Friday, 21 October 2016

Early Neuropathy Detection Can Pay Off Big Time

Today's post from (see link below) looks at the condition known as pre-diabetes, which if identified in time can be treated so that there is much less lasting nerve damage than if it was ignored. By using skin biopsies to identify nerve damage progress. the severity of the neuropathy in the long run may be limited by swift action. It's a complex subject and the truth is that still relatively few skin biopsies are carried out because the symptoms are a very good indicator of active nerve damage and to save money, diagnoses are made based on  the symptoms and lifestyle of the patient and little more. Skin biopsies however, can reveal so much more information and lead to much better treatment. This article is definitely worth a read and maybe worth a little pressure on your doctor to do the most thorough tests possible.

Nerve damage in neuropathy progresses sooner than previously thought, lending urgency to earlier detection and treatment.
By David Glenn
The Fire Within

“If we wait until these patients have large-fiber neuropathy, we’ve needlessly lost time and nerve function. This is one more reason to be aggressive about controlling patients’ glucose levels.”

William Loughran retired from his job as a bank director in northeast Maryland in 2014, when he was 68. Like many new retirees, he vowed to ramp up his exercise routine.

“I started going to the gym three or four times a week and walking every day,” he says. “I felt better than I had in years.”

But then, after a long day of walking with his son during a visit to California, it began: “I went to bed, and the soles of my feet felt like they were on fire,” Loughran recalls. “It was jabbing pain, pins-and-needles pain, and it was pretty severe.”

Within weeks, Loughran’s feet had become so painful that driving his car was a struggle. “Just the slight pressure from the pedals was too much to tolerate,” he says. For months, he spent almost all of his time at home, in bare feet.

Loughran had developed peripheral neuropathy, a condition shared by hundreds of thousands of Americans. Peripheral neuropathy often begins with damage to the unmyelinated small-fiber nerves, resulting in numbness, tingling and lightninglike shooting pains, most commonly in the feet and hands. The best-known causes of peripheral neuropathy are type 2 diabetes and chemotherapy, but there are several other potential culprits. Vitamin B12 deficiency, high cholesterol, smoking and HIV/AIDS have all been implicated. Roughly one-fifth of peripheral neuropathy cases have no clear cause at all.

After several false starts with physical therapists, podiatrists and other specialists, Loughran realized that he needed to see a neurologist. He searched online and learned that Johns Hopkins has a prominent research program in peripheral neuropathy.

In early 2016, Loughran found himself in the Johns Hopkins office of Mohammad Khoshnoodi, an assistant professor of neurology. Here at last he received a thorough workup. “Dr. Khoshnoodi did much more extensive blood work than anyone else had done,” Loughran says. “He did nerve conduction studies to see if I had damage to the large-fiber nerves, which I didn’t. And he took three skin biopsies from my leg.” The idea of having skin samples extracted sounded odd at first, Loughran says. But if that was what was required, he was game.

The technique of using skin biopsies to assess peripheral neuropathy was pioneered at Johns Hopkins in the early 1990s by Justin McArthur, who now chairs the Department of Neurology, and the late John Griffin, one of the best-known neurologists in Johns Hopkins history. A major advantage of these biopsies is that they permit objective, quantifiable measurement of nerve damage. They can be taken sequentially from the same sites over a period of months or years, allowing researchers to see exactly how a patient’s nerves and their supporting structures change over time, and how that neurological damage is affected by changes in the patient’s underlying condition (whether that be diabetes, chemotherapy exposure or something else).

Sequential skin biopsies have become an increasingly powerful tool for uncovering the mysteries of neuropathy. Last spring, Khoshnoodi and five Johns Hopkins colleagues published a much-discussed study in JAMA Neurology that offered some provocative findings. The study considered skin biopsies that were taken sequentially from 52 patients with neuropathy at Johns Hopkins between 2002 and 2010, along with biopsies from 10 healthy volunteers for purposes of comparison.

The study’s first striking finding was that patients with impaired glucose regulation—a condition often known as prediabetes—saw their neuropathies progress just as aggressively as patients with full-blown diabetes. The second finding was that nerve damage increased just as fast at sites on the patients’ upper thighs as it did on patients’ toes and feet, where they actually perceived their symptoms.

“This study reinforces the idea that early neuropathy tends to progress,” says Michael Polydefkis ’93, a professor of neurology and the paper’s senior author. “Primary care doctors should always take it seriously, even if the patient is just talking about slight numbness.”

The fact that prediabetes can cause neuropathies just as severe as full-blown diabetes is relatively well-known among neurologists and endocrinologists, Khoshnoodi says, but it isn’t sufficiently appreciated by generalist primary care doctors. The sequential skin biopsy study should be a wake-up call, he says. “If we wait until these patients have large-fiber neuropathy, we’ve needlessly lost time and nerve function,” he says. “This is one more reason to be aggressive about controlling patients’ glucose levels.”

Left unattended, Polydefkis says, peripheral neuropathy can advance to more severe kinds of neurological dysfunction, including problems with balance, blood pressure regulation and difficulties in walking. In this study, 14 of 52 patients with small-fiber neuropathy progressed to mild large-fiber neuropathy, meaning that their ankle reflexes were reduced and they were less sensitive to the vibrations of a tuning fork. Such problems are often a prelude to more severe deficits in motion and sensation.

Though Loughran arrived at Johns Hopkins too late to take part in that particular sequential skin biopsy study, the three specimens taken from his ankle confirmed that his skin had a significantly reduced density of small-fiber nerves—the classic sign of small-fiber peripheral neuropathy.

Loughran says he was grateful to have a definitive diagnosis after months of confusion and anxiety. While there are currently no treatments that readily reverse neuropathy in Loughran’s situation, peripheral neuropathy pain can be relieved with various combinations of anti-seizure medications, antidepressants and opioid pain relievers.

“We’ve seen some dramatic improvements over time in these patients’ nerves. It’s an example of a severe form of peripheral neuropathy, a fatal form, that appears to be changing before our eyes.”

None of those drugs can cure the condition or even slow its progression. What can slow neuropathy’s progression—at least for many patients—is correction of the underlying cause. If the patient’s neuropathy is caused primarily by diabetes or prediabetes, strict control of blood glucose levels through diet, exercise and medication can do the trick. If the neuropathy is caused by vitamin B12 deficiency, that is usually simple to correct. If chemotherapy is the villain, the patient and his or her oncologist may want to consider a change in treatment.

“Skin biopsies can tell us exactly how much neuropathy you have, but they don’t tell us anything about the cause,” says Ahmet Hoke, a professor of neurology and another of the study’s authors. “The blood work becomes key. The blood work helps us establish the etiology.”

In Loughran’s case, the blood work strongly suggested prediabetes. He is acting accordingly. “I’ve cut out sodas,” he says, “and I’m trying to get back to exercising.”

For many patients, that last step is easier said than done. “We tell them to exercise,” Polydefkis says, “but exercise can be intolerable because of the burning pain and electric shocks in their feet. That’s why it’s so important to find the right combination of medications to get the neuropathy symptoms under control. Those medicines won’t cure the neuropathy, but they’ll allow patients to be more active, which in turn helps with glucose control when diabetes is a factor.” Swimming and other nonweight-bearing exercises are often the best options, Polydefkis adds.

Hoke notes that the sequential skin biopsy study also shed light on the still-unsettled question of why exactly diabetes and prediabetes tend to damage the nerves. Some theories have emphasized the fact that the longest sensory neurons, which extend all the way from the spine to the toes, have huge metabolic needs because of their extreme surface-to-volume ratios. The metabolic dysfunctions associated with diabetes, according to this theory, make it difficult for the long neurons to balance their energy requirements, and they eventually stop working properly. Other scientists have emphasized a simpler, more mechanical model. Diabetes, they say, slowly damages the blood vessels that supply nerves with oxygen and nutrients. Diabetic neuropathy, in this view, is mostly a problem of the vasculature.

For Mark E. Rubenstein, It’s Personal

Much of the recent Johns Hopkins research on peripheral neuropathy, including this year’s high-profile study of sequential skin biopsies, has been financially supported by Mark E. Rubenstein, a trustee emeritus of The Johns Hopkins University and Johns Hopkins Medicine.

This sort of gift is nothing new for Rubenstein. For decades, he has supported several lines of medical research at Johns Hopkins. This one, however, is more personal for him than others, as he himself has contended with one of the most severe types of diabetic neuropathy.

Rubenstein, who retired in 2004 as chief executive of the Rubenstein Company, a major commercial real estate firm, was diagnosed with type 2 diabetes more than 40 years ago. He has long experience with the common symptoms of diabetic neuropathy, including numbness, tingling and shooting pains in the feet. In 2011, those symptoms suddenly blossomed into something much more severe. “Over a period of two weeks, I lost 15 pounds,” he says, “and the muscles in my left leg started to waste away.”

Those were the hallmarks of diabetic amyotrophy, which is sometimes known as Bruns-Garland syndrome. The condition often recedes on its own but sometimes leads to full-blown paralysis in the affected limb. Rubenstein went to see Michael Polydefkis at Johns Hopkins, who prescribed new medications to manage the pain and, more importantly, referred Rubenstein to expert physical therapists for an exercise program that allowed him to rebuild the lost muscle in his leg.

“He’s a fantastic doctor,” Rubenstein says. “He has great empathy for patients. He really got me through this.”

Polydefkis, for his part, is grateful for the research support Rubenstein has provided in the last few years. “For an ambitious program like ours,” he says, “it makes an enormous difference to have this kind of open-ended support.”

The Johns Hopkins studies tend to support the metabolic theory, Hoke and Polydefkis say (though both add that vascular problems probably contribute). “What’s so interesting,” Hoke says, “is that we see damage that is just as bad in prediabetes as in diabetes. That suggests that it isn’t the overall amount of glucose that is causing the neuropathy, but instead that it’s rapid fluctuations in glucose levels. There’s something about those fluctuations that the nerve cells can’t tolerate.”

What about patients who have been diagnosed with diabetes or prediabetes but don’t have any symptoms of neuropathy? “If I were in that situation, I would be vigilant,” Polydefkis says. “There’s reason to believe that nerve damage is already occurring in such patients. I would be very careful about trying to keep my glucose levels stable.”

Howell Todd’s story began much like Loughran’s. He retired as a university president in 2001, moving to a 55-acre farm in rural Tennessee. He looked forward to spending his days reading and raising crops. Not long after retirement, however, he began to notice odd tingling in his feet when he exercised on his elliptical trainer.

“At first, it was just uncomfortable,” he says. “Then, it began to progress. It got to the point where I would wake up at 2:30 in the morning with my feet flaming.”

In 2012, he flew to Johns Hopkins for a workup. Like Loughran, Todd had skin biopsies that clearly indicated peripheral neuropathy. Unlike Loughran, however, Todd turned out to have no identifiable underlying cause—no diabetes or prediabetes, no hyperlipidemia, no B12 deficiency. His is one of the roughly 20 percent of peripheral neuropathy cases that are classified as idiopathic.

These are the cases that Polydefkis finds most frustrating. All he can do as a neurologist is suggest medications to keep the symptoms in check. (He recommended that Todd start a daily regimen of pregabalin and tramadol, a combination that Todd says has served him well for four years.)

Todd says that he is glad he made the trek to Johns Hopkins, even if there is no miracle cure at hand. “Dr. Polydefkis had an excellent bedside manner,” he says. “He and everyone there took the time to talk with me. I’ll be 73 this fall, and I’m still able to do maintenance work on the farm, as long as I watch my limits. I don’t think I could have done that without the medications he suggested.”

While there are currently no treatments that readily reverse peripheral neuropathy, Johns Hopkins researchers are looking at a number of potential molecular targets for medications and are also actively involved in planning clinical trials.

Hoke has been studying medications that might offer protection to cancer patients’ nerve cells before they begin chemotherapy. In 2014, he and his colleagues screened thousands of compounds from a Johns Hopkins drug library. They discovered that ethoxyquin—an antioxidant that is sometimes used as a pet food additive—seems to protect nerves exposed to paclitaxel and cisplatin, two of the most notoriously neurotoxic chemotherapeutic drugs. In recent months, Hoke and Polydefkis have also tested ethoxyquin in animal models of diabetic neuropathy, with promising results. To bring these studies closer to human clinical trials, the team recently received one of the inaugural grants from the Louis B. Thalheimer Fund for Translational Research, a new Johns Hopkins effort to accelerate the development of university discoveries.

“Skin biopsies can tell us exactly how much neuropathy you have, but they don’t tell us anything about the cause. The blood work becomes key.”

Polydefkis is also involved in an international clinical trial of a new medication that may be effective against a rare and devastating inherited neuropathic disorder. The condition, known as transthyretin familial amyloid polyneuropathy, affects roughly 10,000 people worldwide, usually striking in middle age.

“The transthyretin protein normally has a four-leaf clover structure,” Polydefkis says. “But in people who inherit this condition, it has a malformed structure and clumps within the nerves. When those deposits build up, peripheral nerves start to malfunction, and the patient experiences peripheral neuropathy. The disease eventually involves sensory, motor and autonomic nerves, and it is fatal.”

The ongoing clinical trial is assessing a medication known as patisiran, which inhibits the liver’s production of the malformed proteins. Polydefkis and his colleagues have a specific role: to examine skin biopsies sent every few months from trial participants around the world. “We’ve been getting biopsies from Brazil, from Norway, from all sorts of places,” Polydefkis says. “We’ve seen some dramatic improvements over time in these patients’ nerves. It’s an example of a severe form of peripheral neuropathy, a fatal form, that appears to be changing before our eyes.”

Loughran, meanwhile, has signed up for a study that will closely monitor patients’ neuropathic status, glucose control, blood pressure and a wide variety of other variables, with an eye toward developing a deeper understanding of how these factors affect each other.

“My symptoms are gradually improving,” he says. “I’ve finally gotten to the point where I can at least do some exercise. It was initially both feet—front, back, everywhere. Now it’s regressed to just the bottom of the feet. And now that I’ve heard about this possible prediabetes, I’m going to get back to the gym.”

Thursday, 20 October 2016

How Good Is Methadone For Neuropathic Pain?

Today's post from (see link below) takes a look at methadone as an alternative to other opioids for controlling neuropathic pain. Methadone has had an extremely bad rap over the years, mainly because of its association with withdrawal from drug addiction programmes. However, it is an extremely cheap and effective drug for nerve pain and because only low doses are needed, the risks of side effects and addiction are much less than for instance morphine or oxycodone. That said, it is a powerful drug and once you begin, you need to be very careful when and if you want to taper off. Never go cold turkey with methadone - it will react almost instantly. Many doctors are reluctant to issue methadone prescriptions but that's often based on lack of experience rather than factual dangers. If a patient discovers over time that nothing else works, then methadone can be very effective in controlling nerve pain. Remember, all drugs for neuropathy have side effects, so don't be put off by what you may have heard - it all boils down to careful monitoring by your doctor. Discuss it with him or her if you find that almost nothing works for you in reducing the pain of neuropathy.

David E Weissman MD

Background Prescriptions for methadone have greatly increased in the past decade (1). The reason for this increase is likely related to two factors: reduced cost relative to other potent opioids and basic science data suggesting that methadone may be particularly useful in treating neuropathic pain. Two previous Fast Facts (#75, 86) reviewed methadone’s pharmacological properties. This Fast Fact examines the research base regarding methadone and neuropathic pain and reviews the rise in methadone-related deaths.

Historical Context

Prior to 1985, when long-acting morphine preparations were introduced, methadone was commonly prescribed for cancer-related pain as it had a longer duration of action than morphine. However, it was well appreciated that methadone had a higher risk of respiratory depression due to drug accumulation with chronic dosing – an effect not associated with other opioids, for which there is no drug accumulation in the setting of normal renal function.

Prior to 1990 there was a widespread belief that opioids were relatively ineffective in treating neuropathic pain. Since then, there been a much greater understanding that opioids are an effective part of neuropathic pain treatment.

Basic science data Methadone inhibits reuptake of norepinephrine and serotonin in a similar manner to newer anti-depressants, some of which are effective against neuropathic pain (e.g. duloxetine, venlafaxine). Also, methadone binds to the NMDA receptor, a known modulator of neuropathic pain. Finally, methadone has demonstrated efficacy in animal models of neuropathic pain (2).

Patient data Small non-controlled case series and two small randomized study (methadone vs. placebo) have demonstrated that methadone can reduce neuropathic pain in both cancer and non-cancer patients (3-6). There is no data, for or against the proposition, that methadone is superior to other opioids for neuropathic pain. A 2007 Cochrane Collaborative review found, “there is no trial evidence to support the proposal that methadone has a particular role in neuropathic pain of malignant origin” (7). Furthermore, the review cautioned clinicians about the danger of methadone-induced respiratory depression due to its long terminal half-life.

Methadone deaths There is a growing awareness that the increased prescription of methadone is being paralleled by a similar increase in methadone-related deaths. Methadone has been implicated in 30% to 40% of opioid related deaths in the US, even though methadone remains a small minority of opioids prescribed (8). The US Department of Health and Human Services convened an expert panel in 2003 to investigate the rise in methadone deaths and concluded that the rise was largely due to the increasing use of methadone as an analgesic (9). The Center for Disease Control published a report detailing data from Utah in 2005, suggesting that part of the problem was due to increased prescribing (10). The current data seem to suggest that the general increased supply of methadone, via legitimate prescribing, is leading to deaths due to accidental overdose through improper prescribing or illicit diversion/recreational use. In addition to concern about respiratory depression, there has been an observation that methadone, unlike morphine or hydromorphone, can prolong the QTc interval and lead to serious cardiac conduction abnormalities especially when coadministered with antiretrovirals in HIV patients (11). Note: the overall number of opioid-related deaths has increased, not just from methadone. Note: there are no data on untimely deaths related to methadone prescribing in hospice/palliative care patients.

The renewed interest in an old drug holds exciting promise of benefit for the many patients with neuropathic pain. However, clinical research has yet to confirm or deny a unique clinical role for methadone compared to other opioids. The risk of respiratory depression should give clinicians pause before prescribing methadone based solely on the theory that it is a superior opioid in neuropathic pain. Coadministration of methadone with antiretrovirals may pose a particular risk for cardiac arrhythmias and therefore should be avoided if at all possible., Given that diversion of legitimate opioid prescriptions to the illicit market can occur, even in the practice of hospice and palliative care, physicians and hospice agencies need to recognize they also have a larger social responsibility to the public welfare, and prescribe methadone with care and caution.


Warner M, Chen LH, et al. Drug poisoning deaths in the United States, 1980–2008. NCHS Data Brief. 2011; 1-8.

Foley KM. Opioids and chronic neuropathic pain. NEJM 2003; 348:1279-1281.

Morley JS, et al. Low-dose methadone has an analgesic effect in neuropathic pain: a double-blind randomized controlled crossover trial. Pall Med. 2003; 17:576-587.

Altier N, et al. Management of chronic neuropathic pain with methadone: a review of 13 cases. Clin J Pain. 2005; 21:364-369.

Gagnon B, et al. Methadone in the treatment of neuropathic pain. Pain Res Manage. 2003; 8:149-154.

Moulin DE, et al. Methadone in the management of intractable neuropathic non cancer pain. Can J Neuro Sci. 2005; 32:340-343.

Nicholson, AB. Methadone for cancer pain. Cochrane Database Syst Rev 2007; 4.4.

Centers for Disease Control and Prevention (CDC). Vital signs: risk for overdose from methadone used for pain relief – United States, 1999-2010, Morb Mortal Wkly Rep 2012; 61:493-497.

Increase in poisoning deaths caused by non-illicit drugs--Utah, 1991-2003. MMWR Weekly. 2005; 54:33-36.

US Department of Health and Human Services – Division on Pharmacologic Therapies. Report on Methadone Mortality ( - no longer publicly available). Updated Report available at:

Kao D, Bartelson BB, et al. Trends in reporting methadone-associated cardiac arrhythmia, 1997-2011. Ann of Int Med 2013;158: 735-740.

Version History: This Fast Fact was originally edited by David E Weissman MD and published in December 2006. Version copy-edited in April 2009: web-links updated. Revised again in July 2015 by Sean Marks MD: references and epidemiological data updated.

Fast Facts and Concepts are edited by Sean Marks MD (Medical College of Wisconsin) and associate editor Drew A Rosielle MD (University of Minnesota Medical School), with the generous support of a volunteer peer-review editorial board, and are made available online by the Palliative Care Network of Wisconsin (PCNOW); the authors of each individual Fast Fact are solely responsible for that Fast Fact’s content. The full set of Fast Facts are available at Palliative Care Network of Wisconsin with contact information, and how to reference Fast Facts.

Copyright: All Fast Facts and Concepts are published under a Creative Commons Attribution-NonCommercial 4.0 International Copyright ( Fast Facts can only be copied and distributed for non-commercial, educational purposes. If you adapt or distribute a Fast Fact, let us know!

Disclaimer: Fast Facts and Concepts provide educational information for health care professionals. This information is not medical advice. Fast Facts are not continually updated, and new safety information may emerge after a Fast Fact is published. Health care providers should always exercise their own independent clinical judgment and consult other relevant and up-to-date experts and resources. Some Fast Facts cite the use of a product in a dosage, for an indication, or in a manner other than that recommended in the product labeling. Accordingly, the official prescribing information should be consulted before any such product is used.

Wednesday, 19 October 2016

Vitamin B Overdosing A Potentially Serious Problem For Neuropathy Patients

Today's post from (see link below) reinforces the message that you should be careful with how much and how many Vitamin B variants you swallow in an attempt to reduce neuropathy symptoms. The common theme you'll find all over the internet is that nerve damage is often caused by a vitamin B deficiency and although people are warned to get their vitamin B levels tested first to see if this is true; many head straight for the supplement store and pile in extra B12 and Vitamin B compounds without really checking if they're doing the right thing or not. It's a common-held misconception that all vitamin supplements are good for you and while this may be partially true if your lifestyle leads to vitamin deficiencies, you can definitely overdose on many vitamins, causing unnecessary and sometimes serious problems as a result. This article should serve as a warning but in this case, only regarding B9 (folate/folic acid). However, the message applies to all vitamin supplements - check first if you actually need them before supplementing and then stick to the maximum daily intake (at the most).

High folate intake linked with nerve-damage risk in older adults with common gene variant
Date:October 12, 2016 Source:Tufts University

Consuming too much folate (vitamin B9) is associated with increased risk for a nerve-damage disorder in older adults who have a common genetic variant. Although variable by race or ethnic background, an estimated one in six people in the U.S. carry two copies of a genetic variation in TCN2, a gene that codes for a vitamin B12 transport protein. For some of these individuals, the TCN2 variation (referred to as GG) can lead to conditions related to vitamin B12 deficiency even if they consume normal amounts of B12. In an epidemiological study involving 171 adults aged 60 and older, a team led by scientists from the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts (USDA HNRCA) found that individuals with the GG variant of TCN2 were three times more likely to have peripheral neuropathy -- nerve damage commonly associated with vitamin B12 deficiency -- when compared to individuals without the variant.

Among study subjects who consumed more than twice the Recommended Dietary Allowance (RDA) of 800 micrograms per day of folate, individuals with the GG variant had seven-fold higher odds for peripheral neuropathy compared to those without. The team found no significant difference in odds among individuals who consumed less than 800 micrograms of folate a day.

The findings were published in the American Journal of Clinical Nutrition on Oct. 12.

"Due to the prevalence of the TCN2 variant, and because the average daily folate intake for U.S. adults over 50 is already more than twice the RDA, we believe that our findings highlight a potential concern for a large proportion of older Americans," said senior study author Ligi Paul, Ph.D., scientist in the Vitamin Metabolism Laboratory at the USDA HNRCA. "Our data suggest that older adults should keep folate intake close to the recommended amounts, and try to get nutrients from a balanced diet rather than depending on supplements."

Older individuals are at particular risk for vitamin B12 deficiency due to decreased stomach acid production and use of certain medications, which interfere with the absorption of the vitamin from food. Long-term B12 deficiency can cause a range of symptoms, including anemia and peripheral neuropathy -- damage to the peripheral nervous system marked by lack of coordination, weakness, or pain, tingling, and numbness in the hands and feet.

Consumption of folate -- the term for both naturally occurring food folate and folic acid, the synthetic form of folate found in fortified foods and supplements -- is known to alleviate anemia associated with B12 deficiency. However, previous studies have found evidence that excess folate intake could potentially worsen associated neurological deficits, including peripheral neuropathy, in older adults. The new findings now reinforce these observations and suggest that older adults should pay particular attention to their folate intake, especially from supplements or fortified foods.

"Folate is a necessary vitamin and no one should think that it needs to be avoided. But in certain situations, very high intake of folate may be harmful," said lead author Hathairat Sawaengsri, Ph.D., who conducted the study while a doctoral student in the biochemical and molecular nutrition program at the Friedman School of Nutrition Science and Policy at Tufts University and a member of the Vitamin Metabolism Laboratory at the USDA HNRCA. "Vitamins and minerals should be consumed at an optimal level -- not too high and not too low."

The authors caution that the design of the study does not allow for the determination of a cause and effect relationship -- high folate intake is associated with increased risk of peripheral neuropathy, but is not identified as a direct cause. The prevalence of the TCN2 variant differs depending on ethnic background, but the team did not find that it affected the observed association between TCN2 polymorphism and peripheral neuropathy in this study. In addition, increasing sample sizes could improve the accuracy of their findings. The odds ratios for peripheral neuropathy were calculated based on 31 individuals with the GG variant out of 171 individuals in the total study population.

The results, however, add to growing evidence that both low and high folate intake can be associated with negative health outcomes. In previous work, Paul and her colleagues found that excess folic acid consumption is associated with shortening of protective structures (telomeres) on human chromosomes and can reduce the ability of the immune system to destroy cells infected by viruses in aged mice.

Insufficient folate intake by pregnant women can cause birth defects such as spina bifida and neural tube defects, and the Food and Nutrition Board of the National Academies of Sciences, Engineering, and Medicine recommends that all women of childbearing age should get the RDA (400 micrograms) of folate, or 600 micrograms if they are pregnant.

According to the National Institute of Health's Office of Dietary Supplements, approximately 35 percent of people in the U.S. consume folic acid in dietary supplements. Some population groups, particularly adults aged 50 and older, are at risk of consuming excess folate. The federal government's Dietary Guidelines for Americans advises that nutrients are best obtained from natural food sources.

Story Source:

Materials provided by Tufts University. Note: Content may be edited for style and length.

Journal Reference:
H. Sawaengsri, P. R. Bergethon, W. Q. Qiu, T. M. Scott, P. F. Jacques, J. Selhub, L. Paul. Transcobalamin 776C->G polymorphism is associated with peripheral neuropathy in elderly individuals with high folate intake. American Journal of Clinical Nutrition, 2016; DOI: 10.3945/ajcn.116.139030

Tuesday, 18 October 2016

Neuropathy Patients Hate Exercise But They Mustn't Avoid It

Today's short post from (see link below) is a response from a doctor to a question most of us with neuropathy hope the answer to, will be a resounding "No". Unfortunately, the answer is yes to the question as to whether exercise helps with neuropathy. So we need to be prepared to put our bodies through yet more pain and discomfort for their benefit in the long run. The key is, making exercise something that is so obviously valuable that we can't ignore it and making it as pleasurable as possible. You can groan all you want (I do too) but the fact is that neuropathy weakens our muscles and joints to such an extent that it makes the pain considerably worse, never mind the fact that we can't do simple tasks any more. Read the article and think about your best strategy but don't overdo it and listen to your body when it tells you that you're doing just that.

Departments: Ask the Experts
You Ask. We Answer:

Is exercise helpful for peripheral neuropathy?
Ensrud, Erik MD
Neurology Now: October/November 2016 - Volume 12 - Issue 5 - p 31 doi: 10.1097/01.NNN.0000503487.82934.2d
Q Is exercise helpful for PERIPHERAL NEUROPATHY?


Yes, as long as you aren't overdoing it. The same benefits that anyone gets from exercise—improved cardiovascular function, increased mobility, a boost in mood—are realized by people with peripheral neuropathy, regardless of its cause. People with neuropathy may also experience an improvement in function and quality of life, as well as a decrease in pain.


Peripheral neuropathy is a general term for a group of diseases that affects motor and sensory nerves outside the brain and spinal cord. There are different types of neuropathy, and each has different causes and effects. Focal neuropathy, for instance, usually affects just one nerve or group of nerves. A common example is carpal tunnel syndrome, which involves nerve damage in the wrist. Any exercise that involves repetitive motion directly on the joint, such as playing tennis or texting or typing for hours on end, could aggravate the condition. Proximal neuropathy can reduce muscle strength in the legs and hips, so patients with this type of neuropathy might try riding a recumbent bike to avoid putting too much force on a compromised leg or hip joint.


When people think of exercise, they often think of the intense workout regimens of Olympic athletes like Michael Phelps and Katie Ledecky. But for most people, intense exercise is counterproductive. For people with neuropathy in particular, overstressed muscles may not recover as well because of existing nerve problems. A good rule of thumb during exercise is the talk test: If you can maintain a conversation without becoming breathless while exercising, you are likely at the right exertion level.


If physical activity feels like a chore or is inconvenient, you'll eventually stop doing it. Decide what you like to do—swimming, biking, walking, dancing, yoga, tai chi—and how you like to do it—with friends, at home, in nature, as part of a class—and you're more likely to stick with it. The goal is to create a positive association with exercise so you do it more often. Consider an activity tracker, which logs your steps every day; seeing the steps add up can be very motivating for some people.


Before beginning any exercise program, talk to your doctor. You want to be sure you don't have any conditions that may affect the type of exercise you can do or how long you can safely do it. Once you get the all-clear, start out with five to 20 minutes of exercise three times a week. As your fitness improves, gradually add minutes, distance, or intensity. A good way to start is by walking around a large indoor shopping mall or store. The surface is level, the temperature is comfortable, you can use a shopping cart for stability, and it's free—unless, of course, you buy things.

Dr. Ensrud is director of neuromuscular disease rehabilitation at St. Luke's Rehabilitation Institute in Spokane, WA. He is also a member of the American Academy of Neurology.

© 2016 American Academy of Neurology

Monday, 17 October 2016

Physiotherapy For Neuropathy? Worth A Shot

Today's post from (see link below) promotes the use of physiotherapy as part of your neuropathy treatment. It's important at this point to distinguish between physical therapy and chiropractic therapy because in general, chiropractors can have little effect in improving your neuropathy symptoms. Physiotherapy will also do nothing to make your neuropathy better but what it can do, is address the weakness and loss of muscle strength, plus eventual joint problems, that arise due to the effects of nerve damage. In that sense it can make your neuropathy experience more comfortable by improving your physical ability to carry out tasks that have been compromised by nerve damage. Most neuropathy patients will have noticed a marked decrease in muscular function: partly because the pain of neuropathy discourages exercise but also because decrease in muscle density has a direct link to damage of the nerves that stimulate it. Another advantage of physiotherapy is that most insurance covers across the world will at least cover enough sessions to find out whether physio is something for you. Maybe worth consideration: talk it over with your doctor.

Did You Know? Physiotherapy can help with Peripheral Neuropathy!
October 5, 2016 by Christine Campbell, Physiotherapist

Physiotherapists play a vital role in helping individuals improve and maintain functions that may be limited by Peripheral Neuropathy (PN). PN has a variety of causes, types and symptoms and therefore it is essential for each treatment plan to be tailored to help address each patient address their specific needs and goals. Physiotherapy may be helpful in maintaining strength, mobility, and function regardless of the underlying cause of PN.

Research has shown that strengthening exercises for peripheral neuropathy moderately improve muscle strength in people with PN. In addition, exercises to help peripheral neuropathy, when done regularly, may reduce neuropathic pain and can help control blood sugar levels.

The goals and treatment options associated with Peripheral Neuropathy are as follows: 

Decrease pain and numbness
There are many different treatment options to help manage the patient’s symptoms, such as hands-on soft tissue work, stretching, and nerve glides. Nerve gliding/flossing are effective exercises to help ‘unstick’ the affected nerves. This type of treatment helps manage mononeuropathies (peripheral neuropathy where only one nerve is affected) 

Improving overall function by maintaining or improving range of motion
This can be achieved through hands-on soft tissue work, passive range of motion or home exercises/stretching
A physiotherapist can also recommend moderate-intensity exercises that are best suited for the patient, which will help improve their physical function 

Maintain or improve strength
A specific series of exercises would be taught given a patient’s current strength, endurance and tolerance 

Prevention of falls
Balance training and coordination exercises will be prescribed, as well as discussing strategies for home to help prevent a future fall
Physiotherapists can also recommend braces and/or splints to enhance balance and posture 

Your physiotherapist may educate the patient on how to safely manage PN. The education will vary based on individual needs, and may focus on improving safety, preventing further complications, and finding alternative ways to perform certain tasks.

Sunday, 16 October 2016

Watch Out For Commercial Neuropathy Sites: They May Not Be All They Seem

Today's post from (see link below) promotes a new website claiming to be a valuable resource for people suffering from neuropathy. It is created by a 'group of neuropathy professionals' but it is not clear who they are and after a very generalised opening article that seems promising to neuropathy sufferers, it actually turns out to be a commercial site promoting their own supplement products. Now let me say here that the information on this site regarding neuropathy may be perfectly accurate and informative but I take issue with companies that first give the impression that they are independent distributors of information about a disease that afflicts millions and having sucked you in, then go on to blatantly sell their own products with claims that they will help. They may help....who knows but this is just the latest in a long line of subtle and subliminal marketing tricks to get you to part with your money and sorry...long suffering neuropathy patients deserve better than that. If you want to promote your product, fine but don't hide behind a sort of façade that suggests something completely different. In the end it always boils down to 'let the buyer beware' but be aware that advertising is very sophisticated these days.

Neuropathy Professionals Launch Nerve Pain and Neuropathy Relief Website
October 14 02:50 2016

A group of neuropathy professionals has announced the launching of a new website,, that will bring together recommendations for trustworthy products and informative articles that will help those afflicted with chronic nerve pain regain their normal lives through neuropathy relief.

New York, NY – A group of neuropathy professionals has announced the launching of a new website,, that will bring together recommendations for trustworthy products and informative articles that will help those afflicted with chronic nerve pain regain their normal lives through neuropathy relief. Having the right information about a problem like nerve pain is the first step towards seeking the proper treatment. The new website hopes to both inform those suffering from constant discomfort due to nerve pain of the causes and symptoms of the problem, as well as pointing them towards leading options for pain relief.

Kelly Ableman, a spokesperson for the new website, has this to say, “This website hopes to assist people in discovering the truth that lies behind nerve pain and neuropathy. Comprehending the nature underlying the problem is a great first step in finding pain relief methods that work well. Neuropathy is both debilitating and common. Yet many of those who suffer from nerve pain are poorly informed about their condition and their treatment options. We hope to meet a strong need for an informational resource of this nature.” will have everything regarding nerve pain. It will give insights and education that will help those afflicted learn more regarding current conditions, what creates nerve pain, what one can do to manage it, and the ways it affects those suffering and their loved ones. This is irrespective of the pain coming from diabetes, fibromyalgia, or any other range of maladies. This searing, burning, and shocking form of pain could leave people feeling miserable and helpless; which is unacceptable in the eyes of the website’s founders.

Unfortunately, most general physicians have little training where treating nerve pain is concerned. As a last ditch resort, they often prescribe anti-inflammatory medication. These are not effective against nerve pain, prolonging unhappiness, and discomfort for patients. On the website, differing treatment options available include natural methods, medications, supplements, and nutritional support. The website and its social media associates, Facebook and Twitter, aspire to provide diverse reviews and information about solutions and treatments.

The articles and reviews presented here will give patients and caretakers solutions, not only about diverse painkilling medications, but also about various side effects that might come with certain prescriptions. One example is a situation where someone suffering chronic pain could begin to rely too much on painkillers, leading to an addiction. Information available also features vitamins and supplements indicating what role these play to those with nerve damage. Also, there will be insights into various therapies that overcome the discomfort.

The newly launched website,, is a valuable resource to those who are suffering from chronic pain relating to the nerves. This type of pain can be debilitating and is often not easily treated. The new website is based on all things related to neuropathy relief, including information about various forms and causes of nerve pain and natural remedies and therapies.



Kelly Ableman


Saturday, 15 October 2016

Is It Wise To Dismiss Opioids For Chronic Pain?

Today's post from (see link below) is directed at people living with HIV and chronic pain conditions such as neuropathy (around 40% of HIV patients also suffer from nerve damage) but also applies to the general population if they have a chronic pain condition - irrespective of the cause. That said, the article comes over as a little confused; as if the author isn't sure on which side of the fence she sits regarding opioid prescription and use. The underlying message that opioid prescription should be a last resort for chronic pain is indisputable but the idea that the cause of the pain should first be dealt with, is simply inapplicable to people with most chronic pain conditions for which there is no cure and certainly for HIV patients, cancer patients and the like. She also suggests that evidence of opioid effectiveness is limited, when there are countless studies that show that opioids are an extremely effective way of suppressing pain...if handled properly, with sufficient after-care. She also rolls out the addiction problem: "evidence of their risks is mounting, with an estimated 10% of patients on such medications becoming addicted"! Surely this advances the efficacy of opioids because by definition, 90% of patients do not become addicted!! Whether this article will change your opinion on opioids is for you to decide but when it comes to chronic pain conditions, the idea that they can be treated just with behaviour change, is way too simplistic. Experienced neuropathy patients will know all too well the hoops they have to jump through in order to get their pain under control and are well aware of the gamut of other dangerous medications they have to try before reaching the opioid stage. Fear of opioids may lead to much more unnecessary suffering than is needed.

Opioids Are Not a First-Line Treatment for Chronic Pain, Pain Specialist Says
By Barbara Jungwirth From October 6, 2016

When someone living with HIV complains about chronic pain, take their word for it, but try non-opioid therapies and treat underlying psychiatric illnesses before prescribing oxycodone, Jessica S. Merlin, M.D., M.B.A., advised health care providers in a recent webinar. People living with HIV are more likely to suffer from such pain (30%-85% report chronic pain) than the general population (15% report that issue). This may be partly due to greater sensitivity to pain in those with detectable viral loads, Merlin explained.

Providers must understand the impact that this condition has on a patient's daily life, screen for mood disorders and note the patient's coping strategies before suggesting a therapy approach, Merlin advised in the Chronic Pain in HIV Infection: A Practical, Evidence-Based Approach webinar sponsored by the International Antiviral Society-USA on August 18, 2016. An effective technique Merlin has used in her chronic pain clinic is motivational interviewing, which is designed to stimulate people's own motivation for change, rather than simply telling them that they should change their behavior. She counseled providers to educate patients about ways to control pain without resorting to prescription medications, including mind-body techniques and short-term, over-the-counter drugs, such as acetaminophen. The latter, however, has problematic side effects when taken long-term, especially in combination with antiretrovirals, Merlin cautioned. Other approaches include physical therapy and exercise, as well as topical medications.

Providers should develop a team either within their office or within the community; it should include mental health professionals, methadone programs and social workers, among others. Such a team approach allows for better screening and treatment of depression, PTSD and other conditions that may co-occur with chronic pain. These problems need to be addressed first to remove the underlying cause of the pain, rather than treating only the symptoms.

Opioids should not be considered first-line therapy for chronic pain, Merlin emphasized. Evidence of their benefit is limited, and no studies have evaluated their use for longer than one year. By contrast, evidence of their risks is mounting, with an estimated 10% of patients on such medications becoming addicted, as well as a risk of overdose, especially when co-prescribed with benzodiazepines. Providers should take universal precautions when prescribing opioids, rather than deciding who is or is not at risk of opioid use disorder. These precautions include having the patient sign an opioid treatment agreement, with provisions for using only one prescriber and one pharmacy and submitting to frequent urine drug testing. However, urine tests can result in false positives, especially when someone takes multiple medications, as is the case with those living with HIV, Merlin noted. A confirmatory assay, as well as a conversation with the patient, are therefore necessary before jumping to conclusions.

If all non-opioid attempts at managing the chronic pain have failed and oxycodone or a similar drug is prescribed, the lowest effective dose should be used. Patients should be re-assessed at least every three months, other therapies should be optimized, and the opioid dosage prescribed should be tapered off over time with the goal of eventually discontinuing it altogether. Merlin also advocated co-prescribing naloxone for high-risk patients, if they can bring in someone who lives with them and can administer the antidote in case of opioid overdose. However, local laws differ as to whether this approach is permitted. Laws on marijuana use also differ among states, but where legal the substance may be useful in treating chronic pain. Evidence shows that people who are prescribed medical marijuana use opioids less, reducing the risks associated with opioids.

Barbara Jungwirth is a freelance writer and translator based in New York.

Follow Barbara on Twitter: @reliabletran.

Friday, 14 October 2016

How Much Of A Threat Is Zika To Your Nervous System?

Today's post from (see link below) is a response to some questions received here on the blog regarding the possible links between the Zika virus and neuropathic conditions. Just how dangerous is Zika for patients already living with neuropathy or potential patients in the future? This article tells you all you need to know but it seems very likely that this virus is one that likely infects neural stem cells, thus potentially leading to various forms of neuropathy. One thing is sure; ignoring a virus like this is in nobody's interest.

Neurological Manifestations of Zika Virus Infection: What Neurologists Need to Know
Posted on February 17, 2016 • By Avindra Nath, MD, and James Sejvar, MD

In recent years, there has been an emergence of several major viral infections with devastating neurological consequences, including West Nile virus, dengue, chikungunya, enterovirus D68, Ebola and now Zika virus. Increased global travel and climate change, leading to changing patterns of vector distribution and behavior are among the major reasons for the emergence of these infections. Zika virus is the most recent epidemic that is having devastating effects on human populations in affected regions, and is rapidly spreading across the South American continent.


Zika virus was first identified from a primate in 1947 in the Zika forest of Uganda.1 The first human cases occurred in Africa and then in Southeast Asia in the 1960s.2,3 During the intervening years, Zika virus was associated with isolated cases or small outbreaks mainly in Africa. In 2007, there was an outbreak in Yap, the Federated States of Micronesia, where nearly three-quarters of the population was infected.4, 5 This represented the largest outbreak of Zika virus infection to that point. In 2013, there was an epidemic in French Polynesia, which was associated with a reported increase in cases of the autoimmune peripheral nerve disorder Guillain-Barre syndrome, although a causal association between Zika virus and Guillain-Barre syndrome was never established.

In December 2014, Zika virus was first detected in Brazil. Although it is unknown how it was introduced into Brazil, some hypothesize that a traveler attending the 2014 football/soccer World Cup introduced the virus. The outbreak in Brazil was fast moving and large. Tens of thousands of people became ill, and likely millions of people were infected. Similar to French Polynesia, shortly after the beginning of the Zika virus outbreak, clinicians began reporting larger-than-expected numbers of Guillain-Barre syndrome. Many of these people had reported a febrile rash illness compatible with Zika in the days or weeks before their weakness onset. In addition, clinicians in Brazil noted a 20-fold increase in microcephaly in 2015, compared to previous years, with microcephalic babies born approximately eight to nine months after the first recognition of Zika virus. Some of the infants’ mothers reported a rash illness compatible with Zika virus infection while pregnant, leading to the suspicion that the microcephaly was somehow associated with Zika virus infection.

Nearly 90 percent of the cases of microcephaly occurred in the northeastern region of the country,6, 7 areas experiencing some of the heaviest burdens of Zika virus infection as well. French Polynesian health authorities reported an unusual increase in central nervous system malformations in babies born during a Zika virus outbreak on the islands from 2014 to 2015.6 The infection has now spread across most of South America and Mexico. To date, few cases have been reported in the United States among travelers returning from Zika virus-affected regions.8, 9

Virology and Pathophysiology

Zika virus is a positive-sense, single-stranded RNA virus (genome 10.7 K nucleotides) belonging to the flaviviridae family, which includes dengue, yellow fever, Japanese encephalitis, St. Louis encephalitis and West Nile virus. It has the ability to cross the placenta and cause developmental brain abnormalities in children, suggesting that the virus likely infects neural stem cells. The severity of brain malformations may be related to the stage of fetal development at the time of infection. Microcephaly would be the most common manifestation, but if infection were to occur in earlier stages of fetal development, anencephaly or lissencephaly may occur.

The pathophysiology of ascending paralysis and myelitis in adults is unknown. However, mice injected with the virus can develop paralysis, suggesting direct invasion by the virus, although an immune-mediated, post-viral syndrome is also possible. It remains unknown if once infected and recovered if an individual develops long-term immunity or not, and if recurrent infections or relapses can occur. Questions regarding long-term viral persistence in tissue reservoirs also remain unanswered.


The virus is transmitted by the Aedes species of mosquitoes 10, in particular Aedes aegypti, the vector involved with transmission of dengue, a closely related flavivirus. Additionally, experimental evidence suggests the virus can be transmitted by Asian tiger mosquitoes (Aedes albopictus) 11, 12, which can survive in cold temperatures. Most arboviruses have an intermediary host or “reservoir.” For West Nile virus, birds, particularly corvids, serve as these reservoirs. For Venezuelan, Western and Eastern equine encephalitis viruses, horses serve this role, and for Japanese encephalitis virus, it is primarily pigs. However, the transmission of Zika virus generally occurs directly between humans and mosquitos. There is some evidence that human-to-human transmission may occur through sexual intercourse, and the virus has also been detected in saliva, so the potential for oral transmission also exists. The virus has been isolated from the amniotic fluid of pregnant women and blood and tissues of newborns, suggesting materno-fetal transmission.13 So far, an intermediary host has not been identified.

Clinical Manifestations

The majority of Zika virus infections ­­­— 80 percent — are clinically asymptomatic.4 Among persons who develop symptoms, Zika virus infection is generally considered to be mild, causing fever, rash and body aches. Some may develop conjunctivitis. Symptoms usually last one week.

The full spectrum of neurological complications from this viral infection remains unknown. The epidemiological association between microcephaly and the infection seems strong. In Brazil, annual reported rates of microcephaly would generally be somewhere around 150 cases per year. Reportedly, between October 2015 and January 2016, more than 3,500 babies were born with the condition. CT brain scans show evidence of widespread calcification. Other malformations, such as anencephaly and lissencephaly, might also occur. It remains uncertain if other organs may be involved in addition to the brain. However, the differential diagnosis of microcephaly is broad. Hence, when presented with a patient with microcephaly, it remains important to consider other common causes, such as genetic, craniostenosis, and infections, such as toxoplasmosis, rubella, varicella zoster virus and cytomegalovirus. Intrauterine cerebral anoxia, exposure to drugs, alcohol and other toxins, malnutrition and metabolic disorders such as phenylketonuria can also cause microcephaly. Patients with microcephaly often have developmental delay, difficulty with gait and balance, mental retardation, seizures and hyperactivity.

Guillain-Barre syndrome appears to be a recurring possible complication of Zika virus infection. Following the introduction of Zika virus into French Polynesia, clinicians began reporting larger-than-expected numbers of Guillain-Barre syndrome cases on the island.14 Following the introduction of Zika virus to Brazil in December 2014, again, reports surfaced of large numbers of Guillain-Barre syndrome cases. In Brazil, few cases of Guillain-Barre syndrome had laboratory confirmation of Zika virus, but currently the primary method of diagnostic testing is through the detection of viral RNA through polymerase chain reaction. In Guillain-Barre syndrome, by the time the clinical features of limb weakness develop, it is unlikely that there would still be circulating virus, and, as such, detection of viral RNA would not be expected. Less commonly, some patients have been thought to have a myelitis or polio-like manifestations. Currently, it is unclear if these are all related or if indeed both spinal cord and peripheral nerves can be involved. Thus, in Brazil, epidemiologic evidence and the close temporo-spatial clustering of both Guillain-Barre syndrome and Zika virus cases provides intriguing circumstantial evidence for an association.

In other cases in which the virus was newly introduced, reported increases of Guillain-Barre syndrome cases have invariably appeared, including in Colombia, Venezuela and, more recently, El Salvador, which reported 46 Guillain-Barre syndrome cases in a five-week period from December 2015 to early January 2016. That is nearly three times more than the country would normally see in that timeframe. Laboratory substantiation of an association between Zika virus and Guillain-Barre syndrome has proved challenging, however. As noted, by the time of onset of weakness, the virus would be expected to be cleared from the body, and molecular techniques to identify the virus or viral RNA would not be expected to be positive. Detection of Zika virus-specific antibodies would provide evidence of current or prior infection. However, that method also has its challenges. Dengue virus is a closely related flavivirus to Zika, and invariably co-circulates in all areas currently associated with Zika virus. However, dengue virus infection has also rarely been associated with Guillain-Barre syndrome, and laboratory testing by serology is challenging due to the substantial cross-reactivity of antibodies between Zika virus and dengue virus.

Since these viruses are carried by the same mosquito vector and co-circulate at the same times of the year, it can be challenging to differentiate between infection with the two viruses.15 Development of a robust serologic assay that can reliably differentiate Zika virus from dengue and other closely related flaviviruses will be crucial in order to provide laboratory evidence of Zika-associated Guillain-Barre syndrome, as well as other late complications of Zika virus. Currently, the nature of the neuropathy is not known, as results of electrodiagnostics to determine the clinical sub-type of Guillain-Barre syndrome possibly associated with Zika virus has been rarely reported. It would be important to know if it is axonal or demyelinating and if it is immune mediated. This could affect treatment and prognosis. Recovery from demyelinating neuropathies is generally better than those due to axonal injury. Isolated reports suggest that the neuropathy may be demyelinating and may respond to treatment with intravenous immunoglobulin.14
Laboratory Diagnosis

Viremia occurs only during the first few days of the illness, but if blood samples are obtained during that time, virus can be detected by polymerase chain reaction.16 Following this phase, IgM antibodies can be demonstrated by ELISA or Western blot analysis. Previous epidemics have noted that there is cross reactivity between antibodies to Zika and other arboviruses such as dengue.5 The Centers for Disease Control and Prevention (CDC) has issued guidelines for the testing of infants born with possible Zika virus infection.17

Treatment and Prevention

Currently, there is no effective treatment or vaccine against the virus. Hence, prevention is key with control of mosquito populations and prevention of mosquito bites. Travel advisories have been issued for pregnant women not to travel to areas experiencing Zika virus outbreaks. For individuals who suffer from the neurological consequences of the infection, long-term supportive and symptomatic treatment is key. The socio-economic impact of the infection, particularly if the association between Zika virus and microcephaly holds true, will likely be huge and felt for decades. While the large number of cases of microcephaly is tragic, whatever the eventual cause turns out to be, it will result in large numbers of children with developmental disorders and begs for the need to train personnel in a wide variety of health disciplines, including neurology, rehabilitation, specialized nursing, social services, etc., to care for and treat this population. Ongoing surveillance for Zika virus in the Americas and elsewhere, to monitor its continued spread, as well as documentation of infection among travelers returning from affected areas will be critical. Development of more robust serologic assays that can differentiate Zika virus from other closely related flaviviruses will be an important tool to substantiate an association between Zika virus and devastating neurologic conditions, such as Guillain-Barre syndrome and microcephaly. Ultimately, the long-term epidemiologic pattern of Zika virus will be important to monitor.

Weinbren, M.P. and M.C. Williams, Zika virus: further isolations in the Zika area, and some studies on the strains isolated. Trans R Soc Trop Med Hyg, 1958. 52(3): p. 263-8.
Simpson, D.I., Zika Virus Infection in Man. Trans R Soc Trop Med Hyg, 1964. 58: p. 335-8.
Olson, J.G., et al., Zika virus, a cause of fever in Central Java, Indonesia. Trans R Soc Trop Med Hyg, 1981. 75(3): p. 389-93.
Duffy, M.R., et al., Zika virus outbreak on Yap Island, Federated States of Micronesia. N Engl J Med, 2009. 360(24): p. 2536-43.
Lanciotti, R.S., et al., Genetic and serologic properties of Zika virus associated with an epidemic, Yap State, Micronesia, 2007. Emerg Infect Dis, 2008. 14(8): p. 1232-9.
Control, E.C.f.D.P.a., Rapid risk assessment: Zika virus epidemic in the Americas: potential association with microcephaly and Guillian Barre syndrome. 10 December 2015.
Bogoch, II, et al., Anticipating the international spread of Zika virus from Brazil. Lancet, 2016.
Control, C.f.D., CDC telebriefing: Zika virus travel alert. 15 January 2016.
Hennessey, M., M. Fischer, and J.E. Staples, Zika Virus Spreads to New Areas – Region of the Americas, May 2015-January 2016. MMWR Morb Mortal Wkly Rep, 2016. 65(3): p. 55-8.
Li, M.I., et al., Oral susceptibility of Singapore Aedes (Stegomyia) aegypti (Linnaeus) to Zika virus. PLoS Negl Trop Dis, 2012. 6(8): p. e1792.
Grard, G., et al., Zika virus in Gabon (Central Africa)–2007: a new threat from Aedes albopictus? PLoS Negl Trop Dis, 2014. 8(2): p. e2681.
Wong, P.S., et al., Aedes (Stegomyia) albopictus (Skuse): a potential vector of Zika virus in Singapore. PLoS Negl Trop Dis, 2013. 7(8): p. e2348.
Pan American Health Organization and World Health Organization. Epidemiological Alert: Neurological syndrome, congenital malformations, and Zika virus infection. Implications for public health in the Americas., 1 December, 2015.
Oehler, E., et al., Zika virus infection complicated by Guillain-Barre syndrome–case report, French Polynesia, December 2013. Euro Surveill, 2014. 19(9).
Carod-Artal, F.J., et al., Neurological complications of dengue virus infection. Lancet Neurol, 2013. 12(9): p. 906-19.
Faye, O., et al., One-step RT-PCR for detection of Zika virus. J Clin Virol, 2008. 43(1): p. 96-101.
Staples, J.E., et al., Interim Guidelines for the Evaluation and Testing of Infants with Possible Congenital Zika Virus Infection – United States, 2016. MMWR Morb Mortal Wkly Rep, 2016. 65(3): p. 63-7.

Avindra Nath, MD, is intramural clinical director and a senior investigator with the Section of Infections of the Nervous System, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland. James Sejvar, MD is a neuroepidemiologist with the division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia. The authors have no financial relationships relevant to this article to disclose. The findings and conclusions in this article are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention or National Institutes of Health.

Thursday, 13 October 2016

When Neuropathy Hurts And You Need Some Help:- Who Ya Gonna Call?

Today's post from (see link below) is a response to the many readers who ask if I know of a good support group for neuropathy sufferers. It's a difficult question to answer because this blog does not advertise except when it concerns information which is applicable to all and is from a reliable source. is one such resource (no connections whatever) and of course there are more. Their information is widespread, covers most diseases, most medications and just as important for us - most supplements. They are impartial and objective and have no outside concerns pushing them in one direction or another (namely pharmaceutical companies). They also have excellent support systems in the form of support groups for various diseases, including neuropathy. Today's post is a 'snapshot' of their support group page on a day in October 2016 - just to give you an idea of how it works and what's available.

Peripheral Neuropathy Support Group 2016

Related terms: Neuropathy

Questions (529)
News (13)
Members (524)


Our support group for Peripheral Neuropathy has 529 questions and 524 members. Updated 4 Oct 2016.

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Wednesday, 12 October 2016

How To Navigate The Neuropathy Supplement Minefield

Today's post from (see link below) is basically a warning to all neuropathy patients that they need to be really careful which supplements they take to reduce their symptoms, especially, if you're taking drugs for other conditions. The potential for contra-indication (one drug clashing with another) is very real and can often make your condition much worse, especially if you take things over a period of time. Dr Hayes advises consulting a neuropathy specialist (and offers his own organisation as an example). However, specialists in neuropathy in all its forms and all its causes are as rare as hens' teeth: even neurologists have trouble with supplementation for neuropathy. We're therefore easily led by advertisements or word of mouth. It's vital to remember that with neuropathy, what works for one doesn't work for all and this includes standard drug treatments for neuropathy itself. Do your research; consult your doctor(s) and don't try anything until you're reasonably sure that the advice comes from reliable sources. Even then, if you don't notice a difference after a couple of months, stop and look elsewhere. Far too many patients build up a lifetime of supplements to dangerous levels, purely because they 'may' be working but they're not sure! It's a minefield but you're sensible people, so just make the most informed choices possible.

Neuropathy Treatments, Pills, and Potions! 
Posted by john on September 5, 2016

“Just start taking my magic formula and your neuropathy can be GONE!”
Good neuropathy treatment is usually not as simple as taking or rubbing on just one thing.

If only neuropathy treatment was that simple. Or easy.

Now that is not to say that supplements and lotions can’t have a role in good neuropathy treatment. The fact is they often do.

But good neuropathy treatment is usually not as simple as taking or rubbing on just one thing.

Many neuropathy patients don’t know that some supplements should not be taken with drugs. For example, CoQ-10 can be trouble, and should not be taken if you are on Coumadin.

Acetyl-L-Carnitine can interfere with thyroid function, and its use needs to be professionally monitored. This is especially true if you take thyroid medications.

And the list goes on. It seems like some new neuropathy formula is being offered every day! Neuropathy patients need to be very careful.

So what is the he best thing a neuropathy treatment patient should do? Find a neuropathy treatment professional to work with. Find out all you can about them. Are they up on the latest techniques? Are they aware of drugs that may interact with their therapy?

Help treat your neuropathy by providing all your lab and medical records. If your neuropathy is associated with any food or skin allergies, we need to know that too.

Let us know about your family history. Have you had recent surgery, or anesthesia, which can make neuropathy symptoms worse?

Have you tried any neuropathy treatments and what have the results been? What seems to make your neuropathy feel better, and especially does anything you do seem to make it worse?

This is all part of having a neuropathy treatment plan. If you have any questions about what good neuropathy treatment is, ask your trained neuropathy treatment professional.

But just make sure they have actually studied in and are trained in the neuropathy treatment specialty!

For more information on coping with neuropathy, get your Free E-Book and subscription to the Weekly Ezine “Beating Neuropathy” at

Tuesday, 11 October 2016

Neuropathy As Part Of Life With HIV

Today's post from (see link below) is directed at people living with HIV and neuropathy but is applicable to all neuropathy patients who are taking medications concurrently for other conditions (and that's a great many!) It's one person's experience of life with these problems and I'm sure will strike a cord with neuropathy patients who are also living with cancer, diabetes and many other diseases.  It illustrates how important it is to look at a patient holistically (doctors please take note) because the symptoms of neuropathy can be made significantly worse by the symptoms of other problems and of course, vice versa.

Struggling With Nerve Damage, Neuropathy and Bone Damage From Older HIV Meds
By WM From September 8, 2016

Part of the Series Other Sides of HIV: People Taking HIV Meds Share Stories About Side Effects

A lot of us have minimal side effects from our meds but others have many. For myself, over time nerve damage, neuropathy and bone degradation have been the main culprits I have had to deal with and still struggle with. And then there is the social factor of explaining to your dear friends why you just can't make the event or function you want to attend because you're exhausted for some of these reasons, or just plain fatigued from your bodies' catching up with your systems' chemical recovery of the meds on a daily basis.

This month my physician would like to see me change the Atripla (efavirenz/tenofovir/FTC) I am taking to a new medication that will supposedly be easier on my bodies' physiological outlook on my lifetime medication maintenance -- until that miracle cure!

My current condition is HIV positive since Oct. 1983 and 56 years old. I have somewhat stable and damaged nerves and bones at present, my c5 and c6 vertebras are starting to crush; I use MJ to help me sleep. I sleep about five hours a day on average and have much fatigue.

If you had been doing meds this long, and it had pretty much destroyed the nerve function in your feet and ankles and had an impact on your arthritis progression, why would or should you welcome more side effects of another color?

Granted, it might be better in some respects, hopefully. But living on disability as many of you reading this are; happily married to a wonderful man in my life; and working on exercise, daily nutrition and pain management for my deteriorating bone function, I'm doing the best possibly I can!

Fatigue is my worst enemy and then my spine and back issues due to crushing bone loss. I haven't been to the gym on a normal basis in two years, and this also has had a serious impact on my friends, my spouse's family's outlook toward me and on my own social outlook on friends I no longer have or who choose to ignore me. But, I continue to push hard with my daily routine of taking care of our home while my husband is at work and his second job in the summertime. We are stable financially, but we are both approaching retirement in the next five to six years, and this concerns me even though our financial planner assures us that with our investments we should be OK.

The HIV med industry has ruined my physiological system beyond repair, even though I am still able to walk, and with alternative methods of pain management, I'm still kicking. It really is like a slow cancer eating away at your life. And people wonder why I am not happy every day with my husband and beautiful life and our home in Southern California; much of the public still just doesn't get it! I'm not asking for pity but a little respect for what's in my future, which will probably be a wheel chair.

I would love to hear how others are managing the new Odefsey (emtricitabine/rilpivirine/tenofovir alafenamide). If in fact it is easier on bones and kidneys, could this be a better regimen for me? You can write to me here.

Monday, 10 October 2016

Symptoms And Causes Of Neuropathy

Today's post from (see link below) is a no frills, simple neuropathy 123 description of the disease, its symptoms and its causes. You can use it to educate yourself, or friends, family and co-workers and to build up enough basic knowledge to at least have a sensible discussion with your doctor or neurologist. It's amazing how much more respect you get from doctors if you've done a little homework and it enables them to get down to the nitty gritty of treatment without spending too much time on explanation.

Peripheral neuropathy Symptoms and causes
By Mayo Clinic Staff 2016


Every nerve in your peripheral system has a specific function, so symptoms depend on the type of nerves affected. Nerves are classified into:

Sensory nerves that receive sensation, such as temperature, pain, vibration or touch, from the skin
Motor nerves that control muscle movement
Autonomic nerves that control functions such as blood pressure, heart rate, digestion and bladder

Signs and symptoms of peripheral neuropathy might include:

Gradual onset of numbness, prickling or tingling in your feet or hands, which can spread upward into your legs and arms
Sharp, jabbing, throbbing, freezing or burning pain
Extreme sensitivity to touch
Lack of coordination and falling
Muscle weakness or paralysis if motor nerves are affected

If autonomic nerves are affected, signs and symptoms might include: 

Heat intolerance and altered sweating
Bowel, bladder or digestive problems
Changes in blood pressure, causing dizziness or lightheadedness

Peripheral neuropathy can affect one nerve (mononeuropathy), two or more nerves in different areas (multiple mononeuropathy) or many nerves (polyneuropathy). Carpal tunnel syndrome is an example of mononeuropathy. Most people with peripheral neuropathy have polyneuropathy.
When to see a doctor

Seek medical care right away if you notice unusual tingling, weakness or pain in your hands or feet. Early diagnosis and treatment offer the best chance for controlling your symptoms and preventing further damage to your peripheral nerves.


Not a single disease, peripheral neuropathy is nerve damage caused by a number of conditions. Causes of neuropathies include: 

Alcoholism. Poor dietary choices made by people with alcoholism can lead to vitamin deficiencies. 

Autoimmune diseases. These include Sjogren's syndrome, lupus, rheumatoid arthritis, Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy and necrotizing vasculitis. 

Diabetes. More than half the people with diabetes develop some type of neuropathy.

Exposure to poisons. Toxic substances include heavy metals or chemicals.
Medications. Certain medications, especially those used to treat cancer (chemotherapy), can cause peripheral neuropathy.

Infections. These include certain viral or bacterial infections, including Lyme disease, shingles, Epstein-Barr virus, hepatitis C, leprosy, diphtheria and HIV.
Inherited disorders. Disorders such as Charcot-Marie-Tooth disease are hereditary types of neuropathy.

Trauma or pressure on the nerve. Traumas, such as from motor vehicle accidents, falls or sports injuries, can sever or damage peripheral nerves. Nerve pressure can result from having a cast or using crutches or repeating a motion such as typing many times.

Tumors. Growths, cancerous (malignant) and noncancerous (benign), can develop on the nerves or press nerves. Also, polyneuropathy can arise as a result of some cancers related to the body's immune response. These are a form of paraneoplastic syndrome.

Vitamin deficiencies. B vitamins — including B-1, B-6 and B-12 — vitamin E and niacin are crucial to nerve health.

Bone marrow disorders. These include abnormal protein in the blood (monoclonal gammopathies), a form of bone cancer (osteosclerotic myeloma), lymphoma and amyloidosis.

Other diseases. These include kidney disease, liver disease, connective tissue disorders and an underactive thyroid (hypothyroidism).

In a number of cases, no cause can be identified (idiopathic).

Risk factors
Peripheral neuropathy risk factors include:
Diabetes mellitus, especially if your sugar levels are poorly controlled
Alcohol abuse
Vitamin deficiencies, particularly B vitamins
Infections, such as Lyme disease, shingles, Epstein-Barr virus, hepatitis C and HIV
Autoimmune diseases, such as rheumatoid arthritis and lupus, in which your immune system attacks your own tissues
Kidney, liver or thyroid disorders
Exposure to toxins
Repetitive motion, such as those performed for certain jobs
Family history of neuropathy

Complications of peripheral neuropathy can include: 

Burns and skin trauma. You might not feel temperature changes or pain on parts of your body that are numb.
Infection. Your feet and other areas lacking sensation can become injured without your knowing. Check these areas regularly and treat minor injuries before they become infected, especially if you have diabetes mellitus.
Falls. Weakness and loss of sensation may be associated with lack of balance and falling.