How Important Is Vitamin B In The Treatment Of Nerve Damage

Today's post  from cidpneuropathysupport.com (see link below) looks at the role of Vitamin B in both the prevention of and treatment of neuropathy. This article looks at it from the inflammatory neuropathy angle but it can be argued that all neuropathy is inflammatory by nature. The nerves become inflamed and/or damaged through inflammation and a vitamin B deficiency is often seen as contributing to that. That said, you need to be tested by your doctor to establish a deficiency before embarking on vast amounts of supplements. For neuropathy patients with a normal Vitamin B level, there'll be enough extra in your daily multivitamin. There are also different forms of vitamin B and excessive amounts can bring about side-effects - best discuss it with your doctor.

CIDP Type Neuropathy and Vitamin B
Author: Shiraz Abbas May 27, 2017

Studies are now suggesting that vitamin B may have an important role in healing or easing the pain of peripheral neuropathy and CIDP type of neuropathy in particular.

Peripheral neuropathy is a disorder of the peripheral nerves. It is often characterized by weakness of limbs, numbness and pain. CIDP type neuropathy is a form of neuropathy in which there is a progressive and gradual destruction of the nerves through inflammation.

The vitamin B family of vitamins (also known as B complex vitamins) are critical for the proper functioning of the human body. They play a role in our immune system, energy, and red blood cell formation. Vitamin B12 is particularly important for neurological health and is a vitamin of choice to help treat neuropathy.

Vitamin B is commonly used to treat neuropathy. According to one study, people given high doses of vitamin B for four weeks had their pain reduced and saw improvement in their vibration perception threshold (VPT), that is, a testing that is used to measure large nerve fiber function in the body. People with lesser doses in a 8 week span saw lesser improvement.

Deficiency in B vitamins may lead to neurological problems. B12 in particular is important for the development of the central and peripheral nervous system. It has a critical role in maintaining the myelin sheath which ensures the transmission of nerve signals in the central and peripheral nervous system.

In neuropathy, especially CIDP type neuropathy, the signals between the spinal cord and other parts of the body are disrupted. With CIDP in particular, the myelin sheath is gradually but progressively damaged through inflammation and hence leading to an impairment of the transmission of nerve signals. This process of demyelination leads to axonal destruction. The disease is thus characterized by the following symptoms: weakness of the limbs, numbness, tingling sensation and pain. Loss of sensation and activity also happens depending on where the damage is occurring.

As B vitamins, particularly vitamin B12 play a role in maintaining a healthy peripheral nervous system, the vitamin may also play a role in the reconstruction of the nerves and more particularly the myelin sheath and hence helping the reduction of pain and improving sensation.

Some people with neuropathy may not be able to absorb vitamin B12 due to the loss of the “intrinsic factor” that is produced in the stomach and hence the loss of ability to absorb B12 through the digestive tract. In these cases like these, B12 may be injected into the body. Please check with your doctor if you have digestion problems with it comes to B12.

For those who can absorb it through the digestive tract, the following foods are high in B12 in addition to B12 supplements:

Beef Liver (71 mcg for a three-ounce serving, provides 2951% of the daily recommended intake).
Mackerel (16 mcg for a three-ounce serving, provides 661% of the daily recommended intake).
Sardines (8 mcg for a three-ounce serving, provides 333% of the daily recommended intake).
Read Meat (5 mcg for a three-ounce serving, provides 208% of the daily recommended intake).
Salmon (4 mcg for a three-ounce serving, provides 167% of the daily recommended intake).


Shiraz Abbas is the founder and manager of the CIDP Neuropathy Support Group. He is also one of the main community educators of IVIG therapy. He resides in Fresno, California. Shiraz can be contacted through our free CIDP advice service at 1-855-782-0574.

http://cidpneuropathysupport.com/cidp-neuropathy-and-vitamin-b/

Were You Relieved When You Were Diagnosed With Nerve Damage

Today's post from themighty.com (see link below) reflects, by means of a personal story, what millions of neuropathy sufferers across the world feel before they receive their definitive diagnosis. It seems astonishing in this day and age that we have to jump through hoops of disbelief, suspicion, inaccurate evaluations and faulty diagnoses before a medical professional finally comes up with the answer but it still happens continually in 2016. Naturally, the more neuropathy hits the news, the more patients will have light bulb moments and emerge from the darkness but is the medical profession ready for it? Not by a long chalk! Not only are we prescribed the same medications that were issued 30 years ago but the time scale between symptoms and diagnosis is unforgivably long. Add on to that the general lack of expert knowledge among doctors and you have patient frustration on a massive scale. That said, it is changing and the medical profession and pharmaceutical companies are finally waking up to the problem and working on solutions but hey...it's about time! The author of this article's patent relief at being given a diagnosis is therefore perfectly understandable. Do you recognise yourself in her story? I have a feeling you will.
 

Why I'm Happy I Received Diagnoses of Neuropathy and Myopathy  
11/19/16 By Jen Hardy Contributor I write about Hereditary Neuropathies
 
Let me start by saying I do not want to be sick. I am not lazy, or trying to get attention. What I do want is a diagnosis, so medical professionals can treat my symptoms, and if possible, heal me. There are so many people who do not understand people with chronic illness and why we want a diagnosis so badly. I want to share my story so I can help other people understand how difficult it is to live with unidentified health issues.

As a young girl, I spent a lot of time during my non-school hours in bed and on the couch. My parents chalked it up to me being a lazy person, but when I would get bursts of energy, I’d be out doing all I could, and I didn’t feel lazy! In middle school P.E., I would always stop running because of sharp pain and a burning sensation in my chest. Again, I was labeled as lazy and told to work through the pain. (Twenty-five years later, we would discover I had asthma.) My parents had me in soccer and softball for several years, but I would get worn out quickly, begging to be benched after a few quarters or innings. As you see, there was a pattern. High school went on the same way, only with the emergence of back pain on top of everything else.

I started falling down in my early 20s. People just thought that was funny. “Look how clumsy she is,” they said. Everyone thought I was both lazy and clumsy. I had x-rays and all the standard blood tests, but nothing was showing up. After I had a couple of children, my energy plummeted, but after seeing a variety of doctors, and with a chart thicker than a Harry Potter book, I still had no diagnosis. The medical and family consensus was that I was fine, lazy, and maybe a little depressed. I was a little depressed; my body was betraying me and I didn’t know why. Not only that, but no one who was close to me believed what I was saying.

In my 30s, the pain became more intense. It was difficult for me to get around, and I was becoming more unsteady. My pain was mostly in my back, but slowly creeping in a little bit everywhere else too. “Where did it come from? Why was it there?” Those were my questions. What answer did I get? “You must want drugs.”

Through all of this, I would argue with anyone who told me to take so much as an aspirin. I was so anti-any-medicine that wasn’t absolutely life-saving that taking strong pain killers was out of the question. I wanted a permanent solution, not a temporary fix. Again and again and again I was asked, “Why do you want something to be wrong? Why do you keep looking for something to be wrong with you? Why can’t you just do what you’re supposed to do like everyone else?”

I was told by those close to me, “Obviously if the doctor says nothing is wrong, then nothing is wrong.” And, “I’m certainly not going to help you get things done when you are perfectly capable of doing them yourself. Stop being lazy and snap out of it!” But more symptoms kept emerging, and I just kept asking questions, and going to doctors, and not giving up. It’s not easy to keep that up when you feel miserable.

A good personal support system helps not only physically, but emotionally as well. When I was 40, I married a soldier. He not only fought for our country, but he fought for me. He went to doctors with me and explained things when I couldn’t, he helped me to remember to take my medicine when I was too tired to remember by myself, and he always had faith that we would find help and I would get better. With his help, I found a pulmonologist who discovered that I have asthma and sleep apnea. Treating those helped some of my symptoms, but there were still several things going on with my body that no one could figure out.

In my early 40s, my husband got sick with what we thought was a cancerous kidney tumor. I didn’t want to tell him that I’d fallen down the stairs twice in one week, but my sister-in-law did. He immediately sent me to the doctor, where I got an MRI of my back, and they finally found something. Ironically, they didn’t actually find it, they said it was still there! A diffuse atrophy that was found in my back seven years earlier that no one ever mentioned to me. The muscles outside of my lower spine had completely atrophied and been replaced by fat. How could this have happened? Why? We didn’t know, but it explained the pain, weakness, and falling I’d been experiencing for years.

I saw several neurologists. My second one actually told me I had too many symptoms and had to pare down my symptom list for him to be able to help me. “Which symptoms are the right ones?” I cried, but he didn’t know, so it was time to find another neurologist. It is so important for patients to keep searching until they find a doctor who listens to them. If I had listened to the first doctors, I might not be here today. I was misdiagnosed and put through risky treatments that didn’t help, and even a major surgery I didn’t need.

I finally went to a new doctor, my eighth neurologist, who sent me to another neurologist 300 miles away at a medical center that specializes in rare neuromuscular diseases. Finally, the wrong diagnosis was officially ruled out. We also found out answers to the health questions I’d had for years. I don’t have one neuromuscular disease, I have two: neuropathy and myopathy. That’s why I had too many symptoms. That’s why none of it made sense. That’s why no one believed that I was telling the truth. It seemed like too much. Like I was making it up.

We now have names for four out of five of my main diseases: asthma, arthritis, sensory neuropathy, and sleep apnea. The fifth is idiopathic myopathy for now. That means I have a muscle wasting disease and no one knows the cause. I’ve had medical testing, the likes of which I wouldn’t wish on my worst enemy, to get to the root of it, but we’re still waiting for the final results. If they’re negative, it means my disease is so rare, it hasn’t even been discovered yet. But my ninth neurologist has done the testing necessary to know I have a serious disease. My body is like a snowman in February; the thaw is coming, we don’t know when, and little bits of me melt away as we wait.

I don’t want to be sick. I don’t want to have an illness. But I do. And because I have fought to find someone to believe in and help me, I have found answers and now I have help managing my pain and fatigue. I still don’t know what’s causing my muscles to atrophy, but in July 2016 I found out that I have neuropathy and myopathy. That’s where most of my system-wide pain is coming from, that’s why I fall, and the muscles that are left work so hard I get fatigued doing the most mundane things.

I’m very happy to finally have a name for what’s been happening to my body for years. I’m not happy because I’m chronically ill. No one wants to be chronically ill, but we do want to be helped. And that’s what a diagnosis does. It helps us get the treatment we need, and live happier, more productive lives.

https://themighty.com/2016/11/ive-been-diagnosed-with-neuropathy-and-myopathy-so-why-am-i-so-happy/

Antibiotics And Nerve Damage A Professionals View Vid

Today's post from medscape.com (see link below) is text/transcript and video talking about the link between certain antibiotics and nerve damage. There are many more articles here on the blog about the dangers of fluoroquinolone antibiotics for actual and potential nerve pain patients but this one broadens the list to include other antibiotic types as well. The article is not really aimed at patients trying to understand what sort of risks they are facing but it's always useful to hear discussion among professionals on this sort of subject. The conclusion is that if you are prescribed antibiotics by your doctor, it's always wise to have a somewhat deeper discussion, mentioning that you are concerned about the side effects on your nervous system.

Antibiotics and Neuropathy: What's the Latest?
Paul G. Auwaerter, MD Disclosures September 17, 2013

Hello. This is Paul Auwaerter from the Johns Hopkins School of Medicine, talking about peripheral neuropathy and antibiotics. This is not a topic that many in the infectious diseases community spend much time dealing with, but it recently came to our attention because of upgraded warnings to the class of fluoroquinolone drugs (such as ciprofloxacin), which may be associated with an irreversible peripheral neuropathy. The US Food and Drug Administration's Adverse Event Reporting System has received increasing numbers of reports of neuropathy.[1] Peripheral neuropathy has been included on the labeling for fluoroquinolones going back to 2004 as a warning, but there is a paucity of medical literature about this association.[2] These drugs are widely used. Rare adverse effects, such as tendon rupture and tendinopathy, have received increased press as we have had more experience with this drug class. The fluoroquinolones have been very well accepted by most of the medical community because of a generally good side-effect profile, although they have many peculiarities, such as QT prolongation.

Peripheral neuropathy is not generally associated with antibiotics.[3] The drug most often associated with peripheral neuropathy is isoniazid (INH), which is used for tuberculosis.[4] INH interferes with pyridoxine -- the vitamin B6 component of the metabolism of bacteria -- and causes B6 deficiency. This effect is enhanced in humans who might be "slow acetylators," so they accumulate very high levels of isoniazid, which could lead to toxicity. The best estimate of risk for INH toxicity is 0.2%-2% of people on long-term therapy. It usually occurs after 6 months of therapy and is usually reversible when the drug is stopped. Generally, the people who develop this complication also have comorbid conditions such as HIV, alcoholism, diabetes, or renal insufficiency.

By no means is it clear to me, at least from available data, that the story is similar for the fluoroquinolones. Whether neuropathy occurs only with long-term therapy or can occur with short-course therapy is unclear. Other antibiotics can cause neuropathy, and in my experience this typically happens with long-term administration. The drugs capable of causing neuropathy include linezolid, chloramphenicol (a drug that we don't use very much anymore), metronidazole, sulfonamides, colistin, and dapsone. Even the penicillins are capable of causing neuropathy.
The cause is not clear, although some recent work has been done by James Collins and colleagues at Boston University.[5] They are beginning to look at a systems biology approach with respect to the effects of antibiotics, not only on bacteria but also on the host. They have found that some bactericidal (rather than bacteriostatic) antibiotics can increase reactive oxygen radicals and also affect mitochondrial function. These may be some of the ways that these drugs affect different cellular structures in humans.

Antibiotics have been a godsend to our ability to thwart illness, but they do have collateral damage. We have always known this, but it is becoming increasingly recognized. Therefore, it is always good to be as cautious as possible and, when using antibiotics, to be aware of the possible side effects. At least for now, I won't change my practices because of this warning, but with long-term use of fluoroquinolones, I will perhaps be more appreciative of this possibility and stop the antibiotics at the first signs of any numbness or tingling.
References
Medscape Infectious Diseases © 2013 WebMD, LLC
Cite this article: Antibiotics and Neuropathy: What's the Latest? - Medscape - Sep 17, 2013.

http://www.medscape.com/viewarticle/810905

Fluoroquinolones Another Warning About Nerve Damage

Today's post from stonehearthnewsletters.com (see link below) is another forceful article about the dangers of Fluoroquinolone, antimicrobial antibiotics (Levaquin, Cipro,Avelox etc) to nerve damage patients or even those who don't as yet suffer nerve damage. The evidence is now pretty much overwhelming that these antibiotics should be avoided or at least properly discussed with your doctor. Even the FDA has forced manufacturers to clearly state the dangers on their packaging. They can cause mitochondrial toxicity (simply put, they can attack the mitichondria, the energy powerhouses of nerve cells and essential for good working order) and if you already have neuropathy, make it considerably worse and if not, actually cause it. They are so widely prescribed that they're practically medical M&Ms but please talk over any prescription with your doctor or specialist, before taking them - there are alternatives available.
 

Levaquin, Cipro, Avelox May Result In Neurodegenerative Diseases 
Posted on September 2, 2014 by Stone Hearth News

HAMILTON, N.J., Sept. 2, 2014 /PRNewswire-iReach/ – Four years ago, Lisa was a physically active and healthy 45 year old. She would frequently unwind at the local gym after spending a long day on her feet teaching a class of energetic elementary school students. All of that changed dramatically when she took an antibiotic for a sinus infection. Lisa’s doctor prescribed the popular antibiotic, Levaquin, a drug she was told was safe. She became so disabled, she was unable to continue working. Lisa’s doctor was at a loss to explain the sudden onset of these painful, debilitating symptoms, particularly when they continued to worsen months after she had stopped taking the antibiotic.

Levaquin belongs to a class of antibiotics called Fluoroquinolones. Originally manufactured to treat serious, life-threatening infections, they have been increasingly used for minor infections and, in some cases, when no infection exists. A common misconception is that they are safe, despite several Black Box warnings, which include Central Nervous System (CNS) dysfunction and increased risk of tendon rupture. In August 2013, the FDA strengthened Levaquin’s warning to include the risk of Peripheral Neuropathy, which can be permanent.

While doctors have struggled to explain Fluoroquinolone Toxicity Syndrome, part of the explanation may be found in an April 17, 2013 FDA report which indicates Levaquin, Cipro, and Avelox may cause Mitochondrial Toxicity. This report, obtained through a Freedom of Information request, states that Mitochondrial Toxicity is implicated in serious, life-threatening neurodegenerative conditions, such as Parkinson’s, Alzheimer’s, and ALS.

Based on this 2013 FDA report, signed by an FDA Acting Division Director, Dr. Charles Bennett from the University of South Carolina, submitted a Citizen Petition to the FDA requesting a Black Box warning be added to the Levaquin label which would warn doctors and patients of the risk for Mitochondrial Toxicity.

Quinolone Vigilance Foundation (QVF), www.SaferPills.org, a non-profit, charitable organization that fosters, initiates, and funds research on Fluoroquinolone Toxicity, supports the Citizen Petition. Rachel Brummert, QVF Executive Director, herself injured by Levaquin in 2006, was diagnosed four years later with Neurosarcoidosis, a degenerative neurological disorder that is linked to Mitochondrial Toxicity. “The failure by the FDA and drug makers to adequately warn the public puts patients at an alarmingly high risk of developing life-threatening neurodegenerative disorders,” said Brummert. “We call on the FDA and drug makers to protect the American public and issue this important warning immediately.”

John Fratti, also damaged by Levaquin and is a staunch advocate for additional Black Box warnings, agrees with Brummert. “Doctors and patients should not have to obtain drug safety information through a Freedom of Information Act request. The boxed warning requested by the Citizen Petition is needed immediately.”

For Lisa, who still struggles with the aftermath of the damage caused by Levaquin, the requested Citizen Petition Black Box warning will come too late. It may, however, prevent others from suffering a similar fate.

Media Contact: Rachel Brummert, Quinolone Vigilance Foundation, 609-575-9839, rachel@saferpills.org

News distributed by PR Newswire iReach: https://ireach.prnewswire.com

SOURCE Quinolone Vigilance Foundation

http://www.stonehearthnewsletters.com/levaquin-cipro-avelox-may-result-neurodegenerative-diseases/neuropathy/

Socks With Sensors To Prevent Neuropathic Foot Damage Vid

Today's long post from healthline.com (see link below) is nevertheless an easy and interesting read that will appeal to many readers with neuropathy in their feet. It's important to state right from the start that these socks (subject of the article) will do nothing to prevent or improve your neuropathy but will alert you to any physical danger (e.g. ulcers) that you may not notice due to lack of feeling and as such can be seen as a valuable tool in harm prevention. As is clearly stated: "We don't prevent neuropathy, we prevent the complications that come with neuropathy. We prevent ulcers and amputations." That said, the article does read a little like an extended advertisement for a product and this blog tries to avoid anything with potential for commercial gain. However, the story behind the development of these socks does suggest a genuine interest in improving the lot of neuropathy sufferers and more than that...it makes sense. It's also clear evidence of the potential for modern technology to improve people's health. It's long but absolutely not tedious and is well-worth a read.

Siren Socks: Revolutionizing Diabetes Foot Care with the Internet of Things
Written by Amy Tenderich | Published on February 27, 2017

Got neuropathy in your feet?

We hope not, but if you do -- or suspect that you might -- you will absolutely want to know about a new company called Siren Care. It was founded by young Chinese-American entrepreneur Ran Ma, who after completing a Biomedical Engineering degree at Johns Hopkins University, freaked out her parents by spending hours holed up in her bedroom sewing socks.

She had a brilliant idea to embed tiny sensors that would connect to an app to track temperature and localized ulceration risk. It panned out big-time!





The socks she invented recently won the coveted TechCrunch "hottest new hardware" award at CES, and the 2016 Health 2.0 "best newcomer in digital health" competition. And medical experts are now saying "what they have done with embedded IoT (Internet of Things) sensors and smart materials will totally redefine how patients can self-manage complications as a routine part of their daily life." Wow!

Please join us for this chat wth Ran to learn about Siren Socks, and possibly win a set of your own!

Q and A with Ran Ma, on Siren Socks for Diabetic Foot Care

DM) Ran, pioneering ‘smart socks’ for diabetic neuropathy is a pretty unique path... Can you share a bit about how you got here?

RM) I was born in China but I grew up in Texas and then I lived in Baltimore, Chicago, Denmark, Sweden, Germany and now back to the States in San Francisco.

My background is biomedical engineering. I studied at Johns Hopkins, and then afterwards, I actually worked in the Department of Plastic Surgery at Northwestern, under Dr. Maldonado. While I was there, I worked on a project called Biomask. We actually developed a wearable mask that would regenerate your face, using stem cells, and this was targeted for burn victims and war veterans. This was right after the Iraq war and because of the research we did, I learned a lot about wound healing, wound formation, also wound prevention. My lab also worked on diabetic foot ulcers. That's just something that really stuck in my mind.

I also come from three generations of doctors -- so my grandparents, my aunts, uncles, and my parents are doctors. My father's actually a surgeon. He cuts people every day and for me, I want to dedicate my life further up in the chain of medicine, towards the side of prevention. I really want to make great tools that are easy to use, and give people the right data at the right time, so they can take control of their own health. I always say if I do my job right, I could put my parents out of a job.

Do you have a personal connection to diabetes?

No I don’t, but my co-founder Jie Fu has lots of diabetes in his family, and some of his relatives have unfortunately suffered some of the more severe consequences.

As noted, both my parents are physicians in China – my mom does hematology so mostly leukemia, and my father works on cervical and ovarian cancers, so very late-stage cancers and they lose a lot of their patients unfortunately because it is so late-stage. That's why I want to focus on prevention.

For me, it's about knowing that diabetic foot damage is a very serious problem with very severe consequences, but it's preventable and there's strong clinical research showing that temperature monitoring can make a big difference in prevention.

So you came up with this ‘crazy idea’ to embed sensors in socks?

Here I was a biomedical engineer who was going to go to medical school, and I told my parents, ‘You know what? I'm sewing socks in my room by myself.’ My parents thought I had lost my mind. I was buying components off the Internet and just sewing it together… because it's one thing to have an idea in your head, but another to put it into physical form.

So I had this sock that was all misshapen, connected to a circuit board with all these wires coming off it (and) I went to the big annual Diabetic Foot Conference DF Con two years ago and basically said, ‘Hey, podiatrists, I'm gonna make a sock, it's going to detect injuries in real-time and then it's going to connect to a phone and your patients are going to be able to wear this and it will be soft and washable.’ And they looked at me like I was crazy, basically... because the early prototype really was just crazy-looking, but we’ve come a long way.




Fill us in on your current team, headquarters and manufacturing facilities?

The company was founded in February 2015 by myself and two co-founders: Jie Fu, whose background is electrical engineering and hardware mass production, and Henk Jan, whose background is global textiles sourcing -- he worked in the textile industry and he set up one of the world's largest manufacturing groups for textiles.

So our leadership is made up of biomedical engineering (my background), electrical engineering, and textile manufacturing. We have a team of 5 and are currently expanding.

Our headquarters are in downtown San Francisco, and we’re currently doing some manufacturing in China, with final assembly in the U.S. We plan to move more of the production to the U.S., but that's still in the works right now.

Hasn’t it been common knowledge for a long time that temperature monitoring can help with foot health? If so, what’s really so revolutionary about using this technology in socks?

You're absolutely right. Temperature monitoring has been around for at least a decade or more and it's been published in Diabetes Care and other leading journals by Dr. Lavery and Dr. Armstrong. But there's been a lack of technology.

A few years ago the technology didn't exist to make a wearable device for temperature monitoring, right?
 In recent years sensors are getting smaller and cheaper and people are putting them in bands, like Jawbone, etc. and all of this has happened because of the emergence of IoT (Internet of Things) tech. Now sensors have gotten small enough that we can actually incorporate them into fabric.

The other thing that has happened is a revolution in design thinking. As you well know at DiabetesMine, even just a few years ago the focus was, ‘This works in clinic, great!’ but (no one was) thinking about it from the patient’s side – as in:

‘If I were living with diabetes, could I use this tool?’ Even though it works in clinics, even though my doctor can use it, does it actually make sense for me to take these bulky tools home? 


There are other solutions on the market: temperature monitoring wands like the TempTouch foot thermometer, a temperature monitoring carpet and a bathroom scale, and I think those are really great and very pioneering in the field. Our team's goal is at-home prevention, empowering the user by creating something that’s easy to use and monitors continuously, so you can have a sense of security at home. So that's why we're focused on a wearable solution.

OK, so how exactly do new ‘smart’ Siren Socks work?

They monitor six spots on your foot, based on the six most common sites of injury according to clinical trials, and we actually monitor your two feet and compare the temperature difference between the same spot on each foot.

When you have a difference of more than 4 degrees Fahrenheit or 2.2 degrees Celsius, then we know that inflammation is occurring, and that means your body is fighting off injury; that's when we give you an alert on your phone. The point is, something has happened and your body is fighting that injury, reacting with inflammation and that's followed by a rise in temperature. We pick up on that and we alert you. 



And you offer the first continuous temperature monitor for feet, right?

Yes, it's very important for us to be a continuous monitor: All the other solutions mentioned are point solutions, meaning you take one measurement a day. You don’t know what happened before or afterwards -- what about the other 23 hours and 50-something minutes in the day? Since there's no reference, it’s even harder to determine why changes might occur.

Because we take so many measurements over time, we're able to filter out false positives. If it's a random spike (in foot temp), we know that's not normal. Inflammation is a sustained temperature difference averaged over time, it's a very particular signature and that's what we can pick up with our socks.

Another benefit is personalization. Maybe for you, one of your feet is just warmer because you have circulation problems or it’s just genetic. Our technology creates a baseline per user over time, so it's a lot more powerful smart tool that can learn from you over time.

Wait, if you’re targeting people already living with neuropathy or other foot conditions, how are these socks ‘preventative’?

We don't prevent neuropathy, we prevent the complications that come with neuropathy. We prevent ulcers and amputations.

What happens to people with neuropathy is they have a foot injury and don't realize it for a week, two weeks, two months even I've seen. And then you go see your doctor and the first thing they do is wheel you into the surgery room!

With our socks, if you have an injury, you might not feel it but you’ll see it with temperature and we alert you. Then you go see your doctor and he/she makes a diagnosis with the X-ray or with a physical exam and then treats you for it. Just from temperature we cannot possibly know if it's just a callous, or a blister, or Charcot foot – so you need to see your physician. But the early detection helps you avoid ulcers or even needing an amputation.


Don’t the embedded sensors, and that little anklet disc on the side, make the socks lumpy?

No, we take very tiny proprietary temperature sensors, like a grain of sand, and incorporate them into the fabric of the sock, and they send data to our companion app via Bluetooth. The anklet holds the battery and BLE chip. We've designed it to have the thinnest profile and smallest surface area possible, and we are always working to further miniaturize this component.

Back when I was hand-sewing them two years ago, you could definitely feel everything, but now… they are really good diabetic socks. The key point to making smart clothing is you have to make really good clothing first. If I gave you the socks right now, you would never know they were smart socks because you couldn't find the sensors.

Can you wash them like normal socks?

Yes, our socks are machine washable and dry-able, you don't have to charge them, and they're completely soft and flexible. They're super-absorbent and have no seams on the outside or inside, and we all know that's important because diabetic socks should be seamless so you don't have any pressure points on your feet. Right?

So we're really creating a great diabetic sock to start with and then we give it intelligence, to protect your feet.




How does the Siren app work?

The basic functions are of course that you can see the current status of your feet and it's very easy to understand, color-coded green, yellow, and red. And of course we walk you through the recommendations when an injury or potential injury is detected. The app may suggest checking your feet, reducing activity or reaching out to your healthcare professional.

You can see your foot temperature over time, and your foot health over time and that helps you know, when did this inflammation begin? This is why continuous use is important. You can see for example if inflammation was caused because every day you're wearing a certain pair of shoes that are just too small. One of the main causes of diabetic foot ulcers are shoes that are too small -- because if you can't feel pain, you don't realize you're buying shoes that are too small. So our app actually helps people start looking at their habits.




Can you share the data directly with your doctor?

Right now the Siren app basically sends you alerts on your smartphone if there are significant changes in your foot temperature – it’s alerting you to go see your doctor. The data is in the cloud and you access your account on our website or though the app, where you can easily print it or send it to your doctor in file format, but we don’t have direct data-sharing yet. That’s something for the future.

Also, at the end of the year we're going to be rolling out a solution for people living with diabetes that don't have access to a smartphone, like what we're offering but online (instead of app-based) so you can also use our smart socks without a phone.

Eventually we’d like to have a Call Center that can alert users who can’t get those alerts and alarms on a phone.

Can you add notes into the app, like about what shoes you wore or what activity you did that day?

Yes, people can add notes like, ‘Wore my new whatever-shoes,’ and then you may notice the next day after wearing this pair, you're always getting inflamed, so you can think maybe it's those shoes. It really often is the shoes you wear, and that's something you can pick up on.




In the app you can also check the battery life of your socks, track how often you wore them, which ones you're wearing, and how often you washed them. I think one of the key items is, we can tell you this week you only wore your socks 40% of the time, so maybe next week you can aim to wear them 60% of the time. The more often you the wear socks the more protected your feet are. And if you have neuropathy, you have to wear good socks anyway. That's the number one recommendation, right? We help you quantify that.

So this has big potential to help anyone with diabetes, type 2 or type 1?

Neuropathy can happen to anyone. It does happen to people with type 1 and type 2. It's usually a little bit older population, but I've also seen it in people in their 20's and 30's. It just happens, your nerves start dying, getting eaten away and it usually happens in your feet and hands first, because those are your longest nerves. Hands are not as dangerous because you see your hands every day, but you don't check your feet every day or look at them as closely, so damage can go unnoticed. That's why it's very important to take care of your feet.

Have you completed clinical studies on Siren Socks, showing effectiveness?

We did an initial small test and are now scaling. We’re actually recruiting patients right now with Dr. Reyzelman, a podiatric surgeon at UC San Francisco. This will be a published result, ongoing into March including 30 patients.

I'm also giving a talk at this year’s DF Con Diabetic Foot Conference, at the end of March. That’s the biggest diabetic foot conference in the U.S. and I’ll be presenting the background of temperature monitoring, the current form factors, and why it was important to bring up a smart sock to fill the technology gap right now. And hopefully we'll have some initial results that I will present at that conference. It's a huge deal for me to be a speaker there, because as noted, I went to this conference a few years ago with a VERY rudimentary prototype and I think I scared some of the physicians there. So now two years later, we've progressed so much.

What’s the situation with regard to FDA approval?

We are very firm in saying that we are a tool and not a diagnostic, and that doesn't currently fall under FDA scrutiny.

The studies we’re doing are more to test compliance and user experience. We have entry interviews and exit interviews. So we ask, ‘Do you enjoy the solution? Is it easy to use? Do you like the colors?’ Very basic questions like that are important because we already know that temperature monitoring works, there's no doubt about that. But we need to know: can people use this solution? It’s important to do field studies where you even go into people’s homes to see how they use it, how does it work for them?

Tell us about the prestigious TechCrunch award you received for Siren Socks...?

We just won the TechCrunch Hardware Battlefield competition at CES in January, and that was a huge deal, as they screen I think somewhere around 1,000 of the newest, hottest hardware companies and they narrowed it down to 12.




Twelve went on stage and did a live demo and then they narrowed it down to four, who did a final demo, and they picked one, and we were actually that one! It was a huge honor, we didn't think we would get that far because most of the other companies were one or two or three years older than us.

But I think one of the reasons that we made it so far is that we actually brought a patient on stage, Judy, who has been living with diabetes for seven years. She is 73 and has retinopathy and neuropathy – we had to help her on stage because the lights were so bright. She actually wore our socks on stage and we live-streamed her foot data, so it really made the story make sense, you know when you see these socks in action. You could see how much Judy enjoyed wearing them, she was modeling them in front of the judges and we think that’s great because it helps raise awareness that diabetes touches the lives of so many people.

And you won an influential Health 2.0 competition as well?

Yes, in Fall we also won Health 2.0 Launch, which is strictly digital health, encompassing software and hardware. You know, they’ve had some really great companies that have won over the years, like Basis that was purchased by Intel, Glimpse that was a runner-up and they were recently acquired by Apple, and Castlight Health also went through there. They definitely pick winners.

That one is more bragging rights than an investment prize, but TechCrunch… really brought a lot of momentum to our fundraising. We are raising our seed round right now and I must say it's going very well, especially after CES.

Wait, so you did all this pre-seed funding?

Yes exactly. We had a very small pre-seed round of about $500K last year, but most of the other companies that went on stage with us had raised $4-$5 million seed round and they were raising their A Round financing already, so they are one to two years ahead of us. We move fast.

And you got a lot of great exposure… even at home?

Funny story about my mom, who as you know is a doctor in China. I was supposed to go there to visit for Chinese New Year and she was really disappointed that I had to cancel the trip because we had all of this going and we're fundraising.




But two or three weeks ago she turned on the TV to this channel called ‘Chinese People Around the World’ she watches every day during lunch and she actually saw me there, on Chinese National TV! She was making noodles and she almost burned them all because she was running all around the room trying to find her phone so she could record it, then she was texting me all frantically, ‘Oh my God, did you know you were on TV? Can you find it online can and send me the video?’ They even translated all of our presentation to Chinese, and I had no idea.

They look for entrepreneurial Chinese people who've done cool things around the world and they report about it, so I guess they found me somehow. I have no idea where they got my Chinese name from, but it was really cool.

Kudos to proud mamas around the world! So please tell us how you are reaching out to the PWD community in particular. Have you connected with any patient advocacy orgs?


We've been doing a lot of work within the podiatrist community and diabetes HCP groups to get the word out. I am also doing a few podcasts with diabetes experts, and we're coming out with a bunch of blogs (that offer) educational background on temperature monitoring, how important it is and the history of it.

We were also included in an article published in the November ADA Diabetes Forecast magazine on what makes a great diabetic sock.

As far as reaching the patient community directly, that's very important -- getting people involved and getting their feedback. So talking to you at the ‘Mine is one of our avenues…

Glad to help if we can! We see you have an introductory pre-order pricing set up. Tell us about the offer and when the socks are expected to ship?

Our socks are priced at $180 for seven pairs of socks, but right now we’re doing a pre-sale, at a $60 discount. So it’s $120 for a pack of seven, that should last you six months. There's also an option online to purchase smaller packs, of one, three, and five pairs.

Right now it’s all online ordering directly from us, and we expect the socks to ship in Summer. We’re also in talks with distributors to bring the socks into retail stores like Wal-Mart, CVS and Walgreens. But that won’t be rolling out until later this year.

You talked about design, but these socks currently only come in plain black and white versions, correct?

We're going to make our socks as attractive as possible. We have thought about different color variations, (and) we've already come up with Christmas designs, Halloween socks, summer, fashion versions, etc. for the future.





Of course, you shouldn't be wearing high-heeled or other fancy shoes if you have diabetic neuropathy. You should wear comfortable shoes that are well padded and fit your feet properly and we help you with that.

And the life expectancy of a pair of Siren Socks is six months?

Exactly, we replace all your socks every six months because that's standard in diabetic foot care -- every three to six months you need to replace all your socks to minimize spreading infection and also if there's a thin area in the sock material, that's where a foreign object can penetrate and get to your feet. The only line of defense is your socks, so you want to make sure they’re very thick and cushioned and the fabric is in the best shape possible.

And just a reminder: you don’t have to charge these socks, even though they’re outfitted with smart technology.

Finally, what’s a Twitter-style message you might want to send to the Diabetes Patient Community from your vantage point tackling foot damage?

I would say take care of your feet, and the future is here: we’ve dreamt of a world where we can have access to the right data at the right time and that future has arrived!

I don't know if that's a good Twitter message, but I’d want your readers to know there are lots of people – lots of other teams like us – working very hard to make tools easier to use and to bring science into your home in a way that addresses a problem and helps.

Thanks so much Ran -- That’s inspiring to say the least. We thank you for your ingenuity, down to our diabetic toes!

http://www.healthline.com/diabetesmine/siren-socks-revolutionizing-diabetes-foot-care#1

Nerve Damage From Antibiotics

Today's post from neuropathydr.com (see link below) is very short, simple and lacks any evidence to back its claims up. That said, currently the internet is full of articles about certain forms of antibiotics causing neuropathy as a side effect, or making it considerably worse if you already have it. The chief culprits are fluoroquinolones (ciproxin and levaquin amongst others) and as a general rule, it may be wise to discuss the potential for nerve damage with your doctor if he or she prescribes antibiotics for you. Failing that, do your own research by googling both the brand name and pharmaceutical name to see if neuropathy is a potential problem. Fortunately, there are nearly always alternatives you can take. (More articles on this issue can be found in the alphabetical list to the right of this blog).

Antibiotic Neuropathy 
Posted by john on May 12, 2014

Powerful antibiotics are more likely to cause antibiotic neuropathy.

It wasn’t that long ago that human beings just didn’t live that long. In reality it also wasn’t long ago that our life expectancy was half of what it is now! Now no doubt there have been many of reasons over the last 300 years that human beings are living far longer.

Better diet, improved social systems, and better living conditions no doubt account for so much of this.

One key reasons however, in modern societies is we are far better able to deal with infections. Now this is true in modern societies but many underdeveloped countries still suffer and millions die each year from diseases that are largely preventable in our world.

It’s been less than 100 years that antibiotics have been widely available. Now we even have antibiotics for some of the most devastating viral diseases.

Antibiotics also have side effects and for some this is antibiotic neuropathy. This very neuropathy is actually a toxic neuropathy. You see antibiotics are effective because they are by definition toxic products, usually much more so to invaders than humans.

Antibiotics literally help destroy bacteria and viruses so that they don’t kill us, the hosts.

Now we have more powerful antibiotics, which are more likely to cause antibiotic neuropathy. There are also many reasons for what many consider over-prescription of these drugs.

But please keep in mind despite your doctors best efforts, antibiotic neuropathy is a possibility and must be treated as soon as possible.

The most important thing is to recognize and report signs of antibiotic neuropathy as early as possible.

Help your doctor and report any unusual symptoms. This would include things such as tingling, numbness, burning, and loss of sensation. Often times these will occur very suddenly and without warning.

Next time we’ll talk more about the treatment of antibiotic neuropathy but for now understand the best communication between you and your doctor is essential to help prevent it!

Join the conversation all day on Facebook!

http://neuropathydr.com/antibiotic-neuropathy/

Thyroid Hormone Problems And Nerve Damage

Today's short post from mayoclinic.org (see link below) follows up on an earlier post this week concerning thyroid gland problems and the links with neuropathy. The article rightly points out that neuropathy as a result of thyroid hormone under-production is relatively uncommon but nevertheless with thyroid problems now becoming easier to diagnose, there are more and more cases of nerve damage emerging as a result. As with many forms of neuropathy, damage to the nerves because of hypothyroidism, is often the last link in a whole chain of diagnoses that begins with symptoms of another condition or problem. That it remains relatively rare may be because it is so rarely diagnosed as other illnesses take priority. This article just touches the surface really and if you suspect, or are told that you have thyroid hormone problems, it may be worth talking to the doctor about any other symptoms of neuropathy you may have noticed. That discussion alone may cut corners, get more quickly to the nub of the problem and save a lot of time.

Can hypothyroidism cause peripheral neuropathy and, if so, how is it treated? 
Answers from Todd B. Nippoldt, M.D.  March 29, 2017 

Hypothyroidism — a condition in which your thyroid gland doesn't produce enough thyroid hormone — is an uncommon cause of peripheral neuropathy.

Peripheral neuropathy is damage to your peripheral nerves — the nerves that carry information to and from your brain and spinal cord (central nervous system) and the rest of your body, such as your arms and legs.

Peripheral neuropathy may be caused by severe, long-term, untreated hypothyroidism. Although the association between hypothyroidism and peripheral neuropathy isn't fully understood, it's known that hypothyroidism can cause fluid retention resulting in swollen tissues that exert pressure on peripheral nerves.

One of the more common areas this occurs in is the wrists, because the nerve serving the hands goes through a "tunnel" of soft tissue, which can swell, pressing on the nerve, resulting in carpal tunnel syndrome. The vast majority of carpal tunnel syndrome cases are not due to hypothyroidism, but this would be the most likely area for this to occur with hypothyroidism.

Signs and symptoms of peripheral neuropathy may include pain, a burning sensation, or numbness and tingling in the area affected by the nerve damage. It may also cause muscle weakness or loss of muscle control.

See your doctor if you know or suspect you have hypothyroidism and you're having troubling or painful symptoms in your limbs.

Treatment

Treatment of peripheral neuropathy due to hypothyroidism is directed at managing the underlying hypothyroidism and treating the resulting symptoms. This may include:
Levothyroxine (Synthroid, Unithroid, others), which is a medication for hypothyroidism that often improves the symptoms of neuropathy
Exercising and maintaining a healthy weight, which can help minimize stress on your body as well as strengthen affected limbs

http://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/expert-answers/hypothyroidism/faq-20058489

Nerve Damage Repair By Tissue Engineering

Today's post from sciencedaily.com (see link below) is an interesting look at the research showing that by using Schwann cells as the basis (cells that wrap themselves around the nerve and form the protective sheath myelin), nerves can be regenerated. At the moment, a nerve transplant is necessary but is often unsuccessful. Moreover, this can only have a chance of success if the transplant takes place very soon after the initial injury. People with long-term nerve damage have a very small chance of nerve regeneration via transplantation. The new research opens up possibilities of using Schwann cells to regenerate and elongate damaged nerves, so that they better fuse with healthy axons further away. It's a form of tissue engineering with fascinating possibilities for the future.

New Tissue Engineering Breakthrough Encourages Nerve Repair
July 8, 2013 Science News
... from universities, journals, and other research organizations

A new combination of tissue engineering techniques could reduce the need for nerve grafts, according to new research by The Open University. Regeneration of nerves is challenging when the damaged area is extensive, and surgeons currently have to take a nerve graft from elsewhere in the body, leaving a second site of damage. Nerve grafts contain aligned tissue structures and Schwann cells that support and guide neuron growth through the damaged area, encouraging function to be restored.

The research, published in Biomaterials, reported a way to manufacture artificial nerve tissue with the potential to be used as an alternative to nerve grafts.

Pieces of Engineered Neural Tissue (EngNT) are formed by controlling natural Schwann cell behaviour in a three-dimensional collagen gel so that the cells elongate and align, then a stabilisation process removes excess fluid to leave robust artificial tissues. These living biomaterials contain aligned Schwann cells in an aligned collagen environment, recreating key features of normal nerve tissue.

Incorrect orientation of regenerating nerve cells can lead to delays in repair, scarring and poor restoration of nerve function. Much research has taken place into how support cells (Schwann cells) can be combined with materials to guide nerve regeneration. The new technology from The Open University avoids the use of synthetic materials by building neural tissue from collagen, a protein that is abundant in normal nerve tissue. Building the artificial tissue from natural proteins and directing the cellular alignment using normal cell-material interactions means the EngNT can integrate effectively at the repair site.

Dr James Phillips, Lecturer in Health Sciences at The Open University, said: "We previously reported how self-alignment of Schwann cells could be achieved by using a tethered collagen hydrogel, which exploited cells' natural ability to orientate in the appropriate direction by using their internal contraction forces. Our current research shows that cell-alignment in the hydrogel can be stabilised using plastic compression. The compression removes fluid from the gels, leaving a strong and stable aligned structure that has many features in common with nerve tissue."

The team incorporated Schwann cells within the aligned material to form artificial neural tissue that could potentially be used in peripheral nerve repair. The technique could be applied to other regenerative medicine scenarios, where a stable artificial tissue containing aligned cellular architecture would be of benefit.

http://www.sciencedaily.com/releases/2013/07/130708102938.htm

CITY AIR CAN DAMAGE BRAIN STRUCTURES

Air pollution, even at moderate levels, has long been recognized as a factor in raising the risk of stroke. A new study led by scientists from Beth Israel Deaconess Medical Center and Boston University School of Medicine suggests that long-term exposure can cause damage to brain structures and impair cognitive function in middle-aged and older adults

Writing in the May 2015 issue of Stroke, researchers who studied more than 900 participants of the Framingham Heart Study found evidence of smaller brain structure and of covert brain infarcts, a type of "silent" ischemic stroke resulting from a blockage in the blood vessels supplying the brain.

The study evaluated how far participants lived from major roadways and used satellite imagery to assess prolonged exposure to ambient fine particulate matter, particles with a diameter of 2.5 millionth of a meter, referred to as PM2.5. These particles come from a variety of sources, including power plants, factories, trucks and automobiles and the burning of wood. They can travel deeply into the lungs and have been associated in other studies with increased numbers of hospital admissions for cardiovascular events such as heart attacks and strokes.

"This is one of the first studies to look at the relationship between ambient air pollution and brain structure," says Elissa Wilker, ScD, a researcher in the Cardiovascular Epidemiology Research Unit at Beth Israel Deaconess Medical Center. "Our findings suggest that air pollution is associated with insidious effects on structural brain aging, even in dementia- and stroke-free individuals."

Study participants were at least 60 years old and were free of dementia and stroke. The evaluation included total cerebral brain volume, a marker of age-associated brain atrophy; hippocampal volume, which reflect changes in the area of the brain that controls memory; white matter hyperintensity volume, which can be used as a measure of pathology and aging; and covert brain infarcts.

The study found that an increase of only 2µg per cubic meter in PM2.5, a range commonly observed across metropolitan regions in New England and New York, was associated with being more likely to have covert brain infarcts and smaller cerebral brain volume, equivalent to approximately one year of brain aging.

"These results are an important step in helping us learn what is going on in the brain," Wilker says. "The mechanisms through which air pollution may affect brain aging remain unclear, but systemic inflammation resulting from the deposit of fine particles in the lungs is likely important."

"This study shows that for a 2 microgram per cubic meter of air (μg/m3) increase in PM2.5, a range commonly observed across major US cities, on average participants who lived in more polluted areas had the brain volume of someone a year older than participants who lived in less polluted areas. They also had a 46 percent higher risk of silent strokes on MRI," said Sudha Seshadri, MD, a Professor of Neurology at Boston University School of Medicine and Senior Investigator, the Framingham Study.

"This is concerning since we know that silent strokes increase the risk of overt strokes and of developing dementia, walking problems and depression. We now plan to look at more the impact of air pollution over a longer period, its effect on more sensitive MRI measures, on brain shrinkage over time, and other risks including of stroke and dementia."

In addition to Wilker, who is also affiliated with the Exposure Epidemiology and Risk Program in the Department of Environmental Health at the Harvard T.H. Chan School of Public Health (HSPH), and Seshadri, co-authors include: Sarah R. Preis, ScD, of the Boston University School of Public Health, Department of Biostatistics (BUSPH) and the Framingham Heart Study (FHS); Alexa S. Beiser, PhD, of BUSPH, FHS and the Boston University School of Medicine Department of Neurology (BUSM); Philip A. Wolf, MD, of FHS and BUSM; Rhoda Au, PhD of BUSM; Ital Kloog, PhD, of the Department of Geography and Environmental Development , Ben-Gurion University of the Negev, Beer Sheva, Israel; Wenyuan Li, MS, of the Department of Epidemiology of HSPH; Joel Schwartz, PhD, of HSPH; Petros Koutrakis, PhD of HSPH; Charles DeCarli, MD, of the Department of Neurology and Center for Neuroscience, University of California, Davis; and Murray Mittleman, MD, DrPH, of BIDMC and HSPH.

Is Re Myelination Realistic After Nerve Damage

Today's post from journals.lww.com (see link below) talks about spontaneous re-myelination in certain patients with nerve problems. Maybe first, we need to remind ourselves what myelin and myelination actually is. Myelin is the protective sheath around the nerve (axon) and in very many cases of nerve damage, it is the destruction or deterioration of this myelin sheath that causes the neurological problem. You can equate it to a live wire without its insulation. However, by using specialist PET scans, researchers have found that certain people spontaneously regenerate their own myelin and the implications of this may very well provide new forms of treatment for the future. They are looking for the agents involved in maintaining and regrowing myelin sheaths after they've been injured and if these are discovered, the potential for the future is clear.

Multiple Sclerosis: Spontaneous Remyelination, Visualized With PET Tracer, Could Be Marker of Clinical Course
BY DAN HURLEY Thursday, April 23, 2015

WASHINGTON—The first clinical trial of a positron emission tomography (PET) tracer previously shown to bind tightly to myelin in animal models of multiple sclerosis (MS) has identified previously unknown variations in patients’ capacity for remyelination, and has linked those differences to clinical outcomes, according to a paper presented here on Wednesday at the AAN Annual Meeting.

The study used PET with carbon-11 Pittsburgh compound B (11C-PiB), a radioactive compound originally developed as a marker of amyloid plaque but shown in a 2011 paper in the Annals of Neurology to work even better as an imaging marker of myelin loss and repair in animals.

The new study involved 20 patients with active MS who underwent both PET scans and a conventional magnetic resonance imaging (MRI) scan at baseline and at either two or four months later. Indices of myelin content change were statistically correlated with the Expanded Disability Status Scale (EDSS) and the Multiple Sclerosis Severity Scale (MSSS).

The study found no link between changes in demyelination and clinical scores, but identified a strong correlation between remyelination and both EDSS (r = -0.8, p=0.0001) and MSSS (r = -0.57, p = 0.009).

“Our results suggest that there might be an individual remyelination capacity for each individual, which allows them to respond more or less efficiently to a demyelinating insult,” the first author of the paper, Benedetta Bodini, MD, PhD, a neurologist and postdoctoral research fellow in the Brain and Spine Institute at the Hôpital Universitaire Pitié Salpêtrière in Paris, told the Neurology Today Conference Reporter ahead of the presentation.

“Even more interesting, when we correlated this remyelination potential with the clinical scores, we obtained very strong correlations, as if the clinical prognosis is very much influenced by the level of remyelination. If I’m a good remyelinator, I’m going to do better than someone who is not.”

If the findings stand up in larger trials, she said, “This tells us that we really need to shift our therapeutic strategies toward finding remyelinating medications.”

John R. Corboy, MD, FAAN, a professor of neurology at the University of Colorado School of Medicine and co-director of the Rocky Mountain MS Center at Anschutz Medical Campus, welcomed the results, but sounded a note of caution.

“This kind of marker is potentially quite useful,” said Dr. Corboy, who also serves on the Neurology Today editorial advisory board. “MRI scans frequently just tell us there’s been damage of some kind, whereas PET can be tied to very specific molecules on specific cells. If validated in further studies, having a radiological marker of improvement would be incredibly important, especially if it shows areas where you remyelinated brain.”

A study published earlier this year in Brain, he noted, used another PET tracer, PK-11195, to distinguish between activated and non-activated microglia in normal-appearing white matter of patients with clinically isolated syndrome.

“They showed that even in normal-appearing white matter, there was significant activation of microglia,” Dr. Corboy said. “The more activation seen, the higher the patient’s risk for developing MS over two years. So it was prognostic.”

Researchers are aggressively investigating PET markers not only for prognosis, but also to explore pathophysiology and as a means to show whether investigational therapies are working, Dr. Corboy said. “It’s extremely challenging, especially for patients with progressive MS, that we haven’t had a good way to measure improvement.”

A number of potential pro-myelinating agents are already being studied, Dr. Bodini pointed out, including anti-LINGO-1, olesoxime, clemastine, and retinoic acid receptor modulators.

However, Dr. Corboy said, “The phase 2 anti-LINGO-1 study was a little disappointing. It showed only some modest effects on speed of conduction, and did not meet its major outcome measure. Perhaps a marker like 11C-PiB would be useful by showing that perhaps clinical measures weren’t accurate enough.”

The 11C-PiB marker for myelin was developed by the senior author of the paper presented at the AAN meeting, Bruno Stankoff, MD, PhD, a professor of neurology at the Université Pierre et Marie Curie in Paris. Already, Dr. Bodini said, their team is developing another tracer that binds just as tightly to myelin but uses fluorinated compounds rather a carbon-labeled one. “Fluorinated compounds are much more accessible and allow the technique to be used much more widely in different centers,” she said.

For more articles on spontaneous remyelination, browse our archives here.

http://journals.lww.com/neurotodayonline/blog/NeurologyTodayConferenceReportersAANAnnualMeeting/pages/post.aspx?PostID=6

Zebra Fish The New Rats In Nerve Damage Research

Today's fascinating post from medicaldaily.com (see link below) looks at how zebra fish are being used to study how nerve damage progresses with certain neurological diseases (eg neuropathy). The fact that these fish have an 82% likeness with humans in terms of proteins means that results of studies are less likely to be misleading than those involving other research animals. We've heard of various sea creatures being used to study human neurology and developing nerve damage treatments before but apparently studying myelin sheath degradation in Zebra fish brings up many close comparisons with the same cause of nerve damage in humans but how did they ever discover that in the first place!!

Zebrafish, 82% Similar To Humans, Reveal New Insights On Neurological Disorders And Treatments
By Anoopa Singh | Jun 26, 2013

Zebrafish reveal much about neurological disorders and how to treat them.

Neurological disorders in humans are often difficult to study in human brains. As a result, animal models need to be used to simulate the workings of the human nervous system. Usually, scientists will rely on mice, but recently, the use of zebrafish has become popular due to the animal's utility.

Charcot—Marie—Tooth disease (CMT) is causes by a hereditary genetic disorder that affects the nerves that branch throughout the body in young adults. The disease leads to nerve damage and causes a weakness of muscles, foot and hand deformity, loss of muscle mass, and numbness in the lower body. CMT eventually leads to disability and a loss in sensation in the places most affected.

A new study using zebrafish, done by Andrew Grierson, Ph.D., of University of Sheffield, has revealed a great deal about CMT and potential therapies. Humans and zebrafish have proteins that are 82 percent alike — this is important because it indicates that zebrafish are suitable in studies that compare results to potential treatments for diseases in humans. When researchers altered the genes of zebrafish to be the same as patients of CMT, similar symptoms were seen as the fish aged. Once they matured into adulthood, the fish lost the ability to swim properly. The scientists feel that the difficulties in swimming can be paralleled to the difficulties humans face in walking after CMT has fully developed.

Using the zebrafish, researchers were able to identify what goes wrong in neurons as a result of CMT for the first time. They saw that the myelin sheaths around neurons began to degrade. Similarly, the far branches of nerve cells also started to degrade, leading to the sensations of pain, as messages like sensation could not travel up and down this part of the neuron anymore. Both of these issues led to the pain and neurodegeneration suffered by CMT patients.

The researchers have said that all of this would not have been clear in any other animal. In other animals, the disease starts its effects very early in development, but in humans, disease onset is usually in adolescence. This difference in other animals skews results and makes findings inconsistent with the disease's effects in humans. Grierson said, "Using zebrafish we were able to develop a model with an adult onset, progressive phenotype with predominant symptoms of motor dysfunction similar to [what happens in humans]."

He added that while we know much about other neurodegenerative diseases, others seem to escape our grasp. "Motor neurons are the largest cells in our bodies, and as such they are highly dependent on a cellular transport system to deliver molecules through the long nerve cell processes which connect the spinal cord to our muscles," he continued. "We already know that defects in the cellular transport system occur early in the development of diseases such as Alzheimer's disease, Motor Neuron Disease and spastic paraplegia. Using our zebrafish model we have found that similar defects in transport are also a key part of the disease process in CMT

Now that so much has been found out about the way CMT changes neurons for the worst, researchers can start to develop targeted therapies and treatments for the disease. There is currently no cure for CMT, nor are there any drugs that can help manage its symptoms. Patients often depend on physical or occupational therapies or surgeries for relief from symptoms.
 
While a cure may not be made tomorrow, the prospect of it and improved disease management therapies now exist.

Source: Chapman AL, Bennett EJ, Ramesh T, De Vos KJ, Grierson AJ. Axonal Transport Defects in a Mitofusin 2 Loss of Function Model of Charcot-Marie-Tooth Disease in Zebrafish. PLOS ONE. 2013.

http://www.medicaldaily.com/zebrafish-82-similar-humans-reveal-new-insights-neurological-disorders-and-treatments-247168#92xi6cLxdeJUUlFI.99

Are We Close To Restoring Neuropathy Nerve Damage

Today's post from journals.lww.com/ (see link below) is a doctor's answer to a patient's query about the possibility of ever repairing damaged nerves. His answer suggests that gene therapy may well be the answer in the future. He also quite rightly says that more research is urgently needed but research needs funding. Well worth a read.
 

What's on the horizon for restoring nerve function in peripheral neuropathy?
Smith, A. Gordon M.D. Neurology Now:
April/May 2014 - Volume 10 - Issue 2 - p 34
  doi:10.1097/01.NNN.0000446167.75771.61


 Q What's on the horizon for restoring nerve function in peripheral neuropathy? Will there ever be a way to quiet the faulty nerves, as opposed to masking the pain with drugs like gabapentin and oxycodone?

DR. A. GORDON SMITH RESPONDS:

A It is estimated that more than 20 million Americans have peripheral neuropathy, making it one of the most common neurologic conditions. Peripheral neuropathy is caused by damage to the peripheral nervous system, which is responsible for sending information back and forth between the brain and spinal cord to every other part of the body. The condition often causes weakness, numbness, and pain in the hands and feet, but it may also occur in other areas of the body. Because peripheral neuropathy is not a single disease but rather a symptom with many possible causes, it may be difficult to diagnose and to treat.

However, different forms of peripheral neuropathy may also share common mechanisms of nerve injury. This means that discovery of a treatment for one form of peripheral neuropathy might benefit others.

Diabetes is the most frequent cause of peripheral neuropathy. In many cases, the cause of peripheral neuropathy is never known (called idiopathic peripheral neuropathy). Patients, physicians, and researchers are all interested in discovering effective therapies to slow progression, improve pain control, and hopefully reverse nerve injury in peripheral neuropathy.

Recent advances in uncovering the genetics of peripheral neuropathy have been made. Researchers have discovered that some people with painful idiopathic peripheral neuropathy have a mutation in a particular gene. This discovery has led to new studies—including planned human trials—exploring these genetic mutations as potential targets for treatment.

In addition, patients are being actively recruited for a number of exciting clinical trials including studies of growth factors (groups of proteins that stimulate the growth of specific tissues) delivered using gene therapy technology, which allows targeted delivery for peripheral neuropathy caused by diabetes. (Read more on these therapies at bit.ly/1eaBc0H.)

For many neuropathies caused by an immune attack of the nerves, good therapies already exist and others are in development. The outlook for these forms of peripheral neuropathy is even more hopeful. For patients with chronic inflammatory demyelinating polyradiculoneuropathy (a rare and chronic condition characterized by gradually increasing weakness of the legs and, to a lesser extent, the arms), the use of corticosteroids or intravenous immunoglobulin (IVIg)—alone or in combination with immunosuppressant drugs—is effective. However, better treatments are needed for patients who do not respond to currently available approaches.

There is even hope for patients with certain types of genetic neuropathies. Several promising experimental treatments are being studied for familial amyloid polyneuropathy, a rare genetic condition where impaired nerve function is caused by amyloid protein deposits in peripheral nerves.

While the lack of a recognized underlying cause for idiopathic peripheral neuropathy is frustrating, we have learned a great deal about this disorder over the past decade. A number of studies now link obesity and its related metabolic consequences (such as insulin resistance and elevated lipids in the blood) with peripheral neuropathy. In addition, several studies suggest that successful diet and exercise can improve nerve regeneration and improve symptoms including pain. This provides a non-drug treatment approach that would immediately benefit many people with peripheral neuropathy.

Despite all of this good news, more research is urgently needed. Relative to the number of patients who have neuropathy, very few research grants are funded. To help change this, consider joining one of the patient advocacy organizations focused on neuropathy. For example, the Neuropathy Association has many programs to encourage involvement and advocacy: www.neuropathy.org.

© 2014 American Academy of Neurology

http://journals.lww.com/neurologynow/Fulltext/2014/10020/What_s_on_the_horizon_for_restoring_nerve_function.15.aspx