Monday, 27 February 2017

The Inherent Nonsense Of Some Neuropathy Research

Today's post from (see link below) shows yet again that good money is being spent in investigating the blindingly obvious. It's about neuropathy patients' own perceptions of their unsteadiness and lack of balance and whether this affects their state of mind or not. The conclusion is that such people take measures to adjust their walk, step or gait as a result of their own perceived unsteadiness. Well DUH! Why is it that absolutely everything has to be scientifically proved in the modern world; most probably to justify particular amounts of money being spent in certain areas? The cost of the research itself is seldom brought into question. I'm sorry but if you're going to waste our tax-payers' money in this way, there's little chance of genuine progress being made in the treatment of neuropathy symptoms. It's enough to make you choke on your coffee and reach for the walking stick!

Self-perceived unsteadiness influences balance, gait in diabetic neuropathy
February 24, 2017

In adults with diabetic peripheral neuropathy, self-perceived unsteadiness was associated with balance and gait measures, according to published findings.

“Unsteadiness and associated restrictions in activities of daily living predict depressive symptoms in patients with [diabetic peripheral neuropathy], highlighting the negative spiral between [diabetic peripheral neuropathy], unsteadiness, falls and psychological distress,” Neil D. Reeves, PhD, professor of musculoskeletal biomechanics at the School of Healthcare Science at Manchester Metropolitan University, United Kingdom, and colleagues wrote. “However, because unsteadiness has been assessed by self-report in most previous studies, it remains unknown whether a person’s perception of unsteadiness actually correlates with objective measures of balance and gait.”

Reeves and colleagues analyzed data from three groups of patients: adults with diabetic neuropathy (neuropathy disability score ≥ 6; n = 15), patients with diabetes but no neuropathy (n = 15) and matched controls without diabetes (n = 19). All participants completed the neuropathy-specific quality-of-life questionnaire to assess self-perceived unsteadiness during walking and standing. Participants underwent gait analysis using a 10-camera motion analysis system and force platforms while walking at a self-selected speed; dynamic sway was also measured.

Researchers found that the diabetic neuropathy group reported more self-perceived unsteadiness vs. those with diabetes but no neuropathy or controls (P =; .0001). Participants with diabetic neuropathy also had reduced gait velocity and step length vs. controls (P =; .0001), as well as altered body center-of-mass movement (P =; .05). Researchers observed strong correlations between self-perceived unsteadiness and gait velocity, step length and severity of diabetic peripheral neuropathy.

“The novelty of the current study is in showing that [diabetic peripheral neuropathy] patients are not only aware of themselves as being unsteady, but actually attempt to self-regulate their unsteadiness by walking more slowly and taking shorter steps,” the researchers wrote. “These gait adjustments reduce the extent to which [diabetic peripheral neuropathy] patients need to move their body forward, away from their base of support, during each step.”

The researchers noted that self-perceived unsteadiness in participants with diabetes but without diabetic peripheral neuropathy was no different from that of controls without diabetes. The researchers did not assess fear of falling, depression or fall history of participants. – by Regina Schaffer

Disclosure: The researchers report no relevant financial disclosures.

Sunday, 26 February 2017

Finally, A Common Sense Approach To Cannabis For Nerve Pain

Today's post from (see link below) illustrates the new approach and ideas about cannabis as a pain killer perfectly. It reflects the sort of common sense that is finally gaining ground when it comes to cannabis hysteria. The older people in this article clearly benefit from (what seems to be) cannabis oil (CBD) administered to relieve their neuropathic pain and you have to give credit to the authorities that allow this to happen. One thing that comes across very strongly in this article is that people are still afraid of, or suffer, stigma associated with medicinal cannabis. Others seem to be convinced that patients will get high and are even taking it for that very reason, which of course, with cannabis oil is patent nonsense. What the future holds for medical cannabis in the current US climate of right wing political thought, is very much up in the air but neuropathy patients across the world will be hoping that common sense prevails and that even more research and study will be done until medical cannabis becomes as accepted as aspirin.

When Retirement Comes With a Daily Dose of Cannabis
By WINNIE HUFEB. 19, 2017

Ruth Brunn finally said yes to marijuana. She is 98.

She pops a green pill filled with cannabis oil into her mouth with a sip of vitamin water. Then Ms. Brunn, who has neuropathy, settles back in her wheelchair and waits for the jabbing pain in her shoulders, arms and hands to ebb.

“I don’t feel high or stoned,” she said. “All I know is I feel better when I take this.”

Ms. Brunn will soon have company. The nursing home in New York City where she lives, the Hebrew Home at Riverdale, is taking the unusual step of helping its residents use medical marijuana under a new program to treat various illnesses with an alternative to prescription drugs. While the staff will not store or administer pot, residents are allowed to buy it from a dispensary, keep it in locked boxes in their rooms and take it on their own.

From retirement communities to nursing homes, older Americans are increasingly turning to marijuana for relief from aches and pains. Many have embraced it as an alternative to powerful drugs like morphine, saying that marijuana is less addictive, with fewer side effects.

For some people, it is a last resort when nothing else helps.

Marijuana, which is banned by federal law, has been approved for medical use in 29 states, including New York, and the District of Columbia. Accumulating scientific evidence has shown its effectiveness in treating certain medical conditions. Among them: neuropathic pain, severe muscle spasms associated with multiple sclerosis, unintentional weight loss, and vomiting and nausea from chemotherapy. There have also been reports that pot has helped people with Alzheimer’s disease and other types of dementia as well as Parkinson’s disease.

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My biggest Obama disappointment was that he did not use an executive order to make the feds get off our elderly aching backs on the MJ issue...
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Marijuana should be legalized same as alcohol or tobacco. It should be affordable, and people should be able to grow it either for their own...

Across the nation, the number of marijuana users who are in their later years is still relatively limited, but the increase has been significant, especially among those 65 and older, according to recent studies.

Marcia Dunetz, 80, said that she worried at first about what people would think. “It’s got a stigma,” she said. “People don’t really believe you’re not really getting high if you take it.” 

“It’s a bigger issue than we thought,” said Brian Kaskie, a professor of health policy at the University of Iowa who co-wrote a study published in January, “The Increasing Use of Cannabis Among Older Americans: A Public Health Crisis or Viable Policy Alternative?” “This is an elephant we’re just starting to get our hands on.”

A medical marijuana education and support club started by residents of Rossmoor Walnut Creek, a retirement community east of San Francisco, has grown to 530 members — so many that it has changed meeting rooms three times.

“I would be in a lot worse shape if I wasn’t using cannabis, both physically and mentally,” said Anita Mataraso, 72, a grandmother of six who is the program director and takes marijuana daily for arthritis and nerve pain, among other ailments.

In the state of Washington, at least a dozen assisted living facilities have formal medical marijuana policies in response to demands from their residents, said Robin Dale, the executive director of the Washington Health Care Association. The association, an industry group, has posted a sample medical marijuana policy on its website.

In March, an influential group of medical providers, AMDA — The Society for Post-Acute and Long-Term Care Medicine, will tackle the issue at its annual conference. Cari Levy, the group’s vice president, will offer a “Marijuana 101” lesson on the benefits, the risks and the potential pitfalls for providers.

“People are using it, and we need to know how to respond,” she said.

But as older people come to represent an emerging frontier in the use of marijuana for medical purposes, questions are being raised about safety and accessibility. Even in states where medical marijuana is legal, older people who stand to benefit often cannot get it. Most nursing homes do not openly sanction its use, and many doctors are reluctant to endorse pot use, saying not enough is known about the risks in the oldest age groups.

The president and chief executive of RiverSpring Health, Daniel Reingold. He said he administered marijuana to his father as a painkiller shortly before his death.

“This is a target demographic that may have their access limited, if not cut off altogether, simply because they reside in a facility,” said Paul Armentano, deputy director of NORML, a group that advocates the legalization of marijuana. “It is a problem that may infringe on their quality of life.”

While there is no shortage of research on marijuana, relatively little of it has focused explicitly on older users even as their numbers grow — and not just in the United States. In Israel, for instance, older people have been treated with medical marijuana for years. And Americans for Safe Access, an advocacy group, helped open a research center in the Czech Republic that is evaluating its impact on older people.

“It’s an area that’s very important to look at,” said Dr. Igor Grant, the director of the Center for Medicinal Cannabis Research at the University of California, San Diego, adding that older people are now one of the center’s research priorities.

“Older people can be more sensitive to medicine,” he said. “It’s possible a dose safe for a 40-year-old may not be in an 80-year-old.”

Dr. Thomas Strouse, a psychiatrist and palliative care doctor at the University of California, Los Angeles, said that just as sleeping and pain medications could harm older people, marijuana could possibly make them confused, dizzy or more likely to fall.

“There is no evidence that it is particularly helpful to older people, and some reason that it could be harmful,” he said.

Most nursing homes have also taken a cautious position, often resorting to a “don’t ask, don’t tell” approach.

“If residents are taking it, they are taking it undercover without the staff knowing so it’s not part of their care plan,” said Dr. Cheryl Phillips, senior vice president for public policy and health services for LeadingAge, an industry group representing more than 2,000 nursing homes. “I think that creates a safety problem.”

Fred Miles, a Colorado lawyer who represents nursing home operators, said nursing homes — unlike assisted living facilities — were regulated by the federal government, and were fearful of jeopardizing their Medicare and Medicaid funding. Staff members who administer marijuana could also theoretically face criminal prosecution under federal law, he said, though he has never heard of that happening.

The federal Centers for Medicare and Medicaid Services said no nursing home had specifically lost financing or been penalized for permitting the use of marijuana. In New York State, which started a medical marijuana program in 2016, its use is restricted to people with designated medical conditions, including neuropathy, epilepsy, multiple sclerosis, Parkinson’s, H.I.V., AIDS and cancer.

At the Hebrew Home in the Bronx, the medical marijuana program was years in the making. Daniel Reingold, the president and chief executive of RiverSpring Health, which operates the home, said he saw its powers firsthand when his own father, Jacob, was dying from cancer in 1999. To ease his father’s pain, Mr. Reingold boiled marijuana into a murky brown tea. His father loved it, and was soon laughing and eating again.

“The only relief he got in those last two weeks was the tea,” Mr. Reingold said.

When Mr. Reingold requested approval from the nursing home’s board members, there were no objections or concerns, he said. Instead, they joked that they would have to increase the food budget.

Then Dr. Zachary Palace, the medical director, developed a program that seeks to offer marijuana as an option but also comply with federal regulations: Though the nursing home recommends and monitors its use, residents are responsible for buying, storing and administering it themselves.

Last fall, the first three residents started taking marijuana pills. Their families obtain the pills at a dispensary in Yonkers run by Etain, a company licensed by the state to sell medical marijuana to qualifying patients or their designated caregivers, who must live in New York. Dr. Palace said that as the program expanded this month, as many as 50 residents could be using marijuana.

Marcia Dunetz, 80, a retired art teacher who has Parkinson’s, said she worried at first about what people would think. “It’s got a stigma,” she said. “People don’t really believe you’re not really getting high if you take it.”

But she decided to try it anyway. Now, she no longer wakes up with headaches and feels less dizzy and nauseated. Her legs also do not freeze up as often.

For Ms. Brunn, the marijuana pills have worked so well that she has cut back on her other pain medication, morphine.

Her daughter, Faith Holman, 61, said the pills cost $240 a month, which is not covered by health insurance. Ms. Holman, who lives in New Jersey, also has to ask a family friend to go to the Yonkers dispensary.

“Obstacles had to be overcome,” Ms. Holman said. “But I think she was meant to have it because everything has worked out.”

Saturday, 25 February 2017

The Water Babies Of Neuropathy

Today's post from (see link below) revisits an old subject on this blog and that is: exercising to reduce neuropathy symptoms. Now don't rush off just yet, just because of that word! This time the exercising is relatively painless and who doesn't want that! It provides very useful tips for exercising in water...and you don't even have to be able to swim! Really, nobody hates exercise more than me but even I have to admit that this takes the strain out of the whole process and can actually be enjoyable because you can feel the benefits as your body works out in water. Strongly advised for even the most stubborn exerciseophobes! (Be warned: it looks as though the website has used Google translate for this one but you'll get the message)

6 Water Exercises for Neuropathy
Written, Edited or Reviewed By: Pramod Kerkar, MD, FFARCSI Last Modified On: February 14, 2017

For people suffering from neuropathy, performing exercises is just not possible due to the severe nerve pain. Few low impact exercises can help control or reduce the symptoms of neuropathy. Though not all exercises will work for everyone, but there are some water exercises that can be of great benefit to people suffering from neuropathy. Water exercises help reduce the stress on weight bearing joints like knees, ankles, and hips. There is a decreased risk of fall in water exercises for neuropathy patients.

Exercises in water are low-affect movement that takes the weight off your muscles, joint and bones. Water likewise offers regular resistance, for nourishing your muscles. Water exercises can likewise have a few medical advantages, for example, enhanced heart wellbeing, lessened anxiety, and enhanced strong continuance and quality. Practicing in the water can be an awesome approach to incorporate physical action into your life. You can even do sea-going activity on the off chance that you don't know how to swim.

You may begin with water strolling. In water that is about midriff high, stroll over the pool swinging your arms as you do when strolling ashore. Abstain from strolling on your tiptoes, and hold your back straight. Fix your abs to abstain from inclining too far forward or to the side.

To expand resistance as your hands and arms travel through the water, wear hand networks or other resistance gadgets. Water activities are low-influence moves that takes the weight off your bones, joints and muscles. Water exercises also offers regular resistance, which can fortify your muscles against neuropathy

Water activities can moreover have a couple of medicinal points of interest, for instance, improved heart prosperity, diminished uneasiness, and upgraded solid tirelessness and quality level. Honing in the water can be a staggering way to deal with consolidate physical development into your life. You can even do water movement if you don't know how to swim.

6 Water Exercises for Neuropathy

Here are some incredible foot and leg practices for anybody enduring neuropathy.

Water Strolling 

You may begin with water strolling exercise to help with your issues related to neuropathy. In water that is about abdomen high, stroll over the pool swinging your arms as you do when strolling ashore. Abstain from strolling on your tiptoes, and hold your back straight. Fix your abs to abstain from inclining too far forward or to the side.
To expand resistance as your hands and arms travel through the water, wear hand networks or other resistance gadgets.

Leg exercise using a noodle 

If you are running from neuropathy condition, then this water exercise will prove good for you. tie a water noodle (one of those foam tubes that you see at pools these days: Ed.) into a bunch around your foot or water shoe. Remain with your back to the side of the pool in midriff high water, setting your arms on the edge of the pool for solidness. Fix your leg before you, and after that flex your knee to around a 90-degree position.
Come back to the beginning position and rehash 12 to 15 times or until you're exhausted. Tie the water noodle into a bunch around your other foot or water shoe and rehash with the other leg.
Water exercise can be fun at any age, size or wellness level — whether you attempt it all alone or agree to a class. Consider looking at sea-going activity classes offered at a nearby wellness focus or a neighborhood swimming pool. Hop in. The water's fine!

Side Leap 

 Side leap water exercise can be very effective during neuropathy conditions. It is a low impact water exercise with high rate of effectiveness in easing neuropathy pain. Keep your feet all together and draw arms around your sides, crouch somewhat. In one movement, look to one side, raise arms to level of shoulders, and hop around two feet towards one side, extending your leg sideways and arriving on the bundle of your opposite foot. Unite both feet, start pushing up in standing position, and keep your arms lower. Do four bounces with your one leg, then rehash with your other one.

Squat Step 

For patients of neuropathy, Squat steps may prove to be best water exercise. It is designed to get strength in leg muscles and lower body. Keep your feet altogether straight while standing and keep arms down on your sides. Stride left with your left foot after both arms raised to the shoulder level, and start the squat till your thighs come parallel to the base of the pool, while keeping head above water and your mid-section lifted. Bring your correct foot toward your left foot, stand up, and bring down your arms towards your sides and do four snappy strides with left leg, rehash with your privilege. Come back to beginning position.

Resistance Water Exercise for Neuropathy 

 Using a kickboard.  Neuropathy requires resistance training for its cure and exercise using kickboard provides you the exact suitable workout for this purpose. Kickboards give another sort of resistance. Standing up straight with your legs easily separated, and fix your abs. Broaden your correct arm and hold the kickboard on every end.
Keeping your left elbow near your body, move the kickboard toward the focal point of your body. Come back to the beginning position and rehash 12 to 15 times or until you're exhausted. At that point augment your left arm and rehash the practice on the opposite side.

Making Tracks

  Neuropathy patients can discover their cure in low effect water practices since water practices permit your body to take less worry submerged while working out for same stress. Envision you're staying with feet inside tracks of railroads. Keep arms by your sides, whereby forcefully lift right knee and wander over the right track, putting your foot down outside of it. Go over move with your left leg. As your left side foot lands, hunch down while raising your arms towards sides. Stand up, lower your arms, and modify the development, this time wandering inside the track. Rehash it 20 times.

Friday, 24 February 2017

The Absolute Bottom Line With Neuropathy (Vid)

Today's post from (see link below) may seem like a 'post-to-slit-your-wrists-by' but it truthfully reflects the sad reality of living day to day with severe neuropathy. We can read all the self-help articles we like but sometimes we just have to's just too much! Unfortunately, this relentless suffering can occasionally lead to suicidal thoughts and this article offers support links but her main message (after all the depression), is that we shouldn't worry so much about days like this. Let them happen and wallow for a while because they give your brain and body a brief pause to regenerate. Yes you feel like there's no tomorrow but there is and even if that's not a prospect to cheer you up, your body will get you through another day and another and another, until you feel a bit better and less distraught. You may never get back to the old you but you can still get pleasure out of life and the pleasure moments can make the bad moments feel so much less important. Other people's stories can work both ways - you can take comfort in the fact that you don't feel as bad as they do and you can take comfort in the fact that you're not alone in feeling the way you do. Well worth a read.
5 Things I Don’t Admit on My Bad Pain Days 
By Sharilynn Battaglia Contributor I write about Chronic Pain

Have you ever had a day when you just stared off into space? Not staring and thinking deep thoughts about your future. Just empty, with random thoughts floating around occasionally. But nothing coherent. And definitely nothing cheerful. This is the place I am in right now.

My brain has just shut down. The disease has become too much to handle any more and my brain went bye-bye. So, I thought I’d let you into the taboo side of chronic illness and pain. The stuff we really don’t want to admit. The thoughts we may have when our brain and body are at their lowest.

1. I am tired. 

That’s why my brain shut down. Fighting pain is hard. And those of us in daily pain don’t ever get to rest. The constant struggle of trying to stay physically in control of pain is draining. Add to that the daily demands of running a home and raising kids and you have the perfect storm for extreme fatigue. And extreme frustration. And we crack. Because being nice and patient and understanding is also hard work. And when our brains get tired of fighting our disease, we may not care about the niceties anymore. My brain already fled so only fight is left. And it doesn’t matter who gets in the way (sorry)!

2. I am sad. 

It’s emotionally drained. It’s extremely hard to deal with an illness every day and then still be able to deal with what comes in every normal relationship I know of. Disagreements. My husband and I are no different. We argue. It’s not always roses and chocolate. And to be honest, I don’t always have the fortitude to deal with any discord, whether it’s about a burnt dinner or the several hundred bucks he just lost at the casino. I’ll end up in a puddle of tears. (And if it’s about the kids, fuhgetaboutit!) Pain makes everything personal and much more intense. So the small stuff becomes huge and nastiness becomes much more easy.

3. I am depressed. 

It’s hard to stay positive and accepting of a disease that causes so much pain, weakness, degeneration, loss, forgetfulness, uncertainty… I could go on, but you get the point. Obviously, I have accepted my illness. I’ve had to. I would never have gotten out of bed otherwise. But these diseases are progressive and constantly change over time. So we have to constantly readjust our mindset. And let’s be honest, it has to become part of who we are. We can’t exist by putting on rose-colored glasses and ignoring it. So the feelings have to be accepted and allowed to come out, too. But that can cause intense fear that can leave us overwhelmed to the point of motionlessness.

4. I am confused. 

 And confusion is very frustrating. And time-consuming. You see, my body remembers everything it used to be able to do. From dancing to walking miles to rearranging furniture all by myself carrying pieces up and down stairs. So sometimes, I still think I am capable and try to do those things expecting that I will be able to. And when I can’t, I either end up hurting myself or I have to find someone else to help me.

5. I want to give up.

 I know the facts about my disease. I know what my back injuries mean. I know what the future probabilities are for disease progression and pain management. And I worry about where I will end up when I can’t care for myself and who will care for me. I worry about that when I’m tired, hurting, or alone. And I’m alone a lot. And I’m scared. I think about giving up a lot, too. I don’t talk about it, but I think about it. And honestly, in some ways, giving up feels equivalent to being pain-free again and on days like this, that’s all I really want.

When my brain gets like this, what I really need is some sort of regeneration. I’ll watch a movie, find funny shows on TV, watch kittens on YouTube, or bundle up and sleep! These “lost brain” days don’t last forever. And they’re not as common as they may seem, though they do tend to come in clusters. But after 20 years of this, the silver lining seems to be the fact that by letting these days happen, you allow for a mental reset. The negativity gets acknowledged, then let go – and that’s exactly what needs to happen.

If you or someone you know needs help, visit our suicide prevention resources page.

If you need support right now, call the National Suicide Prevention Lifeline at 1-800-273-8255 or text “START” to 741-741.

Thursday, 23 February 2017

Neuropathy: A News Media View

Today's post from (see link below) shows another example of how the media tend to report neuropathy (thinly) and is a mix of information and personal stories but nevertheless useful for people facing neuropathy for the first time. The author does highlight what he calls 'the main' causes of neuropathy but there are many more 'main' causes than these. However, perhaps more interesting is the case study, which led to months of testing, the eventual discovery of a trapped nerve and ensuing surgery. The author then quite rightly points out that surgery is rare in cases of neuropathic damage, partly because they can't repair damaged nerves and in the best of cases may be able to release a trapped nerve (as was the case in this article). If you're new to neuropathy, you should know that surgery is very unlikely, so don't get worried about that being in any way inevitable but unfortunately other forms of treatment are based on subduing the symptoms alone and rarely work 100%. That's the reality in 2017 and it's not very encouraging. This article does have some useful information, especially for people whose neuropathy cause is listed below but you really will need to talk to your doctor and investigate further if you want a thorough explanation of what's going on in your body. This blog has dozens of very good general articles about neuropathy - that could be your start.

Is Peripheral Neuropathy Causing the Numbness or Tingling in Your Feet? 
By Ruben Castaneda | Staff Writer Oct. 31, 2016, 

It affects 40 million people nationwide and can cause serious damage to the nerves that go to your feet.

In September 2015, Rebecca Cole noticed tingling in her toes. Within a few weeks, the tingling changed to numbness, which spread to the soles of her feet.

Cole had never had chronic or serious back ailments, but her parents had suffered from sciatica, a painful condition that affects the back, hips and legs and is caused by the compression of a spinal nerve root in the lower back. Given her parents' experience, Cole suspected the tingling and numbness in her feet could be related to her back. Cole, 31, saw an orthopedist in late October who took X-rays of her back, which showed no problems. Still, the orthopedist believed Cole would benefit from strengthening her back and recommended six to eight weeks of physical therapy. But by May, Cole's condition had worsened, and neither her orthopedist nor physical therapist could pinpoint the source of her problem. "My feet were numb all the time," Cole says. At times, the numbness moved up to her waist; she continued to walk, but slowly and with great difficulty, and she also began experiencing pain in her back.

Cole was suffering from peripheral neuropathy, a condition that develops when the peripheral nervous system – the body's communications network that transmits information between the brain and spinal cord and the rest of the body – is severely damaged. After months of fruitless tests and physical therapy, a neurologist took MRIs of Cole's brain, thoracic spine, lumbar spine and cervical area. The thoracic spine MRI revealed Cole had a herniated disc that was compressing her spinal cord below her shoulder blades. "[The doctor] looked at the images and said the only thing that would prevent me from getting worse is surgery," Cole recalls. So she underwent four hours of surgery, as the surgeon conducted a transpedicular excision of the thoracic herniated disc. After her surgery, Cole spent more than two weeks at a subacute rehabilitation center – less intense than a typical rehab facility – doing physical and occupational therapy exercises six days a week to regain the strength in her legs. Three months later, Cole had recovered about 70 percent of her leg capacity.

Cole's case is unusual. The odds that tingling or numbness in your feet means you need surgery to avoid paralysis are quite long, several physicians say. The symptoms Cole experienced typically signal causes other than a herniated disc for peripheral neuropathy, which affects 40 million people nationwide, according to the Foundation for Peripheral Neuropathy. It could cause serious damage to the nerves that go to your feet, which is why it should be treated promptly, whatever is causing it, says Dr. Steven Neufeld, a foot and ankle orthopedic surgeon and director of the Orthopaedic Foot and Ankle Center in Falls Church, Virginia.

Doctors use an array of methods, including full physical exams with blood tests, MRIs, nerve biopsies and nerve conduction velocity tests, to determine the cause of peripheral neuropathy. Here are the leading causes of peripheral neuropathy and ways to treat them:


 Between 60 and 70 percent of people with diabetes suffer from diabetic neuropathies, a family of nerve disorders that can cause tingling and numbness in the feet, hands, arms and legs. Prolonged exposure to high blood sugar can seriously damage nerve fibers, causing diabetic neuropathy. High blood sugar disrupts the ability of the nerves to transmit signals and weakens small blood vessels that provide the nerves with oxygen and nutrients. These neuropathies are treated by treating the patient's diabetes, says Dr. Kenneth Jung, an orthopedic foot and ankle surgeon at the Kerlan-Jobe Orthopedic Clinic in Los Angeles. An improved diet that lowers the patient's blood-sugar levels and lifestyle changes, such as increased levels of exercise that lead to weight loss, are typical methods of treating the disease, Jung says. Some patients may also require medication, such as insulin. Treating diabetes successfully can slow or stop the nerve damage to the feet, but may not reverse the harm that's already been caused, Jung says. Whether a patient regains the use of nerves depends on how much damage he or she has already sustained.


 Some people who drink excessively experience tingling or numbness in their feet from alcoholic neuropathy. This is caused when peripheral nerves are damaged by the consumption of too much alcohol, which is toxic to nerves. Drinking alcoholically can also alter the body's levels of vitamin B12, vitamin B1 and vitamin B7 – nutrients that nerves need to function properly. Clinical studies have shown between 25 and 66 percent of diagnosable alcoholics suffer from this kind of nerve damage, according to Promises Treatment Centers, which has two for-profit alcoholism treatment centers in Los Angeles. That translates to between 4 and more than 10 million people with alcoholic neuropathy. Successful treatment of alcoholism – getting the patient to stop drinking – can restore the person's nutritional health and prevent future nerve damage. But it may not restore the nerves that are already harmed, Jung says. If the patient drank excessively for years, the nerves may be too damaged to repair.


The toxic effects of chemotherapy attack cancer cells but also damage nerves, which can cause neuropathy. Between 30 to 40 percent of the nation's cancer patients who are treated with chemotherapy experience chemotherapy-induced peripheral neuropathy, according to the Foundation for Peripheral Neuropathy. Some patients may experience neuropathy symptoms right after their first dose of chemo; for others, the effects may not surface for months or even years. Physicians can treat this type of neuropathy with several medications, including pregablin and gabapentin, says Dr. Damon Raskin, an internist in private practice who is affiliated with Concierge Choice Physicians in Pacific Palisades, California. Doctors can prescribe these and other medications by themselves or in combination with other drugs. These drugs "don't always restore the patient back to [their] original baseline, but they can lead to a marked improvement," Raskin says. Whether the patient regains their nerve function depends on how much damage the chemo has caused.

No known cause.

 Doctors cannot determine a specific cause for about 23 percent – or more than 9 million people – of all neuropathy sufferers, according to the Foundation for Peripheral Neuropathy. This is known as idiopathic peripheral neuropathy. Doctors treat this kind of neuropathy with the same medications they would prescribe to patients with chemotherapy-induced neuropathy, Raskin says. As is the case with all kinds of neuropathy, whether the patient's nerves are fully restored depends on how much damage they've sustained. Everyone reacts differently to medication, so what is effective for one patient may not be as successful for another.

Wednesday, 22 February 2017

All You Need To Know About Opioids And Pain Treatment

Today's important post from (see link below) will be of interest to all neuropathy patients who's lives have been so disrupted by the disease and the pain that it brings, that they have had no alternative but to use opioids to quell the symptoms. We go to the doctors and 99% of us dread hearing that opioids are the only remaining option but we have to do it in order to live reasonable daily lives. However, the explanation generally ends there. We know they're the strongest analgesics and we're well aware of the dangers of addiction, let alone the potential side effects but if you're between a rock and a hard place, you accept the prescription in good faith! This comprehensive article tells us all we need to know about these drugs and for that reason it can remove much of the anxiety associated with opioids. More than that, it provides the knowledge we need to justify to ourselves and others that although it may not be the solution of choice, it can be a very effective one. We also sign an invisible contract with the doctor to make sure that we are monitored and controlled throughout our use and any potential dangers are dealt with when they begin and not when they've taken hold. Definitely worth a read then for anyone in this situation - it's amazing how much better you feel when you have knowledge in your armory.

Opioids and the Treatment of Chronic Pain: Controversies, Current Status, and Future Directions
Andrew Rosenblum,1,* Lisa A. Marsch,1 Herman Joseph,1 and Russell K. Portenoy2
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available at Exp Clin Psychopharmacol
See other articles in PMC that cite the published article.

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Opioids have been regarded for millennia as among the most effective drugs for the treatment of pain. Their use in the management of acute severe pain and chronic pain related to advanced medical illness is considered the standard of care in most of the world. In contrast, the long-term administration of an opioid for the treatment of chronic non-cancer pain continues to be controversial. Concerns related to effectiveness, safety, and abuse liability have evolved over decades, sometimes driving a more restrictive perspective and sometimes leading to a greater willingness to endorse this treatment. The past several decades in the United States have been characterized by attitudes that have shifted repeatedly in response to clinical and epidemiological observations, and events in the legal and regulatory communities. The interface between the legitimate medical use of opioids to provide analgesia and the phenomena associated with abuse and addiction continues to challenge the clinical community, leading to uncertainly about the appropriate role of these drugs in the treatment of pain. This narrative review briefly describes the neurobiology of opioids and then focuses on the complex issues at this interface between analgesia and abuse, including terminology, clinical challenges, and the potential for new agents, such as buprenorphine, to influence practice.
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Opioids play a unique role in society. They are widely feared compounds, which are associated with abuse, addiction and the dire consequences of diversion; they are also essential medications, the most effective drugs for the relief of pain and suffering (Portenoy et al, 2004). Historically, concerns about addiction have apparently contributed to the undertreatment of disorders widely considered to be appropriate for opioid therapy, including cancer pain, pain at the end-of-life, and acute pain (Field and Cassel, 1997; Schnoll & Weaver, 2003; Portenoy & Lesage, 1999; Breitbart et al. 1998; Smith et al., 2008). The use of opioids for chronic non-malignant pain (CNMP) remains controversial (Manchikanti, 2008; McQuay, 1999). Following publication of reports on the safety and efficacy of opioids prescribed to small numbers of patients with CNMP (e.g., Portenoy and Foley, 1986; Nyswander and Dole, 1986) and the publication of a seminal article entitled “The Tragedy of Needless Pain”, (Melzack, 1990), the use of opioids to treat CNMP began to be more widely practiced and incorporated into clinical guidelines. Nevertheless, despite the advances in pain medicine and the wider use of opioids for various chronic pain conditions, there is still considerable controversy surrounding the type of conditions that should be treated, whether the treatment can be generally safe and effective in selected patients, and what the clinical goals should be (Ballantyne & Forge, 2007; Streltzer & Johansen, 2006; Stretzler & Kosten 2003).
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History of Opioids

The Sumerians in Mesopotamia were among the first people identified to have cultivated the poppy plant around 3400 BC. They named it Hul Gil, the “joy plant” (Booth, 1986). It eventually spread throughout the ancient world to every major civilization in Europe and Asia and was used to treat pain and many other ailments (Schiff, 2002; Askitopoulou, Ramoutsaki, & Konsolaki, 2002; Booth, 1986; Dikotter, Laaman, & Xun, 2004).

Developments in the 19th century transformed the practice of medicine and initiated the tension between the desire to make available the medicinal benefits of these drugs and recognition that the development of abuse and addiction can lead to devastating consequences for individuals and for society at large (Booth, 1986; Musto, 1999):
In 1803 morphine, an opioid analgesic, was extracted from opium by Friedrich Serturner of Germany;
Dr. Charles Wood, a Scottish physician, invented the hyperdermic needle and used it to inject morphine to relieve pain from neuralgia;
Dr. Eduard Livenstein, a German physician, produced the first accurate and comprehensive description of addiction to morphine, including the withdrawal syndrome and relapse, and argued that craving for morphine was a physiological response.
Diacetylmorphine (brand name heroin) was synthesized and briefly promoted as more effective and less addictive than morphine. In the early 20th century, when heroin was legally marketed in pill form, it was used by young Americans to elicit intense euphoria by crushing the heroin pills into powder for inhalation or injection (Katz et al., 2007, c.f. Meldrum, 2003; Hosztafi, 2001).

Beginning in the twentieth century, there were many research advances and major changes in the way opioids were used for the treatment of pain and addiction (Ballantyne, 2006; Corbett et al., 2006). These included attempts among several nations and international organizations to control the distribution and use of opioids (Musto, 1999); the introduction of opioid maintenance therapy for the treatment of opioid addiction (first with morphine and later with methadone, LAAM (levo-alpha acetyl methadol) and sublingual buprenorphine) (Courtwright, Joseph & Des Jarlais, 1989; Strain & Stitzer, 2006); the discovery of the endogenous opioids (Hughes, Smith, Kosterlitz, Fothergill, Morgan & Morris, 1975); and the recognition that pain is a debilitating and destructive disease and that opioids are essential for the treatment of many forms of acute and chronic pain.

During most of the twentieth century, the widely held perception among professionals in the United States was that the long-term use of opioid therapy to treat chronic pain was contraindicated by the risk of addiction, increased disability and lack of efficacy over time. During the 1990’s, a major change occurred, driven by a variety of medical and nonmedical factors (see below). The use of opioids for chronic pain began to increase, showing a substantial year-to-year rise that continues today. This increased use of opioids for legitimate medical purposes has been accompanied by a substantial increase in the prevalence of nonmedical use of prescription opioids (Zacny, et al., 2003). The National Survey on Drug Use and Health reported that the number of first time abusers of prescription opioids increased from 628,000 in 1990 to 2.4 million in 2004, that emergency room visits involving prescription opioid abuse increased by 45% from 2000 to 2002, and that treatment admissions for primary abuse of prescription opioids increased by 186% between 1997 and 2002 (SAMHSA, 2004a, 2004b). Opioid abuse indices rose most for two frequently prescribed opioids, hydrocodone and controlled-release (CR) oxycodone (Cicero, Inciardi, Munoz, 2005). Although the increase in prescription drug abuse is likely to be multifactorial, it is likely to reflect, in part, changes in available drug formulations and prescribing practices of opioid medication (Compton and Volkow, 2006). This link between increased medical use and increased abuse has driven some of the re-examination of the medical role of these drugs. The challenge, of course, is to reduce the likelihood of opioid misuse while not imposing barriers on the legitimate use of opioid medications, acknowledging both that increased abuse is probably inevitable when a psychoactive drug becomes more accessible and that attempts to control abuse can have the unintentional effects of discouraging treatment and placing severe restrictions on the medical profession.
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Brief Overview of Opioids: Neurobiology and Mechanism of Action

The term opioid refers to all compounds that bind to opiate receptors. Conventionally, the term opiate can be used to describe those opioids that are alkaloids, derived from the opium poppy; these include morphine and codeine. Opioids include semi-synthetic opiates, i.e., drugs that are synthesized from naturally occurring opiates (such as heroin from morphine and oxycodone from thebaine), as well as synthetic opioids such as methadone, fentanyl, and propoxyphene. The term narcotic is a legal designation and should not be used in the clinical setting; it refers to opioids and a few other drugs that are grouped with the opioids by law enforcement.

In the United States, numerous opioids have been commercialized for oral, transdermal and intravenous administration. Oral and transdermal formulations are usually administered for pain in the ambulatory setting. These include combination products, such as those containing hydrocodone and acetaminophen (Vicodin®, Lorset®) or ibuprofen (Vicoprofen®), tramadol and acetaminophen (Ultracet®), oxycodone and acetaminophen or aspirin (Percocet® or Percodan®), and those containing codeine and acetaminophen or aspirin. The single entity formulations on the market include those containing morphine (Avinza®, Kadian®, MS Contin®, MSIR®), oxycodone (OxyContin®), fentanyl (Duragesic®, Actiq®, Fentora®), hydromorphone (Dilaudid®), oxymorphone (Opana®), and methadone.

Opioids act by binding to specific proteins, called opioid receptors. Receptors are widely distributed. Those involved in pain modulation are situated in both the central nervous system and the peripheral nervous system. These receptors also bind endogenous opioid peptides (endorphins), which are involved in pain modulation and numerous other functions in the body. Among these functions are those mediated by deep structures of the brain, which are involved in the modulation of reinforcement and reward mechanisms, mood and stress. Opioid receptors are also found on cells from the immune system (Bidlack, 2000). In studies with rats, activation of these receptors with morphine is associated with varied effects, including sensitization of afferent nerves to noxious stimuli (Raghavendra, Rutkowski, & DeLeo, 2002).

When an opioid given for pain binds to receptors, analgesia may be accompanied by any of a diverse array of side effects related to the activation of receptors involved in other functions. These may include effects mediated by peripheral or by peripheral and central mechanisms, such as reduced peristalsis (leading to constipation) and itch, or primary central nervous system effects, such as miosis, (pupillary constriction) somnolence, mental clouding, and respiratory depression (Jaffe & Jaffe, 2004; Jaffe & Martin, 1990). Central mechanisms also lead to changes associated with hyperalgesia and decreased responsiveness to opioids (tolerance) and it has been speculated that opioid-induced hyperalgesia may be a clinically-relevant phenomenon leading to increased pain in some situations (Deleo, Tanga, & Tawfik, 2004). Activation of other central nervous system pathways by opioids also may produce mood effects, either dysphoria or euphoria.

Presumably, binding to those receptors involved in reinforcement and reward also occurs whenever an opioid is taken. In most individuals, when opioids are taken to treat pain, there appears to be no overt effect from change in these systems. In some cases, however, powerful reinforcement occurs, expressed as efforts to repeat the administration and these reinforcing outcomes may be associated with craving and with positive mood effects such as euphorigenic or pleasurable effects (Di Chiara, 2002; Koob & Bloom, 1988). These outcomes, which are uncommon but potentially serious when they occur (driving the development of an addictive pattern of use), can occur in the presence or absence of pain. Although these effects could be associated with iatrogenic addiction, they appear to be rare in patients who do not have risk factors suggesting the existence of the biological substrate for opioid-induced craving (see below).

Although several types of opioid receptors exist (e.g., mu, kappa and delta), opioid drugs largely produce their analgesic and reinforcing effects via activation of the mu opioid receptor; thus, opioids used for pain are often described as, “mu agonists”. Mu drugs that have the ability to fully activate opioid receptors (e.g., higher doses produce greater receptor activation in a dose-dependent manner) are referred to as opioid agonists or full mu agonists (such as morphine, oxycodone and methadone). Those opioids that occupy, but do not activate, receptors are referred to as opioid antagonists (e.g., naltrexone, naloxone); they can reverse the effects of mu opioid agonists. Those opioids that either have a low intrinsic activity at the mu receptor, or are agonists at another receptor and antagonists at the mu receptor are called agonist-antagonist drugs. Those with a low intrinsic activity are called partial opioid agonists and are characterized by a ceiling on most agonist activity, such that increases in dose will increase the drug’s physiological and subjective effects only to a certain level and further dose increases produce no additional effects (Jaffe & Martin, 1990).

These differences in mu receptor interactions are clearly related to the clinical use of opioid drugs and their abuse liability. Agonist-antagonist drugs are less attractive than pure mu agonists to individuals with addiction and no pain. Although other biochemical and molecular processes are presumably relevant to variation in these effects, relatively little is known about the interactions among these processes in humans.

The clinical use of opioid drugs is influenced by a variety of other characteristics, including pharmacokinetics. With the notable exception of methadone and buprenorphine, most opioids have relatively short half-lives and this has necessitated the development of new delivery systems designed to provide prolonged effects and a longer dosing interval.

Clinically-relevant physical dependence and tolerance (see below) may occur with short-term or long-term use of an opioid compound, particularly a pure mu agonist. These phenomena, which vary greatly in the clinical setting, represent neuroadaptational processes. The neurophysiology of physical dependence and tolerance are closely related to each other and to the phenomenon of opioid-induced hyperalgesia (Mao, 2002). The possibility that opioid administration, particularly at relatively high doses, may lead to increased pain has contributed to the controversy about opioid therapy for non-cancer pain, notwithstanding the limited evidence that this phenomenon occurs in clinical settings.
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Brief Overview of Chronic Pain

Chronic pain has been described as pain that has persisted for at least 1 month following the usual healing time of an acute injury, pain that occurs in association with a nonhealing lesion, or pain that recurs frequently over a period of months. In most clinical and research reports, chronic pain is typically defined as pain that has persisted for at least 3 months (Verhaak, Kerssens, Dekker, Sorbi, & Sensing, 1998).

The prevalence of chronic pain in the general population is believed to be quite high, although published reports have varied greatly. Cautious cross-national estimates of chronic pain range from 10% (Verhaak et al., 1998) to close to 20% (Gureje, Simon, & Von Korff, 2001), which would represent 30 to 60 million Americans. A national survey of 35,000 households in the US, conducted in 1998, estimated that the prevalence among adults of moderate to severe non-cancer chronic pain was 9% (American Pain Society, 1999). A large survey (N=18,980) of general populations across several European countries reported that the prevalence for chronic painful physical conditions was 17.1% (Ohayon & Schatzberg, 2003).

Chronic pain is a highly complex phenomenon, which may or may not be primarily driven by tissue injury. Conventionally, the most common forms of chronic pain are divided into those labeled “nociceptive”, or pain caused by ongoing stimulation of pain receptors by tissue damage, and those labeled “neuropathic”, or pain presumed to be related to damage to or dysfunction of the peripheral or central nervous system. These categories of pain simplify a complex reality in which both acute and chronic pain are induced by multiple peripheral and central mechanisms, which continually interact with each other and with numerous pain modulating systems. The perturbations that ultimately results in pain perception are caused by neurophysiological processes and other related systems. For example, recent evidence has begun to highlight the role of neuroimmune activation following a tissue injury as an important mechanism in the development of chronic pain (DeLeo, 2006). The role of cytokines and other inflammatory mediators is obvious in inflammatory nociceptive pains, such as some types of arthritis, but new data suggest an equally salient role in the development of chronic neuropathic pain associated with central sensitization of neural pathways following peripheral injury (Deleo, 2006).

All chronic pain is profoundly influenced by psychological processing and responses (Turk & Melzack, 2001). Pain severity and pain-related functional impairment are often found to be associated with psychological and social factors, and patients with identical diseases associated with pain, such as degenerative disk disease, may vary greatly in their reports of pain severity and pain behaviors (Aronoff, 1999). There is an extensive literature documenting the importance of operant conditioning factors (Fordyce, 1976) and cognitive-behavioral factors (Turk, Meichenbaum, & Genest, 1983) in the maintenance of chronic pain behaviors.

Chronic pain also is influenced by psychosocial and psychiatric disturbances, such as cultural influences, social support, comorbid mood disorder, and drug abuse (Gatchel, Peng, Peters, Fuchs & Turk, 2007). Classic studies of pain behavior indicate that cultural differences in the beliefs and attitudes towards pain (e.g., Zbrowski, 1969) and the social/environmental context of the pain (e.g., Beecher, 1959) have a significant impact on pain behaviors.

The contribution of psychological, social and psychiatric factors should not lead to the conclusion that a pain syndrome is primarily psychogenic. Pain related exclusively or primarily to psychological factors occurs, but is far less prevalent than pain associated with organic processes that are powerfully influenced by psychosocial mediators and psychiatric comorbidities (Portenoy, Payne, & Passik, 2004).

The “pattern of suffering” or the pain-related disability that often occurs in concert with persistent pain commonly touches on all domains of function. Patients with chronic pain may demonstrate pain-related interference with ability to perform usual activities at home, work, or school; maladaptive or dysfunctional behaviors, social isolation, and poor sleep patterns; and frequent health care utilization (Dworkin & Sherman, 2001). The recognition that acute pain can compromises health has led major medical associations and accreditation committees to designate pain severity as a “fifth vital sign”, along with blood pressure, temperature, heart rate, and respiration (Fishman, 2005). Further recognition of the increased interest in the assessment and management of pain is underscored by the U.S. Federal Law (Pain Relief Promotion Act of 2000) that declared the first decade of the 21st century as the Decade of Pain Control and Research (Gatchel et al., 2007).

Chronic pain is a major public health problem, which is associated with devastating consequences to patients and families, a high rate of health care utilization, and huge society costs related to lost work productivity. The existing treatments for chronic pain are unable to address the problem and better therapies are urgently needed. The need for these therapies is the backdrop for the expanding use of opioid drugs. An extensive clinical experience indicates that long-term opioid therapy is able to help selected patients have a better quality of life, less use of health care, and improved productivity. The medical community is no longer debating the reality of these outcomes, but rather, is now focused on a more fruitful debate about patient selection and the benefits and burdens of these drugs in varied subpopulations. Whether the frame of reference is the individual patient and family, or society-at-large, the issue is about balancing the potential benefits of these drugs in the large and diverse population with chronic pain with its potential risks.
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Terminology of Opioid Abuse: Dependence, Tolerance, Addiction

Concerns that addiction is a frequent iatrogenic consequence of the medical use of opioids may partially be attributed to confusion over terminology, as a well as failure to recognize that both addiction and chronic pain have a multifactorial etiology. In an effort to develop universal agreement on terminology related to addiction, the American Academy of Pain Medicine (AAPM), the American Pain Society (APS), and the American Society of Addiction Medicine (ASAM) approved a consensus document that clarified this terminology (ASAM, 2001; Savage, 2003).

According to the consensus document, tolerance is defined as a decreased subjective and objective effect of the same amount of opioids used over time, which concomitantly requires an increasing amount of the drug to achieve the same effect. Although tolerance to most of the side effects of opioids (e.g., respiratory depression, sedation, nausea) does appear to occur routinely, there is less evidence for clinically significant tolerance to opioids– analgesic effects (Collett, 1998; Portenoy et al., 2004). For example, there are numerous studies that have demonstrated stable opioid dosing for the treatment of chronic pain (e.g., Breitbart, et al., 1998; Portenoy et al., 2007) and methadone maintenance for the treatment of opioid dependence (addiction) for extended periods (Strain and Stitzer, 2006). However, despite the observation that tolerance to the analgesic effects of opioid drugs may be an uncommon primary cause of declining analgesic effects in the clinical setting, there are reports (based on experimental studies) that some patients will experience worsening of their pain in the face of dose escalation (Ballantyne, 2006). It has been speculated that some of these patients are not experiencing more pain because of changes related to nociception (e.g. progression of a tissue-injuring process), but rather, may be manifesting an increase in pain as a result of the opioid-induced neurophysiological changes associated with central sensitization of neurons that have been demonstrated in preclinical models and designated opioid-induced hyperalgesia (Mao, 2002; Angst & Clark, 2006). Analgesic tolerance and opioid-induced hyperalgesia are related phenomena, and just as the clinical impact of tolerance remains uncertain in most situations, the extent to which opioid-induced hyperalgesia is the cause of refractory or progressive pain remains to be more fully investigated. Physical dependence represents a characteristic set of signs and symptoms (opioid withdrawal) that occur with the abrupt cessation of an opioid (or rapid dose reduction and/or administration of an opioid antagonist). Physical dependence symptoms typically abate when an opioid is tapered under medical supervision. Unlike tolerance and physical dependence which appear to be predictable time-limited drug effects, addiction is a chronic disease that “represents an idiosyncratic adverse reaction in biologically and psychosocially vulnerable individuals” (ASAM, 2001).

The distinction between physical dependence and addiction is not always made clear in the pain literature (Ferrell, McCaffery, Rhiner, 1992). Most patients who are administered opioids for chronic pain behave differently from patients who abuse opioids and do not ever demonstrate behaviors consistent with craving, loss of control or compulsive use (e.g., Cowan et al., 2001). Of course, pain and addiction are not mutually exclusive and some patients who are treated for pain do develop severe behavioral disturbances indicative of a comorbid addictive disorder.

Some patients who are treated with opioids for pain display problematic behaviors that, on careful assessment, do not reflect addiction, but rather, appear to relate to a different process. This may be another psychiatric disorder associated with impulsive drug-taking, an unresolved family issue, a disorder of cognition, or criminal intention. In addition, there appear to be some patients who engage in problematic behaviors related specifically to desperation about unrelieved pain. The term pseudoaddiction was coined to describe the latter phenomenon (Weissman & Haddox, 1989).

Behaviors that may represent pseudoaddiction and behaviors that reflect addiction or some other serious psychopathology can occur simultaneously, and presumably, one type of phenomenon may incite the others. The diagnosis of these and other conditions may be challenging and requires a careful assessment of clinical phenomenology, specifically a range of drug-related behaviors during treatment with a potentially abusable drug (Portenoy, 1994, Lue, Passik, & Portenoy, 1998).

The term aberrant drug-related behaviors has been used to indicate the broad array of problematic nonadherence behaviors (Passik, Kirsh, Donaghy, & Portenoy, 2006), the nature of which is uncertain until a diagnosis can be developed based on astute clinical assessment. Some aberrant drug-related behavior strongly suggests the existence of addiction. These may include the use of alternative routes of administration of oral formulations (e.g., injection or sniffing), concurrent use of alcohol or illicit drugs, and repeated resistance to changes in therapy despite evidence of adverse effects; examples of aberrant behavior less suggestive of addiction are drug hoarding during periods of reduced symptoms, occasional unsanctioned dose escalation, and aggressive complaining about the need for more drugs (Portenoy, 1994).
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Distinction between Withdrawal and Chronic Pain

Because addiction is associated with psychological distress and physical discomfort in the form of opioid withdrawal symptoms, it may be difficult to distinguish primary chronic pain complaints from withdrawal pain. Withdrawal also may have the potential to increase baseline pain related to other processes. For example, based on anecdotal evidence from chronic pain patients, withdrawal from opioids can greatly increase pain in the original pain site. These phenomena suggest the need to carefully assess the potential for withdrawal during long-term opioid therapy (e.g, at the end of a dosing interval or during periods of medically-indicated dose reduction).

These phenomena notwithstanding, there also is evidence that experienced drug abusers are able to distinguish withdrawal pain from chronic pain. For example in studies of methadone maintenance patients, both the phenomenology and correlates of chronic pain were different than for withdrawal pain (Karasz et al., 2004; Rosenblum et al., 2003). Chronic pain is typically localized (e.g., back pain, headache) and persists (although with varying degrees of severity) for long periods of time (Gureje, Von Korff, Simon & Gater, 1998). Although certain subjective experiences of withdrawal (e.g., muscle ache) are similar to some distinct pain syndromes, other withdrawal experiences such as yawning, sweating and hot and cold flashes are likely to be more commonly associated with subjective drug withdrawal than with primary pain conditions. Moreover, the constellation of words used to describe withdrawal pain is likely to be different than words used to describe other painful disorders. Qualitative studies of addicts going through withdrawal typically refer to the experience as “being sick” (similar to a moderate to severe flu-like illness) and not as representing a distinct pain (Farrell, 1994). The subjective experience of withdrawal can be validly measured with an instrument such as the Subjective Opiate Withdrawal Scale (SOWS; Handelsman, et al., 1987). Withdrawal from short-acting opioids, such as heroin, is typically short-lived; physical symptoms are likely to reach their maximum intensity over a 36–72 hour period and to reduce in intensity after that (Farrell, 1994).
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Co-occuring Chronic Pain and Opioid Addiction

The prevalence of addictive disorders among chronic pain patients is difficult to determine (Covington and Kotz 2003). One 1992 literature review found only seven studies that utilized acceptable diagnostic criteria and reported that estimates of substance use disorders among chronic pain patients ranged from 3.2% – 18.9% (Fishbain, Rosomoff, & Rosomoff, 1992). A Swedish study of 414 chronic pain patients reported that 32.8% were diagnosed with a substance use disorder (Hoffmann, Olofsson, Salen, & Wickstrom, 1995). In two US studies, 43 to 45% of chronic pain patients reported aberrant drug-related behavior; the proportion with diagnosable substance use disorder is unknown (Katz et al., 2003; Passik et al., 2004). All these studies evaluated patients referred to pain clinics and may overstate the prevalence of substance abuse in the overall population with chronic pain.

A relatively high prevalence of substance abuse disorders among persons with chronic pain can also be inferred by the high co-occurrence of these two disorders. There have been several reports that the prevalence of chronic pain among persons with opioid and other substance use disorders is substantially higher than the pain prevalence found in the general population (Breitbart, et al., 1996; Brennan, Schutte, & Moos, 2005; Jamison, Kauffman, & Katz, 2000; Rosenblum et al., 2003; Sheu, et al., 2008).
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Opioid Treatment for Chronic Pain

Opioid therapy is the mainstay approach for the treatment of moderate to severe pain associated with cancer or other serious medical illnesses (Patt & Burton, 1998; World Health Organization, 1996). Although the use of opioid analgesics for the treatment of CNMP has been increasing in recent years (Joranson, Ryan, Gilson & Dahl, 2000) and has been endorsed by numerous professional societies (AAPM, APS, 1997; American Geriatric Society, 1998; Pain Society, 2004), the use of opioids remains controversial due to concerns about side effects, long-term efficacy, functional outcomes, and the potential for drug abuse and addiction. The latter concerns are especially evident in the treatment of CNMP patients with substance use histories (Savage, 2003).

Other concerns that may contribute to the hesitancy to prescribe opioids may be related to perceived and real risks associated with regulatory and legal scrutiny during the prescribing of controlled substances (Office of Quality Performance, 2003). These concerns have propelled extensive work to develop predictors of problematic behaviors or frank substance abuse or addiction during opioid therapy. Questionnaires to assist in this prediction and monitoring have been developed and used in research and field trials. Examples include the Prescription Drug Use Questionnaire (PDUQ; Compton et al., 1998); the Pain Assessment and Documentation Tool (PADT; Passik et al., 2004) and the Current Opioid Misuse Measure (COMM; Butler et al., 2007). These instruments are not used in practice settings at this time.

Narrative reports on the use of opioids for CNMP have underscored the effectiveness of opioid therapy for selected populations of patients and there continues to be a consensus among pain specialists that some patients with CNMP can benefit greatly from long-term therapy (Ballantyne & Mao, 2003; Trescot et al., 2006). This consensus, however, has received little support in the literature. Systematic reviews on the use of opioids for diverse CNMP disorders report only modest evidence for the efficacy of this treatment (Trescot et al., 2006; 2008). For example, a review of 15 double-blind, randomized placebo-controlled trials reported a mean decrease in pain intensity of approximately 30% and a drop-out rate of 56% only three of eight studies that assessed functional disturbance found improvement (Kalso, Edwards, Moore, & McQuay, 2004). A meta-analysis of 41 randomized trials involving 6,019 patients found reductions in pain severity and improvement in functional outcomes when opioids were compared with placebo (Furlan, Sandoval, Mailis-Gagnon, & Tunks, 2006). Among the 8 studies that compared opioids with non-opioid pain medication, the six studies that included so-called “weak” opioids (e.g., codeine, tramadol) did not demonstrate efficacy, while the two that included the so-called “strong” opioids (morphine, oxycodone) were associated with significant decreases in pain severity. The standardized mean difference (SMD) between opioid and comparison groups, although statistically significant, tended to be stronger when opioids were compared with placebo (SMD = 0.60) than when strong opioids where compared with non-opioid pain medications (SMD = 0.31). Other reviews have also found favorable evidence that opioid treatment for CNMP leads to reductions in pain severity, although evidence for increase in function is absent or less robust (Chou, Clark, & Helfand, 2003; Eisenberg, McNicol, & Carr, 2005). Little or no support for the efficacy of opioid treatment was reported in two systematic reviews of chronic back pain (Deshpande, Furlan, Mailis-Gagnon, Atlas, & Turk, 2007; Martell, et al., 2007). Because patients with a history of substance abuse typically are excluded from these studies, they provide no guidance whatsoever about the effectiveness of opioids in these populations.

Adding further to the controversy over the utility of opioid analgesics for CNMP is the absence of epidemiological evidence that an increase in the medical use of opioids has resulted in a lower prevalence of chronic pain. Noteworthy is a Danish study of a national random sample of 10,066 respondents (Eriksen, Sjøgren, Bruera, Ekholm, & Rasmussen, 2006). Denmark is known for having an extremely high national usage of opioids for CNMP and this use has increased by more than 600% during the past two decades (Eriksen, 2004). Among respondents reporting pain (1,906), 90% of opioid users reported moderate to very severe pain, compared with 46% of non-opioid users; opioid use was also associated with poor quality of life and functional disturbance (e.g., unemployment).

Although this epidemiological study may be interpreted as demonstrating that opioid treatment for CNMP has little benefit, the authors acknowledge that these disquieting findings do not indicate causality and could be influenced by the possibility of widespread undertreatment, leading to poorly managed pain. This latter interpretation is supported by a commentary on the Ericksen et al. study (Keane, 2007). Keane notes that among the 228 pain patients receiving opioids only 57 (25%) were using strong opioids, while the remainder was using weak opioids. European (as well as United States) clinical guidelines generally recommend long-acting formulations of strong opioids for the treatment of chronic moderate to severe pain, which may be supplemented with short-acting opioids for breakthrough pain (Pain Society, 2004; OQP, 2003; Gourlay, 1998; Vallerand, 2003; Fine & Portenoy, 2007).

The possibility of inappropriate opioid treatment is further supported by another Danish study that assigned pain patients who were on opioid therapy to either a multidisciplinary pain center (MPC) or to general practitioners (GP) who had received initial supervision from the MPC staff (Eriksen, Becker, & Sjegren, 2002). At intake, a substantial number of patients in both groups were apparently receiving inappropriate opioid therapy for chronic pain (60% were being treated with short-acting opioids and 49% were taking opioids on demand). At the 12 month follow-up, 86% of MPC patients were receiving long-acting opioids and 11% took opioids on demand. There was no change in the administration pattern in the GP group. These findings suggest that a significant proportion of opioid-treated CNMP patients may be receiving inappropriate opioid treatment and that educating general practitioners in pain medicine may require more than initial supervision.

It is generally acknowledged that there is a wide degree of variance in the prescribing patterns of opioids for chronic pain (Lin, Alfandre, & Moore, 2007; Trescot et al., 2006). Some opioid treatment practices persist despite evidence that they might be harmful or have little benefit, such as the over-prescribing of propoxyphene among the elderly (Barkin, Barkin, & Barkin, 2006; Singh, Sleeper, & Seifert, 2007). Nursing home patients being treated with opioids have been found to be inadequately assessed for pain and to be more likely treated with short-acting rather than long acting opioids (Fujimoto & Coluzzi, 2000). A substantial number of physicians are reluctant or unwilling to prescribe long-acting opioids to treat CNMP, even when it may be medically appropriate (Nwokeji, et al., 2007).

Controversy about the long-term effectiveness of opioid treatment also has focused on the potential clinical implications of opioid-induced hyperalgesia. As noted earlier, exposure to opioids can result in an increased sensitivity to noxious stimuli in animals, and an increased perception of some types of experimental pain in humans (c.f., Koppert & Schmeltz, 2007; Angst & Clark, 2006). Anecdotal reports of hyperalgesia occurring with very high or escalating doses of opioids (Angst & Clark, 2006) has been viewed as a clinical correlate of these experimental findings. The extent to which this phenomenon is relevant to the long-term opioid therapy administered to most patients with chronic pain is unknown. Although experimental evidence suggests that opioid-induced hyperalgesia might limit the clinical utility of opioids in controlling chronic pain (Chu, Clark, & Angst., 2006), there have been no reports of observations in the clinical literature to suggest that it should be a prominent problem. More research is needed to determine whether the physiology underlying opioid-induced hyperalgesia may be involved in a subgroup of patients who develop problems during therapy, such as loss of efficacy (tolerance) or progressive pain in the absence of a well defined lesion.

Outcome studies of long term use of opioids are compromised by methodological limitations which make it difficult to acquire evidence of efficacy (Noble, Tregear, Treadwell, & Schoelles, 2007). Methodological limitations may be unavoidable because of the ethical and practical challenges associated rigorous studies such as randomized controlled trials. Guidelines for opioid therapy must now be based on limited evidence; future evidence may be acquired by utilizing other study designs (Noble et al., 2007) such as practical clinical trials (Tunis, Stryer, & Clancy, 2003). These studies should include at least three criteria to reflect a positive treatment response: i.e., reduction of pain severity (derived from subjective reports or scores on pain scales), recovery of function (improved scores on instruments that measure some aspect of function), and quality of life.

Guidelines for the use of opioids for the treatment of chronic pain have been published (AAFP et al., 1996–2002; OQP, 2003), and recent guidelines have emphasized the need to initiate, structure and monitor therapy in a manner that both optimizes the positive outcomes of opioid therapy (analgesia and functional restoration) and minimize the risks associated with abuse, addiction and diversion (Portenoy et al., 2004). These guidelines discuss patient selection (highlighting the likelihood of increased risk among patients with prior histories of substance use disorders), the structuring of therapy to provide an appropriate level of monitoring and a presumably lessened risk of aberrant drug-related behavior, the ongoing assessment of drug-related behaviors and the need to reassess and diagnose should these occur, and strategies that might be employed in restructuring therapy should aberrant behaviors occur and the clinician decide to continue treatment. They also note that therapy should be undertaken initially as a trial, which could lead to the decision to forego more therapy, and that an “exit strategy” must be understood to exist should the benefits in the individual be outweighed by the burdens of treatment.

The relatively recent recognition that guidelines for the opioid treatment of chronic pain must incorporate both the principles of prescribing as well as approaches to risk assessment and management may represent an important turning point for this approach to pain management. Acknowledging that prescription drug abuse has increased during the past decade, a period during which the use of opioid therapy by primary care physicians and pain specialists has accelerated, pain specialists and addiction medicine specialists now must collaborate to refine guidelines, help physicians identify the subpopulations that can be managed by primary care providers, and discover safer strategies that may yield treatment opportunities to larger numbers of patients.
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Treating Patients with Addictive Disorders

Safe and effective pain treatment is especially important for persons with a drug use history because inadequate treatment or lack of treatment for pain may have problematic consequences, such as illicit drug use (e.g., heroin), misuse of prescription opioids and other pain medications (e.g., benzodiazipines), psychiatric distress, functional impairment and a tendency for health providers to attribute pain complaints and requests for pain medication to an addictive disorder rather than to a pain disorder (Gureje, et al., 2001; Scimeca, Savage, Portenoy, & Lowinson, 2000). Undertreatment of pain among addicted persons may lead to the adverse medical, social and personal consequences associated with continued drug-seeking behavior (Savage, 1996). Pain complaints may be most problematic among persons with opioid addiction, as this group may have lower tolerance for pain than other addicted populations (Compton, 1994; Compton, Charuvastra, & Ling, 2001). Pain and opioid addiction may be further intertwined among persons who have a history of abusing controlled opioid pain medications, such as oxycodone or hydrocodone.
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A Possible Role on the use of Buprenorphine for the Treatment of Chronic Pain

Increasing interest in developing clinical protocols for opioid treatment of chronic pain in the population with substance abuse histories has highlighted the role of opioid medications that may have lower abuse potential. One medication that is beginning to be examined is buprenorphine, a partial opioid mu agonist that is well recognized as an analgesic (Johnson, Fudala, & Payne, 2005). In 2002, a sublingual tablet (both in mono form – Subutex® - and combined with naloxone - Suboxone®) was approved by the U.S Food and Drug Administration as a Schedule III medication for the treatment of opioid dependence. In numerous controlled clinical trials, it has been demonstrated to be highly efficacious in reducing illicit opioid use and promoting treatment retention among opioid abusers (e.g., Johnson, Strain, & Amass, 2003; Kakko, Svanborg, Kreek, Heilig, 2003; O'Connor et al., 1998; Fudala et al., 2003). In opioid addicts, it suppresses the craving and withdrawal symptoms associated with opioid use and also blocks the euphoric effects of subsequent opioid use (See Bickel & Amass, 1995 for a review).

As a partial mu-agonist, buprenorphine has a ceiling effect on its agonist activity (Lewis, 1985; Walsh, Preston, Bigelow & Stitzer, 1995). It is less likely than a full agonist to cause respiratory depression in opioid-naïve patients (Cowan, Lewis & Macfarlane, 1977). This property of buprenorphine increases its safety profile by reducing the risk of accidental overdose (Walsh, Preston, Stitzer, Cone & Bigelow, 1994). The partial agonism of buprenorphine would presumably yield a ceiling effect for analgesia as well, which would limit the clinical use of the drug in pain management, but there is some question about the extent of this ceiling effect in practice (Dahan, et al., 2006).

Although the combination buprenorphine/naloxone tablet (Suboxone) may precipitate withdrawal in opioid-tolerant persons if it is injected, making it relatively unattractive for diversion (CSAT, 2004), there is nevertheless evidence of diversion, as would be expected with any psychoactive drug that has hedonic properties (Cicero & Inciadi, 2005; Smith, Bailey, Woody, & Kleber, 2007). Rates of abuse are relatively low compared to full mu agonists and buprenorphine rarely is endorsed as a primary drug of abuse (Cicero, Suratt, & Inciardi, 2007; Rosenblum et al., 2007; SAMHSA, 2006).

In Europe, a transdermal formulation of buprenorphine has been approved for the treatment of chronic pain (e.g., Griessinger, Sittl, & Likar, 2005; Sittl, 2005). In post-marketing surveillance studies and in a multicenter randomized controlled clinical trial, the transdermal patches were reported to be effective and well-tolerated in the treatment of cancer and non-cancer chronic pain (Griessinger et al., 2005; Sittl, 2005; Sorge and Stittl, 2004; Sittl, Nuijten, & Nautru, 2006). A transdermal formulation of buprenorphine is not presently available in the United States.

The off-label use of sublingual buprenorphine tablets to treat chronic pain has been described in two clinical reports, one describing its use in a series of chronic pain patients who were responding poorly to other opioid analgesics (Malinoff et al., 2005) and the other describing the response of patients with both pain and addiction (Heit & Gourlay, 2008). In both of these reports, the authors reported that their patients were successfully treated with buprenorphine, e.g., pain relief and improved mood and functioning.

In a similar manner, two earlier publications describe the open-label use of the parenteral formulation of buprenorphine administered sublingually to treat patients with chronic pain (Adriaensen, Mattelaer, & Vanmeenen, 1985; Nasar, McLeavy, & Knox, 1986). Although most patients were followed up for less than one month, both studies reported good analgesia and low incidence or time-limited unwanted side effects. There is also evidence from several preclinical studies and one study with human subjects that, in contrast to pure mu-agonists, buprenorphine exerts a lasting anti-hyperalgesic effect (Hans, 2007; Koppert, et al., 2005). The transdermal trials conducted in Europe, the anecdotal reports of sublingual administration in North America, and buprenorphine’s comparatively high safety profile suggest that it would be valuable to systematically study buprenorphine as a treatment of pain in patients with substance use disorders.
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Opioids are among the most effective medications for moderate to severe pain. Although there is a consensus on their utility as a treatment for chronic cancer pain, their long-term use for chronic non-malignant pain remains controversial. Several medical professional organizations acknowledge the utility of opioid therapy and many case series and large surveys report satisfactory reductions in pain, improvement in function and minimal risk of addiction. However, the clinical trials that have been conducted do not provide adequate evidence of long-term effectiveness. Despite the consensus of pain specialists, and the eminently ethical and medically justified commentaries to consider opioid therapy in the armamentarium of treatments for moderate to severe pain (Brennan, Carr, & Cousins, 2007), there is concern that the pendulum has swung from undertreatment to overtreatment (White & Kehlen, 2007). This controversy is enhanced by the increased prevalence of prescription opioid abuse, which has developed concomitantly with an increase in opioid administration in the clinic. The resolution of this controversy will require much more research and the acceptance of treatment guidelines that recognize the dual obligations of the prescriber: to optimize the balance between analgesia and side effects, and promote other favorable outcomes, while concurrently assessing and managing the risks associated with abuse, addiction and diversion. At this juncture, it is important that the opioid treatment debate evolve from a discussion focused on “too little” or “too much” to one focused on identification and training of best treatment practices. Improvement in opioid therapy can occur through research and training to aid practitioners to determine the appropriate patient subpopulations and treatment protocols to achieve satisfactory outcomes.

Finally, it is imperative to advance a research agenda that leads to the identification of methods that would enhance pain relief while reducing the likelihood of addiction and other adverse events when opioids are selected for therapy. This should include the testing of novel medications that may be safer or more differentially effective for select treatment populations (as the proposal to test buprenorphine with high risk patients, discussed above) and the evaluation of treatment protocols incorporating risk management techniques.
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The authors wish to thank two anonymous reviewers who provided extremely thoughtful and helpful comments on an earlier version of this paper. Acknowledgement: Development of this paper was partially supported by a National Institute on Drug Abuse grant R21 DA022675.


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