Gabapentin And Pregabalin Lyrica Really Are A Danger To Your Neuropathic Health!

Today's post from pulsetoday.co.uk (see link below) is an impassioned plea from a home doctor who is seeing the consequences of long-term gabapentin and pregabalin (Lyrica) use in his surgery. Finally, a doctor who stands up to the hype that the pharmaceutical companies use to promote their drugs! Many, many neuropathy patients across the world have been prescribed either gabapentin or pregabalin for their nerve pain and other symptoms. This blog has long warned of the dangers of Lyrica (pregabalin) and advised patient to have serious discussions with their doctors if they are being prescribed these drugs. This article explains why and in terms you can't ignore. These drugs aren't the first and they won't be the last to display dangerous side effects years after the profit on them has been made. As Dr Spence says: "If it quacks like a duck and looks like a duck, then it’s a ducking duck"!

Gabapentinoids - the new diazepam?
Posted by: Dr Des Spence 9 September 2016

The establishment ignores GPs. It prefers the advice and glamour of ‘expert’ or media doctors. But the deference shown to the ‘expert’ is creating overtreatment, medicalisation and iatrogenic harm.

GPs have to ignore this advice. We won’t prescribe statins to everyone because it is irrational and stupid. We don’t accept that ‘pain is what the patient says it is’, because common sense dictates that it isn’t.

And we have seen the damage when experts have free rein. Diazepam was peddled as a safe and effective treatment for anxiety by companies and experts alike. When I started work in the early 1990s the consequence of this advice was evident everywhere. Herds of middle-aged patients zonked out and dependent on benzodiazepines. And benzodiazepines were being widely abused by a younger generation. My surgeries were spent dealing with drug-seeking behaviours, lies, confrontation, rebound agitation, insomnia and withdrawal seizures. It took the establishment decades to realise the harms we caused. Even today, we are still dealing with it.

GPs are first to notice the danger posed by psychoactive drugs. In the past five years my sensor has been off the scale with the gabapentinoids (gabapentin and pregabalin). Patients are seeking them using the crude acting skills that I used to witness with benzodiazepines: anger, tears and threats; constant requests for dose increases; stories of lost scripts; and a tag-team approach with friends who ‘corroborate’ stories.

If you google ‘gabapentinoids’, it is clear they are being widely abused. Large quantities are taken as single doses. Users describe them as the ‘ideal psychotropic drug’ with effects of ‘great euphoria’, ‘disassociation’ and an ‘opiate buzz’ as they boost the effects of these drugs.[1,2]

I wrote an article in the BMJ in 2013[3] highlighting these concerns. Since then, prescriptions have nearly doubled in three years to 10 million scripts and more than £300m in costs.[4] Such rapid increases are the signature of inappropriate prescribing and iatrogenic harm. Many practices started prescribing gabapentinoids on the back of specialist endorsement, despite the existence of effective and less harmful alternatives.[5,6] But requests from pain clinics and psychiatry come thick and fast. We decline many, then weather the storm of protest.

Do we have a problem with gabapentinoid abuse? If it quacks like a duck and looks like a duck, then it’s a ducking duck. Pregabalin is already a controlled medication in the US and there is debate about controls in the UK. The research base for the benefits of gabapentinoids is of short duration and in a small, defined population where as few as one in 10 benefits.[7] We need to change our prescribing policy now and limit the use of gabapentinoids.[2]

We know the pattern: GPs will be blamed even if we just follow orders. I get tired that no one listens to generalists. This is déjà vu. Do we want another benzodiazepines disaster?

Dr Des Spence is a GP in Maryhill, Glasgow, and a tutor at the University of Glasgow

References Schifano F, D’Offizi S, et al. Is there a recreational misuse potential for pregabalin? Analysis of anecdotal online reports in comparison with related gabapentin and clonazepam data. Psychother Psychosom 2011;80:118-22
Advice for prescribers on the risk of the misuse of pregabalin and gabapentin. Public Health England, 2014
Spence D. Bad medicine: gabapentin and pregabalin BMJ 2013; 347 08 November 2013
NHS Prescription Cost Analysis data. NHS Business Services Authority, 2016
Wiffen P, Derry S, et al. Antiepileptic drugs for neuropathic pain and fibromyalgia - an overview of Cochrane reviews Cochrane Database Syst Rev 11 November 2013; (11):CD010567
Moore R, Derry S, et al. Amitriptyline for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2012 Dec 12;12:CD008242
Advice on the anticonvulsant drugs pregabalin and gabapentin. Advisory Council on the Misuse of Drugs, 2106 

http://www.pulsetoday.co.uk/views/blogs/gabapentinoids-the-new-diazepam/20032721.blog

Neuropathy Images And Text To Make You Think

Today's post from recent posts on the Neuropathy Association's Facebook page (see link below) is nothing more than a series of images which may teach you something you didn't know about neuropathy. They are loosely based on the rarer neuropathies. Remember, there are over 100 different types of neuropathy although most people suffer from very similar symptoms, irrespective of the cause. These images may open your eyes to the variety of suffering that neuropathy can bring and you may have to Google a few terms to get an explanation but that's surely not too hard to widen your knowledge! Millions across the world suffer from debilitating nerve damage and we're nowhere nearer any sort of cure than we were 50 years ago!

Selected Neuropathy Association Facebook page Images
2014




Catching up on the Facebook chat is possible via the neuropathy association home page






















 https://www.facebook.com/NeuropathyAssociation

What Can Actually Happen To You If You Have Neuropathy

Today's post from neuropathytreatmentgroup.com (see link below) is actually an article attached to an advertisement for a neuropathy treatment and this blog does not support the treatment offered, nor any other form of advertising for so-called curative neuropathy products. Neuropathy is with you for life I'm afraid and all you can do is reduce the severity of the symptoms using chemical drugs or various alternative treatments and supplements. It can't be cured (at the moment), so please don't believe any website that tells you it can. HOWEVER, this article is packed with such useful and accurate information, I can only applaud the author and recommend the content to readers of this blog. It explains simply and clearly what can happen to you if you have neuropathy. Worth a read.

What No One Tells You About Neuropathy and Muscle Control
2016
 
Have you noticed your muscles acting a little strange since developing neuropathy? Perhaps they affect your ability to walk? Or maybe you find it difficult to use your fingers to pick something up? While we normally associated peripheral neuropathy with symptoms like pain, numbness and tingling – there are other symptoms as well.

The peripheral nervous system is made up of three different kinds of nerves: motor, sensory and autonomic. Each type of nerve controls different functions. Motor nerves send signals from the brain and spinal cord to your muscles – controlling motor functions like walking, dexterity and more. Sensory nerves do the opposite – relaying signals like temperature, pain, etc. from the muscles back to the brain and spinal cord. Finally, the autonomic nerves control involuntary or semi-voluntary functions like heart rate, digestion, blood pressure and more.

Peripheral neuropathy can affect some or all of these nerves. The symptoms you experience will depend entirely upon the type of nerve(s)that have been damaged as a result of your neuropathy. If your sensory nerves have been damaged you will experience symptoms such as pain, numbness, tingling or burning. Damage to the autonomic nerves can lead to problems with dizziness, sweating (either too much or too little), nausea, vomiting, diarrhea, constipation, difficulty urinating and more.

If your motor nerves fall victim to nerve damage – various motor functions can be affected. Lets take a look at five possible symptoms you might experience if your neuropathy has damaged your motor nerves:

Loss of balance and difficulty walking

Damage to the motor nerves can make walking difficulty. Your legs may feel heavy and difficult to move or you may feel constantly off balance. Since damage to the motor nerves disrupts the signals from your brain and spinal cord to the muscles – telling them what to do – even something as simple as walking can become a difficult task.

Damage to the sensory nerves can exacerbate this problem. The pain or numbness usually associated with damage to these nerves often affect the feet – making walking even more problematic.

For those suffering from symptoms related to motor nerve damage – extra caution should be used when walking on stairs or other areas where a fall risk is greater. Allowing extra time and avoiding rushing to perform tasks can also help limit your risk of falling.

Loss of Dexterity

Do you find it difficult to pick things up or use your hands to perform certain tasks? If so, that’s a sign your neuropathy has affected your motor nerves. Damage to the motor nerves can affect the ability of your brain to send signals properly to the muscles in your hands. You may notice somewhat delayed reactions in your hands or the muscles in your hands may feel weak – inhibiting your ability to perform even normal tasks like picking something up or moving your fingers.

Some common difficulties associated with loss of dexterity are inability to grip objects, loss of hand strength, difficulty writing or typing, difficulty performing tasks that require small movements, decreased reflexes and more. While you may not be able to restore complete control or strength to the hands – doing regular hand exercises can help you rebuild and maintain muscle strength and improve dexterity control.

Muscle Weakness; Deterioration

As damage to your motor nerves inhibits the ability of your brain and spinal cord to transmit messages to your muscles – you may find yourself limiting the use of your arms, legs, hands and feet. For many, this decrease in physical activity results in muscle deterioration and weakness. As the muscles deteriorate, you lose muscle mass and tone (this is often referred to as muscle atrophy).

Muscle weakness further contributes to the loss of dexterity, balance and difficulty walking previously mentioned. While exercise is often difficult and pain for those with neuropathy – there are low-impact exercises that will help you retain muscle mass and prevent muscle deterioration.

Try these 5 Low Impact Exercises for Neuropathy if you’re experiencing muscle weakness or deterioration!

Cramps; Spasms

The deterioration of muscle mass and the disruption of signals from the brain to the muscles can also lead to painful cramps, muscles spasms and twitches. For many, the cramping strikes at night and can range in severity from mild to extremely painful. In addition to cramping, many experience uncontrollable spasms or muscle twitching – which is visible just below the skin. While not as painful as cramps, they can be quite bothersome.

Loss of Muscle Control

As we’ve already touched on with the sections on loss of balance and dexterity – damage to the motor nerves affects your ability to control your muscles properly. The motor nerves carry messages from the brain and spinal cord to the muscles – telling them what actions to perform. As this line of communication is disrupted – the ability to control muscles is diminished. This is made manifest in loss of reflexes, inability to move hands or feet quickly, difficulty with fine motor tasks (i.e. buttoning a shirt, writing, etc) and more.

While the most common symptoms associated with peripheral neuropathy are pain, numbness, burning or tingling in the hands or feet – they are not the only symptoms. When the motor nerves fall victim to neuropathy the symptoms can go far beyond pain or numbness. They can affect your ability to control muscles and perform otherwise simple physical tasks. Though you may not be able to completely reverse these negative effects, alternative approaches like exercise can help you build and maintain muscle mass – thus helping to minimize the impact of motor nerve damage.

http://www.neuropathytreatmentgroup.com/what-no-one-tells-you-about-neuropathy-muscle-control/

How To Turn Neuropathy Lemons Into Lemonade!

Today's short post from tellingknots.com (see link below) comes from a blog written by a lady living in Jerusalem, Israel and is a humorous look at an incident in her daily life with neuropathy. If only more of us could be able to bring a smile to other people's faces in such a way, living with neuropathy may not be such a daily grind.

Lemonade: A neuropathy kitchen ballet in one act 
Telling Knots 30th July 2014

Hot day in July, time to make lemonade. Sugar, lemon juice and a little hot water are already mixed up in the bottle. All that remains is to pour the cold water through the funnel and fill the bottle. Pouring from a Brita water-filter pitcher into the funnel. Left hand somehow loses grip on the funnel. Right hand somehow flips off the top of the Brita pitcher. Water, water of blessing, water of life, cold wet water flows over the kitchen counter, over me, onto the floor, onto the other counter, onto the floor of the next room.

I had no idea how much area a liter of water can actually cover.

Then comes the cleaning up part. My balance isn’t great today, but I need to make a choice: toss the floor cloth down and sort of skate around on it to sop up the water? Get down on my hands and knees (which means getting up again) to clean it up?

I start with the skating method, lose my balance (not a huge surprise) and fall over into the water. Nice and refreshing on this hot summer’s day. Since I’m down there anyway, I stay down and finish the clean up. Finally I crawl over to the bed and use it to hoist myself back up.

Cool – I did floor exercises today.
(This post appeared in almost identical form on my Facebook page. It made people smile, so I decided to post it here, too.)

http://www.tellingknots.com/archives/3490

Educating The Nervous System To Ignore Pain

Today's post from pbs.org (see link below) is an excellent explanation of the complexity of chronic pain as a condition and how modern drugs are frequently ineffective in dealing with it. The need is for new drug compounds to address new neural receptors but although progress is being made, it will still take a very long time before the processes and drugs can be explored and refined. It is thought that by interrupting the signal between the pain and the brain (to put it very simply) there is a brief period when old pain memories can be erased. It's working in this area that may bring the most progress for nerve damage patients in the future. A fascinating article - definitely worth a read.

Teaching the Nervous System to Forget Chronic PainBy Eleanor Nelsen on Wed, 13 Aug 2014

“It was an emergency situation,” she says. The horse Sally was riding was barreling straight towards another, younger horse, and the only way to stop him was to pull back on one rein, hard. She felt a pop in her wrist. Heat shot up her arm, excruciating pain fast on its heels.

That was four years ago. No one knows quite what happened to her wrist that day, but whatever it was has left her with constant pain that stretches from her fingertips to her neck, and sometimes creeps into her ribs. On the really bad days, even a hug is unbearably painful.

Sally is my youngest sister, and she is one of an unlucky fraction of people for whom an injury catapults their nervous system into a state of chronic pain. The injury itself heals, but like an insidious memory, the pain lingers. We don’t know why. “The whole issue of the transition from acute pain to chronic pain—why some individuals develop that chronic pain and many don’t—is a major, major question,” says Allan Basbaum, a professor at the University of California, San Francisco. Genetics may play a role. So can the severity of the original injury. 
Today's painkillers are based on well-known compounds like morphine and are often highly addictive.

But what we do know is that once that pain has gotten a foothold, doctors and patients don’t have very many choices. “The irony is that morphine, the 2,000-year-old drug, still remains the number-one weapon against pain,” says Yves De Koninck, a professor of neuroscience at Université Laval in Canada.

And it’s not a weapon that anyone enjoys using. Opioids like morphine and oxycodone are famously addictive, and the numbers of people who abuse them are climbing. Painkiller overdoses now kill more people than cocaine and heroin combined. And while opioids are invaluable for acute pain, they’re less effective for persistent, chronic pain. In fact—in a particularly cruel irony—long-term opioid treatment can actually make pain worse. Non-opioid pain medications exist, but they don’t work for the majority of patients, and even then they are only partly effective. Chronic pain is like “a maladaptive memory.”

Opioids work so well for acute pain because they bind to the receptors the body has designed for its own painkillers—molecules like endorphins and dynorphins that blunt the pain response. Finding good alternatives to opioids for treating chronic pain will mean finding different neurological mechanisms to target—mechanisms that explain not just why people hurt, but why some people hurt for so long.

De Koninck has found such a mechanism. One of the keys to understanding chronic pain, he believes, is to pay attention to the similarities between long-lasting pain and another, very familiar, neurological process that makes some connections stick around longer than others: memory.

Chronic pain is like “a maladaptive memory,” Basbaum explains. Both constitute patterns etched in your brain and nervous system that quicken the connections between “snake” and “poison” or between “bump” and “ouch.” Evidence has been piling up that chronic pain and memory share some of the same cellular mechanisms—and now, De Koninck’s work has shown that a neurochemical trick used to erase memory may be able to turn off chronic pain, too. An Unmet Need

The number of people struggling with chronic pain has been hotly debated, and the fact that chronic pain is broadly defined and difficult to quantify doesn’t help. But even conservative estimates suggest that about 20% of the population have had at least one episode of serious, chronic pain. In the United States alone, that’s more than 60 million people. “It’s a major unmet need,” De Koninck says.

Pain is physically and psychologically debilitating in way that few other conditions are. “In fact, it’s often the most debilitating component of many diseases,” De Koninck notes. And it sharply circumscribes the lives of people who suffer from it. People can find a way to live with the other challenges of painful conditions like arthritis, cancer, even paralysis, he says, but “if you actually ask the patient, their number-one concern, and the one thing that they want us to cure, is the pain.” When pain pathways are functioning properly, they play a protective role.

When chronic pain gets severe, many patients withdraw, sometimes even from their families. Sally says that she’s constantly nervous, afraid to accept invitations or do things that she loves—like riding horses—in case it makes her arm even worse. The ride that day, Sally says, “changed my life.” For some patients, chronic pain can lead to serious mental health problems—it’s strongly correlated with depression and suicide risk.

When pain pathways are functioning properly, they play a protective role. They are a relay of chemical and electrical signals that move from nerve endings to our brains. Pain teaches us to avoid things that are sharp, prickly, or hot. It’s the way our nervous system has adapted to living in a hazardous world. People who can’t feel any pain typically don’t live very long.

Our skin is packed with millions of specialized nerve endings, programmed to detect dangerous conditions like heat or pressure. When one of these pathways is activated, the neuron sends an electrical current shooting up its long, thin axon towards the spinal cord. When it reaches the end of the neuron, that electrical signal prompts the release of chemicals called neurotransmitters into the synapse, or the gap between the first neuron and the next. The neurotransmitters dock in receptors on the next neuron, triggering pores to open in the cell’s membrane. Charged particles rush in through these open pores, creating a new electrical current that carries the signal farther up the nervous system.
Nerve cells, like these seen here from a mouse's spinal cord, send impulses along their axons and connect over synapses.

The first handoff occurs in a region of the spinal cord known as the dorsal horn, a column of grey matter that looks, in cross-section, like a butterfly. From this first relay point, the signal travels to the thalamus, one of the brain’s switchboards, and eventually to the cerebral cortex, where the signal is processed and decoded.

After an injury, it’s normal for the damage sensors near the trauma site to be touchy for a little while. During that time, your nervous system is encouraging you to protect the damaged tissue while it’s healing. But sometimes that extra sensitivity, called “hyperalgesia,” sticks around long after it’s useful. Hyperalgesia is often a major component of chronic pain, and it means that people with chronic pain have to be unceasingly alert. For example, Sally says, before she hurt her arm, hot coffee sloshing onto her hand might have hurt for a few seconds. Now, a careless moment like that means days of burning pain.

Symptoms like this suggest that changes in the nervous system have migrated to the spinal cord. De Koninck believes that a major factor is the number of receptors on the signal-receiving neurons in the dorsal horn. If those neurons synthesize too many receptors, they’ll pick up too many neurotransmitter molecules. Then the neurons’ pores will flutter open to let charged particles in more often than they should, sending electrical signals shooting up to the brain at too high a frequency. The result is a pain signal that’s much stronger than it should be. De Koninck’s work gives us a new window into how it happens, and how to stop it. Recall, Then Erase

The key lies in a study about memory that was published nearly 15 years ago. Long-term memories seem to depend on the synthesis of extra receptors, too, and scientists knew that blocking the synthesis of those receptors during a memorable event could keep memories from forming.

But what a group of researchers at New York University discovered was that there is a brief period when interrupting receptor synthesis can actually erase old memories. Memories are reinforced when they’re retrieved, but, paradoxically, during that process, even well-established memories have a brief window of vulnerability—like jewelry in a safe deposit box, memories are useless when they’re stored but accessible to thieves when they’re being used. A chemical called anisomycin blocks the production of receptors that neurons need to form memories. When the researchers injected anisomycin into rats’ brains right after triggering a particular memory, that memory didn’t just fail to get reinforced—it was erased altogether. The right chemical injected at just the right place at just the right time could erase the physiological “memory” of pain.

Accumulating evidence that pain and memory use similar mechanisms led De Koninck to wonder if this same neurochemical trick could erase chronic hyperalgesia. De Koninck and his colleagues made mice hypersensitive to pain by injecting their paws with capsaicin, the chemical responsible for chili peppers’ fiery bite. Capsaicin activates the same pain sensors that respond to extreme heat and can turn on hyperalgesia without the tissue damage that an actual burn would cause. After their capsaicin injection, the mice’s paws were more sensitive to pressure for hours afterward.

Before that sensitivity had had a chance to wear off, the team gave the mice a second capsaicin injection—and this time, they added an injection of anisomycin. What happened after this second injection is “like magic,” De Koninck says. When the second injection initiated the same flurry of neurotransmitters and electrical signals that encoded the hyperalgesia the first time—the pain analogue of recalling a memory—anisomycin shut down the pain-amplifying mechanism by keeping the spinal cord neurons from making extra receptors. “It’s in the process of reorganizing itself,” De Koninck explains, “and there there’s that window of opportunity to actually shut it back down.” The mice lost seventy percent of their hypersensitivity to pain.

The theory that overdeveloped connections other than memories could be attenuated by retriggering them “is not a new idea,” Basbaum says, “but the fact is, there really has been very little evidence that it’s doable.” De Koninck’s results suggest that the right chemical injected at just the right place at just the right time, can erase the physiological “memory” of pain. Ted Price, a professor at the University of Texas-Dallas, says that this “ paves the road to disease modification instead of just palliatively treating people with these terrible drugs like opioids, which everybody, everybody in the field wants to get away from.” New Options

For now, there are a few other types of treatment doctors can turn to besides opioids. Antidepressants help some people, as do certain antiseizure medications. A controversial technique called “transcutaneous electrical nerve stimulation” may work by making sure that there are plenty of receptors in the dorsal horn for the body’s natural opioid chemicals; a wearable device using this technology was just approved for over-the-counter sale by the FDA.

Treatments based on De Konick’s capsaicin-anisomycin model would constitute an entirely new category of drugs. “When you find a new mechanism,” De Koninck says, “boy, it opens a whole new array of things.” But finding the right combination of chemicals won’t be easy. Capsaicin patches are already sold over the counter at drugstores, but anisomycin is far too indiscriminate for clinical use. Brian Wainger, a physician and researcher at Massachusetts General Hospital, says, “It’s obviously going to be a long time for a discovery like this to work towards a clinical approach, but I think it sort of sets a framework for some options.”

“Options” is a word that seems to come up a lot among pain specialists. One of the reasons chronic pain is so difficult to treat is because “there’s a lot of different forms of chronic pain,” De Koninck says. “But the arsenal that we have so far to treat it is still quite meager.” And the weapons we do have are woefully inadequate.

Still, discovering that this retrigger-and-erase phenomenon works for hyperalgesia, as well as for memory, suggests that it may be useful in other parts of the nervous system. If that’s true, these kinds of treatments could help with pain syndromes more complicated than hyperalgesia—conditions that are so severe that even light touches become painful, or in cases where patients experience pain with no stimulus at all.

One big advantage of De Koninck’s strategy is that it isn’t just an incremental improvement, a way to make a slightly more effective or slightly less addictive analgesic. It’s a totally different angle on the problem. It targets the “chronic” part of chronic pain. “What the field I think really needs is options,” Price says. “And more importantly, patients need options.” For millions of people, and their doctors, a totally different angle is exactly what they’ve been looking for.

Tell us what you think on Twitter #novanext, Facebook, or email.

Eleanor Nelsen
Twitter

Eleanor Nelsen is NOVA's 2014 AAAS Mass Media Fellow. She has also written for QUEST Science and Wisconsin Public Television.

Other posts from this contributor

http://www.pbs.org/wgbh/nova/next/body/chronic-pain

8 Gly Carb To Help Reduce Neuropathic Pain

Today's post from fiercebiotechresearch.com (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 Davisresearchers 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

http://www.fiercebiotechresearch.com/story/uc-davis-team-finds-prime-drug-candidate-neuropathic-pain/2015-02-10

MS Drug To Treat Chemo Neuropathy

Today's post from sciencedaily.com (see link below) talks about the danger of chemotherapy drugs causing neuropathy but also looks at an option to address that threat by using a drug normally used for Multiple Sclerosis. Unfortunately, cancer is more common these days due partly to our increasing age and partly to unwise lifestyle choices. Chemotherapy remains the standard treatment for tumors and as a result, the number of people suffering from neuropathy as a side effect is also increasing exponentially. The chemotherapy drugs most likely to cause neuropathy come from the Taxanes family of drugs but unfortunately, these are also the most effective in treating the cancer. It's a bit of a Catch22 situation but hopefully, progress will be made with this MS option to counteract the threat.

Possible answer to chemo pain found in multiple sclerosis drug
Date: June 23, 2014 Source: Saint Louis University 

Summary:

Two discoveries have been described by researchers: a molecular pathway by which a painful chemotherapy side effect happens and a drug that may be able to stop it. "The chemotherapy drug paclitaxel is widely used to treat many forms of cancer, including breast, ovarian and lung cancers," said one researcher. "Though it is highly effective, the medication, like many other chemotherapy drugs, frequently is accompanied by a debilitating side effect called chemotherapy induced peripheral neuropathy, or CIPN."

In a recently published study in the Journal of Biological Chemistry, Saint Louis University professor of pharmacological and physiological sciences Daniela Salvemini, Ph.D. describes two discoveries: a molecular pathway by which a painful chemotherapy side effect happens and a drug that may be able to stop it.

"The chemotherapy drug paclitaxel is widely used to treat many forms of cancer, including breast, ovarian and lung cancers," said Salvemini. "Though it is highly effective, the medication, like many other chemotherapy drugs, frequently is accompanied by a debilitating side effect called chemotherapy induced peripheral neuropathy, or CIPN."

CIPN can appear as tingling or numbness in the hands and feet, shooting or burning pain in the limbs, or can feel like hot or cold temperature extremes. Symptoms may resolve within weeks or months of stopping the chemotherapy treatment or may last for years. In addition to causing patients suffering, CIPN is often a limiting factor when it comes to treatment.

Physicians estimate that CIPN can occur in 30 to 90 percent of patients treated with taxanes (the class of drugs that includes paclitaxel) and combination chemotherapies.

Salvemini and her colleagues studied paclitaxel, which also is known as Taxol, and discovered that the pain pathway (the series of interactions between molecular-level components) is dependent on activation of sphingosine 1-phosphate receptor subtype 1 (S1PR1) in the central nervous system by engaging a series of damaging neuro-inflammatory processes leading to pain. By inhibiting this molecule, they found that they could block and reverse paclitaxel-induced neuropathic pain without interfering with the drug's anticancer effects.

This finding is particularly encouraging because a drug that modulates S1PR1 is already on the market. A medication called FTY720 (Gilenya) is FDA-approved as a therapy for multiple sclerosis. When Salvemini tested this drug in her lab, she found that the S1PR1 modulator weakened the neuroinflammatory processes, which in turn blocked and reversed neuropathic pain without altering the anticancer properties of paclitaxel. Further, the beneficial effects of FTY720 were not restricted to paclitaxel but also extended to another chemotherapeutic agent, the platinum based drug oxaliplatin which is widely used for metastatic colon cancer and other gastrointestinal cancers.

While clinical trials will be necessary to determine the safety and efficacy of the drug in treating CIPN, researchers are hopeful that they may be able not only to relieve cancer patients of debilitating pain, but also save more lives by permitting the administration of larger, potentially more effective doses of chemotherapy drugs.

"We have identified a critical pathway by which CIPN develops and continues that can be targeted with a drug that is already FDA approved. This does not happen often," said Salvemini. "We need to capitalize on these findings and explore use of these agents in cancer pain patients to improve quality of life and potentially maximize anticancer efficacy as soon as possible."

Story Source:

The above story is based on materials provided by Saint Louis University. The original article was written by Carrie Bebermeyer. Note: Materials may be edited for content and length.

Journal Reference:
K. Janes, J. W. Little, C. Li, L. Bryant, C. Chen, Z. Chen, K. Kamocki, T. Doyle, A. Snider, E. Esposito, S. Cuzzocrea, E. Bieberich, L. Obeid, I. Petrache, G. Nicol, W. L. Neumann, D. Salvemini. The Development and Maintenance of Paclitaxel-Induced Neuropathic Pain Requires Activation of the Sphingosine 1-Phosphate Receptor Subtype 1. Journal of Biological Chemistry, 2014; DOI: 10.1074/jbc.M114.569574 

 http://www.sciencedaily.com/releases/2014/06/140623131335.htm

How To Change Your Lifestyle To Help Neuropathy Pain

Today's post from neuropathydr.com (see link below) is a 'self help' post designed to make you re-evaluate any daily habits you might have that may influence the amount of pain and discomfort you may have. Now nobody is suggesting that your pain isn't real and that your neuropathy symptoms can be cured by simply changing your attitude towards them. If there is any gain to be made by following the suggestions in this article, it's that you may be able to reduce the strength of the symptoms by adjusting certain habits you have and equally adjusting your lifestyle to make choices that will benefit you. Reading the article will probably make you wonder if, indeed, there are a few things that you could do better. Must be worth a try!

Lifestyle Change for Chronic Pain: How Do You Do It?
Posted by Editor on October 16, 2014

Knowing the Benefits Isn’t Enough to Elicit Lifestyle Change for Chronic Pain… So What Is?
By Carol Jeffrey

The World Health Organization (WHO) has defined “health” as not merely the absence of disease but as a “state of complete physical, mental, and social well-being.” That’s a rather rigid utopian view, however; an increasing amount of research is showing that patients fare much better when a multifactorial treatment approach is used to combat disease. In sharing my experience, I will expound on the physical, mental and social factors associated with making a healthy lifestyle change for chronic pain in our mindset and diets.

REFRAMING

Whenever I heard the word “diet” my thoughts went directly to lack of comfort food, deprivation and fear of failure, but these were misguided thoughts. This reminded me of a study which showed that one’s mindset could alter a person’s visual acuity. “Because the letters get progressively smaller on successive lines, participants expected only to be able to read the first few lines on a traditional eye chart. When the participants viewed a shifted and reversed chart, they were able to see letters in which they previously couldn’t identify. This showed that mindset manipulation can counteract physiological limits imposed on vision.” (Believing Is Seeing…, Langer E, Dept. of Psych, Harvard.) Shifting my view allowed me to see not only the gains of feeling better from eating a well balanced diet, but the losses that I had incurred from making poor nutritional choices. I used this information to reframe the word “diet” into new thoughts of nutrition, health, and well-being. The success of healthy eating depends not only on our mindset, but understanding how the mind-body connection affects our eating habits.

MIND-BODY CONNECTION

Let me briefly explain what the mind-body connection is about. It’s important to “be present to one’s self” in a way that fosters self-awareness and acceptance…this allows us to change. I used to work in a physician’s office, and I usually scarfed down my lunch between patients and phone calls. This ended up being a mindless task of squelching my hunger pains with food devoid of nutritional value, leaving me lethargic by the end of the day. Often, after the long commute home I would be too tired to cook, so I’d stop for fast food, only to ingest more food devoid of nourishment. My mindlessness carried on into the late evening when I would find myself absent mindedly munching on snacks as I relaxed. My poor eating habits extended Into my weekend, not due to lack of time but due to the social pressures of eating out with friends…where healthy food choices were limited. I was not psychologically present while eating nor mindful of my food choices.

BEING MINDFUL

Unfortunately, prolonged psychological stress, years of detrimental lifestyle, and poor eating habits had greatly contributed to my poor health. This eventually led to physical disability, unemployment, and the inability to do many of the things that I once loved. I was finally ready to break this cycle, and needed to become aware of the circumstances which led to my poor lifestyle choices and eating habits. I began paying attention to my internal dialogue (i.e., I don’t want to let them down, I’m expected to “…” I know I should choose the salad but I’ve had a difficult day so I deserve to eat what I want. I’m feeling anxious…Ice cream is always soothing. I’m not overweight so it isn’t like I’m pigging out). When I quit accepting my excuses, I became more mindful of my thoughts and choices, and discovered that I had much more control over my health than I had previously realized.

MISGUIDED DEPENDENCE

By this time I had reframed my thoughts about diet, understood the mind-body connection, was mindful of my choices, realized I had control over many aspects of my health. Yet, I was still depending upon my physician to heal me, or at least make me feel better with pharmaceuticals. Which leads me to the next issue I needed to address.

ENCULTURED

I had been encultured into believing that it was my physician’s job to heal, and the pharmaceutical company’s job to relieve my pain. If I failed to get better, it wasn’t my fault, or was it? “In 2012, the pharmaceutical industry spent more than $24 billion on marketing to influence physicians, and over $3 billion in advertising to consumers.” (Cegedim Strategic Data) Traditionally, very few non-M.D. or non-D.O. practitioner appointments or treatments have been covered by insurance. These practices enculture and direct us into accepting the limitations that Western medicine on its own has to offer. It also moves us further away from more natural treatments and the means of self-healing. The strategies used by insurance and BigPharm are contrary to obtaining optimal health, since integrative medicine has shown to be most effective in managing disease. Now that I understood why I was so dependent on my physician, what could I do about it?

SELF-HEALING BEHAVIOR

Fabrega Horacio, Jr. wrote an interesting article (Sickness and Healing and the Evolutionary Foundations of Mind and Minding) which shows how non-human primates (i.e., chimpanzees) are reliant on self-healing behaviors that not only remedy illness but prevent many illnesses, through social functions and diet. I had been relying on my doctors to heal me and a pill to ease my pain, instead of taking personal responsibility, and using preventive and self-healing behaviors…like the chimps. I understood that eating a healthy diet along with living a well balanced life was essential for pain reduction, but I still wasn’t motivated to change.

MOTIVATION

Pain is fundamentally unpleasant, and is designed to protect by promoting motivation and learning. I was now enlightened to the fact that my lifestyle and poor diet were fueling the raging fire within my damaged nerves. However, like many others, I have an aversion to change and even though the reward of pain relief should have provided enough motivation to elicit change…it wasn’t. It is said that most people are motivated by one of two things, “inspiration” or (in my situation) “desperation.” My chronic pain was extremely difficult to handle, but it was the lack of being able to engage in life that made me desperate enough to make changes. My attitude and desire toward change had evolved from I wish, I want, to I must. My reason to change had now been clarified and my need for change had transformed from I should, I intend, to “I am” making a lifestyle change for chronic pain. However, what would keep me motivated? This is where goal setting came into play.

GOAL SETTING

“Remember the word ‘SMART.’ Successful goals are Specific, Measurable, Achievable, Realistic and Timely.” This is based on research conducted by Dr. Edwin A. Lock of the University of Maryland.
Specific: I asked myself what my life was currently missing and what I wanted in my life. Connecting life goals to specific health-related goals clarified the reason I wished to be well and what I would do once my health improved. Thereby answering the questions what, where and why.
Measurable: I then determined how I would accomplish and measure my success. (i.e. Add three new organic, non processed foods to my grocery cart each week. Actively work with my doctor on natural pain relief techniques at each visit. Exercise as tolerated but do it two times a week. Do one thing each day to prepare me for a less stressful career.)
Achievable: I then asked myself if I had the skill, tools, and resources needed. (i.e. I researched YouTube, and I borrowed books from the library to learn about natural pain relief techniques, meditation, healthy diet, etc., and sought out physicians who practiced integrative medicine.)
Realistic: To avoid frustration, I focused on honest goals that I believed were obtainable. There was plenty of evidence to show that changing my lifestyle and eating a healthy diet would decrease my pain and improve my quality of life. It was realistic to train for a less stressful career. Total health and no pain was impossible; however, controlling diet, decreasing narcotic use and learning healthier ways of dealing with pain were within my control.
Timely: I gave myself one year to turn my health around and begin a new career. This goal challenged me but it was possible. I set daily, weekly and monthly goals which were frequently reviewed and revised as necessary.

There aren’t any shortcuts to change, including a lifestyle change for chronic pain. I had to reframe my negative thoughts, become more self-aware and mindful of my decisions, accept personal responsibility for my health, incorporate self-healing behavior, determine what would motivate me, set and commit to my goals.

The rewards of an improved quality of life came by default as I achieved my goals. I have not yet reached the utopia of health that the WHO refers to, but I have significantly decreased my pain level and again live an active and meaningful life. This article reflects my journey, but more importantly, I hope it encourages and guides you to make your own changes so that you too may live life to its fullest.

What is your experience with lifestyle change for chronic pain? Talk with us at our Facebook page.

http://neuropathydr.com/lifestyle-change-for-chronic-pain/

Will Nabilone Prove To Be A Nerve Pain Solution

 Today's post from stonehearthnewsletters.com (see link below) talks about a Canadian discovery, concerning a drug used there to calm feelings of nausea when undergoing chemotherapy. The drug, Nabilone, was tested on 60 diabetic neuropathy patients in the hope of helping with their nerve pain problems. There seemed to be a high rate of success although 60 test cases can hardly be regarded as definitive evidence. However, it strengthens the case for further investigation of Nabilone and other synthetic cannabinoids  that may control neuropathy pain (see earlier post here). Hopefully it will give doctors other options to consider in the future.

Diabetic neuropathy: a new drug, nabilone, on the horizon
Posted on November 1, 2012 by Stone Hearth News

A study from the University of Calgary’s Hotchkiss Brain Institute shows there is evidence to support a new drug therapy called nabilone to treat diabetic neuropathy, or nerve pain. Researchers enrolled 60 patients with diabetic neuropathy in a 12-week placebo controlled clinical study. At the end of the study, patients reported less pain and an improvement in sleep and anxiety when taking nabilone as compared to the placebo.

“This is a good option to help treat nerve pain due to diabetes, with very few side effects,” says Dr. Cory Toth, a neurologist and the study’s lead researcher. Toth is a member of the University of Calgary’s Hotchkiss Brain Institute, Department of Clinical Neurosciences and is the research director of the Calgary Chronic Pain Centre Clinic.

The medication used in the study has the generic name nabilone, and is currently used in Canada to treat nausea in chemotherapy patients. This study gives doctors more evidence to support its prescription for treating neuropathy pain in diabetics. Nabilone is a synthetic cannabinoid, which mimics some of the chemical compounds of cannabis, or marijuana. It is approved for use by Health Canada and the FDA.

This study is a further demonstration of the potential medical benefits of cannabinoids in a difficult pain condition. Dr. Toth and his team have conducted a solid trial which, although small, validates our clinical experience. This study gives physicians support to consider further options in treating this devastating chronic pain disorder,” says Dr. Mark Ware, Associate Professor at the McGill University Health Centre.

Type 2 diabetes is exploding at epidemic rates over the world, and Canada is no exception. Recent studies show that type 2 diabetes is present in close to 10 per cent of Canadian adults and growing at faster than predicted rates.

Diabetic neuropathy is damage caused to the nerves, which results in numbness, tingling, burning and pain. About half of all diabetics suffer from diabetic neuropathy, and about half of this group experiences extreme pain, sleep disturbances, and difficulties walking.

Leslie Bonenfant knows firsthand the pain associated with diabetic neuropathy. She was diagnosed with type 2 diabetes five years ago. Having participated in the study, she experienced positive results, “My pain was so severe that I could barely walk a block. After taking nabilone I can manage my pain and I can function day to day,” say says.

The study was published in the October issue of the medical journal Pain. It was funded by a grant from Valeant Canada.

http://www.stonehearthnewsletters.com/diabetic-neuropathy-a-new-drug-nabilone-on-the-horizon/updates/