6.

Wiffen PJ, Derry S, Moore RA, Aldington D, Cole P, Rice AS, Lunn MP, Hamunen K, Haanpaa M, Kalso EA. Antiepileptic drugs for neuropathic pain and fibromyalgia - an overview of Cochrane reviews. Cochrane Database Syst Rev. 2013 Nov 11;11:CD010567. doi: 10.1002/14651858.CD010567.pub2.

Wiffen PJ, Derry S, Lunn MPT, Moore R. Topiramate for neuropathic pain and fibromyalgia in adults. Cochrane Database of Systematic Reviews 2013, Issue 8. Art. No.: CD008314. DOI: 10.1002/14651858.CD008314.pub3