Monday, 30 March 2015

The Fallacy Of Neuropathy Cures

Today's post from (see link below) is written by a doctor who is as clearly irritated as this blog is, by claims that neuropathy can be cured thanks to one expensive treatment or another. He makes it quite clear that although certain treatments may reduce the effects of the symptoms, neuropathy can not be cured and as of March 2015 (date of this article) that remains the only truth that you can be certain of. Please don't buy into lurid advertisements that claim to be able to 'cure' your neuropathic condition - they can't and the best they may be able to offer is a reduction in the severity of your symptoms.

Confusion regarding neuropathy ‘cures’
By Dr. David Raynor Tuesday, March 10, 2015

Peripheral polyneuropathy is a condition that adversely affects nerves in the peripheral nervous system, which are all the nerves outside the brain and spinal cord. Podiatrists often see patients with peripheral neuropathy in the lower extremities.

The peripheral nervous system has two components. The sensory nerves transmit impulses from sensory receptors to the brain for processing. The motor nerves take impulses from the brain to create an action. Simply stated, sensory nerves are used to feel and motor nerves are used for movement. Peripheral neuropathy can affect motor nerves, but changes are mainly recognized by patients in the sensory nerves because they can feel that their sensation has changed and something “doesn’t feel right.” Patients may not readily notice weakness due to motor-nerve affects, as they may compensate to overcome slight deficits.

Sensory neuropathy symptoms can include exaggeration or diminished sensation of any type due to nerve damage. Common complaints are degrees of numbness or loss of sensation, burning, itching, stiffness and tightness. Pain from neuropathy can be annoying, severe or even debilitating in advanced cases. No one knows exactly what causes neuropathy, but diabetes is the most commonly associated cause, though many other causes exist.

Treating neuropathy symptoms can be difficult, as there is no cure. Unless the causative agent responsible for the neuropathy is cured, you cannot cure neuropathy. Neuropathy can be managed in certain cases, but not cured — regardless of claims made otherwise. Pain and annoying sensation from neuropathy can be managed in many cases with pharmaceutical agents, but no treatment exists to restore “lost” sensation. Pharmaceuticals do not cure or restore sensation, either. Oral or topical methods can effectively be used to reduce neuropathy symptoms to improve quality of life, but these need to be maintained and can have side-effects. Reduction to exposure damaging the nerves may temporarily improve symptoms, such as reeling in uncontrolled diabetes, but in truth the damage is done and symptoms will invariably return.

Neuropathy is unpleasant at minimum and can be debilitating in severe cases. Claims are made regarding surgery, therapy and medicinal options to cure or restore nerves. I know of no cure for neuropathy. Medicinal treatments to reduce symptoms from sensory peripheral polyneuropathy are the most potent or advanced treatments I know of to date.

David B. Raynor. DPM, is a podiatrist in Inverness and can be reached at 352-726-3668 or at with questions or suggestions for future columns.

Sunday, 29 March 2015

Restless Leg Syndrome Or Neuropathy?

Today's post from (see link below) looks at a question that confuses both patients and doctors alike and that is whether you have restless leg syndrome, or neuropathy, or both! Because the symptoms seem to be similar, it's sometimes difficult to distinguish between the two, although people with restless leg syndrom may argue that their symptoms are even more unique than those of neuropathy patients. Also, it may be technically true that RLS is a form of neuropathy in itself. Either way, it's a very annoying complaint and may be treated somewhat differently than 'normal' neuropathy. Your doctor should be able to help and refer you to a specialist if necessary. Useful article.

Is it restless leg syndrome or neuropathy?
Sharon M. O'Brien, MPAS, PA-C March 11, 2015 

Take the time to make the distinction between restless leg syndrome and neuropathy.

This week, a third patient came with a diagnosis of restless leg syndrome (RLS) when a more accurate diagnosis should have been neuropathy. Consequently, I thought I should try to clarify the difference between the two.

RLS is loosely defined as having pain in the extremities, especially during relaxation, that is eased by movement or walking. The symptoms are often characterized as "creepy crawling" or "jumpy legs" but are described as painful at times. However, there are more specific criteria that need to be met in order to make a diagnosis. (See below.)

Restless leg syndrome occurs in about 10% of the population and tends to run in families, so ask patients if anyone else in the family has similar symptoms or has been previously diagnosed with RLS.

The diagnostic criteria for RLS is defined in the International Classification of Sleep Disorders as follows: 

"The patient reports an urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs.
The urge to move or the unpleasant sensations begin or worsen during periods of rest or worsen during periods of rest or inactivity such as lying or sitting.
The urge to move or the unpleasant sensations are partially or totally relieved by movement, such as walking or stretching, at least as long as the activity
The urge to move or the unpleasant sensations are worse, or only occur, in the evening or night.
The disorder is not better explained by another current sleep disorder, medical or neurological disorder, medication use, or substance use disorder."1

Neuropathy is described as burning, shooting, electrical, pins-and-needles type of pain in the extremities. This pain is usually not eased by walking, and many patients complain that movement makes the pain worse. This pain is generally present most of the time and does not change during particular times of the day.

What can make a diagnosis difficult is when a patient has neuropathy and RLS, as the two can occur together. RLS can also be seen in patients with kidney disease, Parkinson's disease, and iron deficiency. It is often seen in pregnancy and can be seen in patients taking antidepressants or antipsychotic drugs.

Besides the patient complaints, check a ferritin level in patients suspected of having RLS. Iron levels should be kept above 50 ng/mL in patients who have symptoms. Add iron if levels fall below. If this does not control symptoms, medications that can be helpful include ropinirole and pramipexole. I often try gabapentin for RLS, especially if there is a neuropathic component as this can help both.

The most important questions to ask your patients are:

When does the pain occur?
Does movement make the pain go away or feel better?

These questions will most likely help you with the diagnosis. In most cases, if the pain is occurring with inactivity, in the evening, and walking makes the pain feel better, then you are safe to assume it is RLS. If not, look for something else.

Have you had a difficult time distinguishing between RLS and neuropathy?

Sharon M. O'Brien, MPAS, PA-C, is a practicing clinician with an interest is helping patients understand the importance of sleep hygiene and the impact of sleep on health.


American Academy of Sleep Medicine. International Classification of Sleep Disorders, 2nd edition, pocket version: Diagnostic and Coding Manual. Westchester, Illinois: American Academy of Sleep Medicine, 2006.

Saturday, 28 March 2015

Autonomic Neuropathy: An Overview

Today's post from (see link below) is another overview of autonomic neuropathy. If your doctor has told you you may have autonomic neuropathy, you are probably experiencing symptoms in various parts of your body. These symptoms can affect the functions you normally take for granted and don't even think about and are very frustrating because many aspects of your daily life may be affected. These symptoms may also appear alongside the more easily recognised neuropathic symptoms involving your feet and hands. Getting as much information as possible is very important in helping you understand what's happening to you and you can find more articles about autonomic neuropathy by using the search facility to the right of the blog.

March 1, 2015 by Douglas Vansant Website:

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

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

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

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

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

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


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

Difficulty beginning to urinate
Feeling of incomplete bladder emptying
Leaking urine


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


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

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

Other tests depend on what type of symptoms you have.


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

Your doctor or nurse may recommend:

Extra salt in the diet or taking salt tablets to increase fluid volume in blood vessels
Fludrocortisone or similar medications to help your body retain salt and fluid
Medicines to treat irregular heart rhythms
Sleeping with the head raised
Wearing elastic stockings
The following may help your intestines and stomach work better:
Daily bowel care program
Medications that increase gastric motility (such as Reglan)
Sleeping with the head raised
Small, frequent meals
Medicines and self-care programs can help you if you have:
Urinary incontinence
Neurogenic bladder
Erection problems


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


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

When to Contact a Medical Professional

Call for an appointment with your health care provider if you have symptoms of autonomic neuropathy. Early symptoms might include:
Becoming faint or lightheaded when standing
Changes in bowel, bladder, or sexual function
Unexplained nausea and vomiting when eating
Early diagnosis and treatment increases the likelihood of controlling symptoms.
Autonomic neuropathy may hide the warning signs of a heart attack. They are sudden fatigue, sweating, shortness of breath, nausea, and vomiting.


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

Alternative Names

Neuropathy – autonomic; Autonomic nerve disease

Friday, 27 March 2015

How Spinal Cord Neurons Control Pain

Today's post from (see link below) is a very interesting look at a study which has identified nerve cells in the spine that regulate pain signals and determine whether they should be forwarded to the brain - like a sort of central sorting office for mail. It's called a 'gate control theory'. It's a fascinating read but it will take some considerable time before scientists will be able to manipulate these neurons by use of specifically delivered viruses and actively control pain in humans. Even itching may be able to be controlled by manipulating these nerve cells in the spine. Fascinating read.
Spinal cord neurons that control pain and itch
Date: March 19, 2015 Source:University of Zurich


The spinal cord transmits pain signals to the brain, where they are consciously perceived. But not all the impulses arrive at their destination: Certain neurons act as checkpoints and determine whether a pain signal is relayed or not. Researchers from UZH identified these neurons and their connections. Moreover, they developed means to specifically activate these neurons, which reduces not only pain -- but astonishingly also alleviates itch.

Sensing pain is extremely unpleasant and sometimes hard to bear -- and pain can even become chronic. The perception of pain varies a lot depending on the context in which it is experienced. 50 years ago, neurobiologist Patrick Wall and psychologist Ronald Melzack formulated the so-called "Gate Control Theory" of pain. The two researchers proposed that inhibitory nerve cells in the spinal cord determine whether a pain impulse coming from the periphery, such as the foot, is relayed to the brain or not. A team headed by Hanns Ulrich Zeilhofer from the Institute of Pharmacology and Toxicology at the University of Zurich did now reveal which inhibitory neurons in the spinal cord are responsible for this control function: As the study published in the science journal Neuron shows, the control cells are located in the spinal dorsal horn and use the amino acid glycine as an inhibitory messenger.

The pain gate can be manipulated with viruses

With the aid of genetically modified viruses, the research group from UZH managed to specifically interfere with the function of these neurons in mice. They discovered that disabling the glycine-releasing neurons leads to an increased sensitivity to pain and signs of spontaneous pain. Moreover, Zeilhofer's team developed viruses that enable these specific pain-control cells to be activated pharmacologically. Mice treated with these viruses were less sensitive to painful stimuli than their untreated counterparts. Activating these nerve cells also alleviated chronic pain. And the surprising additional result: "Evidently, the neurons don't just control pain, but also various forms of itch," explains Zeilhofer.

How light touch controls pain

One key aspect of the Gate Control Theory is that various influences can modulate the pain-controlling neurons' activity. Based on our experience from everyday life, for instance, we know that gently rubbing or holding an injured extremity can alleviate pain in this area. According to the theory, non-painful contact with the skin is supposed to activate the inhibitory cells. Sure enough, the UZH researchers were able to verify this hypothesis and confirm that the inhibitory, glycine-releasing neurons are innervated by such touch-sensitive skin nerves.

Moreover, the pharmacologists were able to demonstrate that neurons on the superficial layers of the spinal cord, where the relay of the pain signals takes place, are primarily inhibited by glycine signals. "These three findings identify for the first the neurons and connections that underlie the Gate Control Theory of pain," sums up Zeilhofer.

Targeted therapy in humans not yet possible

Can these findings be used to treat pain? "The targeted stimulation or inhibition of particular types of neurons in humans is still a long way off and might only be possible in a few decades' time," says Zeilhofer. Another way may well reach the target sooner -- namely via the receptors that are activated by the inhibitory neurons: "As these receptors are located on the neurons that relay pain signals to the brain, their specific pharmacological activation should also block pain," says Hanns Ulrich Zeilhofer. His group has already achieved promising initial results in this field, too.

Story Source:

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

Journal Reference:
Edmund Foster, Hendrik Wildner, Laetitia Tudeau, Sabine Haueter, William T. Ralvenius, Monika Jegen, Helge Johannssen, Ladina Hösli, Karen Haenraets, Alexander Ghanem, Karl-Klaus Conzelmann, Michael Bösl, Hanns Ulrich Zeilhofer. Targeted Ablation, Silencing, and Activation Establish Glycinergic Dorsal Horn Neurons as Key Components of a Spinal Gate for Pain and Itch. Neuron, 2015; 85 (6): 1289 DOI: 10.1016/j.neuron.2015.02.028

Thursday, 26 March 2015

ED Drugs To Treat Neuropathy

Today's post from (see link below) is the second article in two days about the potential benefits of Sildenafil for people living with nerve pain. It backs up yesterday's post with more information, presented in an easily understood manner. An interesting point is that many trial studies fail, or produce unsatisfactory results because the test subjects (frequently rodents) are mainly juvenile, when in fact in humans, neuropathy is often at its worst in later years. In the case of the sildenafil investigation, they used older mice to confirm results that had been seen in humans using viagra. It seems that sildenafil (main ingredient of viagra) may well improve neuropathic symptoms, possibly because of a better blood supply to the sciatic and other nerves.

Erectile Dysfunction Drug Relieves Nerve Damage in Diabetic Mice 
Released: 17-Mar-2015 Source Newsroom: Henry Ford Health System

Newswise — DETROIT – New animal studies at Henry Ford Hospital found that sildenafil, a drug commonly used to treat erectile dysfunction, may be effective in relieving painful and potentially life-threatening nerve damage in men with long-term diabetes.

The research targeted diabetic peripheral neuropathy, the most common complication of diabetes, affecting as many as 70 percent of patients.

The study was recently published online in PLOS ONE.

Lei Wang, M.D., the Henry Ford neuroscientist who led the research, said that although numerous drugs have been shown to be effective in earlier animal experiments, most have not provided benefits in clinical trials.

“Generally, young diabetic animals with an early stage of peripheral neuropathy are used to investigate various drug treatments,” Dr. Wang explains. “But patients with diabetes who are enrolled in clinical trials often are older and have advanced peripheral neuropathy.

“Failure to develop and properly evaluate treatments in the laboratory that properly reflect the target clinical population with diabetic peripheral neuropathy may contribute to the failure of clinical trials.”

To mimic clinical trials in which diabetes patients have advanced peripheral neuropathy, the Henry Ford researchers chose male mice with type II diabetes that were 36 weeks old, roughly equivalent to middle age in humans.

Earlier animal experiments from the Henry Ford group showed that sildenafil, commonly known by the brand name Viagra, improved blood supply to the sciatic nerve.

In addition, it was noted that diabetes patients who took Viagra for erectile dysfunction had fewer symptoms of peripheral neuropathy.

However, it was not known if this therapeutic effect held true for long-term peripheral neuropathy because the diabetic mice used in the previous experiments were relatively young – 16 weeks old.

So the Henry Ford researchers chose diabetic mice that were more than twice as old.

In one group, 15 such mice were treated with an oral dose of sildenafil/Viagra every day for eight weeks. A control group of 15 age-matched diabetic mice were treated daily with the same amount of saline.

After a battery of nerve and function tests were performed on both the drug-treated and control groups, results “revealed that sildenafil markedly improved sensory function starting at six weeks after treatment compared with saline-treated diabetic mice,” Dr. Wang says.

“These data indicate that sildenafil improves neurological function even in middle-aged mice with long-term diabetic peripheral neuropathy.”

While stressing that the findings remain experimental, Dr. Wang says they provide new insights into the underlying mechanisms of long-term diabetic nerve damage and may lead to the development of a sildenafil treatment for long-term diabetic peripheral neuropathy.

Diabetic peripheral neuropathy is particularly insidious because, as it progresses and damages nerves in extremities and other parts of the body, many patients are unaware of it because pain sensors are numbed.

As a result, a cut or sore on the bottom of a foot, for instance, may not be noticed until an infection sets in and spreads, possibly leading to amputation or even death.

Because diabetic neuropathy results from chronically high blood sugar levels, diabetes patients are strongly encouraged to closely monitor those levels and control them through diet.

Over-the-counter and prescription drugs – including antidepressants and opiates – are available to treat neuropathy pain, but often have undesirable side effects.

Wednesday, 25 March 2015

Erection Drugs Help Neuropathy!

Today's post from (see link below) is a rare neuropathy hot topic on the internet at the moment and one you may welcome as being something capable of killing two birds with one stone - if you're a man that is (for women, the benefits may only apply to their neuropathic problems). Basically, the theory is that sildenafil will improve blood flow to the nerves and by testing it on mature mice, it has been found that their neuropathic symptoms improved considerably. More information tomorrow.

ED Medicine Reduces Diabetic Nerve Damage in Animal Study
March 20, 2015 by Diane Fennell

The erectile dysfunction drug sildenafil (brand name Viagra) may be effective at relieving painful neuropathy, or nerve damage, in men with long-term diabetes, according to preliminary animal research recently published in the journal PLOS ONE. Approximately 60% to 70% of people with diabetes have some form of neuropathy, according to the National Institutes of Health.

In previous animal studies, sildenafil has been shown to improve blood supply to the sciatic nerve, which extends from the lower end of the spinal cord into the legs, and it has also been noted that people with diabetes taking the medicine have fewer symptoms of peripheral neuropathy (a type of nerve damage in the arms, legs, hands, and feet).

Many other drugs have been shown to be effective at relieving neuropathy in animal studies but have not demonstrated benefits in human trials. According to scientists at Henry Ford Hospital, this may be because these trials use young animals with an early stage of peripheral neuropathy, while most people used in studies of the condition are older and have an advanced form of peripheral neuropathy.

To better simulate the condition of participants in human trials, the researchers used 30 male mice with Type 2 diabetes that were 36 weeks old, which is roughly equivalent to middle age in people. Fifteen of the mice were given an oral dose of sildenafil every day for eight weeks, while the other fifteen mice served as a control group and were given the same amount of saline daily.

After performing a variety of nerve and function tests on both groups of mice, the researchers found that mice given sildenafil experienced noticeably improved neuropathy symptoms starting at six weeks after treatment compared with the mice that were given saline.

“Generally, young diabetic animals with an early stage of peripheral neuropathy are used to investigate various drug treatments. But patients with diabetes who are enrolled in clinical trials often are older and have advanced peripheral neuropathy,” notes lead study author Lei Wang, MD. “These data indicate that sildenafil improves neurological function even in middle-aged mice with long-term diabetic peripheral neuropathy.”

Although this line of research is still in the early stages, it has the potential to eventually lead to the development of a sildenafil-based treatment for long-term diabetic peripheral neuropathy, Dr. Wang added.

For more information, read the Henry Ford Health System press release “Erectile Dysfunction Drug Relieves Nerve Damage in Diabetic Mice” or see the study in PLOS ONE. And for more information about coping with painful neuropathy, see the article “Controlling Neuropathic Pain: Tips From an Occupational Therapist,” by Erica K. Jacques.

Tuesday, 24 March 2015

8-Gly Carb To Help Reduce Neuropathic Pain

Today's post from (see link below) talks about microglia, which are cells in the spinal cord that are responsible for releasing nitrous oxide when there's nerve damage. This nitrous oxide is partly responsible for the extent of your neuropathic pain at a later stage. Scientists have found a compound which (simply put) can inhibit nitrous oxide release and thus theoretically, reduce pain and other symptoms. The compound is called 6-chloro-8-(glycinyl)-amino-β-carbolin, or 8-Gly carb which hardly rolls off the tongue for patients but the name isn't important, its potential is. As usual, the end product is still somewhere in the future but every little snippet of news increases our general understanding of our condition and puts pressure on the relevant authorities to work as fast as they can to improve our lives with neuropathy.

UC Davis team finds a prime drug candidate for neuropathic pain  
February 10, 2015 | By John Carroll

Neuropathic pain has been linked closely to microglia, immune cells in the spinal cord which are known to release cytokines and other chemicals including nitrous oxide in the wake of peripheral nerve damage. A team of UC Davis researchers says that inhibiting nitrous oxide at the time that nerve damage is done could prevent neuropathic pain from occurring later. And they've found a compound that they say is very effective at doing just that.

The compound is 6-chloro-8-(glycinyl)-amino-β-carbolin, or 8-Gly carb, which belongs to a class of compounds known to blunt nitrous oxide. The
team says that this compound is significantly better at that task than any other known compound. And it appears to do its work without blocking cytokine expression.

Neuropathic pain often doesn't begin until well after physical trauma. And once it does begin it can linger for years as the brain is believed to be misinterpreting nerve signals from the site of the damage.

"A compound like 8-Gly carb that selectively targets nitrous oxide production and does not block cytokine expression makes a promising candidate for drug development aimed at preventing a neuropathic pain syndrome without interfering with recovery," said Fredric Gorin, professor and chair of the UC Davis Department of Neurology and co-principal investigator for the study.

Now new preclinical work is being planned that could set the stage for clinical studies.

- here's the release

Monday, 23 March 2015

Living With Neuropathy: Dean S. Lewis A Personal Story

Today's post from (see link below) is the personal story of Dean Lewis, another neuropathy journalist, patient and analyst with a growing reputation in the neuropathy world. I'm absolutely sure many of you will be able to identify with Dean's story and by following the links, you'll be able to share in his experience and knowledge. There can never be too many reliable sources of information regarding neuropathy and he is certainly one of them.
Dean S Lewis
March 16, 2015 by katrina_world 

Dean S. Lewis

He took some antibiotics, not knowing his life would change forever. This was in 1998. His body reacted negatively to the antibiotics. Every organ in his body except the brain failed. Not even his heart was working. For two months, he lay in the intensive care unit dying. He spent one of the two months in a medically induced coma. Doctors said only a miracle would restore his fortunes. A miracle happened and he has lived to tell the story. However, Dean was left with chronic medical conditions, one being peripheral neuropathy.

Dean has written a book entitled “Peripheral Neuropathy: Nine Simple Steps to Reduce Your Pain” which teaches others with neuropathy how to manage it. He also gives daily tips to people living with neuropathy, in their journey to overcome it.

Dean is a fighter. While his parents worried about his life and whether or not he would leave the ICU alive, he believed he would somehow survive. He is now doing great. He has perfected ‘the art’ of controlling his neuropathy. Dean has a regimen he follows to keep his symptoms at bay. Some of the symptoms he deals with today include tingling in his legs. The tingling has, however, reduced significantly after strictly following his regimen.

He is now a fulltime clinical analyst. He interacts with physicians, nurses and others in the medical field. His work involves implementing the medical practitioners’ requests for information from their database. He is also a life coach. Anyone with a chronic condition can contact Dean for help. He inspires many with his personal story of struggle, endurance and overcoming. Dean pursues his goals. He was able to attend World Cup 2014 in Brazil. He prepared his mind and body for the grueling schedule months before the trip to be in the most optimal condition.


Dean practices gratitude every morning. He knows every day is a gift and is very grateful for one more day of life. He says he experiences numbness in his feet when he wakes up in the morning. So, he starts by getting his body to literally feel his feet. He exerts tension on his feet and muscles to allow his body to wake up in phases.

Once this is done, he steps on the floor and does his cardio, stretches and pushups. This way, his muscles stay strong. This is very helpful when dealing with peripheral neuropathy. Dean says exercise strengthens the muscles and give the nerves the stimulation they need to keep the body fit.

Over the years, Dean has been told over and over again he should share the story of his survival and overcoming peripheral neuropathy. He also used to attend neuropathy support groups and he would listen to people’s frustrations and see their pain. He loved speaking in these gatherings and would inspire those suffering to hope for a life beyond the frustrations of neuropathy. All these happenings pushed him to write the book “Peripheral Neuropathy Nine Simple Steps To Reduce The Pain” which is available on Amazon.

Dean has had moments he wanted to give up. He says it was especially challenging when he experienced so much pain. He says a lot of times when he would skip his regimen or not get enough sleep or push himself a little too far, he would experience so much pain that he would feel like giving up. Dean, however, says he would remember how far he has come and push himself back to his regimen as a way out of his pain.

Dean advices anyone suffering from a chronic illness to gather as much information about the condition as they possibly can. He says this is where it all begins. Once you know the condition you are suffering from, Dean says you can start to understand how you can overcome it. According to Dean, it is also okay to ask for help. “Don’t be afraid to speak to a friend… Don’t feel that there’s something wrong with you. Listen: everyone has something to deal with,” Dean says.

Dean’s mindset was a big contributor to getting his life back on track after the neuropathy experience. Long before he could walk and drive again, he would use his mind to strengthen and reform his neural pathways by imagining himself driving. Though he could not move, Dean believes this helped him recover faster.

Today, he takes no pain killers. He has been liberated. He wants to show others how they can overcome peripheral neuropathy or other chronic conditions. You can contact Dean on Facebook at ‘Overcoming Neuropathy’ or his website He also offers private consultations and more on his website.

Sunday, 22 March 2015

Alternative To Medical Marijuana For Chronic Pain

Today's post from (see link below) is a serious look at medical cannabis, from a serious source and is worth our attention. THC (the active ingredient of cannabis) works very well for people in chronic pain, especially neuropathic pain but it does carry side effects, caused by it acting on cannabinoid CB1 receptors in the brain. Scientists have been working on an agent that works on the CB2 receptors in the brain and they do not produce the side effects associated with THC.  This agent is (as usual) confusingly called AM1710 but that's not really important. What's important is that this agent may end up replacing the need for THC based medical cannabis and working just as well, without the side effects. It sounds trivial but a by-product of this is that a new agent will have a positive image in the eyes of the law and society, which remains stubbornly resistant to the benefits of medical cannabis. It's still a work in progress but looks very promising for the future, where any viable alternative will be welcomed by neuropathy patients and other chronic pain sufferers everywhere.

An alternative to medical marijuana for pain?
Date:March 4, 2015 Source:Elsevier


Medical marijuana is proliferating across the country due to the ability of cannabis ingestion to treat important clinical problems such as chronic pain. However, negative side effects and the development of tolerance limit the widespread therapeutic use of THC, the major psychoactive ingredient in cannabis. THC's side effects are produced via its actions at cannabinoid CB1 receptors in the brain. Thus, scientists theorized that an agent with similar mechanistic actions, but that activate CB2 receptors instead, may eliminate the unwanted side effects while maintaining an equivalent level of efficacy.

Dr. Andrea Hohmann and her colleagues at Indiana University tested this strategy and found that, unlike Δ9-THC, repeated dosing with the cannabinoid CB2 agonist AM1710 suppresses chemotherapy-induced pain in mice without producing tolerance, physical withdrawal, motor dysfunction, or hypothermia. Moreover, the therapeutic effects of AM1710 were preserved in mice lacking CB1 receptors but absent in mice lacking CB2 receptors.

Their findings are reported in the current issue of Biological Psychiatry.

"Our study is important because it demonstrates beyond doubt that activation of cannabinoid CB2 receptors suppresses neuropathic pain without producing signs of physical dependence (i.e., a withdrawal syndrome) or other unwanted side effects associated with activation of CB1 receptors in the brain," said Hohmann.

Their studies used animals that were treated with a chemotherapeutic agent (paclitaxel) to produce pain. When animals were given AM1710, a CB2 agonist, its pain-suppressive effects were fully preserved and its therapeutic effects were maintained even after repeated dosing.

Alternatively, and as expected, when animals were given Δ9-THC, they developed complete tolerance to the pain-suppressing effects of THC and with repeated dosing, THC was no longer effective in suppressing neuropathic pain.

When the THC-treated animals were challenged with a drug that blocks CB1 receptors in the brain, the animals showed a prominent withdrawal syndrome, indicating signs of physical dependence following removal of THC. Strikingly, this was not the case with the CB2 agonist; blocking either CB1 or CB2 receptors produced no signs of withdrawal in animals treated chronically with the CB2 agonist.

Hohmann added, "We think our data suggests that CB2 receptors are an important target for suppressing chronic pain without unwanted side effects (e.g. psychoactivity, addiction)."

"It is important to know whether the benefits of cannabis ingestion for pain could be attributed in large part to the stimulation of CB2 receptors," commented Dr. John Krystal, Editor of Biological Psychiatry. "CB2 agonists, in theory, would present less risk regarding addiction and intoxication than the ingestion of cannabis or THC."

More work will be necessary before CB2 receptor agonists could be prescribed for use in humans, but for now, these data support the therapeutic potential of CB2 agonists for managing pain without the adverse effects associated with cannabis.

Story Source:

The above story is based on materials provided by Elsevier. Note: Materials may be edited for content and length.

Journal Reference:
Liting Deng, Josée Guindon, Benjamin L. Cornett, Alexandros Makriyannis, Ken Mackie, Andrea G. Hohmann. Chronic Cannabinoid Receptor 2 Activation Reverses Paclitaxel Neuropathy Without Tolerance or Cannabinoid Receptor 1–Dependent Withdrawal. Biological Psychiatry, 2015; 77 (5): 475 DOI: 10.1016/j.biopsych.2014.04.009

Saturday, 21 March 2015

How The Brain Processes Chronic Pain

Today's post from (see link below) is a fascinating look at how the brain processes pain signals. It looks at which signals the nerve cells use to respond to a pain stimulus. Slowly but surely, scientists are building up a map of how nerve cells behave in the brain. It's been a largely unexplored area due to the complexity of brain cells but the more is discovered, the better people with chronic pain will be able to be treated in the future.

Brain processes ongoing pain more emotionally
Date: March 11, 2015 Source: Technische Universitaet Muenchen


A momentary lapse of concentration is all it takes for a finger to become trapped or sprain an ankle -- and it hurts. Pain is the body's protective mechanism and a complex neurological phenomenon. Moreover, ongoing pain in the sense of chronic pain can be a disease, clinicians say. Scientists have now demonstrated that already during a few minutes of ongoing pain, the underlying brain activity changes by shifting from sensory to emotional processes.

The picture shows the EEG results during a short (left) and a long-lasting pain stimulus (right). The brain areas with the strongest activity are depicted in red. Short pain stimuli are processed in sensory brain areas, whereas ongoing pain is processed in frontal brain areas which are related to emotional processes.
Credit: E. Schulz et al., 2015, Prefrontal gamma oscillations encode tonic pain in humans, Cerebral Cortex

In their experiments, Prof. Markus Ploner, Heisenberg Professor for Human Pain Research at the TUM School of Medicine, and his team investigated pain perception: How does the duration of pain or the action of a placebo affect activities in the brain? For their measurements they used electroencephalograms (EEGs). The test subject wore a cap with 64 electrodes that can measure nerve cell activity in the brain throughout the experiment. This method makes it possible to chronologically pinpoint which signals nerve cells use to respond to a pain stimulus.

Pain influences emotion

The scientists used the following arrangement for their experiments: Over a period of ten minutes, 41 participants in the study were given painful heat stimuli to the hand which varied in intensity throughout the duration of the experiment. The participants were asked to continuously assess the level of their pain on a scale of one to a hundred with the other hand using a slider.

"We were absolutely amazed by the results: After just a few minutes, the subjective perception of pain changed -- for example, the subjects felt changes in pain when the objective stimulus remained unchanged. The sensation of pain became detached from the objective stimulus after just a few minutes," says Markus Ploner, describing the results.

Previous studies showed that brief pain stimuli are predominantly processed by sensory areas of the brain that process the signals from the sensory organs such as the skin. However, in their experiment with longer-lasting ongoing pain, the EEGs gave the scientists a different picture: in this case, emotional areas of the brain became active.

"If pain persists over a prolonged period of time, the associated brain activity shows that it changes from a pure perception process to a more emotional process. This realization is extremely interesting for the diagnosis and treatment of chronic pain where pain persists for months and years," explains Markus Ploner, who is also senior physician in the Department of Neurology at the TUM Klinikum rechts der Isar.

Placebos change the perception of pain

A second experiment showed that it is not just the duration, but also the anticipation of a pain stimulus that affects perception. Twenty test subjects were initially given different intensities of painful laser pulses on two areas of the back of the hand. The participants then rated verbally how strong they perceived the pain stimuli. As the experiments progressed, the subjects were once again given the same stimuli, the difference this time being that two creams had previously been applied to both areas. Although neither cream contained an active substance, the subjects were told that one of the creams had a pain-relieving effect.

The result according to Markus Ploner: "The subjects assessed the pain on the skin area with the allegedly pain-relieving cream as significantly lower than on the other area of skin." The scientists were further able to demonstrate how the brain implements this placebo effect: although the subjects were given the same pain stimuli, the nerve cells in the second run triggered a different pattern of brain activity.

"Our results show how differently our brain processes the same pain stimuli. Systematically mapping and better understanding this complex neurological phenomenon of 'pain' in the brain is a big challenge, but is absolutely essential for improving therapeutic options for pain patients," in Ploner's opinion.

Story Source:

The above story is based on materials provided by Technische Universitaet Muenchen. Note: Materials may be edited for content and length.

Journal References:
E. Schulz, E. S. May, M. Postorino, L. Tiemann, M. M. Nickel, V. Witkovsky, P. Schmidt, J. Gross, M. Ploner. Prefrontal Gamma Oscillations Encode Tonic Pain in Humans. Cerebral Cortex, 2015; DOI: 10.1093/cercor/bhv043
Laura Tiemann, Elisabeth S. May, Martina Postorino, Enrico Schulz, Moritz M. Nickel, Ulrike Bingel, Markus Ploner. Differential neurophysiological correlates of bottom-up and top-down modulations of pain. PAIN, 2015; 156 (2): 289 DOI: 10.1097/01.j.pain.0000460309.94442.44

Friday, 20 March 2015

d-Methadone For Neuropathic Pain

Today's post from (see link below) looks at d-methadone, a relative of methadone, which is being developed to treat neuropathic pain without the potential side effects associated with methadone and other opioids. Methadone has a bad rap! It's associated with drug addicts weaning off yet stronger drugs, yet is used very successfully with many people with neuropathic pain that doesn't respond to other drugs. Those people may get relief from their pain but have to suffer the unjustified stigma that methadone brings with it. Still in the development phase, d-methadone will achieve the same results without the side effects and that has to be very good news indeed. Unfortunately, parts of this report/article may well appear to be double-dutch to many readers due to the complexity of the science but you will get the gist. d-methadone may end up being a huge breakthrough in efficient treatment of nerve pain.
d-Methadone: A Novel Approach for Neuropathic Pain
 Eliseo Salinas, MD, MSc, President and Chief Scientific Officer, Relmada Therapeutics
Thu, 03/12/2015

At a time when opioid abuse and addiction are making headlines, a new molecule is being studied to treat neuropathic pain without such negative effects. A relative of methadone, a widely known synthetic opioid medication, d-Methadone represents half of methadone’s chemical structure with profoundly different activity on the mu opioid receptor, considered a “gateway for addiction.”

A Gold Standard Treatment

Methadone is a widely known synthetic opioid medication that has been used for decades. It is used to reduce withdrawal symptoms in people addicted to heroin or other narcotic drugs without causing the "high" associated with the drug addiction. Methadone is also used as a pain reliever.

Like many narcotics, methadone suffers from poor safety and tolerability. Some of the adverse effects of methadone include sedation, constipation, dizziness, sleepiness, respiratory depression, and nausea/vomiting. Two enantiomers of a generic amino acid that is chiral Methadone is a chiral compound, meaning that it is comprised of two molecules (optical isomers) with identical composition, but which are arranged in a non-superposable mirror image (see image).

Usually one of the optical isomers of synthetic opioids accounts for most of the pharmacologic activity and the addictiveness of the racemic compound. The other isomer generally exhibits less activity and less addictiveness.

Methadone is an outstanding example of a compound in which greatly different activity and addictiveness occur in the optical isomers. Both the l-optical and d-optical isomers of racemic methadone are noncompetitive inhibitors of N-methyl-D-aspartate (NMDA), a glutamate receptor and ion channel protein found in nerve cells. In view of the fact that upregulation of NMDA plays an important role in neuropathic pain, inhibition of the receptor may provide strong pain relief in neuropathic pain states.

Where the l-optical and d-optical isomers of racemic methadone differ is their effect on the mu opioid receptor. While the l-optical isomer is a potent analgesic with addictiveness greater than or equal to morphine, the d-optical isomer is a weak opioid with potentially low addictiveness. This means d-methadone could be an effective agent to treat neuropathic pain through inhibition of NMDA without the poor safety and tolerability associated with activating the mu opioid receptor.

Early Studies

Leveraging research from Cornell University, d-Methadone is being developed as a novel drug with the potential to treat neuropathic pain. The first Phase 1 study in healthy subjects was initiated in late 2014 to evaluate single ascending doses of d-methadone. The goal of this study is to determine the maximum single dose of d-methadone that can be taken without evidence of the typical opioid effects. The second planned Phase 1 study will evaluate multiple ascending doses. Results from both studies will guide a planned Phase 2 study to assess the effect of d-methadone in patients with neuropathic pain.

While early in clinical development, published clinical studies with low doses of another NMDA inhibitor called ketamine (a psychoactive ‘party drug’ better known as Special K) have produced strong pain relief in neuropathic pain states and serve as proof of concept for d-methadone. Severe side effects limit the use of ketamine, such as hallucinations, memory defects, panic attacks, and nausea/vomiting. In contrast, d-methadone appears to be well tolerated.

Neuropathic pain is defined as a disorder of the sensorimotor system and is distinctly different from nociceptive pain, which is a consequence of trauma, injury, or inflammation. The term neuropathic pain is used to describe a wide range of pain syndromes, including painful diabetic neuropathy, postherpetic neuralgia, and trigeminal neuralgia. According to the Neuropathy Association, neuropathic pain is estimated to affect more than 20 million people in the United States alone.

The main classes of drugs used to treat these neuropathic pain conditions are anticonvulsants, antidepressants, opioids, and topical treatments. However, despite the availability of multiple pain medications only about 50 percent of patients respond to treatment with currently available therapy options, and they present the risk of numerous side effects that reduce their tolerability. Accordingly, the treatment of neuropathic pain represents a large unmet medical need.

Eliseo Salinas, MD, MSc joined Relmada Therapeutics in February 2014. Dr. Salinas has more than 20 years of experience developing therapeutic products for CNS disorders in many key jurisdictions worldwide, including the United States, Canada, the European Union, and Japan. Under Dr. Salinas’ leadership, 15 programs obtained regulatory approval in the United States and other major international markets. Prior to joining Relmada, Dr. Salinas was Executive Vice President and Head of Research and Development at StemCells, Inc. Dr. Salinas has also held high-level positions at Elan Pharmaceuticals, Adolor Corporation, and Shire plc. Dr. Salinas earned his medical degree from the University of Buenos Aires, Argentina, performed a residency in psychiatry in Paris at the Clinique des Maladies Mentales et de l'Encéphale, and obtained a master's degree in pharmacology from the Université Pierre et Marie Curie, Académie de Paris, France.