Neuropathy Patients Hate Exercise But They Mustnt Avoid It

Today's short post from journals.lww.com (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?

ERIK ENSRUD, MD, RESPONDS:

Answer: 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.

PICK AN APPROPRIATE EXERCISE

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.

STAY WITHIN YOUR LIMITS

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.

MAKE EXERCISE ENJOYABLE

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.

START SLOWLY AND BUILD

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

http://journals.lww.com/neurologynow/Pages/articleviewer.aspx?year=2016&issue=12050&article=00019&type=Fulltext

Can Shiatsu Help Neuropathy Patients Sleep

Today's post from news-medical.net (see link below) looks at a very small study into the effects of shiatsu massage techniques, linked with the brain's cognitive processes, to enable pain sufferers to sleep better. The conclusion is that the results are promising enough to deserve further study. Now the article is aimed at people with chronic muscular-skeletal pain and not nerve pain but the disturbed sleep problem is the same end product and the answers probably lie in the brain's relaxation processes - so any therapy that achieves the right result can be seen as valid. Many neuropathy patients have sleep problems due to pain and the other neuropathic symptoms and it may be worth looking further into alternative therapies which aim to block pain signals in the brain. Acupressure, acupuncture, massage, hypnotherapy may all help to ease the problem and don't need medication to back them up. When the problem is affecting your quality of life, it may be worth exploring other possibilities but we all need to realize that what works for one will not necessarily work for someone else.


Researchers explore shiatsu to help people with chronic pain fall asleep
Published on June 18, 2014

There was a time, back in Nancy Cheyne's youth, when she combined the poise and grace of a ballerina with the daring and grit of a barrel racer. When she wasn't pursuing either of those pastimes, she bred sheepdogs, often spending hours on her feet grooming her furry friends at dog shows.

All that seems like a lifetime ago. After 15 years of living with chronic lower-back pain, Cheyne, 64, can't walk from the disabled parking stall to the elevator at work without stopping for a rest. She eats mostly junk food because it hurts too much to stand over the stove and spends most of her spare time in a recliner with a heating pad.

Despite pain patches and opiates, Cheyne often lies awake at night in the same recliner-sleeping in a bed is like torture-after waking every couple of hours in excruciating pain.

"Pain affects everything I do," says Cheyne. "The chronic ongoing lower-back pain, it's all the time."

Researchers at the University of Alberta are exploring the traditional Japanese massage practice called shiatsu as a potential treatment to help Cheyne and others like her find slumber-and stay asleep. A small pilot study followed nine people living with chronic pain as they self-administered shiatsu pressure techniques on their hands at bedtime.

"We know that sleep involves both physiology and learning. You don't just flip a switch and go to sleep," says Cary Brown, an associate professor of occupational therapy in the Faculty of Rehabilitation Medicine. "What we saw with this pilot is that it appears self-shiatsu may help your body to prepare for sleep and help you stay asleep for longer periods."

For the study, occupational therapy and physical therapy students were taught the basic shiatsu techniques and in turn trained participants, who reported falling asleep faster-sometimes even while administering treatment-and slept longer after two weeks and eight weeks of treatment, compared with a baseline measurement.

Cheyne spent about 10 to 15 minutes every night performing the treatments and found that instead of waking up every 45 or 60 minutes, she could stay asleep for 1.5 to two hours. Given she hasn't felt well rested in more than a decade, every minute counts and she still keeps up her treatments months after the pilot concluded.

"Usually within a few minutes of doing the pressure treatments, I'm gone-asleep," she says. "Sometimes I can't even finish, I just go out."

Results promising, but more study required

Brown cautions it's impossible to draw strong conclusions about the pilot given the small sample size, self-reported nature of the data and limitations in gender; however, she believes the results are promising enough to warrant further study.

Brown also notes there's a difference between people with pain passively going to a therapist versus taking control of their sleep problem in the form of self-administering hand shiatsu, which requires more mental effort-a theory of cognitive attention that she would like to explore further. Hand shiatsu, when self-administered, takes some concentration because our minds cannot focus on two demands at one time, she says, making it less likely that negative thoughts would interfere with sleep.

"One of the barriers to falling asleep for people who have pain is they worry about what's going to happen and while you're laying there you're thinking about all these negative things, it occupies your attention," Brown says. "This relates to research on attention in cognitive theory."

The pilot was an attempt to explore low-cost, unintimidating alternatives to drugs to help people with chronic pain fall asleep, noting medication is seldom recommended for long-term use. Brown collaborated on the project with shiatsu therapist Leisa Bellmore of the Artists' Health Centre at Toronto Western Hospital and U of A colleague Geoff Bostick.

For patients suffering from chronic pain due to low-back and other musculoskeletal injuries, the only thing that matters is finding results that work, Brown says. Not only does sleep deprivation lower a person's pain threshold, it also affects their health, from increased risk of obesity, diabetes, cardiovascular disease and traffic accidents.

More research is needed in foundational areas to break the cycle, she adds.

"If you have insomnia, you face a higher risk of experiencing chronic pain. If you have chronic pain, you're not going to get as much sleep."
 
Source:University of Alberta

http://www.news-medical.net/news/20140618/Researchers-explore-shiatsu-to-help-people-with-chronic-pain-fall-asleep.aspx

Can Marijuana Be Moved To The Less Restricted List For Chronic Pain Patients

Today's post from webmd.com (see link below) takes the discussion about medical marijuana a little further and looks at the dilemmas doctors face when confronted by patients' valid questions regarding their pain treatment and the laws that cloud the picture and make them uncertain as to whether they're doing the right thing. It's a call for considerably more research to be done at official drug-enforcement levels and asks for a further loosening of restrictions to enable an unbiased and science-based evaluation of the benefits of marijuana for various conditions. It's a valid point because we already allow several drugs which have the potential to be far more addictive (oxycodon, morphine and many others) to help patients with chronic pain but it seems that marijuana has so many pre-judged labels attached that law enforcers just can't see beyond the decades-old criminality issues. Worth a read.

What DEA Pot Rule Change May Mean for Research WebMD News from HealthDay
By Dennis Thompson HealthDay Reporter TUESDAY, May 10, 2016
 
Agency could move marijuana to a less strictly regulated class of drugs

 (HealthDay News) -- Most doctors approach medical marijuana with a great deal of uncertainty, because drug laws have hindered researchers' ability to figure out what pot can and can't do for sick patients.

That could soon change.

The U.S. Drug Enforcement Administration (DEA) is weighing whether to loosen its classification of marijuana, which would remove many restrictions on its use in medical research.

If that occurs, doctors could start getting answers to the questions they regularly receive from patients regarding marijuana's clinical benefits.

"I am asked as a practicing doctor even in a rural area about medical marijuana use, and I want to make sure I can give patients advice that's evidence-based," said Dr. Robert Wergin, board chair of the American Academy of Family Physicians. "We need those kinds of studies to help us give informed advice to our patients who ask about it now," he explained.

The DEA has said it will decide this summer whether marijuana should be lowered from a Schedule I drug to a Schedule II drug, according to an April memo from the agency to Congress.

Schedule I drugs are considered drugs "with no currently accepted medical use and a high potential for abuse," the DEA says on its website. Heroin, LSD and ecstasy stand alongside marijuana on the DEA's Schedule I list.

On the other hand, Schedule II drugs have a high potential for abuse, but "there is the recognition that they have some medical value as well," said Dr. J. Michael Bostwick, a professor of psychiatry at the Mayo Clinic, in Rochester, Minn.

"This could be an important softening of regulations that make it difficult to do marijuana or cannabis research in this country," Bostwick said.

Morphine, methamphetamine, cocaine and oxycodone are all Schedule II drugs, "because they have medical applications," Bostwick said. "So, it's not as if we don't have precedent for substances that are dangerous from an addictive point of view being useful in certain medical situations."

Studies have shown that marijuana might help decrease chronic pain and nausea, ease seizures, improve the appetite or be useful in psychiatric treatment, Wergin and Bostwick said.

But none of those studies has been large-scale and a definitive clinical trial. The reason: because marijuana's DEA drug status prevents scientists from using large quantities of the plant in medical research, Wergin and Bostwick said.

All marijuana available for research purposes in the United States is grown at the University of Mississippi, which has an exclusive contract with the U.S. National Institute on Drug Abuse (NIDA) to provide the nation's entire research supply, according to the DEA's memo to lawmakers.

In any given year, NIDA sends shipments of marijuana to a small handful of researchers, usually eight or nine, but sometimes as many as 12, the memo states. Researchers must go through a detailed registration process to gain access to the pot.

The American Medical Association (AMA) has come out in favor of loosening drug laws to "develop a special schedule for marijuana to facilitate study of its potential medical utility in prescription drug products," according to a statement its officials provided ABC News.

"While studies related to a limited number of medical conditions have shown promise for new cannabinoid-based prescription products, the scope of rigorous research needs to be expanded to a broader range of medical conditions for such products," the AMA added.

Back in December 2014, the American Academy of Neurology lamented the lack of solid marijuana research in a position paper.

Due to strict drug laws, researchers have not been able to determine whether medical marijuana could help treat neurological disorders such as epilepsy, multiple sclerosis and Parkinson's disease, the academy said.

The academy's paper concluded with a call to deschedule marijuana and open it up to more research.

Expanded research wouldn't necessarily lead to more people smoking pot for medical purposes, Wergin and Bostwick said.

Instead, it's more likely that researchers would focus on how the components of marijuana, such as THC or cannabidiol, interact with the body in ways that might help ease symptoms or illness.

An entire system of receptors has been discovered throughout the body that responds to different components of cannabis, Bostwick said.

"Almost any system you name in the body has a potential cannabinoid receptor that could be manipulated in a way that could be useful," he said. "When the drug was outlawed in 1970, we knew almost nothing about it. In the intervening 45 years, science has shown this endocannabinoid system actually exists. None of that was known when the drug was made illegal."

Such research could result in medications derived from marijuana that would treat conditions without a "high," Wergin said.

Wergin sees two main potential benefits from the descheduling of marijuana and any resulting boom in research.

First, he'd know what to tell patients about pot's particular benefits. And second, he'd feel confident issuing a prescription for a marijuana-based medication, knowing that it's a drug regulated by the U.S. Food and Drug Administration.

"This would result in higher-quality standardized product that's FDA-approved," Wergin said. "If I prescribe you an antibiotic, I'm very confident of what's in it because of the FDA regulations on it. I don't know how to prescribe marijuana to you, or what's even in it."

Paul Armentano, deputy director of the marijuana legalization group NORML, said that at this point a reclassification by the DEA would fall "well short of the sort of federal reform necessary to reflect America's emerging reefer reality."

Armentano added that even with descheduling, federal law still would require researchers to buy pot from NIDA's University of Mississippi marijuana cultivation program.

"Simply rescheduling cannabis from I to II does not necessarily change these regulations, at least in the short-term," Armentano said.

View Article Sources

http://www.webmd.com/mental-health/addiction/news/20160510/what-a-change-in-deas-pot-rules-might-mean-for-medical-research

Why Nerve Cells Die Important To Neuropathy Patients

Today's post from neurosciencenews.com (see link below) provides further information on the subject of an earlier post here on the blog (Sat. 25th April - scroll down to find), concerning the death of nerve cells and how learning about this can lead to new neuropathy treatments in the future. Finding out why nerve cells and axons either die or degenerate is vital to finding out ways to stop that process from happening. This article both fills in the gaps of the earlier article and explains the science in a much easier understood way. It teaches neuropathy patients what goes on in our nervous system and why that can cause such extreme symptoms but more importantly, gives us hope that serious research is being done to improve the situation. Worth a read.

Major Pathway Identified in Nerve Cell Death Offers Hope for Therapies
Neuroscience News April 23, 2015

New research highlights how nerves – whether harmed by disease or traumatic injury – start to die, a discovery that unveils novel targets for developing drugs to slow or halt peripheral neuropathies and devastating neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS).

Peripheral neuropathy damages nerves in the body’s extremities and can cause unrelenting pain, stinging, burning, itching and sensitivity to touch. The condition is commonly associated with diabetes or develops as a side effect of chemotherapy.

The research, by scientists at Washington University School of Medicine in St. Louis, is reported online April 23 in the journal Science.

Nerve cells talk to each other by transmitting signals along communication cables called axons. Such signals underlie vital activities, such as thinking and memory, movement and language.

As part of the study, the researchers showed they could prevent axons from dying, a finding that suggests therapies could be developed to counteract the withering away of nerve axons.

“We have uncovered new details that let us piece together a major pathway involved in axon degeneration,” said senior author Jeffrey Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics. “This is an important step forward and helps to identify new therapeutic targets. That we were able to block axon degeneration in the lab also gives us hope that drugs could be developed to treat patients suffering from a variety of neurological conditions.”

A common thread among many neurological disorders and traumatic nerve injuries is the degeneration of axons, which interrupts nerve signaling and prevents nerves from communicating with one another. Axon degeneration is thought to be an initiating event in many of these disorders. In fact, an unhealthy axon is known to trigger its own death, and researchers are keenly interested in understanding how this happens.

Working in cell cultures, fruit flies and mice, Milbrandt and co-author Aaron DiAntonio, MD, PhD, the Alan A. and Edith L. Wolff Professor of Developmental Biology, and their colleagues showed that a protein already known to be involved in axon degeneration, acts like a switch to trigger axon degeneration after an injury.


Axon degeneration (top), caused by nerve injury or disease, depletes the energy supply within axons, shutting down communication between nerve cells. Washington University scientists blocked axon degeneration by supplementing neurons with a chemical called nicotinamide riboside, which kept the axons energized and healthy (bottom). The image is for illustrative purposes only. Image credit: Milbrandt lab.

Moreover, they found that this protein, once unleashed, causes a rapid decline in the energy supply within axons. Within minutes after the protein – called SARM1 – is activated in neurons, a massive loss of nicotinamide adenine dinucleotide (NAD), a chemical central to a cell’s energy production, occurs within the axon.

“When a nerve is diseased or injured, SARM1 becomes more active, initiating a series of events that quickly causes an energetic catastrophe within the axon, and the axon undergoes self-destruction,” said first author Josiah Gerdts, an MD/PhD student in Milbrandt’s laboratory.

Working in neurons in which SARM1 was activated, the researchers showed they could completely block axon degeneration and neuron cell death by supplementing the cells with a precursor to NAD, a chemical called nicotinamide riboside. The neurons were able to use nicotinamide riboside to keep the axons energized and healthy.

Nicotinamide riboside has been linked in animal studies to good health and longevity, but its benefits have not been shown in people. The researchers said much more research is needed to know whether the chemical could slow or halt axon degeneration in the body.

“We are encouraged by the findings and think that identifying a class of drugs that block SARM1 activity has therapeutic potential in neurological disorders,” Milbrandt said. “The molecular details this pathway provides give us a number of therapeutic avenues to attack.”
About this neurology research

Funding: The research is funded by the National Institutes of Health (NIH), grants RO1DA020812, RO1AG013730, RO1NS065053, RO1NS087632, RO1NS078007 and F31NS074517, and a grant from Vertex Pharmaceuticals.

Source: Diane Duke Williams – Washington University School of Medicine in St. Louis
Image Credit: The image is credited to Milbrandt lab
Original Research: Abstract for “SARM1 activation triggers axon degeneration locally via NAD+ destruction” by Josiah Gerdts, E.J. Brace, Yo Sasaki, Aaron DiAntonio, and Jeffrey Milbrandt in Science. Published online April 23 2015 doi:10.1126/science.1258366

Abstract

SARM1 activation triggers axon degeneration locally via NAD+ destruction

Axon degeneration is an intrinsic self-destruction program that underlies axon loss during injury and disease. Sterile alpha and TIR motif–containing 1 (SARM1) protein is an essential mediator of axon degeneration. We report that SARM1 initiates a local destruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD+) after injury. We used an engineered protease-sensitized SARM1 to demonstrate that SARM1 activity is required after axon injury to induce axon degeneration. Dimerization of the Toll–interleukin receptor (TIR) domain of SARM1 alone was sufficient to induce locally mediated axon degeneration. Formation of the SARM1 TIR dimer triggered rapid breakdown of NAD+, whereas SARM1-induced axon destruction could be counteracted by increased NAD+ synthesis. SARM1-induced depletion of NAD+ may explain the potent axon protection in Wallerian degeneration slow (Wlds) mutant mice.

“SARM1 activation triggers axon degeneration locally via NAD+ destruction” by Josiah Gerdts, E.J. Brace, Yo Sasaki, Aaron DiAntonio, and Jeffrey Milbrandt in Science. Published online April 23 2015 doi:10.1126/science.1258366

http://neurosciencenews.com/peripheral-neuropathy-sarm1-1987/

Will Endomorphin Be The Replacement For Opioids For Neuropathy Patients

Today's post from sciencedaily.com (see link below) follows on from yesterday's post about endomorphin and its potential for chronic pain patients but whereas yesterday's post was from a national newspaper, this one is from the ever-reliable Sciencedaily.com and confirms what you may have read yesterday. If the predictions are correct, then commercially produced endomorphin may replace opioids as the pain killers of choice for those who've tried everything else and as a bonus, will deliver none of the side effects associated with opioids. This is fantastic news for long-term pain patients who not only have to manage their opioid prescriptions properly but have to face the wagging finger of media stigma, however unjust that may be. We still have to wait two years before the first human trials but the eventual benefits may make the wait easier.

New drug could be safer, non-addictive alternative to morphine
 January 28, 2016 Source: Tulane University
The peptide-based drugs, which mimic a natural brain chemical, target the same pain-relieving opioid receptor as morphine

Researchers at Tulane University and Southeast Louisiana Veterans Health Care System have developed a painkiller that is as strong as morphine but isn't likely to be addictive and with fewer side effects, according to a new study in the journal Neuropharmacology.

Using rats, scientists compared several engineered variants of the neurochemical endomorphin, which is found naturally in the body, to morphine to measure their effectiveness and side effects. The peptide-based drugs target the same pain-relieving opioid receptor as morphine.

Opium-based drugs are the leading treatments for severe and chronic pain, but they can be highly addictive. Their abuse results in thousands of overdose deaths in the United States annually. They can cause motor impairment and potentially fatal respiratory depression. Patients also build up tolerance over time, increasing the risk for abuse and overdose.

"These side effects were absent or reduced with the new drug," said lead investigator James Zadina, VA senior research career scientist and professor of medicine, pharmacology and neuroscience at Tulane University School of Medicine. "It's unprecedented for a peptide to deliver such powerful pain relief with so few side effects."

In the study, the new endomorphin drug produced longer pain relief without substantially slowing breathing in rats; a similarly potent dosage of morphine produced significant respiratory depression. Impairment of motor coordination, which can be of particular importance to older adults, was significant after morphine but not with the endomorphin drug.

The new drug produced far less tolerance than morphine and did not produce spinal glial cell activation, an inflammatory effect of morphine known to contribute to tolerance.

Scientists conducted several experiments to test whether the drug would be addictive. One showed that although rats would spend more time in a compartment where they had received morphine, the new drug did not affect this behavior. Another test showed that when the press of a bar produced an infusion of drug, the rats only increased efforts to obtain morphine and not the new drug. The tests are predictive of human drug abuse, Zadina said.

Researchers hope to begin human clinical trials of the new drug within the next two years.

Story Source:

The above post is reprinted from materials provided by Tulane University. Note: Materials may be edited for content and length.


Journal Reference:
James E. Zadina, Mark R. Nilges, Jenny Morgenweck, Xing Zhang, Laszlo Hackler, Melita B. Fasold. Endomorphin analog analgesics with reduced abuse liability, respiratory depression, motor impairment, tolerance, and glial activation relative to morphine. Neuropharmacology, 2016; 105: 215 DOI: 10.1016/j.neuropharm.2015.12.024

Tulane University. "New drug could be safer, non-addictive alternative to morphine: The peptide-based drugs, which mimic a natural brain chemical, target the same pain-relieving opioid receptor as morphine." ScienceDaily. ScienceDaily, 28 January 2016. .

http://www.sciencedaily.com/releases/2016/01/160128155006.htm

Preventing Falling For Neuropathy Patients

Today's post from medivizor.com (see link below) looks at the risk of falling for people in general (especially older people) but also people with nerve damage. It gives some useful explanations as to why this can happen and how to avoid it. Unfortunately, if you have long-term neuropathy, you may have noticed how much more frequently you're stumbling and maybe even falling. It's not surprising, given the confusing signals your feet are receiving from your damaged nerves but there is a serious risk of injury and it's best to be aware of the problem. Many people who feel their balance is fragile, try to grip the ground with their feet and consequently tense up even more when walking, leading to a greater risk of falling. We have to find strategies to avoid this and this article helps with a few tips.

Defying Gravity? Fall Prevention
Posted by Kathleen Hoffman on Jan 22, 2016

Our greatest glory is not in never falling, but in rising every time we fall. ~Confucius

An elephant and a feather would fall from a tall building and land at exactly the same time (in the absence of air resistance). Getting your head around it is hard but it’s just the nature of gravity.

Everyone is affected by gravity. From the time we’re up on our feet as toddlers, we risk stumbling and tumbling. Skinned knees and scraped elbows are a normal part of growing up.

Yet sometimes falls are severe. Every year, over 2 million visits to the emergency department are due to falls.

Although researchers focus on falls that happen to people age 65 and over, according to one insurance company, most falls are not related to age. Certain physical conditions are commonly related to falling.

For example, a recent study comparing adults with and without arthritis found that those with arthritis were twice as likely to experience 2 or more falls. Not getting enough Vitamin D, foot pain and neuropathy, medication side effects like dizziness, weakness in the lower half of the body have all been associated with increased risk of falling. Changes in vision that interfere with balance increase the likelihood of falls.
Another factor associated with falling are the side effects of medications, like dizziness.
Fall Prevention at Home

Certain areas of the house are associated with more frequent falls than others. Here are some ideas to reduce your risk of falling.
What’s The Most Dangerous Room in Your House?

Most people say the kitchen. But according to the CDC, your bathroom is the

most hazardous  

room in the house. Around 235,000 injuries occur in bathrooms every year. Eighty one percent of these injuries are falls. For the young and old alike, getting in and out of the bathtub or shower is treacherous. Adding handrails in the bathroom, in the tub, and by the toilet can help reduce falls.
Step Lively on Stairs

As people walk up and down steps, their nervous systems create a set of expectations about the height of the steps. A difference in height between steps is one of the main reason for falls. Warnings and visual cues that something is amiss in the height of steps is a failsafe but assuring that all steps are the same height can reduce injuries.

Uneven tread, or even broken steps are hazardous. Installing handrails on all stairwells is recommended.
Reduce the Clutter

There are neatniks and then, there are the rest of us. Clutter is a way of life for many. But clutter on the floor, including electric cords and accent or throw rugs are unsafe and increase the risk of falling.
Throw Some Light On the Subject

Okay, here’s where aging research comes in and tells the story. Aging eyes take longer to adjust to changes in the level of light. In addition, physical changes in the eye reduce the amount of light that enters the eye and actually scatters light in the eye. The scattering means that older eyes see more glare and with more glare less detail can be seen. Finally, yellowing lenses, another age effect, makes distinguishing colors more difficult.

So, changes in lighting are essential to safety. Eliminate light fixtures that flicker so that the general lighting of the room is uniform across it. If light can be made uniform between rooms, this can also improve sight and safety. Replace light bulbs so that the house is brighter and use glare free lighting.
Fear of Falling Can Increase the Risk of Falls

Since 20% of falls result in serious injuries, it’s not surprising that after one fall, people become fearful of another. Moreover, that fear can become a reason to be less active. That’s where the paradox lies because being less active weakens muscles in the abdomen, hips and legs, increasing the likelihood of falling. Moving and staying physically fit is key to preventing falls.

Each year, over 700,000 people are hospitalized because of injuries that occur from falling. By taking a few precautions, you can reduce your risk for becoming one of them. Institute fall prevention strategies and Stay safe.

 https://medivizor.com/blog/2016/01/22/fall-prevention/

Swimming Is An Exercise Option For Neuropathy Patients

Today's post from houstonfootspecialists.blogspot.com (see link below) talks about a form of exercise which may not have occurred to some people with neuropathy and that is swimming. Many neuropathy patients shudder at the thought of exercise bringing yet more pain to their feet, legs or arms but swimming solves that problem by taking the weight off your limbs while still giving you a work out.

Have Neuropathy? Try Swimming!
Dr. Jeffrey Bowman is the Podiatrist for Houston Foot Specialists.Tuesday, June 4, 2013

There are many reasons why people have numbness and tingling in their feet. A common disorder that affects the peripheral nerves is neuropathy. Peripheral neuropathy is characterized by nerve damage and results in numbness, tingling or burning sensations. Dr. Jeff Bowman, foot specialist in Houston, TX sees the effects of neuropathy on a regular basis in his patients with diabetes.

The symptoms of neuropathy can be improved especially when the underlying cause is managed well. Another way to manage neuropathy is though exercise.

How can exercise help with neuropathy?

There are many reasons for doing your best to stay active when you have neuropathy:

Reduces pain
Restores balance
Improves blood circulation
Improves your range of motion
Strengthens weak muscles
Reduces foot cramps from contracted muscles

Choosing lower impact options such as cycling, tai chi and Pilates will be safe for feet while still offering a cardiovascular workout. Swimming is a great option suitable for anyone at any age. Swimming works all the major muscle groups in your body and it is great for those with neuropathy since the water holds your body weight. Swimming can lower glucose levels, which ultimately reduces your risk for further nerve damage. You can do some pool walking, swim laps, do water aerobics or try synchronized swimming even.

http://houstonfootspecialists.blogspot.com/2013/06/have-neuropathy-try-swimming.html

Denying Pain Patients Opioids Is That Humane

Today's post from huffingtonpost.ca (see link below) written by a pain specialist, is a sensible article calling for common sense in the opioid debate and lamenting the fact that current systems are either black or white with no common ground to include the needs of chronic pain patients for whom opioids are a godsend. This row is set to go on and on but the fact remains that if you're a severe neuropathy patient, in daily pain ranging from mild to wild and you've been through the whole spectrum of standard drugs to reduce the symptoms, opioids may be the only solution to let you have a reasonable quality of life. To deny them this option is tantamount to torture! Definitely worth a read.

Limiting Opioids Alone Is Not A Sustainable Pain Care Plan  
Beth Darnall Professor, Writer, Opioid Expert Posted: 06/09/2016


Canada and the U.S. have seen alarming increases in opioid prescribing and in opioid-related overdose deaths. Prince's tragic opioid-related death further highlights this international public health problem.

Indeed, the spectre -- and reality -- of opioid limits have sent shockwaves through segments of the chronic pain community. The vast majority of individuals prescribed opioids take them responsibly, yet are now subject to laws created to prevent illicit opioid use.

Patient advocacy groups have loudly decried unjust medical care for chronic pain. Limiting opioids may preclude some opioid overdose deaths, they say, but what about the untold suffering -- and the suicides -- that may occur when patients cannot tolerate severe ongoing pain? The lives of people with chronic pain matter, too, and they should be treated as patients, not as addicts.

It's a Catch-22, of course. The opioid debate engenders strong emotions for both sides: opioid access versus limits. Is it really a zero-sum game where one group must suffer so the other group may survive?

Even when opioids are taken exactly as prescribed by exemplar patients, they come with a range of health risks including overdose fatality. How do we address the need to reduce health risks while treating chronic pain?

Do opioids help some people with chronic pain? Absolutely. For this reason, prescribers must retain discretion to prescribe them, while recalling that it will be for a minority of patients. Opioids may help, but they can't be the whole story.

We don't have good data to show that the average person taking opioids long term gets better in terms of pain or function. Some people do, but studies show that most do not. However, we do have data to show that most people have side-effects that are not trivial. Some opioid side-effects include worsening pain, escalating opioid doses due to increased pain sensitivity or tolerance to the medication, altered hormones, constipation, and sometimes -- fatal overdose.

The problem is, we do not have national systems in place to treat chronic pain otherwise. This is the larger Catch-22 that simply must be addressed. It's time for national governments to put their money where their mouth is and to focus on major pain research initiatives and comprehensive treatment programs that will allow us to treat pain better.

We know that opioids alone are also not a great chronic pain treatment strategy. Studies show that patients improve with combined treatment that includes gradually becoming more active, while also using other key self-management skills. All physical pain is processed in the nervous system (brain and spinal cord). People with chronic pain can regularly use simple skills to dampen pain processing in their own nervous system. They can reduce their own suffering, pain and need and use of opioids.

Will it cure pain? No. Will it help reduce need for medication? Often, yes. Will it reduce suffering?

Absolutely.

As a pain psychologist, I share patients' concerns about limiting opioids without providing access to alternatives. In and of itself, limiting opioids is not a pain care plan. Canada and the U.S. are now tasked with rapidly providing its citizens with access to opioid alternatives for chronic pain.

Ethical pain care should emphasize first the programs and initiatives that empower individuals to best control their own pain. When people are equipped to help themselves feel better, they need fewer doctors and treatments.

Excellent chronic pain self-management programs exist. It's time we subsidize patient empowerment programs; doing so will give physicians and other prescribers the resources needed to treat chronic pain better.

http://www.huffingtonpost.ca/beth-darnall/opioids-limit_b_10374856.html

SKIN CELLS CAN BE ENGINEERED IN TO PULMONARY VALVES FOR PEDIATRIC PATIENTS

Researchers have found a way to take a pediatric patient's skin cells, reprogram the skin cells to function as heart valvular cells, and then use the cells as part of a tissue-engineered pulmonary valve. A proof of concept study published in the September 2014 issue of The Annals of Thoracic Surgery provides more detail on this scientific development

"Current valve replacements cannot grow with patients as they age, but the use of a patient-specific pulmonary valve would introduce a 'living' valvular construct that should grow with the patient. Our study is particularly important for pediatric patients who often require repeated operations for pulmonary valve replacements," said lead author David L. Simpson, PhD, from the University of Maryland School of Medicine in Baltimore.

Dr. Simpson, senior co-author Sunjay Kaushal, MD, PhD, and colleagues designed a process to transform skin cells from a simple biopsy into cells that become an important ingredient in a tissue-engineered pulmonary valve.

The pulmonary valve is a crescent-shaped valve that lies between the heart's right ventricle and pulmonary artery. It is responsible for moving blood from the heart into the lungs.

While the study was conducted in vitro (outside of the body), the next step will be implanting the new valves into patients to test their durability and longevity.

"We created a pulmonary valve that is unique to the individual patient and contains living cells from that patient. That valve is less likely to be destroyed by the patient's immune system, thus improving the outcome and hopefully increasing the quality of life for our patient," said Dr. Kaushal. "In the future, it may be possible to generate this pulmonary valve by using a blood sample instead of a skin biopsy."

Dr. Simpson added that he hopes the study will encourage additional research in tissue engineering and entice more people to enter the field, "Hopefully, growing interest and research in this field will translate more quickly into clinical application."

It is estimated that nearly 800 patients per year could potentially benefit from bioengineered patient-specific pulmonary valves, according to data from the STS Congenital Heart Surgery Database. The Database, which collects information from more than 95% of hospitals in the US and Canada that perform pediatric and congenital heart surgery, shows that approximately 3,200 patients underwent pulmonary valve replacement during a 4-year period from January 2010 to December 2013.

E CIGARETTES UNHELPFUL IN SMOKING CESSATION AMONG CANCER PATIENTS

In a new study of cancer patients who smoke, those using e-cigarettes (in addition to traditional cigarettes) were more nicotine dependent and equally or less likely to have quit smoking traditional cigarettes than non-users. Published early online in Cancer, a peer-reviewed journal of the American Cancer Society, the findings raise doubts about the potential benefits of e-cigarettes for helping cancer patients give up smoking

Because of the risks of persistent smoking, all cancer patients who smoke should be advised to quit. But the rising use of e-cigarettes has raised many questions among patients and their health care providers including whether e-cigarette use helps or hinders quitting efforts. Even regulators are struggling with the complexities associated with e-cigarettes as they weigh the benefits and risks to the general population and subgroups of individuals.

To examine available clinical data about e-cigarette use and cessation among cancer patients, Jamie Ostroff, PhD, of the Memorial Sloan Kettering Cancer Center in New York City, and her colleagues studied 1074 cancer patients who smoked and were enrolled between 2012 and 2013 in a tobacco treatment program within a comprehensive cancer center.

The researchers observed a three-fold increase in e-cigarette use from 2012 to 2013 (10.6 percent versus 38.5 percent). At enrollment, e-cigarette users were more nicotine dependent than non-users, had more prior quit attempts, and were more likely to be diagnosed with lung or head and neck cancers. At follow-up, e-cigarette users were just as likely as non-users to be smoking. Seven day abstinence rates were 44.4 percent versus 43.1 percent for e-cigarette users and non-users, respectively (excluding patients who were lost to follow-up).

"Consistent with recent observations of increased e-cigarette use in the general population, our findings illustrate that e-cigarette use among tobacco-dependent cancer patients has increased within the past two years," said Dr. Ostroff. She stressed that the study had several limitations, and additional studies are required. "Controlled research is needed to evaluate the potential harms and benefits of e-cigarettes as a potential cessation approach for cancer patients. In the meantime, oncologists should advise all smokers to quit smoking traditional combustible cigarettes, encourage use of FDA-approved cessation medications, refer patients for smoking cessation counseling, and provide education about the potential risks and lack of known benefits of long-term e-cigarette use ."

More About The Dangers Of Fluoroquinolones For Neuropathy Patients

Today's important post from peoplespharmacy.com (see link below) takes a fresh look at the current controversy about the antibiotics known as fluoroquinolones. These drugs have been on the market and prescribed for decades which begs the question as to why we weren't warned about the potential for nerve damage and the worsening of neuropathic symptoms earlier. It is entirely possible that your doctor or specialist may prescribe these antibiotics for a particular problem without being aware that they can cause severe nerve damage, In that case, always check the bottle or box or pamphlet for the words '...floxacin' or '...quinolone' in the name of the drug. It can be hidden; Ciprofloxacin for instance can often be called Ciproxin on the label. If you discover that your antibiotic is in fact from the fluoroquinolone family, go straight back to your doctor, discuss it and if necessary, ask for an alternative (there are plenty available). This article is definitely worth reading.

Could Your Antibiotic Cause You Permanent Nerve Damage?
October 7, 2013 in People's Pharmacy Alerts 
 
Did you know that the FDA has issued a safety notification about a class of popular antibiotics called fluoroquinolones (FQs)? The announcement involves the following drugs: 

Ciprofloxacin (Cipro)
Gemifloxacin (Factive)
Levofloxacin (Levaquin)
Moxifloxacin (Avelox)
Norfloxacin (Noroxin)
Ofloxacin (Floxin)

According to the FDA, over 21 million people get a prescription for one of these drugs each year. That makes this class of antibiotics among the most popular in the pharmacy. Doctors love to prescribe FQs because they are effective for a wide range of infections including bronchitis, pneumonia, sinusitis, urinary tract infections, prostatitis and skin infections.

These drugs have been around for decades. Cipro, for example, has been on the market for over 25 years. After all this time, one would think that the FDA would have a clear understanding of the benefits and risks of such drugs. In fact, you might assume that doctors would have been warned about complications of FQ drugs like Levaquin or Cipro from the very beginning. Au contraire. It comes as a great shock to patients to discover that serious fluoroquinolone warnings continue to be issued, decades after these drugs were originally approved.

The most recent FDA announcement relates to nerve damage, aka peripheral neuropathy. Here is the official safety communication issued on 8-15-2013:

"This serious nerve damage potentially caused by fluoroquinolones may occur soon after these drugs are taken and may be permanent... Peripheral neuropathy is a nerve disorder occurring in the arms or legs. Symptoms include pain, burning, tingling, numbness, weakness, or a change in sensation to light touch, pain or temperature, or the sense of body position. It can occur at any time during treatment with fluoroquinolones and can last for months to years after the drug is stopped or be permanent. Patients using fluoroquinolones who develop any symptoms of peripheral neuropathy should tell their health care professionals right away."

In other words, patients can experience this potentially irreversible nerve damage within days of starting drugs like ciprofloxacin or levofloxacin. Even if the drugs are stopped promptly, the side effects can last.

Doctors and pharmacists may not always describe the symptoms patients need to watch out for. And people may not associate weakness, numbness or tingling with an antibiotic, since it doesn't seem logical that a medicine designed to overcome an infection would damage nerves. Such symptoms may not seem that bad, but in some cases peripheral neuropathy can be permanently disabling.

OTHER KINDS OF NERVE DAMAGE

We first became aware of unusual problems brought on by fluoroquinolone antibiotics in July of 1994 after receiving this question:

"I often have side effects from medicines, but have never experienced anything like Floxin. I took it for a severe sinus infection followed by pneumonia last winter. After three days of utter misery and a rash on my back, I started hallucinating. Are there other people who have had a bad reaction to this antibiotic?"

We had to do some digging, but we finally discovered that FQs can cause "hallucinations, visual disturbances confusion, dizziness and seizures."

We talked to journalist Stephen Fried about his wife's experience with Floxin. In the book Bitter Pills, the Frieds describe how one Floxin pill for a urinary tract infection led to debilitating neurological symptoms that lasted for years.

At the time, a lot of doctors didn't believe such long-lasting neurological complications could happen so quickly. It has taken the FDA over 25 years to alert physicians to just such a possibility.

The same can be said about tendinitis or tendon rupture. This is another very serious adverse reaction triggered by FQ antibiotics. The first published report of an Achilles tendon problem appeared in 1983. Thereafter there were many case reports linking drugs like ciprofloxacin and levofloxacin to tendinitis and tendon rupture. These can also be disabling complications of FQ antibiotics. It took the FDA until 2008 to issue "black box" warnings about this problem, 20 years after Cipro was first introduced.

FLUOROQUINOLONE SIDE EFFECTS; COMPLICATIONS: 

Digestive distress, nausea, diarrhea, constipation, stomach pain, heartburn, vomiting
Headache, dizziness
Agitation, anxiety, irritability, restlessness, confusion
Insomnia
Tendon problems, tendinitis, tendon rupture
Retinal detachment
Nerve damage, peripheral neuropathy, nerve tingling, numbness
Allergic reactions, skin rash, anaphylaxis (life-threatening reaction requiring immediate medical attention!)
Super-infections including C. diff diarrhea
Hallucinations, psychosis, seizures
Depression, suicidal thoughts or actions
Irregular heart rhythms, torsades de pointes, QT prolongation
Kidney or liver damage
Blood disorders
Arthritis, muscle pain, weakness

READER REACTIONS:

Here are some stories from visitors to our website. Add your own FQ experience below. If these antibiotics have worked well for you without side effects we would like to hear about that. If you have suffered, we would like to see your story as well. Please comment below.

"I have taken Cipro a number of times over the years and wondered why my tendons, especially the Achilles tendon, were so inflamed. Finally read the side effects and saw it can be a serious side effect to the point of bursting the Achilles tendon. I carry a note with my insurance card in my wallet warning not to give me any of this family of antibiotics." C.G.

"It's been eight months and I've been to two specialists trying to determine if I have arthritis. They say I do not. I took Cipro and Levaquin within a one month period and it has been eight months since then, and I have pain and stiffness EVERY DAY. What started out as plantar fasciitis and wrist tendinitis then moved into my hips and elbows and is now in my upper back and shoulders.

"I ran a low grade fever for 6 months after taking these drugs. The symptoms started within two days of taking the last dose of Levaquin. I have not even addressed the fatigue, irritability and mood changes I experienced during the first three months after taking the drug. I was healthy, active and exercised regularly. Now I don't know what to do--stretching generally aggravates my pain. How can the FDA allow this drug to be prescribed?" Augsdi

"In 2000 I had an adverse reaction to Cipro: inflammation of most of my connective tissue to the point of needing help to get up out of bed or get dressed. I was unable to lift much and could not sit for more than 15 minutes due to the pain. My doctors could not believe it was the Cipro. It was 5 years before I was able to hike and ride my bike again." Jo

"The quinolone drugs, Cipro, Levaquin, Avelox, etc. are extremely strong and dangerous. When they go awry the adverse effects are serious, long term and often permanent.

"The awareness in the medical community of these dangers is extremely poor and often the concerns of patients suffering from adverse effects of these drugs are dismissed as 'not possible,' despite studies and literature citing these very effects i.e. neuropathy, tendon ruptures, neuromuscular damage, cartilage damage and others.

"I struggle to heal from 5 days of Cipro given a year ago and have met hundreds of people now who are going through similar struggles due to quinolone antibiotics. These drugs, though tolerated by many, should only be dispensed when there is no safer alternative due to the severity and permanence of adverse effects." Tao

http://www.peoplespharmacy.com/2013/10/07/popular-quinolone-antibiotics-can-cause-permanent-nerve-damage/