Got Neuropathy Will It Get Better Or Worse

Today's post from neuropathyjournal.org (see link below) asks the question we all want to know and provides the answer, that none of us, including the doctors, know whether our nerve damage will get worse or not. They also don't know if it will improve, yet for some people it does. Some patients seem to get better only for the symptoms to return some time later, maybe in a different place and maybe much worse than before. It's that sort of disease unfortunately and at the moment there's not a damn thing we can do about it except hope we will find the right medication for us that will reduce the symptoms and make life bearable. Of course doctors can predict outcomes but not to any certainty and it is often left to the patient to negotiate his or her way through the minefield of neuropathy medications and treatments. That's character building!

Will My Neuropathy Get Worse?
By LtCol Eugene B Richardson, USA (Retired) BA, MDiv, EdM, MS28 

One issue neuropathy patient’s face is the fear that their neuropathy will grow progressively worse. Neurologists call this a progressive polyneuropathy. The truth: no one really knows if your neuropathy will worsen, stay the same or disappear. A neurologist shared that this may have more to do with the underlying cause of the neuropathy, genetics, and heaven only knows, issues.

I speak of this very fear in chapter twelve, Focus, in the DVD “Coping with Chronic Neuropathy”, and if you have not viewed this chapter, I suggest that you do so. The viewing will provide a better perspective.

Neuropathy patient fears are often increased by the coming and going (remitting and relapsing) of neuropathy symptoms. These patterns are a medically confirmed fact and also occur in many other chronic illnesses. Better recognized are the same patterns for some forms of MS (Multiple Sclerosis)!

Neurologists confirm that there are acute neuropathies that come on suddenly and then the symptoms disappear. In other neuropathies symptoms occur, disappear and then return at the same level. Other neuropathies occur, disappear and then return at increased levels and in more places of the body. Others come, go and then go away for years only to return with a vengeance!

The chronic neuropathies (affect one set of nerves) and polyneuropathies (affect many nerves), which increase for years are often referred to as progressive polyneuropathies. The mystery is increased as there seems to be no rhyme or reason for these patterns. The only thing I noticed is that when I increased activity, I have increased burning, pain or other symptoms and I neurologist tell me that this is due to making damaged nerves work.

For years between the emotional highs when my symptoms remitted (“Hurrah, they’re gone!”) and the emotional lows when they relapsed (“Oh no, they’re back!”), I was tempted to worry that my symptoms were going to worsen and guess what, they did! But one has to ask the question, did the energy spent on worry change anything? No! What I re-discovered was what I learned in Sunday school. It was better to spend my time and energy finding a doctor who was trained (neuromuscular neurologist) in the clinical approaches to neuropathy then to waste energy on worry. I needed a doctor, not worry, to focus on my symptoms. I needed a doctor working with me as a partner, while treating the symptoms and looking for the TYPE and/or CAUSE. Why finding the type of neuropathy important? Because as Dr. Latov in his book tells us, this can often point in the direction of a cause! I needed a medical Sherlock Holmes, not time worrying about what might happen.

This approach maintained a focus on self empowerment by learning all I could, while prodding the doctors with questions that helped them think and act. The most important question for you is not, will my neuropathy get worse, but what is the type of neuropathy and/or the underlying cause? Spend your energy looking for the type and/or cause, as no one knows if your neuropathy will worsen or not.

I know that for so many of you neuropathy has been a progressive illness which worsened over the years. Conversely, my progressive polyneuropathy has not killed me, for my neuropathy symptoms began at age 31 and I am now 76. Thirty-five years into the symptoms with a million denials with a diagnosis from mentally ill to idiopathic neuropathy. I was given one drug which drove me to talk backwards and then another that reduced pain by 80%. Five years later with the miracle of IVIg I am able to keep breathing and the chest muscle spasms stopped while reducing other mind numbing symptoms. This took many doctors, lots of research and knowledge, while asking good questions and giving doctors documents from experts. It may have been fear and anger which drove me forward, but it was these focused actions that brought help, not dwelling on my fears!

It is important to know which issue is important as you set goals for getting help. It is important to focus your energy on learning, getting help with symptoms and finding the cause and solutions for the diagnosed illness. I do not mean idiopathic neuropathy (of unknown cause). It is very difficult to find a solution, other than for symptoms, when the neuropathy is of unknown cause. Help the doctor think and pushing the system to do the testing that is now available. Click here to read about my opinion on Idiopathic Neuropathy.

Tests that are available will allow the doctor to know if the neuropathy is large or small fiber, motor, sensory or autonomic, axonal, immune-mediated, demyelinating or inflammatory and these clues can lead to a possible identification of the type and/or cause that is more helpful than idiopathic.

RESOURCE: Read Dr. Scott Berman’s book, as this book may provide insight on these issues. Click here to view the recommended Books On Neuropathy. Dr. Berman has untreatable CIDP (chronic inflammatory demyelinating polyneuropathy) and his book speaks to all neuropathy patients as one who has been in our shoes with many neuropathies. Dr. Berman empowers us to face creatively the emotional issues we ALL face in chronic illness.

https://neuropathyjournal.org/will-my-neuropathy-get-worse/

Will a Better Attitude Towards Opioids Help Neuropathy Sufferers

Today's article from an unknown author writing for opioids.co.uk (see link below)is not an easy read but one that definitely stimulates discussion. The writer is clearly someone with a deep scientific knowledge of how opioids work and his or her political agenda aside, he makes a powerful case for a more open-minded approach to using opiods in the treatment of pain. It's not as if it's a new drug source; it's been used for thousands of years but it is a controversial one because of the perceived dangers of addiction and substance abuse. Much like marijuana, the authorities both political and medical, seem to see it always as a potential threat to society, rather than an effective weapon in the fight to control severe pain. Of course, as many of you know, it's already widely used in the treatment of neuropathic symptoms but almost always as a last-resort measure, when all else has failed.
This article tries to show that opioids are not something to be feared but an age old pain suppressor that deserves much better research, so that it may be possible to use it at an earlier stage. After all, the anti-depressants and anti-convulsants which are generally prescribed first, are not without unpleasant side effects of their own and are very often ineffective. However, it's a real hot potato as far as the FDA in the States and most governments across the world are concerned. They seem to have a vision based in the 19th century of half the population living in a drug-induced stupor. Time to trust the people a little more maybe?

FUTURE OPIOIDS

THE BIRTH OF A NEW GENERATION

A significant minority of the population only feel truly well on opioids. In effect, they self-medicate, taking responsibility for their own mental health in defiance of medical orthodoxy.

It would indeed be extraordinary if - alone among the neurotransmitter systems of the brain - the endogenous opioid families were immune from dysfunction. Enkephalins are critical to "basal hedonic tone" i.e. whether we naturally feel happy or sad. Yet the therapeutic implications of a recognition that dysfunctional endogenous opioid systems underlie a spectrum of anxiety-disorders and depression are too radical - at present - for the medical establishment to contemplate. In consequence, the use of opioid-based pharmacotherapies for "psychological" pain is officially taboo. The unique efficacy of opioids in banishing mental distress is neglected. Their unrivalled efficacy in treating "physical" nociceptive pain is grudgingly accepted.

Later this century and beyond, however, the development of highly selective, site-specific designer drugs and innovative gene-therapies may enhance our native opioid function and revolutionise mental health. Therapeutic intervention targeted on the opioid pathways will potentially enrich the quality of life of even the nominally "well", not least because - by the more enlightened health standards of posterity - we may all be reckoned mentally ill.

Today, by contrast, immense energy is devoted by the authorities into persecuting "illicit" narcotic users. Many drug-"abusers" feel well thanks only to the "non-therapeutic" use of opioids. They are stigmatised, pilloried and criminalised in a futile War Against Drugs. In the "Inquisition against pleasure", victims of medically-sanctioned human-rights abuses - e.g. the hundreds of thousands of drug "offenders" incarcerated in the Amerikan gulag - are officially supposed to believe their malaise-ridden drug-naïve states were "normal", "natural" and mentally healthy. In the course of our ill-conceived Drug War, vast resources are dissipated by the state-apparatus in an effort to choke off narcotic production and supply. When these efforts are temporarily successful, drug-deprivation makes the habitual opioid user feel ill; [s]he "cold-turkeys" with characteristic irritability, anhedonia, depression, sickness behaviour and sometimes raw physical pain. The ill-effects felt from involuntary deprivation of opioids are taken to demonstrate the likely ill-effects of legalised access, a paradox that might be thought laboured were its human costs not so tragic.

When caught up in the criminal justice system, users may be pressured into taking opioid antagonists like naltrexone (Trexan). Such drugs can induce dysphoria and suicidal despair. At best, their use subtly diminishes the victim's capacity ever to feel well. Meanwhile Chinese military surgeons have developed (2003) a new treatment weapon against narcotic users: surgical destruction of the pleasure centres. Western doctors are said to be following these procedures with interest, but are more likely to achieve their functional equivalent by non-surgical means.

Even where it is acknowledged that many opioid users have a pre-existing anxiety or depressive disorder in urgent need of relief, those so afflicted are fobbed off with often third-rate psychotropics instead. For a start, the monoamine hypothesis of depression - and the new classes of drug it has spawned (SSRIs, NARIs, SNRIs, NaSSAs, RIMAs etc to complement the dirty old tricyclics and irreversible unselective MAOIs) - is radically incomplete. A minority of people, admittedly, find such drugs effective. Often taking a licensed antidepressant is better than nothing at all - perhaps in part because of their positive effects on endogenous opioid peptide release. Yet even in the context of controlled clinical trials with relatively high dosage-regimens and artificially good rates of patient-compliance, it's rare for response-rates to reach more than 70%. Rates of full remission of depressive symptoms are far lower, perhaps 25-30%. Out "in the field", the picture is worse still. Adverse side-effects are common. Response may take weeks. Withdrawal reactions can be unpleasant.

A recognition of the crucial role of dopamine, and selective dopamine reuptake blockers, in sub-types of depressive mood-disorders might push response and remission rates higher. The mesolimbic dopamine system is critical to vitality, motivation, libido and a capacity to anticipate reward. Dopaminergics can also act as analgesics. They can also reverse the apathetic sedation induced by some antidepressants and opioid agonists. Yet the FDA stymies the licensing of effective dopamine reuptake-blocking mood-brighteners at home; and applies pressure to deny access to them abroad. This is because of worries about their (sometimes) faster efficacy - and mild psychostimulant effect - raise the spectre of "abuse-potential"; and proscription, persecution and indiction are favoured over consumer education. For Big Brother knows best.

More controversially, adding customised opioids, enkephalinase-inhibitors and kappa-antagonists to our therapeutic armamentarium may prove critical to boosting response- and remission-rates towards 100% in the decades ahead. Crudely, whereas dopamine mediates "wanting", mu opioid agonists mediate "liking". Both systems can be fruitfully enhanced. Depressive and dysthymic people often suffer from a dysfunctional opioid system and anhedonia - an incapacity to experience pleasure. Sometimes orthodox "antidepressants" may even make them feel worse. Yet controlled clinical trials of designer narcotics for refractory and/or melancholic depression, let alone their use by "normal" people with "ordinary" mood-disorders, are not imminent.

So what is to be done? Even in the context of today's crude agents, would some of us be better off as legalised junkies?

No, usually not, at least in contemporary society. Self-medicating users with enough resources to maintain a regular supply may indeed find they can function as well as, or better than, their drug-naïve state. Popular mythology aside, users don't seek to escalate dosage indefinitely: both humans and laboratory monkeys with unlimited access tend slowly to increase injection-frequency until eventually they self-administer a stable and subjectively optimal amount of the drug. Most users take heroin, not primarily to stave off the abstinence syndrome, but because they find life on heroin better than their pain-ridden life without it. Yet the existence of a typical heroin addict in prohibitionist society can still be exceedingly unpleasant at times. Contemporary opioid drugs, natural and synthetic alike, are flawed. The problem is not the euphoric well-being they can induce - an ill-named "adverse side-effect" - but their tendency to induce a financially ruinous tolerance; perhaps insidiously to dull the intellect; trigger nausea; slow digestive processes; and sometimes induce a parodoxical hyperalgesia. Most seriously, when taken in acute excess, today's opioids can cause respiratory depression. This is a consequence of their stimulation of the mu-2 receptors in the medullary respiratory centres of the brain. These problems are exacerbated a thousandfold, however, by the illegal status of narcotics in contemporary society. Dosage, purity and regularity of supply cannot be guaranteed; prices are inflated; quality-control is negligible; good hygiene is difficult. Pharmacological education is non-existent, whereas it ought to be part of the core curriculum. Opioid users are frequently forced into crime to pay for pharmacotherapies that should be cheaply and safely available; and damned for seeking a state of mind which will one day be their birthright: invincible happiness.

To promote emotional superhealth both durably and effectively, designer-opioids must be synthesised that are also subjectively nicer, richer and cleaner than today's product-line. For one of our three major endogenous opioid families is implicated in profoundly dysphoric psychological effects: a cruel negative-feedback system exists between the mu and kappa systems that "corrects" any "excess" tendency to well-being. Thus dynorphin activity at the kappa receptors tonically inhibits the release of dopamine from the mesolimbic terminals. By contrast, the mu-opioid receptor selective endomorphins, especially endomorphin 1, are potent antidepressants: they enhance mu opioid receptor-mediated dopamine release in the nucleus accumbens. If our well-being is to be sustainably enhanced, the balance between the two opposing opioid systems must be shifted.

The role of the mu receptors appears to be crucial in another respect. Today, people vary hugely in their sensitivity to pain. This sensitivity is genetically regulated. Pain perception - and, conversely, emotional well-being - is closely linked to the number of neuronal mu receptors. This number is controlled by a single gene, the mu opioid receptor gene. Pain-sensitivity is diminished when the receptors are present in relative abundance. When the receptors are reduced in number or missing altogether, relatively minor noxious stimuli may be perceived as painful.

In the short-to-medium term, then, we need better-targeted opioids, safer and more site-specific than the present crop. Smarter opioids can potentially be combined with cholecystokinin antagonists (e.g. proglumide); nitric oxide (NO) synthase inhibitors; peroxynitrite-blockers; and also, perhaps, better-designed NMDA receptor antagonists - co-analgesics with potential antidepressant efficacy that inhibit the onset of tolerance. Although mu receptor agonists are the best analgesics and euphoriants, selective delta receptor agonists and enkephalinase inhibitors may prove clinically valuable antidepressants. The development of centrally active and more selective kappa antagonists - which block the endogenous excess production and reuptake of dynorphin underlying many depressive and anxiety disorders - is also a priority. Orally active JDTic, a potent, exceedingly long-acting selective kappa antagonist, is currently undergoing preclinical testing. Kappa Therapeutics, the world's first conference dedicated to the kappa opioid receptor, was held in Seattle July 2011. In the meantime, Buprenorphine (Buprenex, Temgesic, Subutex), for instance, is certainly no panacea; but it would probably benefit a far wider section of the population than its current restriction to use in "detoxifying" heroin-addicts. Its role as a mixed mu agonist reduces buprenorphine's addictive potential as a euphoriant while increasing its safety in overdose. Buprenorphine's kappa receptor antagonism may contribute to its superior efficacy as an antidepressant. Even the humble codeine analogue tramadol (Ultram), a selective partial mu agonist analgesic with noradrenaline and serotonin reuptake inhibiting properties, can serve as a useful mood-brightening stopgap. Weak but non-negligible kappa agonism limits its therapeutic benefit. But contemporary medico-legal opiophobia ensures such usage remains strictly off-label.

THE QUEST FOR A DRUG-FREE SOCIETY

In the longer-run, however, irrespective of how clever our pharmacological interventions may one day be, we'd arguably be better off taking no drugs at all. For if there were nothing fundamentally wrong with our default-state of consciousness, then we wouldn't now try so hard to change it. Thus our sophisticated descendants may opt instead to rewrite the vertebrate genome and allow themselves life-long genetically pre-programmed bliss. They may "naturally" be animated by gradients of well-being beyond the bounds of normal human experience as an everyday part of mental health.

Wouldn't lifelong happiness make us stagnate? No. In our genetically-enhanced post-human successors, the functional analogues of aversive experience can potentially perform an analogous functional role to mental and physical pain in our Darwinian past, but without its textures of phenomenal nastiness. Our descendants' enriched dopamine function will enhance their drive, energy and will-power, not just hedonic capacity. Thus outright abolitionism is not technically infeasible - just ideologically problematic.

Tomorrow's bioscientists face another challenge. Taken in excess, opioid-based drugs of today tend to dull consciousness, inducing a dreamy warm contentment. The name "narcotic" derives from the Greek word for stupor. Indeed smacked-out bliss is typically used as the archetype of what any drug-or-gene-underwritten chemical utopia would be like. Most notably, soma in Aldous Huxley's Brave New World is depicted as a cross between a non-addictive opioid and a hangover-less tranquilliser. Thus Huxley's utopians enjoy only an empty imbecilic happiness, not life-enriching peak experiences. Unlike dopaminergics, soma doesn't increase incentive-motivation, nor does it heighten the felt intensity of experience. You can use soma to drift off to sleep.

Yet this negative stereotype of synthetic bliss is profoundly misleading. Addictive tranquillity is only one option among many. It reflects a poverty in our conception of the range of options for paradise-engineering that biotechnology puts on offer. In reality, the quality of our consciousness can be intensified, sharpened and radically diversified by creative psychopharmacology. Intellect and empathy, and not just mood, can be prodigiously enhanced when the ideology of Better Living Through Chemistry finally enters mainstream culture.

Better still, when a wholesale genomic rewrite - and not just piecemeal genetic tinkering - unfolds in the millennium ahead, then any chemical manipulation of our descendants' emotionally- and intellectually-enriched superminds may be redundant. At most, lifestyle drugs will offer an optional fine-tuning for the parameters of their well-being - set against a backdrop of native-born bliss. In the wake of any such Post-Darwinian Transition, a wide variety of social interactions will "naturally" trigger a far richer endogenous opioid release than occurs today; and do so from a much higher baseline of emotional well-being.

However, our present restrictive definitions of mental illness, and the technical challenges posed by large-scale genetic-rewrites, make germline gene-therapy seem a pipe-dream for now. In the present era, lifetime pure dysthymia afflicts far too many people; and periods of "mild" anxiety, malaise and depressive episodes blight the lives of hundreds of millions more. Meanwhile countless victims of chronic pain-disorders are condemned to a life of needless suffering by institutionalized opiophobia. Victims of the most unspeakable, spirit-crushing neuropathic or central pain are liable to be fobbed off with pain-management courses - "helping you to manage your pain" - rather than given the potent pain-relief they deserve. For with a bit of creative psychopharmacology, both the tolerance and adverse side-effects of chronic opioid use are manageable even with today's crude agents. Thanks to tomorrow's biotechnology, the real obstacles to curing the nasty side of life are set to become doctrinal, not technical. Suffering of any kind is due to become optional. It remains to be seen how quickly the ideological baggage of the past can be overcome.

http://opioids.co.uk/

Will Glycene be Able to Help with Neuropathy

Today's post comes from ezienarticles.com (see link below) and talks about the possibility of using the amino acid Glycene to interfere with neuropathic pain signals by blocking them between the nerve cells. Glycine is a non-essential amino acid that may be useful for conditions such as schizophrenia and strokes and can be bought as a supplement. HOWEVER, nobody should buy and use this supplement without discussing it with their doctors first. Without all available information and a recommendation from a doctor, it wouldn't be sensible to use Glycene. That said, this is an interesting and reasonably easy to follow article what may have far-reaching consequences for neuropathy patients.

A New Approach to Neuropathy Pain Relief, The Glycine Transporter
By George Kukurin D.C.

There are numerous explanations why individuals acquire peripheral neuropathy and sad to say only a few reliable strategies to decrease the discomfort and other symptoms connected with it. There are a minimal number of different types of prescription drugs which have recognized treatment success. One example of these types of medication operates by elevating the amount of a neurotransmitter called GABA. This substance, GABA functions like a braking mechanism on the nervous system. It is presumed that GABA decreases neuropathy pain by diminishing or decreasing the pain impulses that travel from the hands and feet to the brain. An additional category of drug works by raising the neurotransmitters serotonin and norepinephrine. Precisely how this inhibits neuropathy pain is uncertain. Another important additional neurotransmitter, glutamate acts much like the gas pedal inside the nervous system. It ramps up signaling of pain transmission in sensory neural fibers. In nerve injuries which includes chemotherapy associated neuropathy, glutamate concentrations may be heightened or their transporters pumps depressed. The net consequence is an heightened action of glutamate function, which due to the excitatory character of glutamate, in due course translates into neural hypersensitivity in pain pathways. Drug treatments that reduce glutamate or obstruct its receptors may work to diminish pain signaling. Even though neuropathy is a common and incapacitating sickness and huge amounts of money have already been invested in investigation of its treatment, no one method is universally successful to help persons who must endure neuropathy. Each and every patient reacts in different ways to these medications and sad to say none of them deliver exceptional benefits for most of patients suffering with peripheral neuropathy.

Considering that the diverse types of prescription drugs utilized to address different types of neuropathy render, by and large, insufficient or discouraging benefits there is always a continuous search for unique and perhaps more potent biological pathways with which to handle neuropathy signs or symptoms.

Yet another neurotransmitter and its receptor is attracting particular attention from the neuropathy research community. The amino acid glycine is what is referred to as an inhibitory neurotransmitter. It functions at the junction in between neural cells known as a synapse. Whenever glycine is introduced in the junction between two nerves it decreases or halts the transmission of impulses (like pain signals) traveling to the brain. For this reason Glycine is labeled as an inhibitory neurotransmitter. Glycine's inhibition of pain signaling however does not continue long since the nerve ending at the junction of synapse possess pumps that push the glycine out from the gap between the nerves and sequester it within the neural cell. When returning within the cell Glycine is less active and generates no more inhibition of nerve signaling.

Consequently pain impulses like those seen in neuropathy can once more start along their path from the toes and fingers towards head, making life dismal for individuals affected by neuropathy. At least one group of experts has confirmed that substantial levels of glycine consumed by mouth can elevate blood and cerebrospinal glycine concentrations considerably. On the other hand due to the glycine transporter positioned in between nerves cells, we can't be certain that glycine concentrations in the synapse, the place it is effective in reduction of neurological impulses can be obtained by glycine supplementation by itself.

So providing excess glycine within the diet might not be the optimal strategy to decrease neuropathy discomfort. Considering that glycine transporter pump can be so effective it might call for significant doses of oral glycine and it may well nevertheless be challenging to get adequate glycine into the synapse between nerves and to retain it there long enough to obtain important reductions of nerve associated suffering.

If only we're able to inhibit the glycine transporter?

Investigation into pharmaceutical development designed to inhibit the glycine transporter is exploding. Without a doubt preliminary research shows that boosting the effects of glycine by means of curbing the removal of this neurotransmitter out of the gap between nerve cells lessens pain related patterns in animal models of neuropathy. Therapies created for blocking the glycine transporter is an interesting new avenue and offers something genuinely unique in the treatment of patient struggling with neuropathy.

Using the concepts of pharmacognosy to approach this problem suggests some fascinating opportunities. For hundreds of years and over numerous cultures various varieties of the Ash Tree have been utilized for therapeutic applications. Native American herbalists used the bark from the Northern Prickly Ash tree for many different ailments. One of the most intriguing conditions that pertains to neuropathy is toothache. It sounds as if the ability of the bark from this prickly ash was so recognized for its tooth pain relieving qualities that it was frequently call toothache tree or toothache bush. Very recently scientists studying the effects of compound from various ash species on transmission of pain signals within a nerve complex known as the Trigeminal Ganglion (the nerve complex that is associated with toothache and other facial pains), found that chemical substances contained is ash tree bark suppressed nerve pain within this system. Their research further implied that the mechanism for this nerve pain alleviation was in connection with the capacity of prickly ash constituents to inhibit the glycine transporter pump.

This raises the prospect of utilizing prickly ash derived compounds to control the glycine transporter at the synapse while supplementing the diet with oral glycine, methylglycine or trimethylglycine that are different forms of the naturally occurring amino acid glycine.

Make sure you keep in mind not to try this or any other treatment recommendations that are publicized on the net. This short article should be used for educational purposes exclusively. Every patient is a unique individual and medical treatments truly should only be tried using the advice, approval and the direction supervision of a qualified healthcare physician.


Dr. Kukurin is a board certified chiropractic neurologist, with certification in acupuncture. He has over 25 years experience in treating neurological disorders with alternative medicine techniques. The techniques he has pioneered to treat neuropathy have been included in scientific conferences sponsored by Johns Hopkins Medical School and the at the Peripheral Nerve Society. The results his patients have obtained have been published in journals indexed in the National Library of Medicine. Dr. Kukurin has post-graduate continuing medical education through Harvard Medical School, Johns Hopkins, the Mayo Clinic and the Russian People's Friendship Medical School.

http://ezinearticles.com/?A-New-Approach-to-Neuropathy-Pain-Relief,-The-Glycine-Transporter&id=6938562

How Soon Will A Pregnancy Test Work

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View the latest health news and explore articles on fitness,t, nutrition, parenting, relationships, medicine, diseases and healthy living at CNN Health..Live a healthier life with TODAY's health tips and find the latest news for personal wellness, fitness,t and relationships..Build tests better. We've helped test and certify millions of people in thousands of organizations. By test.com Learn More.TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..What's in a Name? What Every Consumer Should Know About Foods and Flavors; 4 Medication Safety Tips for Older Adults; FDA: Cutting-Edge Technology Sheds Light on .Tech 2/16/2012 @ 11:02AM 3,063,735 views How Target Figured Out A Teen Girl Was Pregnant Before Her Father Did.

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Xixx Regina Krilow On Vimeo

Build tests better. We've helped test and certify millions of people in thousands of organizations. By test.com Learn More.What's in a Name? What Every Consumer Should Know About Foods and Flavors; 4 Medication Safety Tips for Older Adults; FDA: Cutting-Edge Technology Sheds Light .TODAY Parents is the premiere destination for parenting news, advice community. Find the latest parenting trends and tips for your kids and family on TODAY.com..View the latest health news and explore articles on fitness,t, nutrition, parenting, relationships, medicine, diseases and healthy living at CNN Health..Live a healthier life with TODAY's health tips and find the latest news for personal wellness, fitness,t and relationships.. Tech 2/16/2012 @ 11:02AM 3,063,735 views How Target Figured Out A Teen Girl Was Pregnant Before Her Father Did.

Will Quell Be The Device That Actually Works For Neuropathy Patients

Today's post from healthline.com (see link below) looks like an advert for a new product, something which this blog tries to avoid but at the same time, if something comes on the market, it is our duty to inform people who may or may not benefit and ask for user reactions and experiences. After all, it's not as if neuropathy is overwhelmed with health devices that actually work is it? Take a read and make up your own minds, then do your own research and discuss it with your doctor or neurologist. One of these days, one of these products may well turn out to be a eureka moment but in the meantime, always maintain a healthy dose of scepticism!

Got Neuropathy? Quell Offers “World’s First Pain Relief Wearable”
Written by Amy Tenderich | Published on 01 July 2015



Amongst the current flurry of wearable sensors and mHealth apps that appear to be so many elaborate toys, a new system called Quell stands out. It seems to have real potential to change lives… for many people with diabetes and beyond.

Quell is a first-of-its-kind, drug-free option for reducing the pain of neuropathy, sciatica, and other chronic pain through neural pulses — delivered by a band wrapped just below the knee, with a companion app that allows users to change settings and track sessions via a smartphone or iPad.

Its makers boast that it is “clinically proven to start relieving chronic pain in as little as 15 minutes… (with) FDA cleared prescription-strength technology that works with your own body by stimulating your nerves and blocking pain signals in your body.”

Approved by FDA last summer, Quell is just being launched now, following a highly successful Spring Indiegogo crowdfunding campaign. It was debuted to the diabetes world in a decent-sized booth at the ADA Scientific Sessions in Boston a few weeks ago. The big expo signs touting “Wearable Pain Relief Technology” were hard to ignore. I spent about 40 minutes in the booth myself, talking with their experts and getting a demo of this insipid-looking Velcro band that’s creating such a stir.

Check out their marketing video here.



My first thought was that for many of our friends in the Diabetic Community who suffer from the pain of neuropathy, Quell could certainly be a boon!

From Calf to Brain

I learned that the device, made by a startup called NeuroMetrix in the Boston area, was developed in collaboration with the renowned design firm IDEO. Users simply wrap it around their upper calf, just below the knee, and turn it on for intermittent sessions of up to 60 minutes, followed by a rest period of another hour (more than 60 minutes at a time can cause overstimulation), we’re told.

The first time you use it, you calibrate the unit by testing different vibration intensity levels and pressing when you feel stimulation (user tip: the unit needs to be held upright while you do this). The companion app remembers your settings and tracks your sessions, for your own records and to share with a doctor, if desired.

Quell works by stimulating nerves in your upper calf with neural pulses, that trigger a pain relief response in your central nervous system that blocks pain signals in your body. So it helps treat pain in the back, legs, or feet –- the pain does not have to be located at or even near the spot on your leg where the unit is worn.

“A Huge Difference”

“There’s been a ton of excitement around this because there really are so few options for treating chronic pain. Some patients are on three to five different medications, which can be addictive or have other unwanted effects,” said Alyssa Fenoglio, NeuroMetrix Director of Marketing.

Indeed, the Quell Indiegogo campaign (“The World’s First Pain Relief Wearable!”) launched in March raised $100,000 in just 1.5 days, and over $387,000 in one month, Fenoglio says. As part of that, the company pre-sold nearly 2,000 units at an introductory discount of $199 per device.

The company’s been collecting user testimonials, with dozens of people saying things like “it makes a huge difference” and “I’m getting my life back” by being able to enjoy many activities again.

"It elevates your inherent pain-modulating chemicals — at a molecular level, it's what painkillers do synthetically. But you can essentially cause a similar effect without any of the downsides by electrically stimulating to induce your brain to produce these chemicals," CEO of NeuroMetrix Shai Gozani told Fast Company recently.

The use of electrical stimulation to fight pain has apparently been around since the 1970s. But NeuroMetrix has developed a novel, convenient way to deliver its benefits.

NeuroMetrix itself began as a spinoff of the Harvard-MIT Division of Health Sciences and Technology in 1996, and has “spent nearly two decades of designing, building and marketing medical devices that stimulate nerves and analyze nerve response for diagnostic and therapeutic purposes.” Its Board of Directors includes Nancy Katz, who some may recognize as a diabetes expert who serves as VP of Consumer Marketing and Market Development at Medtronic.

Supply and Demand

Quell likely will not be covered by insurance, but it can be purchased using FSA debit cards. You can obtain Quell through selected physician’s offices (they’re expanding that network) or by purchasing it directly from the company online. The price is $249 for the device, plus $30 for a package of two replacement electrode strips, which need to be changed out every two weeks because sweat and oil from the skin wear them out, Fenoglio says.

OK, so if used regularly, the cost adds up to a little over $600 for the first year, and then ca. $360 in following years, which is less than the annual cost of prescription pain relief meds like Lyrica and Cymbalta — but without the side effects of weight gain, foot swelling, drowsiness and more. Not to mention potential negative drug interactions and long-term effects.

The Quell companion app is free to download and lets users track the number of sessions per day (time and intensity), change settings, and get alerts, such as when they are nearing the point of overstimulation or when it’s time to change the electrode strip.



The app also includes an accelerometer that can track activity and sleep (Quell has FDA clearance for nighttime use), so users could track the correlation of decreased pain with better sleep and more exercise over time, for example. With users’ permission, the company also plans to use data from the app to study Quell’s performance.

Got Neuropathy?

Seriously, who wouldn’t be interested in a non-invasive, drug-free, relatively affordable and easy-to-use wearable to reduce chronic pain?

My hope is that NeuroMetrix gets connected with efforts like the Diabetes Hope Conference, where people with diabetes meet online to discuss living well with complications like painful neuropathy. Because this is one Internet of Things/Health Wearable Gadget that the Diabetes Community ought to take seriously, IMHO.

http://www.healthline.com/diabetesmine/quell-neuropathy-pain-relief-wearable#1

How Much Longer Will Lyrica Be A First Choice Neuropathy Drug

Today's post from sciencedaily.com (see link below) needs to be taken seriously, if only because it comes from sciencedaily.com, which is one of the most trusted medical sites on the internet. You may wonder what an article about birth defects has to do with neuropathy but the common link is the drug pregabalin (Lyrica). Despite Pfizer withdrawing its own recommendation for Lyrica for many forms of neuropathy as long ago as 2013 and despite the mounting evidence of the harm it can do, it remains one of the most widely prescribed mainstream drugs for nerve pain across the whole world. The reasons for this are unclear but you have to suspect the mass marketing of the drug still goes on and of course doctors still make use of so-called 'off-label prescribing because the right information is not getting through. This particular article looks at the evidence of the potential for birth defects due to pregabalin but this is just the latest in a long line of contra-indications for Lyrica. If it is prescribed for your neuropathy symptoms, you should probably have a serious discussion with your doctor and maybe take along some of the evidence you can find here on the blog (type 'pregabalin' in the search box to the right of the page) because there's a distinct possibility that it may do you more harm than good.

Drug used for pain, anxiety may be linked to birth defects 
Date: May 18, 2016 Source: American Academy of Neurology (AAN)

A drug commonly used to treat pain, epilepsy, anxiety and other brain health disorders may be associated with an increased risk of major birth defects, according to a study published in the May 18, 2016, online issue of Neurology®, the medical journal of the American Academy of Neurology.

The drug pregabalin is approved by the FDA to treat epilepsy, fibromyalgia and neuropathic pain, such as pain from diabetic neuropathy or pain after shingles or spinal cord injury. It is also used for generalized anxiety disorder and other mental health issues. This is called off-label prescribing.

For the study, information was collected in seven countries from 164 women who took pregabalin during a pregnancy and 656 pregnant women who were not taking any anti-seizure drugs. The women or their practitioners were then contacted again after their expected date of delivery.

Pregnancies of the women who took pregabalin during the first trimester of pregnancy were three times more likely to result in major birth defects than those of the women who did not take anti-seizure drugs. Seven of the 116 pregnancies in women taking anti-seizure drugs, or 6 percent, had major birth defects, compared to 12 of 580 pregnancies, or 2 percent, in women who did not take the drug. Birth defects due to chromosomal abnormalities were not included in these results.

The major birth defects included heart defects and structural problems with the central nervous system (CNS) or other organs. The women taking pregabalin were six times more likely to have a pregnancy with a major defect in the central nervous system than women who were not taking the drug, with four CNS defects out of 125 pregnancies, or 3.2 percent, compared to three CNS defects out of 570 pregnancies, or 0.5 percent.

Of the women taking pregabalin, 115 were taking it to treat neuropathic pain, 39 were taking it for psychiatric disorders, including depression, anxiety, bipolar disorder and psychosis, five were taking it for epilepsy and one was taking it for restless leg syndrome.

A total of 77 percent of the women started taking pregabalin before they became pregnant. The women in the study stopped taking the drug at an average of six weeks into their pregnancies. Of the women taking pregabalin, 22, or 13 percent, were also taking another anti-seizure drug.

"We can't draw any definitive conclusions from this study, since many of the women were taking other drugs that could have played a role in the birth defects and because the study was small and the results need to be confirmed with larger studies, but these results do signal that there may be an increased risk for major birth defects after taking pregabalin during the first trimester of pregnancy," said study author Ursula Winterfeld, PhD, of the Swiss Teratogen Information Service and Lausanne University Hospital in Lausanne, Switzerland.

Winterfeld said, "Pregabalin should be prescribed for women of child-bearing age only after making sure that the benefits of the drug outweigh the risks and after counseling them about using effective birth control. In cases where women have taken pregabalin during pregnancy, extra fetal monitoring may be warranted."

Story Source:

The above post is reprinted from materials provided by American Academy of Neurology (AAN). Note: Materials may be edited for content and length.

Journal Reference:
Ursula Winterfeld, Paul Merlob, David Baud, Valentin Rousson, Alice Panchaud, Laura E. Rothuizen, Nathalie Bernard, Thierry Vial, Laura M. Yates, Alessandra Pistelli, Maria Ellfolk, Georgios Eleftheriou, Loes C. de Vries, Annie-Pierre Jonville-Bera, Mine Kadioglu, Jerome Biollaz, and Thierry Buclin. Pregnancy outcome following maternal exposure to pregabalin may call for concern. Neurology, May 2016 DOI: 10.1212/WNL.0000000000002767

https://www.sciencedaily.com/releases/2016/05/160518170014.htm