AGONIZING RABIES DEATHS CAN BE STOPPED WORLDWIDE

The deadly rabies virus--aptly shaped like a bullet-- can be eliminated among humans by stopping it point-blank among dogs, according to a team of international researchers led by the Paul G. Allen School for Global Animal Health at Washington State University.

Ridding the world of rabies is cost-effective and achievable through mass dog vaccination programs, the scientists report in a paper that appears in the Sept. 26 issue of Science magazine. What's more, they write, because infections occur as a result of interactions between animals and people, a "One Health" approach is necessary, where veterinary, medical and public health professionals collaborate to eliminate the disease worldwide.

Publication of the article, "Implementing Pasteur's vision for rabies elimination" coincides with the 119th anniversary of French scientist's Louis Pasteur's death and a global campaign to wrench an ancient disease in the shadows to the forefront.

A rabies vaccine has long existed, developed by Pasteur in 1885. Even so, the disease kills an estimated 69,000 people worldwide -- that's 189 each day. Forty percent of them are children, mostly in Africa and Asia. The disease is spread primarily through the saliva of infected dogs. Once a person develops symptoms, the chance that he or she will die is nearly 100-percent.

"The irony is that rabies is 100 percent preventable. People shouldn't be dying at all," said veterinary infectious disease expert Guy Palmer, who directs WSU's Allen School and is co-author of the paper.

The disease persists, partly due to political complacency but also because of a lack of international commitment, researchers state in the article. And yet, eliminating it "meets all the criteria for a global health priority: It is epidemiologically and logistically feasible, cost-effective and socially equitable," they conclude.

The authors cite the success of mass dog vaccination clinics held in the East African country of Tanzania. Working in 180 villages, members of the Allen School and the Serengeti Health Initiative vaccinate as many as 1,000 dogs in a single day. Since the program began in 2003, the number of people killed by rabies has dropped from an average of 50 each year to almost zero, according to Allen School researcher Felix Lankester, based in East Africa, who is the paper's lead author. Vaccinating 70-percent of the dogs in the region broke the route of transmission from dogs to humans, he explained.

Though human rabies is rarely seen in developed nations that conduct mass dog vaccination programs, the disease should be viewed as a global public health problem that can be solved, writes Lankester, Palmer and co-authors from the Nelson Mandela African Institution of Science and Technology, the University of Glasgow in Scotland and the Global Alliance for Rabies Control.

Will HGF Injections Be The Answer For Neuropathy

Today's post from type2nation.com (see link below) talks about injecting HGF (hepatocyte growth factor - a protein associated with tissue regeneration) to treat neuropathy. Notice, I say neuropathy and not neuropathy symptoms because this is designed to help regenerate nerve growth where damaged and not just the symptoms of nerve pain or tingling. However and this is a big however, in the study, the majority of subjects did not respond to the treatment, which leaves the whole idea open to doubt. The article author suggests that this still shows HGF injections to be potentially useful for neuropathy patients but it seems that many more studies and lots more research may be needed first before this can be assumed.
 

Injections May Combat Diabetic Neuropathy
Published on January 25th, 2016 | by Travis Manni

One common side effect of living with diabetes can be painful diabetic neuropathy, which is nerve damage in the arms, hands, legs, or feet; the condition is caused by chronically high blood sugar levels. There are limited treatment options to deal with diabetic peripheral neuropathy, or the pain it causes.

However, a new multi-center study showed hepatocyte growth factor (HGF) injections helped treat the condition for a good amount of study participants. The study was published in the May 2015 issue of the journal Annals of Clinical and Translational Neuropathy. However, the treatment did not work for the majority of individuals studied, meaning HGF may be a good treatment option, but not necessarily a silver bullet in treating diabetic peripheral neuropathy.

According to the National Center for Biotechnology Information, HGF is a protein in the body that is associated with organ development, tissue regeneration, and wound healing in adults. It also supports the growth and nourishment of neuron cells. In the double-blind Phase II study, 96 individuals were given either a placebo or HGF intramuscular injections in the leg twice over two weeks; the experimental group received either 8 mg (low-dose) or 16 mg (high-dose) of HGF. Participants were asked to record information in a pain and sleep diary.

The low-dose experimental group showed the greatest reduction in pain after three months, according to a MedScape article. In particular, those who were not not already taking other prescription drugs that treat this type of pain reported a statistically significant decrease on the pain measurement scale. Additionally, 48% of those surveyed in the low-dose group reported their pain was either “improved” or “very much improved” after three months; 31% of people in the high-dose group also reported “improved’ or “very much improved” pain levels. Improvement in touch sensitivity was also observed in those treated with HGF.

Researchers hope this form of treatment, which would require only eight injections a year, will eliminate the need for patients experiencing painful diabetic neuropathy to take daily medication. The HGF injections also could be seen as an alternative option for those who do not experience pain relief with currently available prescription drugs. Further study will be needed before the treatment might become available on the market, and researchers expect to conduct a new trial in 2016.

http://www.type2nation.com/treatment/new-injection-treatment-may-combat-diabetic-neuropathy/

Guru Is A Scary Word But Janice Wiesman May Just Be A Neuropathy Guru!

Today's post from practicalneurology.com (see link below) may seem to have a slightly uninspiring title but trust me, this is an article which fills a glaring gap in internet information, in that it's addressed towards neuropathy patients directly and talks to us as if we are part of the process and not just a footnote at the end of a complex disease. Please read this because you will find your own neuropathy reflected here and may realise that what Janice Wiesman says is true...if science is currently failing neuropathy patients, then we have to empower ourselves to make the best improvements we can in our daily lives. The pay off is not a cure, or even a dazzling new medication but its an almost guaranteed improvement (however small) in our symptoms - most of you will pay good money for that!

Peripheral Neuropathy: Keys to Diagnosis, Management, and Patient Communication
By Janice Wiesman, MD October 2016

 Empowering patients to make lifestyle changes plays an essential role in managing peripheral neuropathy.
  
An estimated 20 million people in the US have peripheral neuropathy. That is one in 15 persons. Patients presenting with symptoms referable to the peripheral nerves—which include numbness, pain, paresthesia, and weakness— are common in neurology practice. And yet, residency programs are skewed towards the diagnosis and management of inpatient neurological disorders, which means that practicing neurologists may not become comfortable with diagnosing and treating neuropathy until early in the course of practice.

This article provides an overview of neuropathy diagnosis and management. It will also offer strategies for talking to patients about the disease and avenues for addressing it therapeutically.

Making the Diagnosis

Neuropathy itself is not usually a disease but a symptom of an underlying illness. The most common cause is diabetes mellitus. Heavy alcohol use and inherited forms also top the list. Medication-associated neuropathy may be overlooked. When we speak of inherited neuropathies we must distinguish between neuropathy that is inherited as a disease unto itself, such as Hereditary Motor and Sensory Neuropathy, versus inherited illness that has neuropathy as a symptom, such as familial amyloidosis or Pompe’s disease.

In unpacking the word “neuropathy” we recognize that this word can mean a lesion of a single nerve (mononeuropathy), multiple nerves scattered throughout the body that are affected at different times (mononeuropathy multiplex), or a disease of all nerves (peripheral neuropathy, also called polyneuropathy or simply neuropathy). Within the diagnosis of peripheral neuropathy there are three types: axonal, demyelinating, and dysmyelinative (which describes inherited disorders of myelin). Demyelinating neuropathies account for approximately 10 percent of all acquired neuropathies. The most common type is axonal, length-dependent, dying back polyneuropathy, which account for almost 90 percent of acquired neuropathies.

Sensory symptoms that patients describe with axonal neuropathy can range from a feeling as if bugs are crawling on their skin to shooting, electrical, or burning pains. When autonomic nerves are involved, common symptoms include lightheadedness when standing or sitting up, dry eyes and mouth, diarrhea, difficulty with vision and, in men, erectile dysfunction.

On examination, characteristic findings include symmetrically depressed or absent tendon reflexes at the ankles, atrophy of the extensor digitorum brevis, weakness of distal muscles in the legs and decreased or absent sensation in a stocking distribution. In most axonal neuropathies, small fiber modalities such as pain and cold sensation are affected first with large fiber modalities of vibration and joint position affected later. Careful examination of cranial nerve III may reveal a partial palsy associated with diabetes. With autonomic involvement, the skin over the legs may be shiny and dry with loss of hair distally. In patients whose symptoms are caused by vitamin B12 deficiency, the exam may instead show decreased large fiber sensation with preserved small fiber sensation and brisk, rather than depressed, reflexes. This is due to subacute combined degeneration of the spinal cord. Patients with this topsy-turvy exam in the face of symptoms suggestive of neuropathy should have a careful diet history taken and vitamin B12 level checked.

Evaluation of peripheral neuropathy includes testing of blood and urine, nerve conduction studies, and electromyography and lumbar puncture, if demyelinating neuropathy is suspected. Routine blood testing includes complete blood count, thyroid stimulating hormone, renal functions and tests for diabetes including hemoglobin A1c, fasting glucose and two-hour glucose tolerance test. Then, obtain serology for human immunodeficiency virus and hepatitis C. Depending on the patient’s history, you may also investigate less common causes, such as heavy metal exposure and inherited neuropathy. While you can test for syphilis, it is important to note that syphilis does not cause neuropathy. Tabes dorsalis can cause “lightening pains,” shooting into the legs and trouble with balance, but these symptoms are different from symptoms of neuropathy and I do not typically obtain this test.

Nerve conduction studies and electromyography can characterize neuropathy as axonal or demyelinating, sensory or motor or both and can give an idea as to the severity and chronicity of the neuropathy. In addition, it can exclude neuropathy look-a-likes such as lumbosacral radiculopathy. Nerve biopsy is typically not necessary except in cases where infiltration of the nerve (such as with lymphoma or amyloid) or vasculitis is suspected and treatment depends on a tissue diagnosis.

Treatment Options and Patient Communication

In the treatment phase, management of patients’ concerns is essential. Over the years I have found that patients think about treatment of neuropathy from three perspectives. These are expressed in the following questions: “Can I treat the cause of neuropathy?” “What can I do to help the nerves grow back?” “What can I do about the pain, tingling, weakness and autonomic symptoms?” After the history, examination and testing reveal the type of neuropathy, we still may not know the etiology but we can address the patients’ questions.

If the etiology is known, it can be addressed: for example, with better glucose control, treatment of hepatitis C, Vitamin B12 repletion and cutting back or abstaining from alcohol. I like to use this time to empower patients to help themselves: In the case of heavy alcohol use or poorly controlled diabetes mellitus I tell the patients that they are fortunate in that the key to control of their neuropathy is already in their hands. While this may lead patients to think they are being blamed for their trouble, I never say this. I instead use the opportunity to partner with patients in improving their health. If the etiology is not known, I discuss this candidly and make a plan for a follow-up examination with repeated testing in the future. I take a few minutes to explain the anatomy of neuropathy and emphasize that there is no magic medicine or treatment to help the nerves repair more quickly. This is disappointing for patients but it leads to a discussion of what can be done, whether or not the cause of their neuropathy is known.

When discussing treatment of sensory symptoms, my first question is: “Do you need or want to be treated?” I explain that treatment is for symptoms only and will not help the nerves heal. I also emphasize that there is no treatment for numbness. For some patients, symptoms are mild and they prefer to stay away from medication. Others prefer to control their symptoms with occasional non-steroidal anti-inflammatory medication or over the counter topical treatments such as local anesthetic or capsaicin creams. For patients who are interested in treatments, I categorize these as: non-medication treatments, medications that are not pills and medications that are pills.

Non-medication treatments include use of a warm water vibrating foot bath for 15 minutes before bed. This may calm down the pain long enough to fall asleep. The theory is that the input from large fibers mediating vibration and pressure will block the input from small pain fibers at the level of the spinal cord. Some people get relief from wearing tight socks. Percutaneous nerve stimulation, done by a professional, may relieve pain temporarily, though there is conflicting evidence regarding the usefulness of transcutaneous nerve stimulation. I have been asked about oral and smoked marijuana. There is conflicting data about marijuana’s usefulness for neuropathic pain, while the side effects and legal restriction for both oral and smoked marijuana also complicate the discussion.

Medications that are not pills include local anesthetic applied as a cream, spray, or patch. These are not recommended for people with cardiac arrhythmias or seizures. Capsaicin cream can be effective, but requires three times daily use and is messy. Recent studies show that botulinum toxin injections into the foot may relieve neuropathic pain by blocking the release of Substance p and other factors from sensory nerves.

Oral medications fall into two main categories: anti-seizure and antidepressant. These may be used on- or off-label. The FDA has approved only two medications specifically for this use: pregabalin and duloxetine, however others such as gabapentin, amitriptyline, and nortriptyline are sometimes used. I do not recommend the use of sedatives, such as carisoprodol and methocarbamol, due to their lack of efficacy and potential for addiction.

What if none of these approaches provides relief? The use of opioid medication for neuropathic pain is controversial, and, in my opinion, should be handled by an expert. It is reasonable to refer the patient to a pain management specialist who is comfortable with intravenous pain medications and less frequently used oral agents.

Motor symptoms are less amenable to treatment. I explain to patients that muscles require nerve stimulation to stay healthy and suggest physical and occupational therapy to try to preserve strength, endurance and function.

Autonomic symptoms are sometimes the most serious impediment to the enjoyment of daily life. Orthostatic hypotension can lead to falls and broken bones, daily diarrhea limits socializing and travel, dry mouth can lead to dental decay and erectile dysfunction can lead to depression. Depending on how comfortable you are with the treatment of gastrointestinal, orthostatic, and sexual dysfunction, the neurologist can, at least, initiate treatment and refer to the appropriate specialist.

As with any illness for which there is no satisfactory treatment, neuropathy treatment scams run loose on the Internet. I encourage patients to bring to my attention items they have found online or through patient forums before they buy and use them. While transcutaneous nerve stimulation devices, anodyne light therapy and supplements have hopeful and encouraging descriptions and testimonials, there is no evidence that they are effective in reducing neuropathic pain. In addition, many supplements and vitamins are advertised for the treatment of neuropathic pain. I make it a point to tell my patients that supplements are not regulated by the FDA, therefore consumers have no idea what is actually in the bottle they buy. In addition, supplements may interfere with medications they are taking and may contain filler ingredients, such as ground walnut shells that may trigger allergies.

The Importance of Setting Expectations

As physicians we have certain expectations for the treatment of neuropathy—reducing or alleviating pain and maintaining function. However, patients may have different expectations and these may be greater or lesser than we imagine. When all is said and done, the patient and his family must live every day with the symptoms and disabilities of neuropathy. The most important aspect of the discussion comes after review of the diagnosis, etiology, and treatment. I like to start out by asking what improvements are most important to the patient: Does he seek better mobility and endurance, relief from pain or autonomic symptoms, avoidance of foot complications?

I emphasize what patients can do to feel better. Exercise, regardless of the degree of disability, is important. Some patients require a physical therapy evaluation prior to partaking in exercise due to other health problems but for those who do not require this, keeping active with walking, biking, formal exercise classes, sports (including swimming and dancing) is always worth encouraging. Some patients question whether exercise could further damage the nerves and I tell them that, on the contrary, exercise will not damage nerves and that nerve input to muscle is required to keep muscles healthy. Occupational therapy is useful for those with weakness or sensory loss in the hands and physical therapy with gait training is suggested for those with trouble walking.

I always speak with patients about foot care. In fact, this may be the most important lifestyle issue I address. If they cannot feel their feet, hot water, cuts, a rock in shoe or blister on the heel will not be felt and all can lead to infection. I advise patients to look under and between their toes every day, to keep feet well moisturized, wear proper fitting shoes with socks, not to go barefoot and, most important of all, to not cut their own toenails. I advise filing the nails or seeking professional nail care from a podiatrist or pedicurist. I say, many times a day, “I want you to have all ten toes, all the time.”

Other lifestyle suggestions include limiting alcohol and tobacco use, good blood glucose control, and healthy diet. Some patients argue that it is difficult to give up smoking, while others can be defensive about the quantity of alcohol they drink, but I implore them not to “kick your nerves when they are down.”

After discussing with patients their concerns, I bring up issues they may be thinking about but are not bringing forward. By this time, I have seen the patient a few times and we have gotten comfortable with each other. I can now ask if there are concerns around sexual function and prognosis. It can be a tricky discussion, and I find it best to speak with the patient alone, including the spouse later if the patient requests. Patients with preserved sexual function are often surprised and relieved to hear that neuropathy is no barrier to sexual activity. For those whose function is impaired I offer referral to a urologist. As for prognosis, this depends very much on the cause of neuropathy and I like to use this discussion as an opportunity to encourage patients to undertake lifestyle changes that may not only improve or stabilize their neuropathy but also improve their general health. There often comes the question: “Doctor, will I end up in wheelchair?” Every patient’s circumstance is different and predicating the future is tricky so I like to emphasize what can be done to avoid that fate while still being realistic.

Conclusion: Empowering Patients

Peripheral neuropathy affects many aspects of life. As physicians, we concentrate on diagnosis, treatment of etiology when possible, and treatment of sensory symptoms, but we must not forget to think about day-to-day life from the patient’s point of view. Empowering patients affected by neuropathy to make lifestyle changes that can improve their overall health and make their lives as normal as possible is something we can always do. n

Include the Patient in the Process

After history and examination, it is important to bring the patient into your thought process and include them in the treatment discussion. It’s important to share questions such as: Is this peripheral neuropathy or something else? Do the symptoms and exam lead to a diagnosis of something that looks like neuropathy but is not, such as lumbo-sacral radiculopathy or plexopathy, myopathy or even a disease of the central nervous system, like multiple sclerosis? If the diagnosis is peripheral neuropathy, is testing needed to determine if this is the correct diagnosis? Am I certain of the cause or is testing needed? Is treatment appropriate at this time and if so, what kind? Would medications or lifestyle modifications help? I encourage patients to make sure the doctor tells them what she is thinking–this should not be a secret!

While patients are typically not familiar with the anatomical structures known as nerves, I find they are very interested in knowing what is causing their symptoms and with a small investment in patient education, they are able to understand. Educating patients about their disease is not isolated to those with neuropathy and is important for a number of reasons:
There is personal dignity in understanding what is wrong with your own body and why.
It encourages patients to participate the diagnostic
process.
It empowers patients to participate in their treatment
It may inspire lifestyle changes that will improve overall health
It protects patients from dangerous treatments
It protects patient’s wallet from useless treatments

— Janice Wiesman, MD


Janice Wiesman, MD, FAAN, is the author of Peripheral Neuropathy: What It Is and What You Can Do To Feel Better, Johns Hopkins Press, 2016. Go to amazon.com/author/janicewiesman to purchase.
 
http://practicalneurology.com/2016/10/peripheral-neuropathy-keys-to-diagnosis-management-and-patient-communication/

California Poppy Photos Dont Worry Be Happy

Lasers May Be Able To Repair Damaged Nerve Sheaths

Today's post from diabetesqld.org (see link below) is an article from an Australian website that reports on what could be the next big thing regarding neuropathy treatment. I know...I can hear you sighing...after so many 'next big things' that turn out to be false dawns, we tend to view new findings with some skepticism don't we? However, the science behind this one seems to be solid and although many more studies are needed (as always), the idea that non-invasive laser treatment may be able to repair damaged myelin sheaths (insulation around the nerves) is a very attractive one. Also encouraging; the Brazilian lab admits it doesn't know why this seems to work but they have some theories that time will either prove or disprove. It may be a question from a dumb onlooker but precisely where do you apply the laser treatment? The very nature of peripheral neuropathy means that the damaged nerves can be very hard to pin down and identify. Just because the pain is in the feet or hands, doesn't mean that the damage is there also. I guess we'll just have to wait and see but this is one of those research discoveries you hope will turn out to be true and workable for us long-term sufferers.

Neuropathic pain? Science says lasers can help.
31 March 2017 /

 Recent studies at the University of São Paulo's Biomedical Science Institute (ICB-USP) in Brazil shows low-level laser therapy to be a non-invasive and effective alternative for treating neuropathic pain, a chronic condition caused by nerve damage, spinal cord injury or diseases such as diabetes.

The treatment in a model of diabetic neuropathy, one of the most common chronic and incapacitating complications of diabetes, was tested. Neuropathic pain in diabetes occurs when the disease is not properly controlled and excessive amounts of blood sugar cause oxidation of the myelin sheath, damaging the structure of peripheral nerves. As well as causing pain, this degenerative process impairs communication among neurons and can even lead to amputation of the lower limbs.

"We tested laser therapy in different rat neuropathy models, and behavioral responses improved in all of them," Professor Marucia Chacur, the principal investigator, said. "One of the beneficial effects observed was myelin sheath recovery. The myelin sheath is a lipid layer that covers the axon and acts as electrical insulation to assist nerve impulse propagation."

With the aid of a transmission electron microscope, the researchers found that as diabetes progressed, the structure of the sciatic nerve's myelin sheath changed. After four sessions of the treatment, however, the myelin had almost completely recovered.

"The condition of the nerve practically returned to baseline levels after treatment. We're now continuing the study by analyzing protein expression and the release of inflammatory cytokines to understand exactly what's happening," Chacur said.

In a second study, treatment focused on the sciatic nerve, and found that astrocytes - star-shaped cells that play an active role in brain function and inflammatory responses - were the first type of cell to migrate to the site of a nerve injury or inflammatory process. These cells release several inflammatory mediators, which in turn trigger the release of other inflammatory substances.

"We believe the laser curtails this chain reaction as if it were anti-inflammatory medication, by reducing the migration of astrocytes to the site of the injury," Chacur said.

The third model used to test low-level laser therapy focused on orofacial pain, involving the inferior alveolar nerve, one of the branches of the trigeminal nerve responsible for innervating the face. Phototherapy started two days after injury and improvement was observed after two sessions.

"We set out to understand the mechanisms and mediators involved because we believed phototherapy could be used in association with pharmacological treatment because it acts via a different pathway. In this way, it may be possible to reduce the drug dose and mitigate the systemic effects of the treatment," Chacur said.

The results suggest that all three models of neuropathic pain studied share a common mechanism involving myelin sheath regeneration and reduced astrocyte migration to the site of the lesion, she added.

"Evidence in the literature also suggests an effect on mitochondria. The laser apparently facilitates the flow of calcium in these organelles, boosting production of ATP [adenosine triphosphate, the body's cellular fuel] and leading to enhanced healing as well as the release of mediators that assist remodeling. In future studies, we plan to investigate this effect on mitochondria more thoroughly," Chacur concluded.

http://www.diabetesqld.org.au/media-centre/2017/march/neuropathic-pain-science-says-lasers-can-help.aspx

CROHNS AND COLITIS MAY BE TIED TO RISK OF HEART ATTACK STROKE

People with inflammatory bowel disease may be at increased risk for heart attack and stroke, a new study suggests.

Researchers analyzed data from more than 150,000 inflammatory bowel disease (IBD) patients who took part in nine studies. They found that these patients had a 10 percent to 25 percent increased risk of stroke and heart attack, and that this increased risk was more prevalent among women.

Doctors need to be aware of this link and should focus on controlling other stroke and heart attack risk factors, such as smoking, high blood pressure and diabetes, study author Siddharth Singh, of the Mayo Clinic in Rochester, Minn., said in a news release from the clinic.

The study was scheduled for presentation Monday at the annual meeting of the American College of Gastroenterology, in San Diego. Research presented at medical meetings should be viewed as preliminary until published in a peer-reviewed journal.

Crohn’s disease and ulcerative colitis — the most common forms of IBD — affect 1.5 million Americans. In these patients, inflammation of the intestine leads to rectal bleeding, diarrhea, abdominal cramps and pain, fever, and weight loss.

Patients with IBD need to work with a doctor to manage their condition, control their stress, eat a healthy diet and get moderate exercise. Smoking is a major risk factor for IBD patients, and those who smoke should try to quit, the researchers said.

Although the study found an association between IBD and an increased risk for heart attack and stroke, it did not prove a cause-and-effect relationship.

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Why Cannabis Must Be At Least An Option For Neuropathic Pain

Today's post from whaxy.com (see link below) returns to a common theme on this blog and that is the potential cannabis has for relieving nerve pain. It's not that we are for or against cannabis, it's just that cannabis remains one of the very few proven treatments for dulling nerve pain and for that reason, deserves the best research and trustworthy conclusions. Not only that but the moral (but non-scientific) objections to cannabis form a considerable barrier to making progress with its development as a truly useful analgesic for neuropathy sufferers. This article is easy to follow and gives a breakdown of what it is, how it works and why it's so effective. Definitely worth a read.
 

Study Reveals Cannabis Significantly Reduces Neuropathic Pain
By Marie Veksler February 14, 2015 

A study published in the The Journal of Pain: Official Journal of the American Pain Society found that low-doses of vaporized cannabis provide significant improvement for neuropathic pain sufferers. The study, a double-blind crossover, was placebo-controlled, and tested the efficacy of cannabis to treat the neuropathic pain of patients who were not responding to traditional treatments.

In the study, patients with central and peripheral neuropathic pain were administered either a medium-dose of 3.53 percent, a low-dose of 1.29 percent, or a placebo through vaporizing. Each patients’ pain was then rated using a visual analog scale of intensity. Psychoactive side effects and brain function were also monitored and evaluated throughout the study.

Analyzed results revealed that the cannabis provided at least the equivalent pain reduction as other patients reported from using traditional neuropathic pain medication. The low-dose (1.29%) and medium-dose (3.53%) were equally as effective, proving that even the lower dose of cannabis improved symptoms.

As a result, the study revealed that “even at low doses, [cannabis] may present an effective option for patients with treatment-resistant neuropathic pain.” The study conclusion also stated that “one might not anticipate a significant impact on daily functioning.”

What is neuropathic pain?

Neuropathic pain is the result of nerve damage to the peripheral nervous system, which includes all nerves outside of the brain and spinal cord. It is usually described by patients as chronic. The damaged nerves send incorrect signals to the body that there is pain. The damage to nerve fibers is most often the result of a tissue injury caused by trauma or infection. Patients describe this kind of pain as “shooting and burning” or “tingling and numbness.”
What causes neuropathic pain?

The one, specific cause of neuropathic pain is often unknown unless it is the result of amputation (phantom limb syndrome). However, people diagnosed as suffering from neuropathic pain often also had or have one or more of the following:

Diabetes
Alcoholism
Back, leg, and hip problems
Chemotherapy
Facial nerve problems
HIV infection or AIDS
Multiple sclerosis
Shingles
Spine surgery 

Why is cannabis effective as a neuropathic pain reliever?

Cannabis is made up of many, diverse chemical compounds known as cannabinoids. There are more than 60 cannabinoids found in marijuana that we know to exist, and each of them reacts differently in the human body and produces different responses. Cannabinoids are responsible for producing all of the effects experienced when using cannabis.

Unfortunately, we know very little about most of them because researchers have difficulty gaining access to cannabis to study because of it’s current listing as a Schedule I substance under the Controlled Substances Act of 1970. Being listed as a Schedule I, deemed the worst of the five categories, means that it has “no accepted medical value in the United States.” Because of this, researchers are rarely granted federal permission to study it.

Scientists have been able to identify the most common medicinal benefits produced by only seven different cannabinoids. Four of those seven are known to be analgesic, or pain relieving. The four known to act as strong pain relievers are:

Tetrahydrocannabinol (THC)
Cannabidiol (CBD)
Cannabichromene (CBC)
Cannabinol (CBN)

Another reason that many patients report having a preference to medical marijuana is because the side-effects produced by cannabis, including those that are psychoactive, are less debilitating than those produced by many of the strong opiod pain reliving pharmaceuticals like Oxycontin.

Such heavy-hitting pharmaceuticals make it difficult for patients to function during normal day-to-day activities, and can cause serious addiction or result in accidental overdoses and deaths. A cannabis overdose has never resulted in the death of a person. A recent report even revealed that opiod overdoses were reduced by 25 percent in states where medical marijuana is legal because patients in those states were more likely to use cannabis.

Although much more research needs to be completed on this topic to make any certain conclusions, there is at least enough evidence to prove that cannabis as a viable treatment option for neuropathic pain should be explored further.

https://www.whaxy.com/learn/marijuana-treatment-neuropathic-pain

How Neuropathy Patients Should Be Tested And Diagnosed

Today’s post from podiatrytoday.com (see link below) takes a good look at diagnosing neuropathic problems. Many of you will be familiar with several aspects of these processes but maybe not all. It seems to me that this is a good blue print for how people presenting neuropathic symptoms should be examined, tested and diagnosed. The problem is that doctors are busy people and may not follow through with all these tests, yet they perhaps should, if they are interested in accurate diagnosis and prognosis. Thanks to the unique symptoms and features of neuropathy, this blog always supports the doctor who listens to a patient's story and background and makes a correct neuropathy diagnosis based on pretty much those alone. However, if demands are made on him or her to 'prove' their diagnosis for bureaucratic reasons or record keeping, then the least they can do is conduct a thorough examination and this article demonstrates how that should be done. Neuropathy patients may learn quite a bit about their disease just by reading this guide for health professionals.

Mitigating Some Guesswork In Treating Neuropathic Pain
Wednesday, 05/20/15 | 1018 Issue Number: Volume 28 - Issue 6 - June 2015
Author(s): Cynthia Cernak, DPM, Eric M. Larsen, DPM, and Robert H. Odell, MD, PhD
 
Diabetic Neuropathy
 
Neuropathies take many forms depending on anatomic location. A mononeuropathy affects a single spinal or peripheral nerve with the cause likely to be a distinct anatomic lesion (such as lesions due to disc disease or tarsal tunnel syndrome). Systemic neuropathies often cause symmetrical issues in the limbs. Common causes are diabetes, alcohol, chemotherapy, etc.

Accordingly, let us take a closer look at the differentiation and treatment of distal neuropathies. Peripheral neuropathies come from damage or diseases affecting nerves that produce symptoms related to dysfunction in the nerve itself. This is in contrast to nociceptive pain, in which the nerve’s performance is normal.

Consider the following patient. A 76-year-old female presents with diabetes and a HgbA1c of 7.6. The patient was in a severe car crash 15 years ago and has had low back pain since. She had breast cancer five years ago and had chemotherapy. The patient describes the pain as an “aching, burning pain” that makes it hard to sleep. She notes there is some reduction of the pain with walking. The patient reports seeing three other doctors who could not help address her pain.

The most crucial elements of the history are the symptoms and location of the neuropathy. See “A Guide To Signs And Symptoms Of The Onset Of Neuropathy” at right. It is important to document positive and negative findings because improvement in any of these can be valuable in tracking the progress of your patient.

Perhaps more crucial to the diagnosis, in our opinion, is the location of neuropathy. If it is peripheral, circumferential and roughly symmetric, one can be reasonably sure there is a systemic cause (such as diabetes or a toxin). The causes of asymmetric neuropathies, which are prevalent in the lower extremities, are typically associated with isolated lesions. Causes include disc disease, trauma and entrapments.

A proper history is crucial to find a cause. Did the patient work in an environment where she would have been exposed to heavy metals? Was she exposed to Lyme disease? One must know the social history and nutritional history to look for vitamin deficiencies of B6, B12, folate, vitamin D, etc.

Two useful tools are a peripheral arterial disease questionnaire and the neuropathy function index. These are easy surveys that will help in triaging, treatment and measuring a patient’s progress. 

How does one differentiate among the various causes of peripheral neuropathy? 
Developing an algorithmic approach can save time and medical resources. Ordering tests to rule out all possible causes could be very expensive. Clinical judgment can help narrow the list of possibilities.

Conducting An Effective Physical Examination
The physical examination should include a limited back exam and full lower extremity exam. As part of the foot exam, we utilize several objective tests. Standard tests include the Semmes Weinstein monofilament test, the Rydel-Seiffer eight-point vibration scale, sensory testing with a sharp and a dull instrument, temperature testing, Tinel’s sign, two-point discrimination, and pressure specified sensory testing. While exhaustive and time-consuming, these tests will serve to map the location (e.g. proximal spread) and quantitate the nature and severity of the neuropathy. These tests are quite useful in tracking a patient’s progress.

The loss of vibration and/or light touch sensation around the entire limb may mean undiagnosed diabetes or idiopathic peripheral neuropathy. Often, these findings represent a decrease in the function of the small nerve fibers. If these findings are confined to a single dermatome, one should suspect a lumbar radiculopathy, a more proximal entrapment syndrome or another type of neuropathy.

What Diagnostic Testing Can Reveal About The Cause Of Neuropathy
Blood tests can be useful in finding a specific cause for neuropathy. Hemoglobin A1c reflects the average blood sugar and can track a patient’s adherence over three months. To maximize the treatment of neuropathy, an HgbA1c of 7.0 or below should be the goal. The GlycoMark test (GlycoMark, Inc.) is a blood test that reports a two-week average measure of the maximum blood glucose.

Nutritional screening is important because the B vitamins and vitamin D are often deficient. Clinicians should check blood levels to minimize potential toxicity if patients are taking high doses of fat-soluble vitamins.

Comprehensive neuropathy testing includes: lead, mercury, arsenic levels, vitamin B6 level, B12 levels, a Lyme titer, RPR (rapid plasma reagin) syphilis test and complete blood cell count with differential to evaluate for possible anemia. Comprehensive testing should be individualized to each case and be the decision of each practitioner. Bear in mind that testing can be very expensive and may not influence treatment.

The “standard” in objective nerve testing remains nerve conduction/electromyography (EMG), especially if one suspects nerve entrapment. We believe there is little evidence for ordering these tests in diagnosing systemic neuropathies. Often, the report states “diffuse peripheral polyneuropathy with both axonal and demyelinating features,” which one would already know.

The A-delta nerve conduction study, a relatively new test for small fiber neuropathy, has been in use for over 10 years. We believe this test is more useful to evaluate efficacy of the neuropathy treatment but it is not widely available at this time.

The epidermal nerve fiber density test is a new gold standard that has emerged for the diagnosis of peripheral neuropathy.1 Physicians and labs advocate using one to three biopsy sites with a 2 mm punch biopsy. Common testing sites are: the proximal thigh (10 cm from the hip), the distal thigh (10 cm from the knee), 10 cm above the lateral malleolus and on the lateral midfoot. Systemic neuropathies often show a decrease in small nerve fiber density and this simple test can quantify improvement in neuropathy.

What You Should Know About Diabetic Neuropathy Treatments
Nutritional. Alpha lipoic acid, vitamin B complexes and vitamin D supplementation have shown improvement in neuropathic symptoms in numerous studies. According to a Cochrane Review in 2008, most studies did not show significant improvement in peripheral neuropathy using vitamin B only.2 
Using epidermal nerve biopsy, Jacobs found that a combination of L-methylfolate, methylcobalamin and pyridoxal 5’-phosphate (Metanx, Pamlab) decreased neuropathic symptoms and showed an increase in epidermal nerve fiber density.3

Pharmacological. Gabapentin (Neurontin, Pfizer) received FDA approval in 1993 and has been the subject of multiple double-blind studies. According to Moore and colleagues, the number needed to treat ranged between 4.8 to 8.7.4 Sixty-six percent of patients experienced adverse events and 12 percent withdrew because of adverse events. Serious events were no more common in the treatment group than placebo (4 percent).

Pregabalin (Lyrica, Pfizer) received FDA approval in 2004. Finnerup and coworkers state that the number needed to treat ranged from 3.3 to 4.7.5 In studies, 22 to 38 percent of patients taking pregabalin experienced adverse events with rare withdrawal from therapy due to side effects.5

Compound creams. An enticing treatment option to prevent systemic side effects, compound creams have shown mixed results for us. To our knowledge, no high-powered studies have demonstrated efficacy with compound creams.
 Most compounding pharmacies use their own specific combinations, which makes it difficult to determine which compounds are most effective and in determining the number needed to treat.

Current Insights On An Emerging Treatment
Combined electrochemical treatment (CET) has shown promising results in several small studies.6-9 We have covered our current treatment protocol in other previous published papers.7,8 These studies have shown up to 80 percent of patients experiencing significant relief from their neuropathic symptoms.6-8 

Before and after epidermal nerve biopsies have proven that combined electrochemical treatment increases the epidermal nerve fiber density. The combined electrochemical treatment shows very impressive results in comparison to traditional therapies for systemic neuropathies.

Larger studies are needed to improve the acceptance of combined electrochemical treatment by third-party payers. As long-term patient success continues to be documented at substantially reduced overall costs for neuropathy treatment, the third-party payers will be more forthcoming with appropriate reimbursement.

Dr. Cernak is affiliated with Weil Foot & Ankle Institute in Kenosha, Wis.
Dr. Larsen is affiliated with Weil Foot & Ankle Institute in Kenosha, Wis.
Dr. Odell is affiliated with Neuropathy & Pain Centers of America in Las Vegas.

References
Saperstein DS, Levine TD. Diagnosing small fiber neuropathy through the use of skin biopsy. Practical Neurology. 2009; 8(1):37-40
Ang CD, Alviar MJM, Dans AL, Bautista-Velez GGP, Villaruz-Sulit MVC, Tan JJ, Co HU, Bautista MRM, Roxas AA. Vitamin B for treating peripheral neuropathy. Cochrane Database Syst Rev. 2008; 16(3):CD004573.
Jacobs AM, Cheng D. Management of diabetic small-fiber neuropathy with combination L-methylfolate, methylcobalamin, and pyridoxal 5’-phosphate. Rev Neurol Dis. 2011; 8(1-2):39-47.
Moore RA, Wiffen PJ, Derry S, McQuayHJ. Gabapentin for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev. 2011 16;(3):CD007938
Finnerup NB, Jensen TS. Clinical use of pregabalin in the management of central neuropathic pain. Neuropsychiatric Disease Treat. 2007; 3(6):885-891.
Odell RH, Sorgnard RE. New device combines electrical currents and local anesthetic for pain management. Practical Pain Management. 2011; 11(6):52-68
Cernak C, Marriott E, Martini J, Fleischmann J. Electric current and local anesthetic combination successfully treats pain associated with diabetic neuropathy. Practical Pain Management. 2012; 12(3):23-36.
Cernak C, Odell R, Carney P. Can combined electrochemical treatment have an impact for diabetic peripheral neuropathy? Podiatry Today. 2014; 27(7):20-24.
Carney PM. Quantum theory treats neuropathy better than pharmacology. The Pain Practitioner. 2014: 28-31
For further reading, see “Can Combined Electrochemical Treatment Have An Impact For Diabetic Peripheral Neuropathy?” in the July 2014 issue of Podiatry Today.

http://www.podiatrytoday.com/mitigating-some-guesswork-treating-neuropathic-pain

FRUIT AND VEGETABLE CONSUMPTION COULD BE AS GOOD FOR YOUR MENTAL AS YOUR PHYSICAL HEALTH

Fruit and vegetable consumption could be as good for your mental as your physical health, new research suggests.

The research, conducted by the University of Warwick's Medical School using data from the Health Survey for England, and published by BMJ Open focused on mental wellbeing and found that high and low mental wellbeing were consistently associated with an individual's fruit and vegetable consumption.

33.5% of respondents with high mental wellbeing ate five or more portions of fruit and vegetables a day, compared with only 6.8% who ate less than one portion. Commenting on the findings Dr Saverio Stranges, the research paper's lead author, said: "The data suggest that higher an individual's fruit and vegetable intake the lower the chance of their having low mental wellbeing."

31.4% of those with high mental wellbeing ate three-four portions and 28.4% ate one-two.

Other health-related behaviours were found to be associated with mental wellbeing, but along with smoking only fruit and vegetable consumption was consistently associated in both men and women. Alcohol intake and obesity were not associated with high mental wellbeing.

Commenting on the findings Dr Saverio Stranges, the research paper's lead author, said: "Along with smoking, fruit and vegetable consumption was the health-related behaviour most consistently associated with both low and high mental wellbeing. These novel findings suggest that fruit and vegetable intake may play a potential role as a driver, not just of physical, but also of mental wellbeing in the general population."

Low mental wellbeing is strongly linked to mental illness and mental health problems, but high mental wellbeing is more than the absence of symptoms or illness; it is a state in which people feel good and function well. Optimism, happiness, self-esteem, resilience and good relationships with others are all part of this state. Mental wellbeing is important not just to protect people from mental illness but because it protects people against common and serious physical diseases.

Discussing the implications of the research, co-author Professor Sarah Stewart-Brown says that: "Mental illness is hugely costly to both the individual and society, and mental wellbeing underpins many physical diseases, unhealthy lifestyles and social inequalities in health. It has become very important that we begin to research the factors that enable people to maintain a sense of wellbeing.

"Our findings add to the mounting evidence that fruit and vegetable intake could be one such factor and mean that people are likely to be able to enhance their mental wellbeing at the same time as preventing heart disease and cancer."

Mental wellbeing was assessed using the Warwick-Edinburgh Mental Wellbeing Scale (WEMWBS), in which the top 15% of participants categorised as having High mental wellbeing, the bottom 15% Low and the middle 16-84% as Middle.

The research involved 14,000 participants in England aged 16 or over, with 56% of those being female and 44% male, as part of the Health Survey for England -- which saw detailed information collected on mental and physical health, health related behaviours, demographics and socio-economic characteristics.