Anti Epileptic Drugs For Neuropathic Pain

Today's post from pallimed.org (see link below) will be of interest for those neuropathy patients being treated with anti-convulsion, anti-epileptic or seizure medications. The information using case studies, is meant for student or colleague doctors and nurses and as such is slightly more technical in nature but is nevertheless quite easy to follow. It's always interesting to know how your doctor is thinking when he or she prescribes a certain type of drug for your complaint. It also helps you understand why that particular drug has been chosen. Remember too, anti-epilepsy drugs are on the treatment list for neuropathy and if you aren't taking them now, they may well be prescribed for you in the future - it's worthwhile knowing what you may be dealing with.

Cases: Anti-epileptic Medicines for Pain Management
Posted by Christian Sinclair on Friday, August 30, 2013

 
Personal details in the case have been altered to protect patient privacy. These cases may reflect a composite image of many different cases to illustrate a teaching point.

Case: Mr. LF is a 58 year-old gentleman with a history of metastatic lung cancer with metastases to the bone including the sacrum. He is seen in a palliative care clinic for severe right lower extremity burning pain lasting several months. Noting LF’s pain appeared to be neuropathic in nature, LF’s primary care physician prescribed, in succession, duloxetine and then amitriptyline. Unfortunately, neither of these interventions decreased his pain. His oncologist prescribed a fentanyl patch and oxycodone 5-10mg as needed. LF reports the opioid pain medications make him tired but do not relieve his pain. He wonders if there is anything else to try for his pain.

Discussion: Tri-cyclic antidepressants (TCAs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and anti-epileptic drugs (AEDs) are the mainstays of adjuvant therapy for neuropathic pain. This Case of the Month will focus on oral anti-epileptic neuropathic pain analgesics. Due to lack of head-to-head data, evidence is presented as numbers needed to treat (NNT) and numbers needed to harm (NNH). For instance, an NNT of 5 for 50% pain reduction means for every 5 patients treated with a drug, only 1 of them would achieve a 50% reduction in pain. Gabapentin (Neurontin) and pregabalin (Lyrica) are considered first-line anti-epileptics for the treatment of neuropathic pain.

Gabapentin is effective in treating central and peripheral neuropathic pain. According to a 2011 Cochrane review of the effect of gabapentin on chronic neuropathic conditions (including post-herpetic neuralgia, painful diabetic neuropathy, mixed neuropathic pain), the NNT is 5.8 (4.8-7.2) to achieve at least moderate benefit. This NNT is more conservative than those previously published due to better definitions of efficacy outcomes and an increased number of participants and studies evaluated.

Adverse effects are frequent and include drowsiness, dizziness and edema. Typically, if the dose is increased slowly these side effects are tolerable (1). Gabapentin should be dose adjusted for renal dysfunction. It should be withdrawn gradually to avoid precipitating seizures (2).

Pregabalin is effective in treating peripheral and central neuropathic pain. Since both gabapentin and pregabalin are chemical analogs of GABA, they are not used simultaneously in clinical practice. There are no comparison studies of gabapentin versus pregabalin. Pregabalin’s effectiveness increases as the dose approaches 600 mg/day. Based on a recent meta-analysis, at a dose of 600 mg/day the NNT to decrease pain by 50% for the following conditions is: 3.9 (range 3.1-5.1) for post-herpetic neuralgia; 5.0 (range 4.0-6.6) for diabetic neuropathy; and 5.6 (range 3.5-14) for central neuropathic pain. There was no difference in incidence of side effects among participants taking pregabalin vs. placebo and no indication of a dose response to side effects (3 - Open Access (OA)).

Carbamazepine is effective in treating neuropathic pain, specifically trigeminal neuralgia, but is not considered first-line therapy due to its adverse effects. A 2011 meta-analysis focused on the use of carbamazepine for chronic neuropathic pain reported carbamazepine reduced pain compared to placebo (NNT of 1.7, range 1.5-2.0). However, adverse events occur frequently: NNH = 2.6, range 2.1-3.5 (4). Common side effects include leukocytosis, thrombocytopenia, dizziness, drowsiness, ataxia, nausea/vomiting and blurred vision. Additionally, there is a risk of agranulocytosis, aplastic anemia, and Stevens Johnson syndrome. Laboratory tests (BUN, complete blood count, sodium, liver function tests, urinalysis) and serum drug levels should be checked at baseline and during treatment. Oxcarbazepine is an analogue of carbemazepine which is equally effective at treating trigeminal neuralgia as carbemazepine (5) but with fewer side effects (6 - OA).

Valproic acid was evaluated in a 2011 meta-analysis for the treatment of neuropathic pain. There were insufficient data for reliable pooled analysis, and the authors recommend against its use as first-line therapy (7).

Several small studies (n less than 60) showed benefit of the use of valproic acid (maximum of 1200 mg/day in divided doses) over placebo in the treatment of diabetic neuropathy (8 - OA). However, this data is not convincing. Other studies of valproic acid have failed to find an effect (9). Adverse effects include liver function test abnormalities, dizziness, drowsiness and nausea (2).

Topiramate was evaluated in a 2010 systematic review for the treatment of neuropathic pain. Of four randomized placebo-controlled trials, three were negative and one positive for the treatment of painful polyneuropathy. No studies were found to evaluate its efficacy in the treatment of post-herpetic neuralgia, peripheral nerve injury or central pain (9). Serious adverse events thought to be related to topiramate included convulsion and bradycardia plus syncope. Additional adverse effects include sedation, nausea, diarrhea and metabolic acidosis (2).

Summary: Neuropathic pain remains best treated with TCAs, SNRIs, and the AEDs gabapentin and pregabalin. For patients who are intolerant to or who experience pain unresponsive to those medications, one can consider therapy with other anti-epileptics. However, these agents are associated with more side effects and lower rates of efficacy.

Resolution of the case: LF was started on gabapentin and titrated up to a dose of 900mg three times a day with moderate pain relief. His opioids were tapered and discontinued.

References:
Moore RA, Wiffen PJ, Derry S, McQuay HJ. Gabapentin for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database of Systematic Reviews. 2011, Issue3, Art No.: CD007938. DOI: 10.1002/14651858.CD007938.pub2
Micromedex® Healthcare Series [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
Moore RA, Straube S, Wiffen PJ, Derry S, McQuay HJ. Pregabalin for acute and chronic pain in adults. Cochrane Database of Systematic Reviews. 2009, Issue 3. Art. No.: CD007076. DOI: 10.1002/14651858.CD007076.pub2. Open Access PDF
Wiffen PJ, Derry S, Moore RA, McQuay HJ. Carbamazepine for acute and chronic pain in adults. Cochrane Database of Systematic Reviews. 2011, Issue 1. Art. No.: CD005451. DOI: 10.1002/14651858.CD005451.pub2.
Zakrzewska J, Linskey M. Trigeminal Neuralgia. Clinical Evidence. 2009; 3(1207). Retrieved Nov 15, 2011 from http://clinicalevidence.bmj.com/ceweb/conditions/nud/1207/1207.jsp
Finnerup NB, et al. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain. 12005; 18:289-305.PMID: 16213659. Open Access PDF
Gill D, Derry S, Wiffen PJ, Moore RA. Valproic acid and sodium valproate for neuropathic pain and fibromyalgia in adults.Cochrane Database of Systematic Reviews. 2011, Issue 10. Art. No.: CD009183. DOI: 10.1002/14651858.CD009183.pub2.
Kochar DK, et al. Sodium valproate for painful diabetic neuropathy: A randomized double-blind placebo-controlled study. Quarterly J Med. 2004; 97:33-8. PMID: 14702509 Open Access PDF
Finnerup NB, et al. The evidence for pharmacological treatment of neuropathic pain. Pain. 2010; 150: 573-581. PMID: 20705215

Original Case by Rene Claxton, MD, Edited by Christian Sinclair, MD
Originally posted at the Institute to Enhance Palliative Care,
University of Pittsburgh Medical Center
Original PDF

Pallimed Case Conference Disclaimer: This post is not intended to substitute good individualized clinical judgement or replace a physician-patient relationship. It is published as a means to illustrate important teaching points in health care.

http://www.pallimed.org/2013/08/cases-anti-epileptic-medicines-for-pain.html

Can We Learn About Medication Via Internet Chatrooms

Today's video from www.live.wsj.com (see link below) is an interesting one for people with neuropathy and other illnesses (including HIV) because it highlights something many people already know. There is much more information available on the internet about drug interactions and reactions than your doctors may themselves be aware of. Visiting a trustworthy forum and seeing how other people have reacted to certain drugs, can help build up your knowledge base before discussing it with your doctor. That's not to say that you should believe everything you read on internet forums; far from it but if you notice that a significant number of people have had the same experience, it may be worth taking that information with you to your appointment. For people with neuropathy and HIV for instance, the number of different drugs being taken can be alarmingly high. Knowing what they can potentially do to you may be very useful - knowledge is always power in this respect.





Can Web Chatter Make Medication Safer?
From live.wsj.com - October 10, 2012

Is it possible to make medication safer by analyzing information publicly available on the internet, such as patient complaints on web chats? The medical community is starting to think so, reports Shirley Wang on Lunch Break.

http://live.wsj.com/video/can-web-chatter-make-medication-safer/46F629BD-8D3A-4BF2-8917-F6201DB60C9E.html#!46F629BD-8D3A-4BF2-8917-F6201DB60C9E

HOMOEOPATHIC REMEDIES FOR AILMENTS DUE TO SUPPRESSION

One of the most important contributions of homeopathy to the theory of health and disease is the concept of suppression of symptoms.

Both in conventional and in some alternative forms of medicine reduction of symptoms and alleviation of suffering are viewed as the towering goals of treatment.

The clinical philosophy shared by naturopathic and homeopathic medicine holds, in contrast, that a symptom is an expression of inner disharmonyrather than a problematic thing in itself, and that the disappearance of a symptom may or may not be an indication of cure when health is considered holistically.

In homeopathy it is very important to distinguish between a curative and a suppressive effect because the goal of treatment is healing of the entire person at the deepest possible level. To achieve this the homeopath first needs to know the patient’s medical history in order to determine whether any past treatments have been suppressive; second, the homeopath needs to evaluate the response of the patient to homeopathic treatment, in order to determine whether or not the patient is progressing in the desired direction toward greater health.

Some common treatments that unnecessarily lead to suppression of symptoms include:-Antibiotics,Anti-inflammatory medications (especially corticosteroids), Surgeries (tonsillectomies, nasal polypectomies, removal of benign skin lesions, and more),Anti-fever medications,High doses of certain supplements,Homeopathic remedies used symptomatically (these include remedies prescribed with the help of machines, muscle testing, and complex formulations (mixtures), Improper long-term administration of single homeopathic remedies

HOMOEOPATHIC REMEDIES

ABROTANUM 30-Rheumatism after suppression of diarrhea

AMMONIUM MUR. 30- Hemorrhoids due to suppression of leucorrhea

CAUSTICUM 200- Diseases like asthma , arising on account of suppression of skin diseases like itching of skin or eczema

MEDORRHINUM 1000- Bad effects following suppression of gonorrhea

OLEUM ANI 200- Asthma due to wetting of feet or chilling them, when perspiring

PLATINUM MET. 200- Mental problems due to suppression of menses. Physical symptoms disappear as mental problems develop

SARACA INDICA Q- Headache due to suppression of menses, better as the flow starts

SILICEA 200-Convulsions due to suppression of menses, better as the flow starts

SULPHUR 200- Skin problems when suppressed with ointments cause some other problems , especially respiratory. In such cases a dose of Sulphur 200 every day in the morning for four days will bring out the original diseases, which can then be cured by the indicated remedies. Insanity due to suppression is also cured by this remedy

THLASPI BURSA Q- After effects suppressed uterine diseases

ZINCUM METATALLICUM 200- Mania due to suppression of eruptions 

Leg Pain not always Neuropathy

This blog almost always relates HIV-related, foot and leg pain to Neuropathy but that's not always the case and it's always worth bearing in mind that there are other possible causes, before jumping to conclusions. When you're HIV positive, it's easy to pin a label on a problem at the first sign of trouble, after all, when it comes to secondary infections, virus, or drug related conditions, we're prone to almost everything (and they wonder why some people become hypochondriacs!) This article from Pain.com (see link below) outlines the commonest causes of leg pain. The true cause will eventually be discovered by your doctors but keeping an open mind before you get the diagnosis weeks or months later, is always advisable.

Leg Pain
May 21, 2011

In addition to injuries and muscle cramps, various medical conditions can cause leg pain. This article covers some of the medical conditions that can cause leg pain. Medical conditions involving the cardiovascular system will be discussed in a separate article in this series about leg pain.

Peripheral neuropathy is not a disease in itself, but a symptom of nerve damage in the limbs that is caused by other medical conditions. Peripheral neuropathy is common in patients with diabetes, HIV/AIDS, vitamin B12 deficiency, cancer, lupus, syphilis, lyme disease, rheumatoid arthritis, sarcoidosis, hypothyroidism, toxic exposure, certain genetic diseases and so on. Peripheral neuropathy is a common symptom and it can be inherited, caused by an infection, caused by exposure to certain chemicals, experienced as a side effect of some medications, caused by metabolic disorders or nutritional deficiencies, caused by inflammatory diseases, caused by oxygen starvation or caused by trauma to a peripheral nerve.

Peripheral neuropathy commonly affects the feet and legs. If a nerve that carries sensation from the body to the central nervous system is damaged, a person may experience pain, burning, numbness or tingling in the leg or foot. Proprioception, or the ability to sense where a body part is without looking, can also be affected and a person can become more uncoordinated. If a motor nerve that supplies a muscle is damaged, a muscle becomes weak because it can not contract as well. It is possible for some muscles to become paralyzed, depending on the extent of the nerve damage. In some cases, muscles may cramp up instead of becoming flaccid and weak. Treatment of peripheral neuropathy involves treating the underlying cause of the problem, along with symptomatic care for pain and physical or occupational therapy if necessary.

Another possible medical cause of leg pain is a bone infection, called osteomyelitis. Osteomyelitis is a bacterial infection that can be caused by several different types of bacteria. People can contract a bone infection via a wound, such as when an open fracture occurs or when a person has surgery, or an infection can spread to the bone from a different part of the body. A type of skin infection called cellulitis can spread to underlying tissues and bones in the leg, or an internal infection like a bladder infection can spread to other parts of the body through the bloodstream.

Any patient with a suppressed immune system due to aggressive immunosuppressive therapy or an immune deficiency like HIV/AIDS is more likely to develop infections, including osteomyelitis. Treatment for osteomyelitis includes antibiotic medications to get rid of the infection and medications to control pain. If the infection is not treated early, it is possible for the infection to spread to other tissues in the leg, making amputation of the leg necessary. It is also possible for a person with an untreated infection to go into septic shock when the bacteria infect the bloodstream.

If your leg pain is in your joints, you may have arthritis, or joint inflammation. There are many different types of arthritis, including osteoarthritis, gout and rheumatoid arthritis. More information about the various types of arthritis can be found at http://pain.com/library/2011/05/01-arthritis-awareness-month/. Infections in the joint capsule itself can also cause joint pain. Osteoarthritis, the most common type of arthritis, is caused by “wear and tear” on the cartilage of the joint. Rheumatoid arthritis is an autoimmune disease. Gout is caused by having too much of a substance called uric acid in your body, which builds up in the joints and causes pain and inflammation. Common symptoms of many different types of arthritis include joint pain, joint stiffness or decreased joint mobility and joint swelling. Treatment for arthritis varies depending on the type of arthritis. Talk to your doctor if you think you may have arthritis pain.

Fibromyalgia is a medical condition that can cause muscle pain in the legs and in other parts of the body. In addition to muscle pain, people with fibromyalgia may also have chronic fatigue, sleep disorders, tension headaches and mood disorders. The cause of fibromyalgia is unknown, but researchers think that people with fibromyalgia have a lowered tolerance to pain because of abnormalities in the way that their brains process pain signals. Treatment for fibromyalgia is symptomatic and aims to control pain, improve sleep and treat mood disorders. Not all aspects of fibromyalgia can be treated medically; for example, the frustration that a patient with fibromyalgia may feel in not knowing how to deal with chronic pain and fatigue may benefit from counseling.

Peripheral neuropathy, infections, arthritis and fibromyalgia are just a sampling of the medical conditions that may cause leg pain. These conditions are not as common as muscle cramps and injuries, but a good proportion of older people develop some degree of osteoarthritis and peripheral neuropathy can be caused by a variety of medical conditions. Always talk to your doctor if you have persistent leg pain and you do not know what is causing it.

http://pain.com/library/2011/05/21-leg-pain-3/

How Good Is Methadone For Neuropathic Pain

Today's post from mypcnow.org (see link below) takes a look at methadone as an alternative to other opioids for controlling neuropathic pain. Methadone has had an extremely bad rap over the years, mainly because of its association with withdrawal from drug addiction programmes. However, it is an extremely cheap and effective drug for nerve pain and because only low doses are needed, the risks of side effects and addiction are much less than for instance morphine or oxycodone. That said, it is a powerful drug and once you begin, you need to be very careful when and if you want to taper off. Never go cold turkey with methadone - it will react almost instantly. Many doctors are reluctant to issue methadone prescriptions but that's often based on lack of experience rather than factual dangers. If a patient discovers over time that nothing else works, then methadone can be very effective in controlling nerve pain. Remember, all drugs for neuropathy have side effects, so don't be put off by what you may have heard - it all boils down to careful monitoring by your doctor. Discuss it with him or her if you find that almost nothing works for you in reducing the pain of neuropathy.

METHADONE FOR NEUROPATHIC PAIN
David E Weissman MD FAST FACTS AND CONCEPTS #171

Background Prescriptions for methadone have greatly increased in the past decade (1). The reason for this increase is likely related to two factors: reduced cost relative to other potent opioids and basic science data suggesting that methadone may be particularly useful in treating neuropathic pain. Two previous Fast Facts (#75, 86) reviewed methadone’s pharmacological properties. This Fast Fact examines the research base regarding methadone and neuropathic pain and reviews the rise in methadone-related deaths.

Historical Context

Prior to 1985, when long-acting morphine preparations were introduced, methadone was commonly prescribed for cancer-related pain as it had a longer duration of action than morphine. However, it was well appreciated that methadone had a higher risk of respiratory depression due to drug accumulation with chronic dosing – an effect not associated with other opioids, for which there is no drug accumulation in the setting of normal renal function.

Prior to 1990 there was a widespread belief that opioids were relatively ineffective in treating neuropathic pain. Since then, there been a much greater understanding that opioids are an effective part of neuropathic pain treatment.

Basic science data Methadone inhibits reuptake of norepinephrine and serotonin in a similar manner to newer anti-depressants, some of which are effective against neuropathic pain (e.g. duloxetine, venlafaxine). Also, methadone binds to the NMDA receptor, a known modulator of neuropathic pain. Finally, methadone has demonstrated efficacy in animal models of neuropathic pain (2).

Patient data Small non-controlled case series and two small randomized study (methadone vs. placebo) have demonstrated that methadone can reduce neuropathic pain in both cancer and non-cancer patients (3-6). There is no data, for or against the proposition, that methadone is superior to other opioids for neuropathic pain. A 2007 Cochrane Collaborative review found, “there is no trial evidence to support the proposal that methadone has a particular role in neuropathic pain of malignant origin” (7). Furthermore, the review cautioned clinicians about the danger of methadone-induced respiratory depression due to its long terminal half-life.

Methadone deaths There is a growing awareness that the increased prescription of methadone is being paralleled by a similar increase in methadone-related deaths. Methadone has been implicated in 30% to 40% of opioid related deaths in the US, even though methadone remains a small minority of opioids prescribed (8). The US Department of Health and Human Services convened an expert panel in 2003 to investigate the rise in methadone deaths and concluded that the rise was largely due to the increasing use of methadone as an analgesic (9). The Center for Disease Control published a report detailing data from Utah in 2005, suggesting that part of the problem was due to increased prescribing (10). The current data seem to suggest that the general increased supply of methadone, via legitimate prescribing, is leading to deaths due to accidental overdose through improper prescribing or illicit diversion/recreational use. In addition to concern about respiratory depression, there has been an observation that methadone, unlike morphine or hydromorphone, can prolong the QTc interval and lead to serious cardiac conduction abnormalities especially when coadministered with antiretrovirals in HIV patients (11). Note: the overall number of opioid-related deaths has increased, not just from methadone. Note: there are no data on untimely deaths related to methadone prescribing in hospice/palliative care patients.

Summary The renewed interest in an old drug holds exciting promise of benefit for the many patients with neuropathic pain. However, clinical research has yet to confirm or deny a unique clinical role for methadone compared to other opioids. The risk of respiratory depression should give clinicians pause before prescribing methadone based solely on the theory that it is a superior opioid in neuropathic pain. Coadministration of methadone with antiretrovirals may pose a particular risk for cardiac arrhythmias and therefore should be avoided if at all possible., Given that diversion of legitimate opioid prescriptions to the illicit market can occur, even in the practice of hospice and palliative care, physicians and hospice agencies need to recognize they also have a larger social responsibility to the public welfare, and prescribe methadone with care and caution.

References

Warner M, Chen LH, et al. Drug poisoning deaths in the United States, 1980–2008. NCHS Data Brief. 2011; 1-8.

Foley KM. Opioids and chronic neuropathic pain. NEJM 2003; 348:1279-1281.

Morley JS, et al. Low-dose methadone has an analgesic effect in neuropathic pain: a double-blind randomized controlled crossover trial. Pall Med. 2003; 17:576-587.

Altier N, et al. Management of chronic neuropathic pain with methadone: a review of 13 cases. Clin J Pain. 2005; 21:364-369.

Gagnon B, et al. Methadone in the treatment of neuropathic pain. Pain Res Manage. 2003; 8:149-154.

Moulin DE, et al. Methadone in the management of intractable neuropathic non cancer pain. Can J Neuro Sci. 2005; 32:340-343.

Nicholson, AB. Methadone for cancer pain. Cochrane Database Syst Rev 2007; 4.4.

Centers for Disease Control and Prevention (CDC). Vital signs: risk for overdose from methadone used for pain relief – United States, 1999-2010, Morb Mortal Wkly Rep 2012; 61:493-497.

Increase in poisoning deaths caused by non-illicit drugs--Utah, 1991-2003. MMWR Weekly. 2005; 54:33-36.

US Department of Health and Human Services – Division on Pharmacologic Therapies. Report on Methadone Mortality (http://dpt.samhsa.gov/reports/methodone_mortality-05.htm - no longer publicly available). Updated Report available at: http://www.dpt.samhsa.gov/pdf/MethadoneBackgroundPaper_72007_2_.pdf.

Kao D, Bartelson BB, et al. Trends in reporting methadone-associated cardiac arrhythmia, 1997-2011. Ann of Int Med 2013;158: 735-740.

Version History: This Fast Fact was originally edited by David E Weissman MD and published in December 2006. Version copy-edited in April 2009: web-links updated. Revised again in July 2015 by Sean Marks MD: references and epidemiological data updated.

Fast Facts and Concepts are edited by Sean Marks MD (Medical College of Wisconsin) and associate editor Drew A Rosielle MD (University of Minnesota Medical School), with the generous support of a volunteer peer-review editorial board, and are made available online by the Palliative Care Network of Wisconsin (PCNOW); the authors of each individual Fast Fact are solely responsible for that Fast Fact’s content. The full set of Fast Facts are available at Palliative Care Network of Wisconsin with contact information, and how to reference Fast Facts.

Copyright: All Fast Facts and Concepts are published under a Creative Commons Attribution-NonCommercial 4.0 International Copyright (http://creativecommons.org/licenses/by-nc/4.0/). Fast Facts can only be copied and distributed for non-commercial, educational purposes. If you adapt or distribute a Fast Fact, let us know!

Disclaimer: Fast Facts and Concepts provide educational information for health care professionals. This information is not medical advice. Fast Facts are not continually updated, and new safety information may emerge after a Fast Fact is published. Health care providers should always exercise their own independent clinical judgment and consult other relevant and up-to-date experts and resources. Some Fast Facts cite the use of a product in a dosage, for an indication, or in a manner other than that recommended in the product labeling. Accordingly, the official prescribing information should be consulted before any such product is used.

http://www.mypcnow.org/blank-ari0c

TUMORS MIGHT GROW FASTER AT NIGHT

They emerge at night, while we sleep unaware, growing and spreading out as quickly as they can. And they are deadly. In a surprise finding that was recently published in Nature Communications, Weizmann Institute of Science researchers showed that nighttime is the right time for cancer to grow and spread in the body. Their findings suggest that administering certain treatments in time with the body's day-night cycle could boost their efficiency.

This finding arose out of an investigation into the relationships between different receptors in the cell -- a complex network that we still do not completely understand. The receptors -- protein molecules on the cell's surface or within cells -- take in biochemical messages secreted by other cells and pass them on into the cell's interior. The scientists, led by Dr. Mattia Lauriola, a postdoctoral fellow in the research group of Prof. Yosef Yarden of the Weizmann Institute's Biological Regulation Department, working together with Prof. Eytan Domany of the Physics of Complex Systems Department, focused on two particular receptors. The first, the epidermal growth factor receptor, EGFR, promotes the growth and migration of cells, including cancer cells. The second binds to a steroid hormone called a glucocorticoid (GC). Glucocorticoids play a role in maintaining the body's energy levels during the day, as well as the metabolic exchange of materials. It is often called the stress hormone because its levels rise in stressful situations, rapidly bringing the body to a state of full alert.

With multiple receptors, the cell receives all sorts of messages at once, and some of these messages can take precedence over others. In the experiment, Lauriola and Yarden found that cell migration -- the activity promoted by the EGF receptor -- is suppressed when the GC receptor is bound to its steroid messenger.

Since the steroid levels peak during waking hours and drop off during sleep, the scientists asked how this might affect the second receptor -- EGFR. Checking the levels of this activity in mice, they found that there was a significant difference: This receptor is much more active during sleep and quiescent during waking hours.

How relevant are these findings for cancers, particularly those which use the EGF receptors to grow and spread? To find out, the scientists gave Lapatinib -- one of the new generation of cancer drugs -- to mouse models of cancer. This drug, used to treat breast cancer, is designed to inhibit EGFR, and thus to prevent the growth and migration of the cancer cells. In the experiment, they gave the mice the drug at different times of day. The results revealed significant differences between the sizes of tumors in the different groups of mice, depending on whether they had been given the drug during sleep or waking hours. The experimental findings suggest that it is indeed the rise and fall in the levels of the GC steroids over the course of 24 hours that hinder or enable the growth of the cancer.

The conclusion, say the scientists, is that it could be more efficient to administer certain anticancer drugs at night.

"It seems to be an issue of timing," says Yarden. "Cancer treatments are often administered in the daytime, just when the patient's body is suppressing the spread of the cancer on its own. What we propose is not a new treatment, but rather a new treatment schedule for some of the current drugs."

Molecule PSR 1 Can Repair Damaged Nerve Cells

Today's post from sciencedaily.com (see link below) looks at the discovery of a unique 'wonder' molecule that can eliminate diseased cells but also apparently regenerate damaged nerve cells. The fact that it can re-join and fuse together broken axons in the central nervous system (frequent causes of neuropathic symptoms) is astonishing and has many implications for the future of neuropathy treatment. That said, as with so many of these findings, we're a long way from translating the theory into effective treatment models but take comfort from the fact that new discoveries are being made and will lead to improvements for future generations

Research findings have implications for regenerating damaged nerve cells 
Date:January 7, 2015 Source:University of Colorado at Boulder
 
Summary:

Two new studies have identified a unique molecule that not only gobbles up bad cells, but also has the ability to repair damaged nerve cells. Known as the phosphatidylserine receptor, or PSR-1, the molecule can locate and clear out apoptotic cells that are pre-programmed to die as well as necrotic cells that have been injured and are causing inflammation. Programmed cell death, or apoptosis, is a natural process that kills billions of cells in a typical human body each day.
 
Two new studies involving the University of Colorado Boulder and the University of Queensland (UQ) in Brisbane, Australia have identified a unique molecule that not only gobbles up bad cells, but also has the ability to repair damaged nerve cells.

Known as the phosphatidylserine receptor, or PSR-1, the molecule can locate and clear out apoptotic cells that are pre-programmed to die as well as necrotic cells that have been injured and are causing inflammation, said CU-Boulder Professor Ding Xue, who led one study and co-authored the other. Programmed cell death, or apoptosis, is a natural process that kills billions of cells in a typical human body each day.

But it is the finding that the PSR-1 molecule also can help reconnect and knit together broken nerve fibers, called axons, that has caught the attention of both science teams.

"I would call this an unexpected and somewhat stunning finding," said Xue of CU-Boulder's Department of Molecular, Cellular and Developmental Biology. "This is the first time a molecule involved in apoptosis has been found to have the ability to repair severed axons, and we believe it has great therapeutic potential."

Xue is the lead author on a paper being published Jan. 7 in Nature Communications that details how PSR-1 recognizes and removes cells that are pre-programmed to die or damaged. He also is co-author of the companion paper being published in Jan. 7 in Nature led by Associate Professor Massimo Hilliard of the UQ's Queensland Brain Institute that shows the major role played by PSR-1 in the regeneration of nerve axons, a holy grail of sorts for neurologists involved with patients who have suffered central nervous system damage from accidents or diseases.

Both studies relied on a popular lab organism known as C. elegans, a nearly microscopic nematode that is fast growing, translucent and has a sequenced genome showing that nearly half its genes are closely related to corresponding human genes.

"This will open new avenues to try and exploit this knowledge in other systems closer to human physiology and hopefully move toward solving injuries," said Hilliard. In the future, neurosurgery may be combined with molecular biology to deliver positive clinical outcomes and perhaps treat conditions like spinal cord or nerve injuries, he said.

During programmed cell death, apoptotic cells flag themselves for elimination by moving a specific cell membrane component known as phosphatidylserine (PS) from the inner membrane to the cell surface, setting them up to be engulfed. "These are what we call 'eat me' signals," said Xue.

In contrast, broken axons in nerve cells send PSR-1 molecules an SOS alert. "The moment there is a cut to the nerve cell we see a change in the cell membrane PS composition, which acts as a signal to PSR-1 molecules in the other part of the nerve that essentially says "I am in danger, come and save me," said Xue.

One of the most encouraging finding is that PSR-1 plays an early role in the axonal fusion process required for neuroregeneration, said Xue. "Whether human PSR has the capacity to repair injured axons is still unknown," he said. "But I think our new research findings will spur a number of research groups to chase this question."

While biomedical researchers have had some successes in repairing peripheral nerves and nerve clusters outside the brain and spinal cord in humans, there currently is no effective way to regenerate broken nerve cells in the central nervous system, said Xue. Such nerve damage can cause partial or total paralysis.

Xue, who first identified the PSR-1 receptor in 2003, said the collaboration between CU-Boulder and UQ has pushed scientific discovery forward. "We are trying to understand how PSR-1 removes cells through apoptosis and necrosis, and they are trying to understand if molecules involved in apoptosis also play a role in the neuroregeneration process," said Xue.

CU-Boulder postdoctoral researcher Yu-Zen Chen, a Nature Communications paper co-author, said the team currently is trying to find ways to raise the level of the PSR-1 in nematode cells, which likely would promote faster healing in nerve axons. "We think the higher the PSR-1 level, the higher the repair capacity of the molecule," said Chen.

Xue said C. elegans is an ideal organism to use in the hunt for new therapeutics to treat nerve damage because of its relatively small, well-known genome and short life span -- just a few days. "This makes drug screening much easier, faster and less expensive than using a mouse model, for instance," said Xue.

"The big finding is that we have a single receptor that does two different jobs," Xue said. "We don't have a solution yet for treating people with nerve damage, but we feel these findings offer promise in seeking new and effective therapeutics."

Story Source:

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

Journal References:
Hengwen Yang, Yu-Zen Chen, Yi Zhang, Xiaohui Wang, Xiang Zhao, James I. Godfroy, Qian Liang, Man Zhang, Tianying Zhang, Quan Yuan, Mary Ann Royal, Monica Driscoll, Ning-Shao Xia, Hang Yin, Ding Xue. A lysine-rich motif in the phosphatidylserine receptor PSR-1 mediates recognition and removal of apoptotic cells. Nature Communications, 2015; 6: 5717 DOI: 10.1038/ncomms6717
Brent Neumann, Sean Coakley, Rosina Giordano-Santini, Casey Linton, Eui Seung Lee, Akihisa Nakagawa, Ding Xue, Massimo A. Hilliard. EFF-1-mediated regenerative axonal fusion requires components of the apoptotic pathway. Nature, 2015; 517 (7533): 219 DOI: 10.1038/nature14102

http://www.sciencedaily.com/releases/2015/01/150107122912.htm

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HIV Related Neuropathy

Today's video is an Australian view of how HIV can cause neuropathy, whether from the virus itself or the drugs. It comes from PainClinician.com (see link below) and is basically a teaching video for other medical professionals. The difference with most of the other neuropathy videos posted here on the blog, is that if this is what medical students are learning, then we can look at the disease from the point of view of the doctors who treat us. It seems to be full of up to date information and reflects modern medical thinking but apart from the odd scientific term here and there, which may not be so easily understood, the vast majority of the 11 minutes, is pretty interesting to the average neuropathy and HIV patient and explains a few areas which may have previously seemed vague.




http://painclinician.com/video/hiv_related_neuropathy

Hepatitis C And Neuropathy

Today's post from hepcsupport.org (see link below) talks about the link between hepatitis C and neuropathy. It is suspected that the blood condition EMC which is associated with hepatitis C, is responsible for causing nervous system abnormalities, thus explaining why so many people with hepatitis C also display symptoms familiar to many neuropathy patients. In this case, new treatments for hepatitis C are emerging and becoming more widely available. There's even a good chance that a combination therapy similar to the HIV anti-viral combos will be available for Hepatitis C patients. The research so far however, on the links between Hep C, EMC and Neuropathy, is thin on the ground to say the least.

A PAINFUL CONNECTION: HCV, CRYO, NEUROPATHY

By Mary Lou Reazor|March 24th, 2013|

There is a very strong association between HCV and a blood condition called Essential Mixed Cryoglobulinemia (EMC). People with hepatitis c, who suffer numbness or tingling of their extremities, know from experience there is also an association between HCV and Neuropathy. Increasingly, their claims are finding support according to researchers and clinical physicians.

Among other symptoms, EMC can cause nervous system abnormalities. Researchers have not explained the connection between HCV, Neuropathy and EMC, nor have they found significantly effective treatments, but knowledge is sure to increase as more people are diagnosed with HCV and its symptoms.

Neuropathy refers to any disease of the nervous system, resulting from localized inflammation of nerves. Patients complain of numbness, tingling and muscle weakness. Symptoms appear in the body’s extremities, the condition is called “Peripheral Neuropathy”. A physical exam may also reveal decreased deep tendon reflexes.

In both Encephalopathy and Neuropathy, the key change is inflammation of blood vessels (Vasculitis). The vessels are responding to immune system products floating in the blood vessels directly. The immune-globulins that are involved are called Cryoglobulins because they turn into a cool gel at cool temperatures. Since cold temps readily affect the small and middle-sized vessels in the extremities, the Cryoglobulins are more likely to form in them. Cryoglobulemia is the condition of having cyroglobulins in the blood.

There are several possible new treatments in “the pipeline”. There are several anti-viral agents that have shown promise in clinical trials, and researchers are developing several HCV specific protease inhibitors similar to those used for HIV retro-virus.

http://hepcsupport.org/a-painful-connection-hcv-cryo-neuropathy/

B Vitamins Alpha Lipoic Acid and other Nutrients for Neuropathy

There have been other posts on the blog (see alphabetical list on the right) about both Alpha Lipoic Acid and nutrients in general which may or may not help with neuropathy. Today's post comes from MDJunction (see link below) and is an excellent account, though without any indication of the writer's qualifications. That said, she says nothing that isn't found on most related sites on the Web (and provides more detail than most) and that may, in your opinion, be verification enough.
The general concensus from neurologists is that they support B-Vitamins and both Alpha Lipoic Acid and Acetyl-L Carnitine as supplements which may improve neuropathic problems but you should be aware that neither is cheap and in most countries, neither is covered by any sort of insurance policy. If the case is proved, it seems unfair to discriminate on the basis of who can and who can't afford a treatment but that's a whole other story!
Also, always take extra B-vitamins with advice from your doctor - it's easy to create an imbalance in your body and cause more harm than good.
If you decide to try supplements, (after consultation with your doctor) shopping around on the Net may help reduce costs.

Peripheral Neuropathy- Nutrients
Jackie
Mar 23 2011

Neuropathy: Nutrient Therapies

Although there has been virtually no research on the use of nutrient therapies for HIV-related neuropathies, there has been a fair amount of research (mostly in other countries) on their use for diabetic neuropathies. Since it appears likely that at least some of the mechanisms for the nerve damage may be similar in the two diseases (inflammation and oxidative damage to the nerves combined with B vitamin deficiencies), there is reason to believe that therapies which have proven useful for diabetics may also work for at least some people living with HIV who develop neuropathy. Many people living with HIV have reported to me that they have successfully eliminated neuropathy with some combination of the nutrient therapies discussed here. Thus, in addition to the other treatments mentioned, I would stress the importance of therapy with the B vitamins and other nutrients, especially acetyl-L-carnitine, gamma-linolenic acid, alpha-lipoic acid, magnesium, and chromium. I would definitely consider including the nutrients that have been shown to help rebuild the myelin sheath around nerves and/or improve nerve functioning such as choline, inositol, gamma linolenic acid, B6, B12, niacin, thiamine, biotin, folic acid, and magnesium.

Biotin, choline, inositol, and thiamine are B vitamins that have all been found useful in treating the peripheral and autonomic neuropathies found in diabetes and may also help with HIV-related neuropathies. In a study at the University of Athens, it was shown that regular, long-term use of biotin in diabetics was very effective both for improvement in nerve conduction and relief of pain. Improvement in nerve conduction occurred after only 4-8 weeks of therapy. In this study, biotin was given via daily intramuscular injection (10 mg/day) for 6 weeks; then 3 times per week (10 mg), intramuscularly, for 6 weeks; then 5 mg/day taken orally for up to two years. The researchers hypothesize that deficiency, inactivity, or unavailability of biotin in diabetics may result in disordered activity of the biotin-dependent enzyme, pyruvate carboxylase, leading to an accumulation of pyruvate and/or a depletion of aspartate, either of which could adversely affect nervous system metabolism. There are a number of reasons why HIV-positive persons may be deficient in biotin and, thus, potentially at risk for a similar problem. It has been suggested that those with neuropathy symptoms might try 10-15 mg/day orally, taken in conjunction with the other B vitamins found useful for improving nerve function.

B12 deficiency is a known cause of neuropathy so this vitamin, along with its coworker folic acid, should certainly be included in any program aimed at eliminating this symptom. Typical symptoms of peripheral neuropathy related to B12 deficiency include the type of leg and foot pains experienced by many. B6 deficiencies are also known to cause both carpal tunnel syndrome (with symptoms of numbness, tingling, and pain in the hands and wrists) and degeneration of peripheral nerves and may be responsible for some peripheral neuropathy problems.

Choline and inositol also seem to be very important parts of the combination of vitamins needed for neuropathy resolution. Diabetic neuropathy is known to be associated with a reduction in myo-inositol levels in nerves and tissues. The decreased level of myo-inositol is believed to cause a decrease in the activity of the sodium-potassium pump and, thus, to change the sodium permeability of nerves. Both diets high in inositol and inositol supplementation have been shown to improve diabetic neuropathy. Researchers at the University of Alabama found a statistically significant improvement in nerve function in diabetics placed on a diet high in inositol. Included in the diet were high-inositol foods such as cantaloupe, peanuts, grapefruit, and whole grains. Other researchers have reported that supplementation with inositol in doses of 2-6 grams per day has resulted in improvements in neuropathy. Robert Atkins, M.D., has reported his successful use of 2-6 grams per day for reversing diabetic neuropathy, and notes that physicians at St. James Hospital in Leeds, England, have reported good results with even smaller dosages.

In addition to the use of inositol itself, treatment with acetyl-L-carnitine can help raise nerve myo-inositol content. Florida researchers have found that peripheral nerve function in diabetes is linked to nerve myo-inositol content and that acetyl-l-carnitine can raise the levels of myo-inositol in the nerves of animals with experimentally induced diabetes. It also apparently protects the nerve membranes from free-radical damage, as evidenced by reduced malondialdehyde levels in the animals treated with acetyl-l- carnitine.

Thiamine has also been seen to be useful in treating diabetic neuropathy. Stanley Mirski, M.D., has reported that a large percentage of his diabetic patients who suffer from neuropathy have achieved improvements with daily thiamine supplementation in doses of 50-100 mg. Using a fat-soluble form of thiamine such as thiamine tetrahydro-furfuryl disulfide may be preferable because of the relatively poor absorption of water-soluble forms of this vitamin. This type is contained in Cardiovascular Research's Allithiamine. A large number of HIV-positive people have reported to me their successful elimination of neuropathy with the combined use of the B vitamins discussed here. The information on acetyl-l- carnitine is too recent for much in the way of anecdotal reports to have surfaced, but it might be an important addition to improve the chances for successful elimination of neuropathy.

Alpha-lipoic acid has long been used in Europe for the treatment of peripheral neuropathy in diabetics. A number of controlled clinical trials have shown its usefulness for reducing both the pain and numbness suffered by those with diabetic neuropathy, and its use for this condition is approved in Germany. Its antioxidant properties may help protect the nerves from the inflammation and oxidative damage that HIV induces, as has been shown to be true with diabetic neuropathy. Because of its liver protective and antioxidant benefits, it has been included as a component of the programs of many of my clients for several years now. It may have contributed to the success of the neuropathy elimination programs some of them have used.

Gamma linolenic acid is an essential fatty acid found in borage oil, grape seed oil, black currant oil, and evening primrose oil that has been shown to be successful in reversing nerve damage in diabetics suffering from peripheral neuropathy. In a double-blind, placebo-controlled study using 480 mg of GLA daily, all the diabetics given the fatty acid experienced gradual reversal of nerve damage and improvement in the symptoms related to the peripheral neuropathy, while those on placebo gradually worsened. It is thought that GLA may help to rebuild the myelin sheath around the nerves, thus restoring proper nerve conduction.

Magnesium is also known to be necessary for nerve conduction; deficiency is known to cause peripheral neuropathy symptoms. Thus, including optimal amounts of magnesium might contribute to elimination of neuropathy. There have also been reports of chromium deficiency causing peripheral neuropathy. I learned this too recently for chromium to have been included in most of the neuropathy therapy programs used by my clients in the past and, thus, I'm not sure what it might contribute. However, chronic infection is known to deplete body stores of chromium, so adding a dose of perhaps 200-400 mcg/day to a complete nutrient protocol might be reasonable.

In addition to all the nutrient supplements, an analysis of data coming out of the Immune Enhancement Program in Portland, Oregon, appears to show that their program, which includes Chinese herbs along with acupuncture and various other therapeutic approaches, results in improvement in neuropathy for some.

If you are considering supplementation with any of the B vitamins discussed above, never forget that although B vitamins are by and large non-toxic, any individual B vitamin should always be taken along with the full B complex to prevent imbalance in the body. Long-term use of very high doses of individual B vitamins taken alone, without the rest of the B complex, can induce imbalances or deficiencies in other B vitamins.

About Alpha Lipoic Acid

Alpha-lipoic acid (ALA), also known as lipoic acid (or thioctic acid), is a sulfur-containing fatty acid found inside every cell of the human body. The main function of alpha-lipoic acid is to generate the energy required to keep living organisms alive and functioning. Lipoic acid plays a key role in a variety vital energy-producing reactions in the body that turn glucose (blood sugar) into energy.

Alpha-lipoic acid is a potent biological antioxidant that has been shown to slow the oxidative damage in cells, and in many cases stabilize or even reverse cell damage. Alpha-lipoic acid is so effective as an anti-oxidant because it works on both water and fat-soluble free radicals that cause oxidation and cell damage in the body. Notwithstanding its popularity, the exact mechanism responsible for the medicinal affects of alpha-lipoic acid is still not fully understood.

Some research suggests that certain nerve diseases may occur as a result of free radical damage. Since alpha-lipoic acid can reach all parts of a nerve cell it can potentially protect nerve cells against such damage. This is the rationale behind studies on the potential benefits of alpha-lipoic acid for diabetic neuropathy.

Experimental studies show that alpha-lipoic acid may exhibit a renal protective effect in individuals with diabetes. Alpha-lipoic acid increases glucose uptake in the cells and appears to reduce symptoms of diabetic complications including cataract formation, vascular damage, and polyneuropathy (nerve damage). A study published in Diabetic Medicine in 1999 showed that patients treated with 600 mg of ALA 3 times daily for 3 weeks had improvement of diabetic symptoms from polyneuropathy. In another study using 600 to 1,800 mg of ALA daily, individuals treated showed improved insulin sensitivity. Most studies supporting the use of alpha-lipoic acid to reduce symptoms of diabetic peripheral neuropathy employed intravenous alpha-lipoic. Evidence for the use of oral lipoic acid, in connection with diabetes remains weak and contradictory.

Another group of nerve cells in diabetics, the autonomic nerves, which control the function of internal organs, may also become damaged. When this same phenomenon occurs in the heart, a condition known as cardiac autonomic neuropathy, it leads to irregularities of heart rhythm. There is some evidence that alpha-lipoic acid may be helpful for this condition.

Some in the scientific community believe that alpha-lipoic acid can actually reverse the damage in aging cells of the brain. Alpha lipoic acid has also been used both in oral and topical forms as a way for keeping skin healthy and young in appearance. There have been studies documented in medical literature indicating that supplemental ALA may even be beneficial in patients with glaucoma.

NutritionalTree.com is a great consumer resource that collects user reviews for alpha lipoic acid products.

Dosage

The common dosage of alpha-lipoic acid for complications of diabetes is 100 to 200 mg three times daily. In studies that found benefit of supplementing with alpha-lipoic acid, several weeks of treatment were often necessary for effects to develop. However, some studies have indicated as much as 600-1,800 mg per day of alpha-lipoic acid for optimal benefit in people with specific health concerns such as diabetes, liver cirrhosis and atherosclerosis.

If you are healthy and want to promote optimal health, a dose of 30 - 300 mg per day may be sufficient.

Lipoic acid appears to have no significant side effects at dosages up to 1,800 mg daily.

http://www.mdjunction.com/diary/jackies-journey-back-to-health/peripheral-neuropathy-nutrients

HOMOEOPATHIC REMEDIES FOR DYSENTERY

Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in which the loose or watery stools contain visible red blood. Dysentery is most often caused by Shigella species (bacillary dysentery) or Entamoeba histolytica(amoebic dysentery).

HOMOEOPATHIC REMEDIES

MERCURIUS COR 30- MERCURIUS SOL 30- Begin the treatment with Merc cor. if there is much blood  or with Merc sol. If there is much mucus. Cutting pains are present and stools are scanty. Tenesmus before and after stools.

NUX VOMICA 30- Stools contain much mucus. There are abdominal pains before stools and these are relieved after stool

ALOE SOC. 30—Stools contain a lot of mucus or are jelly like. There is burning and pain in the rectum . Patient is afraid of passing flatus as he is not sure whether the urge is for stool or flatus. Bleeding from the rectum

CHAPARRO- It is an excellent remedy for chronic dysentery and diarrhea

COLCHICUM AUTUM. 30- Autumnal dysentery when days are hot and nights are cold

TROMBIDIUM 30—Dysentery worse by eating and drinking. Stools only after eating. Much pain, before and after stool. Burning in the anus

THUJA OCC. 200- An excellent remedy for amoebic dysentery

SEPTICAEMINUM 30- It cures magically the dysentery which is produced in camp life

BAPTISIA TIC. 30- Dysentery  of old people. Dysentery during typhoid fever

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Will Neuropathy Diagnosis Go Over The Fiscal Cliff

 Today's post comes from the Neuropathy Association E-news letter for November 2012 (see link below) and highlights a potentially very difficult time for neuropathy patients in the United States. Hopefully solutions can be found, now that plunging off the fiscal cliff has been temporarily averted but these sort of spending cuts are just the sort that will remain on the statute books irrespective of macro decision making in Washington. Not that EMGs are the be all and end all of neuropathy testing (a patient's account of symptoms is more often than not enough to confirm diagnosis) but EMGs and the like are useful tools in establishing the extent of neuropathic damage and certainly in measuring its progress. If you are living in the USA it may well be worth reading and supporting this  campaign by the Neuropathy Association.

 

A MESSAGE FROM THE PRESIDENT AND CEO
Tina Tockarshewsky November 2012

Dear Friend,

A clear and present danger for our community is now upon us, and your support is essential.

It was recently announced in the 2013 Medicare Physician Fee Schedule from the Centers for Medicare & Medicaid Services (CMS) that reimbursement payments to physicians for needle electromyography (EMG) tests and nerve conduction studies (NCSs) will be severely reduced by 30%-70% beginning on January 1, 2013. EMG and NCSs are the primary diagnostic tools for peripheral neuropathy as well as other neuromuscular diseases like ALS, MS, and Parkinson’s. Implementing these cuts will deny millions access to proper diagnosis and care.

We are hearing from many physicians that they will no longer be able to afford to practice neuromuscular medicine...and many currently in practice will simply stop seeing Medicare patients!

This Neurological Fiscal Cliff Will Hurt Neuropathy Patients!

 

This is a crisis unlike any we have ever known before…and is a potential game changer for ALL patients and medical professionals working with the neuropathy community. Early diagnoses will be reduced and misdiagnoses will increase. Patient access and care will suffer, exacerbating the challenges already facing neuropathy patients.

A 2010 poll by The Neuropathy Association showed that many patients already face significant delays in diagnosis, during which irreparable nerve damage continues:

 

Two Ways You Can Help

First: In the coming days, we will announce a process for contacting members of Congress and posting comments on these proposed changes on the Centers for Medicare & Medicaid Services website. Please watch your emails for this announcement and respond immediately. Please also know that we are working with our medical professional society partners to respond to this crisis.
And keep in mind that other insurers follow Medicare’s actions. So, even if you are not on Medicare, this change has the potential to impact everyone in the neuropathy community.

Second: Support our year-end fundraising efforts, and KEEP US IN THE FIGHT. In these difficult times for the economy and the Association, your generous contributions are our lifeline – and help protect your interests as well as those of untold numbers of future patients.
Thank you for taking action.

Neurologists to See Cuts in 2013 Medicare Payments
The Center for Medicare and Medicaid Services (CMS) recently released new code values that could result in decreased payments to neurologists. Specifically, physicians who provide nerve conduction and needle EMG services will face dramatic cuts of more than 50 percent for some services starting January 1, 2013. This is a drastic cut that will be especially hard on neurology practices large and small, many of which rely on these services to meet their bottom line. Patients also will pay the price with less access to these services. Private health insurers often follow Medicare payment rules as well, which will exacerbate the situation.
- American Academy of Neurology

Editor’s Note: Please refer to the President and CEO's message above for more information about this breaking issue that negatively impacts access to critical evaluation and care for people with neuropathy, and how The Neuropathy Association is working with the American Academy of Neurology, the American Association of Neuromuscular & Electrodiagnostic Medicine, and the American Academy of Physical Medicine & Rehabilitation to address this issue.

http://www.neuropathy.org/site/PageServer?pagename=Resources_PubArchivesM_E

BED BUGS CAN TRANSMIT PARASITE THAT CAUSES CHAGAS DISEASE

The bed bug may be just as dangerous as its sinister cousin, the triatomine, or "kissing" bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.

The role of the bloodsucking triatomine bugs as vectors of Chagas disease -- which affects 6 to 8 million worldwide, mostly in Latin America, and kills about 50,000 a year -- has long been recognized. The insects infect people not through their bite but feces, which they deposit on their sleeping host, often around the face, after feeding. Bed bugs, on the other hand, are usually considered disease-free nuisances whose victims are left with only itchy welts from bites and sleepless nights.

In a study published online this week in the American Journal of Tropical Medicine and Hygiene, senior author Michael Z. Levy, PhD, assistant professor in the department of Biostatistics and Epidemiology at the University of Pennsylvania's Perelman School of Medicine, and researchers at the Universidad Peruana Cayetano Heredia in Peru conducted a series of laboratory experiments that demonstrated bi-directional transmission of T. cruzi between mice and bed bugs.

In the first experiment run at the Zoonotic Disease Research Center in Arequipa, Peru, the researchers exposed 10 mice infected with the parasite to 20 uninfected bed bugs every three days for a month. Of about 2,000 bed bugs used in the experiment, the majority acquired T. cruzi after feeding on the mice. In a separate experiment to test transmission from bug to mouse, they found that 9 out of 12 (75 percent) uninfected mice acquired the parasite after each one lived for 30 days with 20 infected bed bugs.

In a third experiment, investigators succeeded in infecting mice by placing feces of infected bed bugs on the animal's skin that had either been inflamed by bed bug bites, or scraped with a needle. Four out of 10 mice (40 percent) acquired the parasite by this manner; 1 out of 5 (20 percent) were infected when the skin was broken by the insect's bites only. A final experiment performed at the Penn bed bug lab in Philadelphia demonstrated that bed bugs, like triatomines, defecate when they feed.

"We've shown that the bed bug can acquire and transmit the parasite. Our next step is to determine whether they are, or will become, an important player in the epidemiology of Chagas disease," Levy said. "There are some reasons to worry -- bed bugs have more frequent contact with people than kissing bugs, and there are more of them in infested houses, giving them ample opportunity to transmit the parasite. But perhaps there is something important we don't yet understand about them that mitigates the threat."

T. cruzi is also especially at home in the guts of bed bugs. "I've never seen so many parasites in an insect," said Renzo Salazar, a biologist at the Universidad Peruana Cayetano Heredia and co-author on the study. "I expected a scenario with very low infection, but we found many parasites -- they really replicate well in the gut of the bed bugs."

Wicked Cousins

Bed bugs and kissing bugs are distant cousins but share many striking similarities. Both insects hide in household cracks and crevices waiting for nightfall and the opportunity to feed on sleeping hosts. They are from the same order of insects (Hemiptera) and both only feed on blood. (One main difference is their size: kissing bugs are five times as big as a bed bug). With so much in common, it seemed logical to the authors that the kissing bug's most infamous trait, the transmission of T. cruzi, is also shared by the bed bug.

Other investigators have shared this suspicion. In 1912, just three years after Carlos Chagas described the transmission of the disease by kissing bugs, French parasitologist Émile Brumpt recounted that he had infected almost 100 bed bugs exposed to an infectious mouse, and then used them to infect two healthy mice. Decades later an Argentine group replicated his work. These experiments, largely ignored during the recent bed bug resurgence, missed one key point.

"Mice can hunt and eat bed bugs," said Ricardo Castillo-Neyra, DVM, PhD, coauthor and postdoctoral fellow at the Universidad Peruana Cayetano Heredia and Penn. "The older studies were almost certainly only documenting oral transmission of the parasite. Our work shows for the first time that bed bugs can transmit the parasite when their feces are in contact with broken skin, the route by which humans are usually infected."

Emerging Problem

More people in the U.S. are infected with T. cruzi now than ever before. The Centers for Disease Control and Prevention estimates that the number of Chagas disease cases in the U.S. today could be as high as 300,000.

"There have always been triatomine bugs and cases of Chagas disease in the U.S., but the kissing bugs we have here don't come into homes frequently like the more dangerous species in South and Central America do," Levy said. "I am much more concerned about the role of bed bugs. They are already here -- in our homes, in our beds and in high numbers. What we found has thrown a wrench in the way I think about transmission, and where Chagas disease could emerge next."

Equally worrying is the invasion of bed bugs into areas where Chagas disease is prevalent, especially in countries where traditional insect vectors of the parasite have been nearly eliminated, Levy said. In these areas, bed bugs will be repeatedly exposed to T. cruzi, and could re-spark transmission where it had been extinguished.

"Bed bugs are harder to kill than triatomines due to their resistance to common insecticides." Levy said. "No one is prepared for large scale bed bug control. If the parasite starts to spread through bed bugs, decades of progress on Chagas disease control in the Americas could be erased, and we would have no means at our disposal to repeat what had been accomplished."

Often referred to as a silent killer, Chagas disease is hard to diagnose in its early stages because the symptoms are mild or absent. The parasites are hidden mainly in the heart and digestive muscle and over time can cause cardiac disorders and sometimes digestive or neurological problems. In later years, the infection can lead to sudden death or heart failure caused by progressive destruction of the heart muscle. Although there are some drugs to treat Chagas disease, they become less effective the longer a person is infected.

The long asymptomatic period of Chagas disease complicates surveillance for new outbreaks of transmission. In Arequipa, Peru, thousands became infected with the parasite before a case appeared in the hospital. The same could happen in cities in the United States if the parasite were to emerge in the bed bug populations, the authors say.

"Carlos Chagas discovered T. cruzi in triatomine insects before he saw a single case of the disease," Levy said. "We need to learn from his intuition -- check the bugs for the parasite."