Substance P Nerve Pain Killer Or Pain Promoter

Today's post from the ever-reliable sciencedaily.com (see link below) is an interesting one because it explains in terms we can all understand, a peculiar paradox that occurs in both the central and peripheral nervous systems concerning a mysterious substance called 'Substance P'. Now apparently, if substance P is found in the central nervous system (brain and spinal cord) it excites pain cells and causes more pain but if it is found in the peripheral nervous system (the rest of the body) it acts as a natural pain killer and prevents pain cells from becoming over-stimulated. So, what does all this mean? It means that drugs used to suppress substance P have actually caused more pain, when targeted at the peripheral nerve system and that has led to new drug 'failures' when in fact, they should have been used to suppress substance P in the central nervous system. Scientists are excited by this discovery because drugs that will promote substance P in the peripheral system will act as genuine pain killers. It's a question of targeting the right places. The article explains it much better but it's worth a read to see how research is progressing on our behalf.

'Pain paradox' discovery provides route to new pain control drugs
Date:July 28, 2016 Source:University of Leeds

A natural substance known to activate pain in the central nervous system has been found to have the opposite effect in other parts of the body, potentially paving the way to new methods of pain control.

The discovery could explain the repeated -- and costly -- failure over the last 20 years of clinical trials of potential pain-killing drugs that targeted the substance, known as 'Substance P'.

Substance P is produced in both the central nervous system (CNS) -- the brain and spinal cord -- and in our peripheral nervous system (PNS) -- all the other nerves and nerve cells that send signals to the brain.

The new research, by the Hebei Medical University in China and the University of Leeds in the UK, has found that, in the peripheral nervous system, Substance P makes nerve cells less responsive and excitable, thereby reducing sensations of pain. This is in direct contrast to its role in the central nervous system, where it triggers very different signals, exciting neurons and so promoting pain.

Lead researcher Professor Nikita Gamper, from the University of Leeds, explains: "We were really surprised by the results -- Substance P is described in the literature as a molecule that gets nerve cells excited and promotes pain. But we've discovered a paradox -- that in the peripheral nervous system it acts as one of the body's natural painkillers and actually suppresses pain.

"This means that when drugs were used in trials to suppress Substance P's action in the central nervous system, they may have also prevented it from acting as a painkiller in the peripheral system. So, although the drugs looked like they worked in the lab, when they moved to clinical trials, they failed."

Substance P works in the peripheral system by modulating the action of certain proteins that control the ability of pain-sensing neurons to respond to 'painful' stimuli. In particular, Substance P makes one type of these proteins extremely sensitive to zinc, so that natural trace levels of zinc in circulation are enough to dampen their activity and suppress the neuronal responses.

Professor Gamper -- who is also a visiting professor at Hebei Medical University -- believes this discovery could open the door to new drugs that don't have the negative side effects currently associated with stronger painkillers.

"Drugs like morphine hijack the body's natural painkilling mechanisms, such as those used by endorphins, but because they act within the central nervous system, they can affect other brain cells that use similar pathways, leading to side effects such as addiction or sleepiness," says Professor Gamper. "If we could develop a drug to mimic the mechanism that Substance P uses, and ensured it couldn't pass the blood brain barrier into the CNS, so was only active within the peripheral nervous system, it's likely it could suppress pain with limited side effects."

The study -- which looked at the action of Substance P within nerve cells in the lab and in animal models -- focused on acute pain, but Professor Gamper aims to look at its role within chronic pain as well.

Story Source:

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

Journal Reference:
Dongyang Huang, Sha Huang, Haixia Gao, Yani Liu, Jinlong Qi, Pingping Chen, Caixue Wang, Jason L. Scragg, Alexander Vakurov, Chris Peers, Xiaona Du, Hailin Zhang, Nikita Gamper. Redox-Dependent Modulation of T-Type Ca2 Channels in Sensory Neurons Contributes to Acute Anti-Nociceptive Effect of Substance P. Antioxidants & Redox Signaling, 2016; 25 (5): 233 DOI: 10.1089/ars.2015.6560

https://www.sciencedaily.com/releases/2016/07/160728105608.htm

d Methadone For Neuropathic Pain

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

d-Methadone: A Novel Approach for Neuropathic Pain
 Eliseo Salinas, MD, MSc, President and Chief Scientific Officer, Relmada Therapeutics Thu, 03/12/2015
 
At a time when opioid abuse and addiction are making headlines, a new molecule is being studied to treat neuropathic pain without such negative effects. A relative of methadone, a widely known synthetic opioid medication, d-Methadone represents half of methadone’s chemical structure with profoundly different activity on the mu opioid receptor, considered a “gateway for addiction.”

A Gold Standard Treatment

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

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

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

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

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

Early Studies

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

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

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

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

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

http://www.dddmag.com/articles/2015/03/d-methadone-novel-approach-neuropathic-pain

Do People Really Understand Their Neuropathic Pain

Today's post from healthskills.wordpress.com (see link below) asks the question as to whether people really understand the nature of their neuropathic pain. It's a very interesting study which concludes that people do much better with their problem if they receive a cogent explanation of what's happening to them. Unfortunately, with neuropathy that's rarely the case, as doctors assume that the medical science is often too complex for their patients to understand. It is pretty much a given that patients can cope much better with symptoms if they know why they are happening and what's going on inside their bodies. After that, an explanation of any treatment is also useful.

How well do people understand their neuropathic pain? 
 Martin, S., Daniel, C. Williams,  (2014)

When coming to terms with a chronic pain problem, one of the important steps involves obtaining a diagnosis that fits with both the individual’s personal experience of their pain, and also their knowledge (drawn from what is available in the general population). If the label doesn’t square with their experience, people continue searching until they find something that does.

There has been an enormous wave of excitement about giving people good “pain education”. I’ve always been a bit anxious about the term “education”, because it can so often mean giving an information dump, leaving the person being “educated” with little or no relevant knowledge about their personal concerns – and it’s the individual and unique concerns that influence how a person interprets what is happening, and how they respond. As a result, I prefer “helping people to develop a personal pain formulation” or “reconceptualising” their pain. Putting the pedantics aside, it seems really important for health professionals to not only understand what people with pain already know about their health condition, but also to understand how people interpret what they’re told – if they’re told anything.

In this study, 75 people with neuropathic pain were asked to sort a series of statements about neuropathic pain according to their level of agreement with them. This is known as Q-methodology. The sorted statements are then analysed to identify common features amongst them.

 Four factors were identified:
Neuropathic pain is a nervous system problem, psychology influences the pain experience and acceptance, and being open to psychological interventions – this group of respondents had tried psychological treatments, their pain was on average about 6 – 7 years.

Neuropathic pain is nerve damage, psychology is irrelevant in pain experience, neutral about psychological treatments – this group of people had not tried psychological treatments, but had tried surgery and medications.

Neuropathic pain is irreparable nerve damage, symptom management is needed, psychological factors play a part in pain perception but psychological treatment is not OK – this group of individuals had pain for an average of 10 years, and they had used breathing, positive thoughts, medications and physical treatments.

Neuropathic pain cause should be identified, psychological influences may play a part, and treatment can include both medical and psychological – this group had pain for an average of 1 -2 years, and they had tried a range of medications, physical methods, yoga, meditation and complementary therapies.

The authors point out several limitations of this study – people were not recruited on the basis of an particular characteristics, there could be a number of recruitment biases, and they were all identified via online recruitment processes, therefore it’s hard to generalise. What it does indicate is that there is no coherent biopsychosocial explanation put forward by participants, they appeared to have received very little explanation about their problem, and this affected their readiness for psychological or self management interventions.

Another interesting point is how many of these participants, across all the four factor groups, described experiencing being given psychosomatic explanations of their pain. The authors write :”Across all accounts, participants’ comments indicated that they had received psychosomatic explanations of their pain and had been distressed and offended, consistent with other studies which use open-ended methods to sample patients’ experiences. (p. 353).” The influence of psychological factors was found to be associated more with adjusting to chronic pain, rather than to developing an integrated model of pain. Factor 1 were the only group to endorse the notion of acceptance, or learning to live with pain – and the groups in Factors 3 and 4 were strongly against the idea that pain could be lived with.

I find this study interesting, not so much in what it has discovered, but rather more in terms of the discussion about psychological factors and medical factors – but nothing on social factors. I find myself wondering again whether we have a biopsychological model of pain, rather than a more complex biopsychosocial model.

That being said, I agree with a point made in the conclusion: people with chronic pain value a coherent explanation for their pain, it helps resolve their worry and enables them to approach their pain differently. The problem facing people with chronic pain is how to access evidence-based and accessible information about neuropathic (or indeed any type of) pain. Often people find out about neuropathic via biomedical models, and they rarely get exposed to the complexity of a biopsychological model, let alone a biopsychosocial one.

We desperately need to understand the best ways to personalise an explanation for an individual with chronic pain. I think a case formulation approach is the most useful, but I’ve found that many clinicians think this takes “too long” and is “too complex”. I wonder about this. A formulation might take a couple of sessions, but it’s a lot less expensive and has lower risk than surgery.

In light of the very limited range of interventions for people with neuropathic pain, perhaps taking the time to respond to the person’s unique questions about their pain would be time and money well spent.

People who have chronic pain are often very reluctant to consider the influence of psychological factors on their pain, reflecting their fear that by accepting this, their pain is being dismissed as “not real”, or not legitimate. This means people may not accept (or indeed be referred for) psychological interventions. Treatment approaches based on a cognitive behavioural approach have good evidence to support them, but they don’t do much good if people are not ready for them, or even referred for them.

Martin, S., Daniel, C., & Williams, A. (2014). How do people understand their neuropathic pain? A Q-study PAIN®, 155 (2), 349-355 DOI: 10.1016/j.pain.2013.10.021

http://healthskills.wordpress.com/2014/03/11/how-well-do-people-understand-their-neuropathic-pain/

Opioids For Chronic Pain Vid

Some very sensible advice and information in this short YouTube clip about the use of opioids in tackling both neuropathic pain and pain in general. The debate goes on but maybe be overhauled by over-hasty political reactions, leading to patients not being able to get the proper treatment any more.

Dr. Charles Argoff on Opioids as Treatment for Neuropathic Pain
Published on 19 Apr 2012


Charles Argoff, MD, from the Albany Medical Center, in Albany, NY, discusses the use of opioids as an effective treatment option for neuropathic pain, along with guidelines clinicians should consider when evaluating patients for treatment with opioids.

Is Zonisamide A Good Idea For Neuropathic Pain

Today's post from onlinelibrary.wiley.com (see link below) looks at Zonisamide as a possibly effective drug for reducing neuropathic pain. Zonisamide is one of the anti-epileptic/ anti-convulsant drugs that are designed to treat epilepsy. Like some other anti-convulsants, it's now being prescribed to treat neuropathic pain and discomfort. However, this study shows that there is very little evidence to support its effectiveness in suppressing nerve pain and that other anti-epileptics are far more effective - for instance, Gabapentin and pregabalin (Lyrica). However, there are also questions surrounding the effectiveness of pregabalin especially for neuropathy caused by diabetes and HIV (see other articles on this blog), not least from the manufacturers themselves! Gabapentin has a far better reputation but as this article shows, Zonisamide hasn't proved to be effective at all. Worth discussing with your doctor or neurologist, if anti-convulsants are being prescribed for you.
 

Zonisamide for neuropathic pain in adults
R Andrew Moore1,*, Philip J Wiffen1, Sheena Derry1, Michael PT Lunn2 
Editorial Group: Cochrane Pain, Palliative and Supportive Care Group
Published Online: 22 JAN 2015

Abstract

Background

Antiepileptic drugs have been used in pain management since the 1960s; some have shown efficacy in treating different neuropathic pain conditions. The efficacy of zonisamide for the relief of neuropathic pain has not previously been reviewed.

Objectives

To assess the analgesic efficacy and associated adverse events of zonisamide for chronic neuropathic pain in adults.

Search methods

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (via CRSO), MEDLINE, EMBASE, and two clinical trials databases (ClinicalTrials.gov. and the World Health Organisation Clinical Trials Registry Platform) to 1 August 2014, together with reference lists of retrieved papers and reviews.

Selection criteria

We included randomised, double-blind studies of at least two weeks' duration comparing zonisamide with placebo or another active treatment in chronic neuropathic pain. Participants were adults aged 18 and over. We included only full journal publication articles and clinical trial summaries.

Data collection and analysis

Two review authors independently extracted efficacy and adverse event data, and examined issues of study quality. We considered the evidence using three tiers. First tier evidence derived from data meeting current best standards and subject to minimal risk of bias (outcome equivalent to substantial pain intensity reduction, intention-to-treat analysis without imputation for dropouts; at least 200 participants in the comparison, 8 to 12 weeks duration, parallel design); second tier evidence derived from data that failed to meet one or more of these criteria and were considered at some risk of bias but with adequate numbers in the comparison; and third tier evidence derived from data involving small numbers of participants that were considered very likely to be biased or used outcomes of limited clinical utility, or both.

We planned to calculate risk ratio (RR) and numbers needed to treat (NNT) and harm (NNH) for one additional event using standard methods expected by The Cochrane Collaboration.

Main results

We included a single study treating 25 participants (13 zonisamide, 12 placebo) with painful diabetic neuropathy over 12 weeks. No first or second tier evidence was available for any outcome. The small size of the study and potential major bias due to a high proportion of early study withdrawals with zonisamide precluded any conclusions being drawn. There were two serious adverse events (one death) in zonisamide-treated participants, which were apparently not related to treatment.

Authors' conclusions

The review found a lack of evidence suggesting that zonisamide provides pain relief in any neuropathic pain condition. Effective medicines with much greater supportive evidence are available.

Plain language summary

Zonisamide for neuropathic pain in adults

Neuropathic pain can arise from damage to nerves and injury to the central nervous system. It is different from pain messages carried along healthy nerves from damaged tissue (a fall, or cut, or arthritic knee). Neuropathic pain is treated by different medicines than those used for pain from damaged tissue. Medicines like paracetamol or ibuprofen are not usually effective in neuropathic pain, while medicines that are sometimes used to treat depression or epilepsy can be very effective in some people with neuropathic pain.

Zonisamide is one of a type of medicine normally used to treat epilepsy. Some of these medicines are also useful for treating neuropathic pain. We looked for clinical trials that used zonisamide to treat neuropathic pain. We found a single study with 25 participants treated either with zonisamide or placebo. Study reporting may have led to major over-estimation of any treatment effects because most (8/13) participants treated with zonisamide withdrew before the end of 12 weeks of treatment for a variety of reasons, mostly adverse events (side effects).

There was too little information, which was of inadequate quality, to give any guidance as to whether zonisamide works as a pain medicine in any neuropathic pain condition. Other medicines have been shown to be effective in some types of neuropathic pain.

http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD011241.pub2/abstract

Pain For HIV ers A Growing Problem

Today's article from pain.com (see link below) is the first of a week-long examination of living with pain for people living with HIV in general and pays special attention to neuropathy as being one of the main causes of pain. It is useful for people who are experiencing pain, in that it may help identify the cause more easily. The symptoms of neuropathic pain can't really be mistaken for anything else but that's not to say that people with HIV don't also suffer from pain from other sources. 

Treating Pain in the HIV/AIDS Patient

December 8, 2011

Treating pain in HIV/AIDS patients is a concern, as at least half of HIV/AIDS patients report some kind of pain complaint related to their disease. Pain related to HIV/AIDS can be categorized into three general categories: general complaints, neuropathy and pain from AIDS-related cancers. Each of these types of pain are treated differently.

General complaints of pain in HIV/AIDS patients comprise both acute pain related to HIV/AIDS and chronic pain problems. Some of the pain problems related to HIV/AIDS that patients experience include muscle aches, chest pain and chronic headaches. These are problems that are present in the general population, but more common in people who are ill with a disease such as HIV/AIDS. If these symptoms are caused by a complication of the disease, the root cause must be treated. For example, people with HIV/AIDS are prone to getting a lot of opportunistic bacterial, viral and fungal infections because of their immune system deficiency. Chest pain in some HIV/AIDS patients may be caused by an infection of the lungs, such as pneumonia. In these cases, the pneumonia must be treated, and medications may be given to control the pain and other symptoms that the underlying condition is causing. These general complaints of pain that HIV/AIDS patients may have can be treated with prescription pain medications, such as narcotics. For some conditions, such as chronic headaches, other medications or treatments may work better and are safer for long-term use because they are not as habit-forming as the opioid drugs.

Peripheral neuropathy is another type of pain that HIV/AIDS patients can experience. Peripheral neuropathy is damage to the nerves that go to the extremities. This nerve damage is widespread in HIV/AIDS patients, as opposed to affecting just one part of the body. Peripheral neuropathy causes symptoms such as burning or tingling pain in the hands and feet, numbness in the hands and feet and muscle weakness in the extremities. Pain that is caused by damage to the nerves themselves does not respond as well as other types of pain to narcotic pain medications. Thankfully, there are alternative medications that can have an affect on pain due to nerve damage. Certain medications that are used to treat seizures and depression are also useful for reducing nerve pain due to peripheral neuropathy. Examples of these medications include the anti-seizure drugs gabapentin and phenytoin. Antidepressants of the tricyclic antidepressant and mixed reuptake inhibitor classes have been shown to help control nerve pain. Other remedies that may be prescribed for peripheral neuropathy are topical medications containing the numbing medication lidocaine or the substance capsaicin, which is responsible for giving chili peppers their heat and can reduce pain sensations when applied topically.

Because HIV/AIDS creates severe immune system deficiency, people with this infection are more prone to not only opportunistic infectious diseases, but they have a greater chance of getting certain types of cancer. The immune system usually finds and destroys abnormal cells before they can become a cancerous tumor, but if the immune system is deficient, cancers arise more frequently. People with HIV/AIDS are much more likely to get a type of rare skin cancer called Kaposi sarcoma than the general population, and HIV/AIDS patients also have high rates of non-Hodgkin lymphoma. Some other types of cancer are also more likely to arise in patients infected with HIV. As pain can be caused by a cancerous tumor itself, chemicals that are present in the body because of the cancer and the effects of cancer treatments, palliative care is an important part of any cancer treatment. Not all people with cancer experience cancer-related pain, but many people do. There are a lot of different pain medications that can be used for cancer pain. If the pain is severe, strong opioid medications may be used to control it.

http://pain.com/library/2011/12/08-treating-pain-hivaids-patient/

Sciatic Nerve Pain During Pregnancy

Sciatic Nerve Pain Relief

3 Sciatic Stretches for Pregnancy Prenatal Safe Stretch Routine Relief for insomnia, restless leg syndrome, sciatica more - Duration: 22:03..By Pregnancy.org Staff. Sciatic nerve pain often comes on suddenly, creating immediate distress. And while it usually resolves in a few weeks, the pain may linger for .How to treat sciatic nerve pain during pregnancy? Sciatica causes pain and weakness from the lower back down through the legs and to the feet..Pregnancy is a never ending group of changes. The sciatic nerve can be a great source of pain during pregnancy, but women can avoid and treat the condition with rest .What is sciatica? Sciatica is pain, tingling, or numbness produced by an irritation of the nerve roots that lead to the sciatic nerve. The sciatic nerve is formed by .Sciatic Nerve Pain During Pregnancy: Causes and Treatment. The sciatic nerve is the largest nerve in the body, providing sensory and motor function to the lower .The sciatic nerve goes across the buttock and runs down the leg clear to the toes. People complain of a pain that radiates from the hip down the thigh clear to the .I admit it. I am lousy at being pregnant. While other first trimester moms are being complimented on their healthy glow, I spend the first trimester of my pregnancy .Causes of Sciatic Nerve Pain. The biggest reasons for sciatic nerve pain development are herniated spinal discs and inflammation. For the majority of .Sciatic nerve paint is common during pregnancy, as the uterus can put pressure on the lower spine, but a few simple stretching exercises can help relieve .

Sciatic Nerve Pain Relief

Triple Threat Triathlon Ttt Mysteries Nervous Breakdown The Case Of

Sciatic Nerve Pain During Pregnancy: Causes and Treatment. The sciatic nerve is the largest nerve in the body, providing sensory and motor function to the lower .By Pregnancy.org Staff. Sciatic nerve pain often comes on suddenly, creating immediate distress. And while it usually resolves in a few weeks, the pain may linger .How to treat sciatic nerve pain during pregnancy? Sciatica causes pain and weakness from the lower back down through the legs and to the feet..Pregnancy is a never ending group of changes. The sciatic nerve can be a great source of pain during pregnancy, but women can avoid and treat the condition with rest .I admit it. I am lousy at being pregnant. While other first trimester moms are being complimented on their healthy glow, I spend the first trimester of my pregnancy . Sciatic nerve paint is common during pregnancy, as the uterus can put pressure on the lower spine, but a few simple stretching exercises can help relieve .What is sciatica? Sciatica is pain, tingling, or numbness produced by an irritation of the nerve roots that lead to the sciatic nerve. The sciatic nerve is formed by . Causes of Sciatic Nerve Pain. The biggest reasons for sciatic nerve pain development are herniated spinal discs and inflammation. For the majority of . 3 Sciatic Stretches for Pregnancy Prenatal Safe Stretch Routine Relief for insomnia, restless leg syndrome, sciatica more - Duration: 22:03..The sciatic nerve goes across the buttock and runs down the leg clear to the toes. People complain of a pain that radiates from the hip down the thigh clear to the .

Are There Non Opioid Alternatives For Nerve Pain

Today's post from medscape.com (see link below) is an important one because it highlights the dilemmas facing doctors and patients alike when it comes to medicating severe neuropathic pain. The situation at the moment is clear: there is a global (but mainly North American) outcry at the use and abuse of opioid-strength medications and this has triggered a frantic search amongst the scientific community for non-opioid medications that are both strong and effective enough to combat nerve pain at its worst. This article is directed at trainee doctors and nurses and examines the problem in a sensible and well-balanced way and for that reason it's very interesting for neuropathic patients who have no option at the moment but to use the only means available for suppressing their pain and that is the opioid family of medications. It may seem a little technical but it will provide you with so much information about the thinking behind nerve pain drug prescription.

Non-Narcotic Options for Pain Relief with Chronic Neuropathic Conditions
Donna V. Wright, MS, RN, FNP
Journal for Nurse Practitioners. 2008;4(4):263-270.

Neuropathic pain is a misunderstood, usually inadequately treated condition. This article discusses the types of pain, mechanisms of pain, diagnosis, and rationale for treating neuropathic pain. The importance of working with patients to achieve their functioning goals is also addressed.

Tom Jacobson, a bail bondsman, is not getting adequate pain relief from hydrocodone/acetaminophen 10/500 (Lortab) four times a day. He is suffering from chronic low back pain with peripheral neuropathy secondary to a motor vehicle accident. He knows that his back pain is a long-term condition (with chronic pain, the recommended daily dose of acetaminophen is 2000 mg to minimize the risk of liver damage; therefore, increasing his daily doses is not an option). He has tried the generic equivalent with less acetaminophen and with less than satisfactory results. He does not want to take the next step up the pain ladder to oxycodone/acetaminophen (Percocet) at this time. He knows that in South Carolina, by changing his prescription to a schedule II medication, he will be required to obtain a new prescription monthly and that his nurse practitioner can no longer prescribe independently of her physician preceptor (in 29 states, prescription of scheduled drugs requires physician collaboration.)[1] This increase in required medical supervision and possible change of caregiver can be a deterrent for some patients. The most important consideration for Tom is the nature of his work. He does not believe that he can function effectively in his role unless he feels "totally in control." The nature of narcotic medications makes this a concern.

To better understand some of the mechanisms of neuropathic pain, a review of the types of pain, the mechanisms, the diagnosis, and the treatment of neuropathic pain is in order. Cadden describes three types of pain: acute, chronic, and acute on chronic.[2] Tom is experiencing chronic pain, which simplifies his care. When chronic pain sufferers have acute pain as well as chronic pain, they are at risk for undertreatment of pain. Table 1 reviews terms used to describe pain. There are basically three ways to treat pain: alter the central pain perception (inhibit mechanisms of pain perception in the dorsal horn of the spinal cord"'how most narcotics work), modify the pain source, and block transmission of pain impulses by modulating the transmission of the pain impulse.[2] The last mechanism is the area in which we will focus.

"Chronic neuropathic pain is the net result of sensory input greater than the central inhibitory response" the uniqueness of chronic neuropathic pain is that its multiple etiologies share a common pathway."[5] The pain signal is processed via the dorsal horn of the spinal cord and transmitted in the central nervous system (CNS). After an injury, the healing process may be altered and actually increase rather than decrease the pain response. The development of dendritic growth (neuroplasticity) can increase the number of alternate neural pathways, which may actually increase the sensitivity to pain. These alternate pathways may have an accumulation of Na+ channels that become "leaky" and fire spontaneously or with very little provocation. "Neurons fire, or spontaneously produce electrical impulses on a regular basis" they may fire more or less slowly depending on whether or not they are excited or inhibited from firing by various types of chemicals called neurotransmitters" naturally occurring chemicals i.e. substance P, glutamate and aspartate excite neurons responsible for pain transmission" drugs that block the action of these substances diminish our awareness of pain. Our body's narcotic chemicals in the brain and the spinal cord inhibit the transmission of pain impulses."[6] By decreasing the rate of impulse firing, these chemicals can help modulate the pain response. The chemicals or neurotransmitters involved are commonly affected by anticonvulsants, antidepressants, neuroleptics, and antiarrythmics (ie, betabockers, sodium channel blockers, acetycholinesterase inhibitors) ( Table 2 , Table 3 ). This very simplified explanation helps provide rationale for the diagnostic criteria and the management of neuropathic pain.

The initial goals for diagnosis according to Gilron[8] include: rule out treatable conditions (ie, a neoplasm), confirm the diagnosis of neuropathic pain, and identify the clinical features (ie, insomnia) that help individualize treatment. Neuropathic pain is most frequently diagnosed by history and examination. A common presentation would be a level of pain intensity that is disproportionate to the injury received. There may be a history of sensory disturbance (numbness, abnormal sensations, itching, burning, pricking) that worsens as the day progresses. This pain pattern may initially follow a dermatonal distribution but can begin to deviate as neuronal plastic changes advance. The development of new "leaky" neural pathways (neuroplasticity) after an injury can set the stage for development of chronic burning or electric (tingling, shocking, jolting) sensations. These overly sensitive pathways can become "exquisitely painful" or sensitive to sensations that are normally not considered painful (allodynia). Other manifestations of neuropathic pain are dysesthesia, altered or abnormal sensations, paresthesias, or hyperalgias. These pains can occur spontaneously due to regrowth connections to sympathetic nerve fibers or can be evoked. It may become difficult for the sufferer to perform his or her usual daily activities.

It is important to determine which medications or treatments have been attempted. Acetaminophen and nonsteroidal antiinflammatories (NSAIDs) are usually not effective. Concurrent alcohol or substance use and abuse issues can complicate treatment. This delayed symptomology combined with a tendency for the pain path to follow a dermatonal distribution meet the diagnositic criteria for neuropathic pain.[9]

On physical examination, disturbances in light touch, response to pin pricks, vibration, and proprioception may be noted. Sensory disturbances may be beyond the discrete nerve territory. There may be pain with a straight-leg raise exam, which suggests irritation of a lumbar root; Phalen's test or Tinell's sign may be positive (usually indicates carpal tunnel). Deep tendon reflexes may be abnormal. A skin examination may show temperature, color, and hair growth changes, along with abnormal sweating.[8] Stimulus-evoked hypersensitivities may be present and can occur in areas that have loss of sensation. "The symptoms most associated with neuropathic pain were dysesthesias, evoked pain, paroxysmal pain, thermal pain, autonomic complaints, and descriptions of the pain as being sharp, hot or cold, with high sensitivity."[10] It is common for there to be a relatively modest demonstration of clinical neurological deficits or an essentially normal examination.[10]

Confirmatory diagnostics include computed tomography (CT) scans and magnetic resonance images (MRIs) that may show compromised nerve root pathways and structural damage; electromyography and nerve conduction studies, which can show the extent of neuroplastic changes; quantitative sensory testing (QST "' measures sensory thresholds for pain, touch, vibration, and temperature); and three-phase nuclear medicine bone scans that may help diagnose complex regional pain syndrome (CRPS).[10] During the diagnostic phase, a physiatrist (a physician who specializes in physical and rehabilitation medicine) can be an invaluable ally who can perform and interpret many of these examinations as well as suggest other diagnostic tests that might be appropriate.

Once the diagnosis has been confirmed, the practitioner may want to consider using conservative nonpharmacologic treatment options. These options can be crucial if the patient has a history of alcohol and/or substance abuse. Consider the physical conditions and activities that may increase pain. Watch the patient walk, move, and transfer. Large wallets, improper shoes (especially heels and boots), inappropriate canes and walkers, and gaits that favor one leg or another can increase neuropathic pain. Also, evaluate physical activities that may be exacerbating pain. Riding lawnmowers, all-terrain vehicles, and post-hole diggers are among the common culprits.

Physical therapy may be an appropriate referral for gait training; to determine the need for assistive devices; to determine whether use of a TENS (transcutaneous electrical nerve stimulation) unit would be appropriate; to initiate the use of massage, therapeutic exercises, cold, heat, hydrotherapy, electrical stimulation, or light therapy; to improve the general physical condition and reduce stress levels;[9] or to assist with the development of a set of guidelines for patient activity. A physiatrist may not only be able to assist in confirming the diagnosis but also in performing nerve blocks (injection of an anesthetic to "deaden" a specific nerve pathway), facet injections (use of a corticosteroid to decrease inflammation around a nerve root), and in recommending appropriate physiologic therapies.

The other specialists that you may wish to consult include a pain clinic referral[9] (a facility supervised by a physician, usually an anesthesiologist, who specializes in pain management) for nerve blocks and other injections; a chiropractor[9] (a practitioner who uses spinal manipulation to treat disorders of the nervous system); or a homeopath[9] (a practitioner who uses a system of therapeutics based on the theory that "like cures like"). Due to the emotional impact of chronic pain, a referral to a behavioral therapist may be appropriate. This therapist may suggest various therapies to improve the patient's coping level, reduce stress, and raise the pain threshold, which include relaxation, biofeedback, distraction, or attendance at a support group.[9] "Early referrals for nerve blocks and injections can promote the effectiveness of physiotherapy and pain rehabilitation."[8] While you hate to discourage activity with chronic pain, management of pain requires that the patient achieve a balance between activity and rest.

What pharmacologic options are available for the nurse practitioner who wants to help his or her patients maintain their functional levels? "Pharmacologic interventions follow the guidelines of the three-step analgesic ladder for pain control as developed by the World Health Organization (WHO). Step 1: Mild pain is usually treated with aspirin, acetaminophen, or nonsteroidal antiinflammatories (NSAIDs).[11] This is usually not an appropriate treatment level for neuropathic pain. Step 2: "Step 2 of the WHO three-step ladder includes mild opiates" along with the adjuvant medications."[9] In this instance, the nurse practitioner may be delaying or minimizing the use of stronger opiods (i.e. morphine) which are reserved for moderate-to-severe pain (Step 3 of the WHO ladder). This combination can decrease the incidence of side effects and increase the functional level of patients. Which medication is best? Table 4 suggests options. However, the bottom line is "how functional is your patient with this medication?" Current guidance is that for neuropathic pain, "tricyclic antidepressants are the initial drugs of choice" .amitryptyline, nortriptyline, imipramine, or desipramine." "Second line medications are anticonvulsants that include phenytoin, carbamazepine, and valproic acid" . (they) are especially helpful in cases of neuralgia and paresthesia."[15] Atypical anticonvulsants have had a role in neuropathic pain treatment, ie, gabapentin (Neurontin). The Food and Drug Administration (FDA) also has recommendations based on research.

Antidepressants should be used with caution in patients whose psychiatric history is unknown. A patient with an undiagnosed bipolar disorder can be placed in a hypomanic state or in a state of rapid cycling subsequent to initiation of an antidepressant.[15] Tricyclic antidepressants, ie, amitriptyline (Elavil) have been used as an adjunctive in treatment of neurogenic pain. They are believed to inhibit reuptake of serotonin and norepinephrine. Amitriptyline has multiple drug effects and antiarrythmic effects. Dosing this medication at bedtime can help reduce the impact of sedation. It is a pregnancy category D.[15] It is investigational for adjunctive analgesia with phantom limb pain, migraine, diabetic peripheral neuropathy, peripheral neuropathy pain, and post herpetic neuralgia.[14] Doxepin (Sinequan) works similarly to amitriptyline but with more sedation. Its pregnancy category is NR.[15] Nortriptyline can be used for chronic severe neurogenic pain.[14] Desipramine is investigational for severe neuropathic pain.[14] Imipramine has been used for severe neuropathic pain but has a seizure risk with high therapeutic dosages.[14]

Other antidepressants used for pain control include venlafaxine (Effexor), which potentiates neurotransmitter activity in the CNS, especially serotonin and norepinephrine with weak potentiation of dopamine. This medication should not be discontinued abruptly. It is a pregnancy category C.[15] Duloxetine (Cymbalta) works similarly to venlafaxine. It was the first medication to have FDA approval for diabetic peripheral neuropathy. With duloxetine, you must use caution with severe renal and hepatic disease. It is a pregnancy category C (Lilly insert). With any medication that increases serotonin levels, be aware of the risk of serotonin syndrome. This is especially true when "triptans" (medications used to prevent migraines) and SSRIs (selective serotonin reuptake inhibitors) are used together.[13]

Anticonvulsants have been considered second line for neuropathic pain. One of the most commonly used drugs is gabapentin (Neurontin). It is believed to be a competitive and reversible inhibitor of acetycholinesterase, which decreases the available acetycholine for nerve impulse transmission. The dosage needs to be reduced if the patient has altered renal function. It is a pregnancy category C.[15] It is considered an investigation drug for neuropathic pain and prevention of migraines. It has been approved for treatment of post herpetic neuralgia (PHN). It can be dosed up to 1800 mg/day in three divided doses.[14] Pregabalin (Lyrica) has obtained FDA indications for post herpetic neuralgia, diabetic peripheral neuropathy, and primary fibromyalgia syndrome. It is believed to be a GABA analog that reduces calcium dependent release of several neurotransmitters. The dosing for pregabalin is more linear than that of gabapentin (Pfizer insert).[13]

Another anticonvulsant, carbamazepine (Tegretol) is commonly used for trigeminal neuralgia and restless leg syndrome. It reduces the post tetanic potentiation of synaptic transmissions (it possibly depresses activity in the nucleus ventralis anterior of thalamus, thus decreasing polysynaptic responses).[14] This medication is well known for its multiple drug interactions, especially with warfarin, tricyclic antidepressants, and monamine oxidase inhibitors. It is a pregnancy category D.[15] Valproic acid (Depakene) acts by increasing levels of GABA, an inhibitory transmitter. It may also improve membrane stability by affecting the potassium channel. It has been used for prophylaxis of migraine headache.[14] Concerns include decreased hepatic function, multiple drug interactions, and that it is pregnancy category D.[15] Phenytoin (Dilantin) has also been indicated for neuretic pain"'migraine, trigeminial neuralgia, Bell's palsy. This medication acts by stabilizing neuronal membranes by decreasing the influx of sodium ions across the cell membranes in the motor cortex during generation of nerve impulses. Concerns include hydantoin hypersensitivity, slowed cardiac conduction, and hepatic dysfunction. This medication is also a pregnancy category D.[15] It is considered investigational for trigeminal neuralgia.[14] In theory, any anticonvulsant could be used as an adjuvant. However, be wary of medications not commonly used for pain control. In my practice, the drug Gabitril (tiagabine) has precipitated seizures in nonepileptic patients and should not be used "off label." In fact, an FDA alert was issued February 28, 2005 discouraging off-label use of this medication due to seizure risk in nonepileptics.[13]

Other medications that can be used include skeletal muscle relaxants, ie, lioresal (Baclofen), which has a twofold effect. It inhibits transmission of monosynaptic and polysynaptic reflexes and it causes muscle relaxation. It has indications for analgesia and trigeminal neuralgia. This medication should not be withdrawn abruptly.[15] Its function is related to GABA with CNS depressant effects. It is investigational for trigeminal neuralgia, prevention of migraines, and neuropathic pain.[14] Chloroxazone (Parafon forte) modifies the central perception of pain through its sedative effects. Possible side effects can include angioedema and anaphylaxis.[15]

Do not overlook topical analgesics. In fact, some authors suggest that topical lidocaine should be the first pharmacologic intervention.[8] The three classes most commonly used include[5]:

Local anesthetics "' lidocaine and mexiletine (Mexitil) interfere with the exchange of sodium in the sodium channel. (Some patients find Biofreeze effective at decreasing pain.)

Formulations containing antiinflammatories

Topical capsaicin "' depletes substance p and decreasing transmission of pain impulses.

Consider having a compounding pharmacist tailor topical medications. Consult with the pharmacist regarding the specific compounds and their concentration. Table 5 provides a reference for discussion. Topicals are ideal when patients desire decreased side effects and decreased liver involvement.

Another consideration when choosing an adjuvant is the associated conditions that interfere with pain management. Has the patient recently started on a "statin" for lowering cholesterol levels? Does the patient also suffer from arthritis, muscle spasms, restless leg syndrome, insomnia, diabetes mellitus, or depression? Sometimes treating other conditions allows medications for chronic pain syndromes to work more effectively. Comorbidities may point to appropriate adjuvants. Tricyclic antidepressants are helpful if insomnia is a concern. Baclofen has been known to help with neuropathic pain due to its neurotransmitter and CNS effects. "Steroids have been and continue to be administered by multiple routes for complex regional pain syndrome therapy."[12] Methylprednisolone (Medrol dose pak) is an antiinflammatory and immunosuppressant that can provide significant relief when inflammation is present. It is not for long-term use.[15] "Nonsteroidal anti-inflammatory drugs, physical therapy, accupuncture, antidepressants, and antiepileptics have been used as adjunctive treatment for chronic low back pain."[12] Clonidine (Catapress) stimulates the alpha andrenergic receptors in the CNS, which inhibits the sympathetic vasomotor center and decreases nerve impulse transmission, thus decreasing pain. Side effects include bradycardia and hypotension. This medication has been used for post herpetic neuralgia and restless leg syndrome.

"Pain management requires ongoing evaluation, patient education and reassurance. Diagnostic evaluation of treatable underlying conditions (eg, spinal cord compression, herniated disc, neoplasm) should occur concurrently with pain management."[8] For many patients with neuropathic pain, the nurse practitioner who has developed a comprehensive plan of care and has a strong network for referrals can be the most appropriate primary care provider. However, severe intractable pain may require referral to a pain clinic or neurosurgeon (if significant damage is identified during diagnostic studies). In most cases, "treatments with the lowest risk of adverse effects should be tried first."[8]

There is both an art and a science to pain management. Rowbotham states that the "Treatment of complex regional pain syndrome is largely empirical."[12] Sometimes trial and error is the best guide with any neuropathic pain. Both the practitioner and the patient need a willingness to try various options. If "pain is whatever the person experiencing the pain says it is, existing whenever the patient says it does,"[17] perhaps optimal functioning can be defined similarly. Can optimal functioning be defined as being achieved when the patient can satisfactorily perform at their chosen activity level? My bail bondsman, Tom, is a case in point. After multiple trials, he started using pregabalin as an adjuvant. His pain was more controlled, he felt as if he was "in control," and he became better able to function without excessive sedation. An unqualified success. 

There is both an art and a science to pain management. Rowbotham states that the "Treatment of complex regional pain syndrome is largely empirical."[12] Sometimes trial and error is the best guide with any neuropathic pain. Both the practitioner and the patient need a willingness to try various options. If "pain is whatever the person experiencing the pain says it is, existing whenever the patient says it does,"[17] perhaps optimal functioning can be defined similarly. Can optimal functioning be defined as being achieved when the patient can satisfactorily perform at their chosen activity level? My bail bondsman, Tom, is a case in point. After multiple trials, he started using pregabalin as an adjuvant. His pain was more controlled, he felt as if he was "in control," and he became better able to function without excessive sedation. An unqualified success. 

References (click to open)
Journal for Nurse Practitioners. 2008;4(4):263-270. © 2008 Elsevier Science, Inc.

http://webcache.googleusercontent.com/search?q=cache:DtqGKvHZDuoJ:www.medscape.com/viewarticle/576064+&cd=1&hl=en&ct=clnk&gl=nl&client=firefox-b-ab

New Discovery Curbs Nerve Pain Without Drug Side Effects

Today's post from sciencedaily.com (see link below) is one of those complex technical ones that often leave us scratching our heads to wonder how it could possible affect our own personal situations. However, if you take a little time to read it, you should get the gist of what it's saying and what the implications are. It starts off with a neuropathy-patient-friendly call for treatments that work well on people and not just laboratory mice. We are so used to the newest developments being announced at the rodent-testing stage, that we lose faith that they will ever be translated to human treatment. This article tries to show that the gulf between lab-rats and humans in this case, is not so large after all. Worth a read.

Potent approach shows promise for chronic pain
Inhibitor discovered through human, mouse genetic studies curbs pain without narcotic side effects 
Date:June 17, 2015 Source:Boston Children's Hospital

Non-narcotic treatments for chronic pain that work well in people, not just mice, are sorely needed. Drawing from human pain genetics, an international team led by Boston Children's Hospital demonstrates a way to break the cycle of pain hypersensitivity without the development of addiction, tolerance or side effects.

Their findings, reported June 17 in the journal Neuron, could lead to treatments for chronic pain conditions caused by nerve damage, such as diabetic peripheral neuropathy (DPN) and post-herpetic neuralgia (PHN), as well as chronic inflammation, like rheumatoid arthritis. Current treatments provide meaningful pain relief in only about 15 percent of patients.

"Most pain medications that have been tested in the past decade have failed in phase II human trials despite performing well in animal models," notes Clifford Woolf, MD, PhD, director of Boston Children's F.M. Kirby Neurobiology Center and a co-senior investigator on the study with Michael Costigan, PhD. "Here, we used human genetic findings to guide our search from the beginning."

In 2006, Costigan, Woolf and colleagues showed in Nature Medicine that people with variants of the gene for GTP cyclohydrolase (GCH1)--about 2 percent of the population--are at markedly lower risk for chronic pain. GCH1 is needed to synthesize the protein tetrahydrobiopterin (BH4), and people with GCH1 variants produce less BH4 after nerve injury. This suggested that BH4 regulates pain sensitivity.

"We wanted to use pharmacologic means to get the same effect as the gene variant," says Alban Latremoliere, PhD, also of Boston Children's Kirby Center, who led the current study along with Woolf and Costigan.

In a "reverse engineering" approach, the researchers modeled the human biology in mice. They first showed that mice with severed sensory nerves produce excessive BH4, churned out both by the injured nerve cells themselves and by macrophages--immune cells that infiltrate damaged nerves and inflamed tissue. Mice engineered to make excess BH4 had heightened pain sensitivity even when they were uninjured, suggesting that BH4 is sufficient to produce pain. On the flip side, mice that were genetically unable to produce BH4 in their sensory nerves had decreased pain hypersensitivity after peripheral nerve injury.

"We then asked, if we could reduce production of BH4 using a drug, could we bring about reduction of pain?" says Latremoliere.

The answer was yes. The researchers blocked BH4 production using a specifically designed drug that targets sepiapterin reductase (SPR), a key enzyme that makes BH4. The drug reduced the pain hypersensitivity induced by the nerve injury (or accompanying inflammation) but did not affect nociceptive pain--the protective pain sensation that helps us avoid injury.

Fine-tuning pain relief

Because BH4 is active all over the body, with important roles in the brain and blood vessels, the goal of any treatment would be to dial down excessive BH4 production, but not eliminate it entirely. Latremoliere and colleagues showed that blocking SPR still allowed minimal BH4 production through a separate pathway and reduced pain without causing neural or cardiovascular side effects.

"Our findings suggest that SPR inhibition is a viable approach to reducing clinical pain hypersensitivity," says Woolf. "They also show that human genetics can lead us to novel disease pathways that we can probe mechanistically in animal models, leading us to the most suitable targets for human drug development."

Story Source:

The above post is reprinted from materials provided by Boston Children's Hospital. Note: Materials may be edited for content and length.

Journal Reference:
Clifford J. Woolf et al. Reduction of Neuropathic and Inflammatory Pain through Inhibition of the Tetrahydrobiopterin Pathway. Neuron, June 2015 DOI: 10.1016/j.neuron.2015.05.033

http://www.sciencedaily.com/releases/2015/06/150617135409.htm

Can Osteopaths Improve Nerve Pain Symptoms

Today's post from health.clevelandclinic.org (see link below) is both helpful and should maybe carry a health warning to people with long-term neuropathy. We're all looking for ways of reducing the symptoms without resorting to bucketloads of pills but whether, as suggested here, an osteopath is the answer, is an important question. Typically, osteopaths treat joint and muscular pain but more and more nerve pain patients find their way to the osteopath, having unsuccessfully tried just about everything else. As the article suggests; both acupuncture and massage are genuine ways of relieving  inflammatory pain with out medications. Similarly, diet and exercise are important components of treating nerve pain and possibly most importantly, most neuropathy patients are begging for doctors to treat them holistically (looking at the whole body and history of the patient before treatment). However, purely because of an osteopath's specialisation and concentration on muscles and joints, that may not be the best way forward for people with nerve damage - in fact it may make matters worse. Many doctors are dismissive of osteopaths and rightly or wrongly, you should still consult them as to whether visiting an osteopath will help you or not. Try to get your doctor to explain to you why they are anti osteopath if that's the case and armed with that information, you may be able to make a better decision for your own body.

You Can Manage Your Pain Without Medications
Contributor: William Welches, DO, PhD 

 Diet, exercise and gentle ‘manual medicine’ can help 

Too often, we treat pain with medications. Unfortunately, many pain medications have bad side effects. They also can be addictive. As a pain management physician, I encourage patients struggling with pain to consider all of their alternatives before resigning themselves to long-term medication use.

Many of my patients are able to achieve significant relief of pain throughout their body (back, neck, shoulder, knees, chest and more) with osteopathic manipulation therapy (OMT) and acupuncture. Both are in-office procedures and typically are gentle.

In OMT, the physician uses his or her hands to manipulate patients’ bodies into proper alignment as a way to ease pain. Such “manual medicine” is the hallmark of osteopathic physicians.

OMT generally is covered by insurance. Acupuncture, the strategic placement of very thin needles to stimulate nerves and relieve pain, is not always covered.
 
Diet and exercise

Osteopathic physicians are trained to be holistic in their approach to patients. They try to treat the whole patient, not just one part of the body. As part of my holistic approach to pain, I strongly encourage my patients to improve their diet and exercise. These two acts alone can achieve positive results without medication.

I often suggest an anti-inflammatory diet. This can be a big change from the typical American diet. An anti-inflammatory diet involves eating a lot of vegetables (corn and potatoes don’t count) and fish. The diet includes some fruit and limited amounts of dairy and whole grains and very little red meat, flour or sugar. It is 80 percent to 90 percent vegan.

Following it is a challenge, but it is well worth it. Some patients start to feel much better in as little as two weeks. They have substantial pain relief. They also see lower blood pressure and lower lipid, cholesterol and blood sugar levels. All this without bad side effects.

With these approaches, I have seen patients overcome disabling pain and resume an active life without medications. If you think you might benefit from these steps, consider seeking a referral to a physician who specializes in a holistic approach to pain management.

https://health.clevelandclinic.org/2014/09/you-can-manage-your-pain-without-medications/

Can Essential Oils Help With Nerve Pain

The title alone of today's post from healthyfocus.org (see link below) may put you off reading it unless you have some sort of faith in alternative treatments for neuropathy. But consider this; medical science currently provides treatments which either don't work, or are limited, or have side effects worse that the nerve problem itself - is it not worth at least considering that there may be alternative treatments which may work for you? Believe me, I'm with the doubters but have studied neuropathy for long enough to realise that some things really do work for some and not for others and that includes non-chemical treatments. This article provides a good overview of the subject and gives helpful hints as to how to use the oils in question. It may be worth not dismissing out of hand - worth a read.

Essential Oils for Neuropathy
Wellness By Angela Deckard / June 12, 2015

Chances are, you either suffer from neuropathy yourself or may know someone with this disorder. Neuropathy is a painful condition that occurs when there is damage to the peripheral nervous system.

The peripheral nervous system connects the nerves from the central nervous system (brain and spinal cord) to the rest of the body, including the internal organs, skin, muscles, hands, feet, legs, mouth, and face.

These are responsible for sending messages about physical sensations back to your brain. However, when these nerves have suffered significant damage or are destroyed, these nerves may no longer do their job, resulting in a disorder called neuropathy.

This means that you may not feel physical pain when something is hurting you or your brain may send pain signals when you have not suffered injury. There are three different nerve groups and neuropathy can affect one or all three:

Sensory nerves, connected to your skin, which receive messages such as pain, heat, or touch.
Motor nerves, connected to your muscles, which dictate how they move.
Autonomic nerves, connected to your internal organs, which control such functions as heart rate, blood pressure, bladder function, and digestion.

Despite the grim nature of this disorder, there are many treatments, such as the use of essential oils, which can alleviate these painful symptoms and make living with neuropathy more manageable.



Symptoms
 
The symptoms of neuropathy may limit a person’s activities and decrease their ability to live a normal life. These symptoms may include:

Tingling in the hands and feet, which may eventually extend to the arms and legs
Numbness in the hands and feet
​Sharp, stabbing pains or a burning sensation
​A decrease in motor function such as dropping things from your hands
Lack of coordination and falling down
​Extreme sensitivity to touch
​Muscle weakness or heavy feeling limbs

If the autonomic nerves are affected, you may experience the following symptoms:

Digestive and bladder problems
A heat intolerance or a change in sweating patterns
Change in blood pressure which may result in a feeling of being light headed or dizziness

Causes

Neuropathy is a common disorder that can occur due to a number of factors, which include:

Hereditary: People who have a family history of neuropathy have a higher risk of developing the disorder.
Diabetes: Diabetes is one of the #1 factors contributing to the development of neuropathy, affecting over half of diabetes sufferers. This is the result of unregulated blood sugar levels, obesity, and high blood pressure in the diabetes patients over the age of 40.
​Autoimmune diseases: Disorders affecting the immune system such as lupus or rheumatoid arthritis are known to contribute to the development of neuropathy.
​Disease: Other diseases such as liver disease, kidney disease, hypothyroidism, and connective tissue disorders may lead to the development of neuropathy.​
​Alcoholism: People with severe alcoholism are at a higher risk for developing neuropathy as alcohol can have a toxic effect on nerve tissue.
Medications: Taking certain medications may result in developing neuropathy. These drugs may include medications that treat cancer, seizures, blood pressure, and blood pressure.
​Toxins: Exposure to insecticides, solvents, and toxic chemicals can result in nerve damage. Exposure to heavy metals such as mercury and led can also contribute to the disorder.
Infections: Certain viruses and bacterial infections can cause neuropathy, which include Lyme disease, herpes simplex, hepatitis C, leprosy, chicken pox, shingles, Epstein-Barr virus, and HIV.
​Vitamin deficiencies: Lacking vitamins E, B1, B6, and B12 may cause neuropathy. These vitamins are vital to nerve health and functioning.
Injury: Suffering physical injury is the most common way people damage their nerves. This may be the result of car accidents, falls, sports injuries, and fractures. Carpal tunnel syndrome is a form of neuropathy, which is the result of placing increased pressure on the nerves of the wrist from repeated motions such as typing.
Tumors: The development of tumors can create pressure on surrounding nerves, causing damage.


Treatment with Essential Oils

Many find that living with neuropathy isn’t really living at all. They may limit their activities because they are scared they may fall, injure themselves, or may simply find it too painful to participate in activities they once enjoyed.

Fortunately, there are natural and non-invasive treatments that can help control the symptoms of neuropathy, dramatically increasing the quality of life for those suffering from neuropathy.

Essential oils address many problems associated with neuropathy, such as pain management, circulation, energy, sleep disorders, stress, anxiety, depression, and overall mood.

Research has found that several essential oils are effective in alleviating the pains associated with nerve damage

Peppermint

Peppermint essential oil increases circulation and provides nervous system support. It is also a pain reliever, controls muscle spasms, improves respiration, and relieves flatulence. 

Black pepper

Black pepper is an antiviral essential oil that provides nervous system support, increases circulation and is a known pain reliever. This powerful essential oil also gives skin a healthy ruddy glow, aids in digestion and relieves flatulence.

Geranium Rose

Geranium rose provides circulatory support, increasing sluggish circulation. This antimicrobial essential oil is also a pain reliever, anti-inflammatory, balances hormones, stops bleeding, and can be used as an astringent.

Eucalyptus

Eucalyptus oil is an antiseptic, antimicrobial, and antibacterial, anti-inflammatory oil that offers a host of benefits such as relieving muscle spasms and improving respiration.

Rosemary

Rosemary increases circulation, relaxes muscle fibers, and removes lactic acid. This incredible essential oil is an antifungal, antimicrobial, anti-rheumatic that also suppresses muscle spasms, improves respiration, and is a mild pain reliever. 

Spruce

Spruce essential oil that improves circulation, stimulates the immune system, and promotes muscle repair. This essential oil relieves muscle spasms, helps clear cell receptor sites, and is an anti-inflammatory, antiparasitic, and antiseptic.

Frankincense

Frankincense stimulates the immune systems and relaxes the muscles. This essential oil also is an antiseptic that improves respiration, clears up mucus, and works as antidepressant and sedative. 

Blue Tansy

Blue tansy is an anti-inflammatory and a pain reliever. It also relieves itch, helps clear cell receptor sites and clears excess debris from soft tissues to help improve oxygenation.

Lavender

Lavender is a pain reliever and anti-inflammatory. This hardworking essential oil is also an antidepressant and helps to reduce the damaging effects of stress on the body.

Rosewood

Rosewood is a pain reliever and increase immune system function. Rosewood essential oil an anti-inflammatory and an antibacterial that works overtime to increase mood by working as an antidepressant and stress reliever.

Roman Chamomile

Roman chamomile is a pain reliever that soothes achy muscles. This essential oil is also mood booster and promotes relaxation.
Helichrysum

Helichrysum essential oil is an anti-inflammatory that is a known pain reliever. It also helps to relieve muscle spasms and helps to calm the nerves.

How to Use Essential Oils

There are many ways you can apply essential oils to help relieve the symptoms of neuropathy:

Massage: Mix 10 to 12 drops of essential oil with one ounce of carrier oil. The most recommended carrier oil for this method is coconut oil as it is clear, and light, and does not oxidize. Massage the mixture onto the effected area.
Bath: Mix 4 to 8 drops of essential oil with one teaspoon of carrier oil. Once again, coconut oil is the recommended carrier oil. To relieve achy muscles, add Epsom salt. Fill the tub with warm water and immerse yourself for duration of 15 minutes, making sure to massage the affected areas.
Compress: Fill a container with water. Use warm water to inspire relaxation and increase circulation or use water to energize and relieve inflammation. Add 3 to 5 drops of essential to the container and then stir. Soak a washcloth in the container of water, wring, then apply to the affected area.

Some recommended oils are listed in the table below. These are reasonably priced oils that are good brands who make therapeutic grade oil.

 http://healthyfocus.org/essential-oils-for-neuropathy/

The Sodium Switch And Neuropathic Pain

Today's post from genengnews.com(see link below) is a technically, difficult to grasp description of how sodium acts as an on/off switch for neurotransmitters in the brain. The Kainate receptor plays a role in receiving pain signals and as such, if it can be switched off in isolation from other receptors, there's a chance that pain information can be blocked without affecting other brain functions. Sodium might be able to do just that. These sorts of snippets of information are not going to mean much to most people but they do show how deeply researchers are looking in trying to come up with solutions to irregular nerve behaviour that causes neuropathy patients so much discomfort. We may not understand what's going on but we should be grateful for it, especially if one day, they come up with a really effective treatment for the pain we have to put up with.

New Pharmacological Drug Target Identified in the Brain

A research team says it has found that sodium serves as a unique on/off switch for a major neurotransmitter receptor in the brain. The kainate receptor is fundamental for normal brain function and is implicated in numerous diseases, such as epilepsy and neuropathic pain, according to the investigators.

Derek Bowie, Ph.D., and his colleagues in McGill University’s department of pharmacology and therapeutics worked with University of Oxford scientists to make the discovery. They believe that by offering a different view of how the brain transmits information, their research highlights a new target for drug development. Their findings are published in the Nature Structural & Molecular Biology.

Balancing kainate receptor activity is the key to maintaining normal brain function, explained Dr. Bowie. For example, in epilepsy, kainate activity is thought to be excessive. Thus, drugs which would shut down this activity are expected to be beneficial.

“It has been assumed for decades that the ‘on/off’ switch for all brain receptors lies where the neurotransmitter binds,” continued Dr. Bowie, who also holds a Canada Research Chair in Receptor Pharmacology. “However, we found a completely separate site that binds individual atoms of sodium and controls when kainate receptors get turned on and off.”

The sodium switch is unique to kainate receptors, which means that drugs designed to stimulate this switch should not act elsewhere in the brain. This would be a major step forward, since drugs often affect many locations, in addition to those they were intended to act on, producing negative side-effects as a result.

“Now that we know how to stimulate kainate receptors, we should be able to design drugs to essentially switch them off,” said Dr. Bowie, who added that Philip Biggin, D.Phil., and his lab group at Oxford University used computer simulations to predict how the presence or absence of sodium would affect the kainate receptor.

http://www.genengnews.com/gen-news-highlights/new-pharmacological-drug-target-identified-in-the-brain/81248754/

Using The Herpes Virus To Target Pain

Today's post from idse.net (see link below) looks at a surprising development concerning the herpes virus and its relationship to pain treatment. It is hoped that by using the herpes virus in its latent stage (before it becomes active and leads to the complications many people are aware of) to act as a postman and deliver pain-blocking messages to nerve cells. The article is short but heavy on medical terminology, yet it's not difficult to get the idea of what they mean. Definitely an interesting development worthy of a read.

Harnessing the Herpes Virus To Precisely Target Pain
by Damian McNamara ISSUE: FEBRUARY 2014 | VOLUME: 1

The herpes simplex virus might start getting some good press for a change. Anesthesiology researchers at the University of Miami Miller School of Medicine, in Florida, are using the virus to deliver genetic instructions in the hope of rewriting chronic pain signals at the source.

Spurred by success in animal models and encouraged by results from initial trials in cancer patients, Shaunglin Hao, MD, PhD, Roy C. Levitt, MD, and their colleagues use the virus’s predilection for neurons to their advantage in delivering anti-nociceptive neuromodulating molecules directly to the dorsal root ganglia to treat chronic pain.

Herpes simplex virus (HSV) bears a genome big enough to carry a relatively large “payload” of genetic instructions compared with other vectors, according to the Miami researchers. In addition, HSV remains latent after it enters the neurons of sensory ganglia, a feature that allows gene transfer to continue while evading an immune system reaction, another positive aspect of this approach. Importantly, HSV rendered to prevent replication (“replication-defective”) can still deliver genes during the latency phase exclusively within the sensory nerves targeted.

“We are one of the few centers worldwide working with this innovative technology in preclinical studies,” said Dr. Levitt, director of translational research and clinical professor of anesthesiology, perioperative medicine and pain management at the institution. “We certainly hope to continue this close collaboration with the inventors and develop new applications and innovative uses of this technology to anesthesiology.”

The inventors are David Fink, MD, of the University of Michigan, Joseph C. Glorioso, PhD, of the University of Pittsburgh, and their colleagues at Periphagen Holdings, a team that pioneered this HSV-mediated gene-transfer strategy. The group has brought HSV vectors into the clinic in Phase I (Ann Neurol 2011;70:207-212) and Phase II clinical trials for the treatment of intractable cancer pain.

Blocking Pain Signals

The trials have assessed the effectiveness of a modified HSV that delivers a gene that encodes for preproenkephalin. Preproenkephalin is a precursor protein that cleaves to produce the endogenous opioid peptides met-enkephalin and leu-enkephalin. These enkephalin peptides inhibit pain signals in the spinal cord.

Dr. Fink, a neurologist, said his group plans another trial with the enkephalin vector. With funding from the National Institutes of Health and from the Department of Veterans Affairs, they are progressing toward clinical trials of an HSV vector expressing glutamic acid decarboxylase for neuropathic pain and an HSV vector expressing a neurotrophin for the prevention of neuropathy, he said.

Dr. Levitt said the applications of the approach for clinical medicine “seem almost limitless.” For instance, in anesthesiology, “I can envision an approach where we might treat a patient preoperatively with a nerve block and ‘activate’ the dormant pain treatment just before the surgery to treat acute pain, and possibly post-op to treat and/or avoid chronic pain development in susceptible individuals.

“Only time will tell us the true risk–benefit ratio of this approach as these clinical trials and large-scale patient-use progress and new applications are developed,” Dr. Levitt added. He predicted if the current trajectory of research continues and HSV-mediated gene transfer continues to prove safe and effective, a product launch could come within three to five years.

“This is the frontier of modern medicine and where our specialty will benefit enormously in the future,” Dr. Levitt said. “HSV-mediated gene therapy with localized delivery to sensory nerves important to the care of patients who experience pain will transform our specialty, and as a consequence, change the paradigm of current practice.”

Dr. Levitt reported no relevant financial disclosures. Dr. Fink is a co-inventor on patents related to this research.

http://www.idse.net/ViewArticle.aspx?d=Public%2BHealth&d_id=212&i=February+2014&i_id=1034&a_id=25906

Management of Neuropathic Pain

This article is all about how neuropathic pain is currently managed and is useful because it explains in one go, how and why the various types of drugs are used. It comes from a commercial Pain Management Centre,(see link below) with no traceable home address on the website and the only contact possibility being a toll-free number. That makes you immediately suspicious but the article is factually correct and therefore of value. It is also true that private, specialist, American health care clinics abound and this sort of advertising is commonplace - in this case, there is no reason to doubt their intentions but contacting them is of course, your own choice.
The lists of medications may also be different to those you are used to and several commonly prescribed medications seem to be missing but can of course be found in other posts here on the Blog or website.

Management of Neuropathic Pain

Today, there is no efficient way to treat neuropathic pain. Because each patient reacts differently to their problem, it usually takes a combination of different pharmacologic treatments. Recently, science has made headway into understanding neuropathic pain by using randomized controlled trials to provide some sort of guideline for treatment.

Antidepressant Pain Treatment

Although an antidepressant may seem odd for treating pain, it is the forerunner in managing neuropathy. Antidepressants work differently for pain sufferers than people that are treated for depression by activating descending norepinephrinergic and seretonergic signals through the spinal cord, limiting pain signals to the brain. People that are prescribed antidepressants for their pain management treatment
may not have suffered from depression.

Below are common antidepressants prescribed for neuropathic pain management:
■Duloxetine
■Venlafaxine
■Milnacipran

Also, tricyclic antidepressants can also work through sodium channels of peripheral nerves.

Anticonvulsant Pain Treatment

Where an antidepressant may work through sodium channels on nerves, anticonvulsants work both through sodium and calcium channels by blocking their neurons.

Below are common anticonvulsant drugs prescribed for neuropathic pain management:
■Neurontin
■Lyrica
■Tegretol
■Trileptol
■Lamotrigine

Opioid (Narcotic) Pain Treatment

Narcotics usually aren’t the first treatment for neuropathic pain but are still
prescribed for their combination and effectiveness. Although opioids are powerful painkillers, patients must exercise extreme care and supervision because of their tendency to be addictive.

Below are common opioid drugs prescribed for neuropathic pain management:
■Methadone
■Ketobemidone

Topical Pain Treatment

Topical pain relievers are typically modest, although they are still prescribed. Lidocaine is the most common including a transdermal patch. Capsaicin may also be prescribed and can help by reversing the degeneration of epidermal nerve fibers.

Cannabinoid Pain Treatment

The active ingredient in marijuana (THC) and its use is one of the more controversial subjects of neuropathic pain treatment. Because it is illegal, marijuana has a harder time finding prominence among medical context.

Neuropathic Pain Management Dependence

Fortunately, the best treatments for neuropathic pain are antidepressants, however doctors can and will prescribe opioids and/or marijuana where it is legal if additional options are needed. Patients who are prescribed these types of treatment need to take care to tell someone about their program. Narcotics and marijuana use can lead to extreme dependence and addiction, and can lead to more powerful drugs that can further damage the body, creating more problems outside of pain management.

Neuropathic Painkillers Addiction

Opiate or narcotic type painkillers prescribed for neuropathic pain are some of the most widespread, addictive, and readily available drugs today. Regular use results in physical and psychological damage and dependence.

There are thousands of people that have used, gone through treatment, and now live normal, healthy lives. If you or someone you know is a narcotic or marijuana abuser due to their neuropathic pain, most likely they are already an addict or are quickly becoming one.

http://pain-management-treatment.com/management-neuropathic-pain