CHIN STRAP HARVESTS ENERGY FROM CHEWING

A chin strap that can harvest energy from jaw movements has been created by a group of researchers in Canada.

It is hoped that the device can generate electricity from eating, chewing and talking, and power a number of small-scale implantable or wearable electronic devices, such as hearing aids, cochlear implants, electronic hearing protectors and communication devices.

The first results of the device's performance have been published today, 17 September, in IOP Publishing's journal Smart Materials and Structures.

Jaw movements have proved to be one of the most promising candidates for generating electricity from human body movements, with researchers estimating that an average of around 7 mW of power could be generated from chewing during meals alone.

To harvest this energy, the study's researchers, from Sonomax-ÉTS Industrial Research Chair in In-ear Technologies (CRITIAS) at École de technologie supérieure (ÉTS) in Montreal, Canada, created a chin strap made from piezoelectric fiber composites (PFC).

PFC is a type of piezoelectric smart material that consists of integrated electrodes and an adhesive polymer matrix. The material is able to produce an electric charge when it stretches and is subjected to mechanical stress.

In their study, the researchers created an energy harvesting chin strap made from a single layer of PFC and attached it to a pair of ear muffs using a pair of elastic side straps. To ensure maximum performance, the chin strap was fitted snugly to the user, so when the user's jaw moved it caused the strap to stretch.

To test the performance of the device, the subject was asked to chew gum for 60 seconds whilst wearing the head-mounted device; at the same time the researchers recorded a number of different parameters.

The maximum amount of power that could be harvested from the jaw movements was around 18 µW, but taking into account the optimum set-up for the head-mounted device, the power output was around 10 µW.

Co-author of the study Aidin Delnavaz said: "Given that the average power available from chewing is around 7 mW, we still have a long way to go before we perfect the performance of the device.

"The power level we achieved is hardly sufficient for powering electrical devices at the moment; however, we can multiply the power output by adding more PFC layers to the chin strap. For example, 20 PFC layers, with a total thickness of 6 mm, would be able to power a 200 µW intelligent hearing protector."

One additional motivation for pursuing this area of research is the desire to curb the current dependency on batteries, which are not only expensive to replace but also extremely damaging to the environment if they are not disposed of properly.

"The only expensive part of the energy harvesting device is the single PFC layer, which costs around $20. Considering the price and short lifetime of batteries, we estimate that a self-powered hearing protector based on the proposed chin strap energy harvesting device will start to pay back the investment after three years of use," continued Delnavaz.

"Additionally, the device could substantially decrease the environmental impact of batteries and bring more comfort to users.

"We will now look at ways to increase the number of piezoelectric elements in the chin strap to supply the power that small electronic devices demand, and also develop an appropriate power management circuit so that a tiny, rechargeable battery can be integrated into the device."

Writing A Free Distraction From Chronic Pain

Today's post from paincommunity.org (see link below) talks about a form of therapy that won't reduce the painful symptoms of neuropathy but may serve as a distraction and therefore lessen its impact. Not only that but it may help you put into writing (and therefore words) how long-term neuropathy affects your personality and quality of life. The article urges you to start writing! I don't need to say any more than that but if you do start writing and are looking for an outlet, or an audience, this blog will be happy to publish your work. Let me know that you're intending to write something and I'll provide an email address to which you can send your word file, or whatever. Fiction or non-fiction - it's all good and you may be surprised how much positive energy the simple act of writing can give. If while you're doing it, you don't notice your discomfort as much, then it's a win-win situation.

Writing as a Form of Therapy
by The Pain Community | Apr 21, 2017 | Daily Living
by Guest Blogger – Maria Miguel

All of us encounter stressful and traumatic experiences in our lives. We could be fighting everyday battles of anxiety, depression and other mental health disorders. For me, I find a special comfort in the written word. I can read countless novels and teleport myself into the writer’s worlds. The characters come alive on the pages, and I can visit faraway places conjured up in the minds of the author.

As a writer, I use words to relay emotions and thoughts I can’t exactly form orally. Over the years, writing has been the consistent and most therapeutic method to ease my stress. As someone with obsessive compulsive personality disorder, this is sometimes a challenging task. When I am writing, either about my life or creating my own characters and stories, I am able to work through the best — and worst — times in my life. Through this introspection, I find some of my greatest strength. For me, it’s easier to write about how I am feeling versus talking about every single rumination. Writing allows me to collect my thoughts.

Even if you aren’t a seasoned writer, give it a shot. After all, you don’t have to share your musings with anyone but yourself. Writing can help you assess patterns in your behaviors, increase your sense of self-identity and determine goals and objectives. For example, if you have been struggling with depression, writing about your feelings could help you determine that you are depressed because you are in a failing relationship, don’t enjoy your current job or feel overwhelmingly hopeless because you see the world through a loved one’s sickness.

Here are some tips to use writing as a form of therapy in your own life:

Keep a journal.

Write in this journal as often as needed. I recommend writing every day. It’s OK if your journal writing isn’t structured and is more stream of consciousness. Make your journal an extension of your personality. I write all of my dates in French and tend to purchase journals that are vintage, Parisian or “Wizard of Oz” themed.

Write a letter to yourself or someone else.

If you’re in the midst of letting go of something or someone, writing a “goodbye” letter could work for you. If you weren’t able to say what you wanted to say, then this could be a way to get your feelings out in the open without ever sending the letter or email. You will tell your truths in your internal narrator’s voice, which can be extremely therapeutic. You won’t be bottling up your emotions.

Detail your emotions in poetry.

We all probably had to read and write poetry in high school. For some of us, we didn’t understand the stanzas in front of us; however, poets draw from their own experiences and emotions to pen their poetry. If you feel overwhelmed and don’t know where to start, make a list of images, such as in your bedroom, from your childhood days, from a stressful situation, etc. Then, write a list of senses you experienced associated with these images. Write down your emotions related to the images and senses. After this process, write a poem containing these words and images. You will be able to show yourself — and potential readers — how you are feeling without having to put blatant labels on your emotions.

Be prepared to uncover good and bad memories.

During the writing process, your mind could rediscover thoughts and emotions associated with something bad that happened in your life. For example, if you are writing about lost loves, you may think of a former significant other who wasn’t faithful. You may feel helpless as you write about your parents’ divorce. However, you could also relive the best parts of your life, such as the birth of your child, achieving a goal, traveling to your favorite location and more. Using writing as therapy can help you forgive yourself and others. You can reflect on situations and improve into your best self because you have learned from your successes and mistakes.

Write fiction based on your nonfiction experiences.

Often, when we use writing as therapy, we talk about our personal journeys. Use your own story and craft your own characters. If you are uncomfortable writing about a traumatic experience of your own, have your character experience the event. Writing about specific emotions can help you in the healing process. If you decide to share your writings with someone else — or even a mass audience — the works centered on your experiences and emotions could help others going through the same type of situation. This gives you a new role and gives your writings even more meaning that is greater than you.

To figure out if writing could be therapeutic for you and to find more therapy options, seek out a licensed professional to talk with you about your mental health disorder and its effects and solutions.

Marie Miguel is an avid internet researcher. She is fueled by her determination to answer the many questions she hasn’t been able to find the answer to anywhere else. When she finds these answers she likes to spread the knowledge to others seeking help. She is always looking for outlets to share her information, therefore she occasionally has her content published on different websites and blogs. Even though she doesn’t run one for herself she loves contributing to others.

http://paincommunity.org/writing-form-therapy/

Foot Damage From Neuropathy

Today's post from wecare.ca (see link below) discusses ulceration, one of the foot problems that can arise from neuropathy. Most people manage to avoid severe ulceration but for many it can be a serious problem. Loss of feeling and numbness in areas on the feet can lead to small cuts and wounds becoming ulcerated without you even noticing it. Normally the feet are very sensitive to injury and we can respond immediately to any warning pain but sensory loss removes that early warning system. Ulceration can severely affect the quality of your life and it is vital that you see a doctor the moment you notice it. As a general rule for people living with neuropathy, checking your feet daily is a good idea - they need looking after; they've got to carry you a long way yet!

The Pins and Needles of Peripheral Neuropathy

November 12th, 2012 | Posted by SueKelly in Care Connections

 
Most people know what it is like to experience the numbing effect of ‘pins and needles’. But if you are diabetic or suffer from circulatory problems – this ailment can be a serious and ongoing concern.

Peripheral neuropathy is damage to the nerves in the limbs and particularly the feet where the body’s nerves are the longest. The risk of developing neuropathy increases the longer a person has been afflicted with diabetes or congestive heart failure or other circulatory problems. The nerve damage prevents people from knowing when their feet are too hot, too cold or sore or painful. Therefore a person loses the warning signs that their feet could be in jeopardy. This is called “loss of protective sensation”.

Loss of protective sensation (LOPS) contributes significantly to ulcer development. In healthy individuals, irritants like bunions, blisters or calluses may cause an unconscious change of gait. In people living with diabetes who experience LOPS as a result of peripheral neuropathy, no discomfort is felt, so pressure on specific sites is continued, directly affecting the development of ulcers. Early detection of LOPS and implementation of preventative strategies will reduce the rates of limb-threatening complications.

Many foot ulcers begin in innocent ways. As a visiting nurse I was always curious how a problem started and would ask my clients what was the first sign that brought them to the doctor? Often the response was one of embarrassment and foolishness as they described the simple way it began – a blister, a piece of torn skin or a small amount of bleeding. The harmless scratch burgeoned from a trivial occurrence to a condition that threatened the maintenance of limbs and in some cases, life.

The following signs may be an indication that you have peripheral neuropathy or decreased circulation. If you have any one of these symptoms, make an appointment to see your health care professional.

Signs of Peripheral Neuropathy

Signs of Poor Circulation

Pain, tingling, burning and numbness that starts in the feet and slowly progresses up the calves; tends to be worse at night Inability to detect excessive heat such as in a bath or a heating pad Any small sore, cut or ingrown toenails Weakness in small muscles of the feet that cause the toes to claw, or in more serious cases foot drop will develop A change in gait Swelling or redness on any part of the foot The existence of a bunion, callus, corn or wart

Absence of foot pulses A pale colour of the feet when the feet are raised Feet that feel cold Pain at rest Pain at night relieved by hanging the feet over the side of the bed A blue colour to the toes A reddish colour of the feet Swelling of the feet

Given the alarming statistics of foot problems in patients living with diabetes, it is prudent to assess all diabetics for their level of risk related to foot problems. Special attention needs to be paid to the elderly and over-weight clients. In older clients limited mobility and poor eyesight may prevent them from properly examining their feet – a task that should be done daily. In obese patients, excessive weight will be an impediment to easy foot inspection.

People with diabetic foot ulcers face incredible challenges in their family, social and work lives, which sometimes affect their sense of self-worth. From the ease with which the ulcers seem to develop, to the future unpredictability imposed by the condition, people describe the dramatic impact that having a foot ulcer has on their activities of daily living. There is a great deal of stress and fear that comes with the uncertainty of not knowing when and if the ulcer will heal and in some cases whether or not amputation will become an eventuality.

http://www.wecare.ca/blog/?p=562

BIO ENGINEERED DECOY PROTEIN MAY STOP CANCER FROM SPREADING

A team of Stanford researchers has developed a protein therapy that disrupts the process that causes cancer cells to break away from original tumor sites, travel through the blood stream and start aggressive new growths elsewhere in the body.

This process, known as metastasis, can cause cancer to spread with deadly effect.

"The majority of patients who succumb to cancer fall prey to metastatic forms of the disease," said Jennifer Cochran, an associate professor of bioengineering who describes a new therapeutic approach in Nature Chemical Biology.

Today doctors try to slow or stop metastasis with chemotherapy, but these treatments are unfortunately not very effective and have severe side effects.

The Stanford team seeks to stop metastasis, without side effects, by preventing two proteins -- Axl and Gas6 -- from interacting to initiate the spread of cancer.

Axl proteins stand like bristles on the surface of cancer cells, poised to receive biochemical signals from Gas6 proteins.

When two Gas6 proteins link with two Axls, the signals that are generated enable cancer cells to leave the original tumor site, migrate to other parts of the body and form new cancer nodules.

To stop this process Cochran used protein engineering to create a harmless version of Axl that acts like a decoy. This decoy Axl latches on to Gas6 proteins in the blood stream and prevents them from linking with and activating the Axls present on cancer cells.

In collaboration with Professor Amato Giaccia, who heads the Radiation Biology Program in Stanford's Cancer Center, the researchers gave intravenous treatments of this bioengineered decoy protein to mice with aggressive breast and ovarian cancers.

Mice in the breast cancer treatment group had 78 percent fewer metastatic nodules than untreated mice. Mice with ovarian cancer had a 90 percent reduction in metastatic nodules when treated with the engineered decoy protein.

"This is a very promising therapy that appears to be effective and non-toxic in pre-clinical experiments," Giaccia said. "It could open up a new approach to cancer treatment."

Giaccia and Cochran are scientific advisors to Ruga Corp., a biotech startup in Palo Alto that has licensed this technology from Stanford. Further preclinical and animal tests must be done before determining whether this therapy is safe and effective in humans.

Greg Lemke, of the Molecular Neurobiology Laboratory at the Salk Institute, called this "a prime example of what bioengineering can do" to open up new therapeutic approaches to treat metastatic cancer.

"One of the remarkable things about this work is the binding affinity of the decoy protein," said Lemke, a noted authority on Axl and Gas6 who was not part of the Stanford experiments.

"The decoy attaches to Gas6 up to a hundredfold more effectively than the natural Axl," Lemke said. "It really sops up Gas6 and takes it out of action."

Directed Evolution

The Stanford approach is grounded on the fact that all biological processes are driven by the interaction of proteins, the molecules that fit together in lock-and-key fashion to perform all the tasks required for living things to function.

In nature proteins evolve over millions of years. But bioengineers have developed ways to accelerate the process of improving these tiny parts using technology called directed evolution. This particular application was the subject of the doctoral thesis of Mihalis Kariolis, a bioengineering graduate student in Cochran's lab.

Using genetic manipulation, the Stanford team created millions of slightly different DNA sequences. Each DNA sequence coded for a different variant of Axl.

The researchers then used high-throughput screening to evaluate over 10 million Axl variants. Their goal was to find the variant that bound most tightly to Gas6.

Kariolis made other tweaks to enable the bioengineered decoy to remain in the bloodstream longer and also to tighten its grip on Gas6, rendering the decoy interaction virtually irreversible.

Yu Rebecca Miao, a postdoctoral scholar in Giaccia's lab, designed the testing in animals and worked with Kariolis to administer the decoy Axl to the lab mice. They also did comparison tests to show that sopping up Gas6 resulted in far fewer secondary cancer nodules.

Irimpan Mathews, a protein crystallography expert at the SLAC National Accelerator Laboratory, joined the research effort to help the team better understand the binding mechanism between the Axl decoy and Gas6.

Protein crystallography captures the interaction of two proteins in a solid form, allowing researchers to take X-ray-like images of how the atoms in each protein bind together. These images showed molecular changes that allowed the bioengineered Axl decoy to bind Gas6 far more tightly than the natural Axl protein.

Next steps

Years of work lie ahead to determine whether this protein therapy can be approved to treat cancer in humans. Bioprocess engineers must first scale up production of the Axl decoy to generate pure material for clinical tests. Clinical researchers must then perform additional animal tests in order to win approval for and to conduct human trials. These are expensive and time-consuming steps.

But these early, hopeful results suggest that the Stanford approach could become a non-toxic way to fight metastatic cancer.

Glenn Dranoff, a professor of medicine at Harvard Medical School and a leading researcher at the Dana-Farber Cancer Institute, reviewed an advance copy of the Stanford paper but was otherwise unconnected with the research. "It is a beautiful piece of biochemistry and has some nuances that make it particularly exciting," Dranoff said, noting that tumors often have more than one way to ensure their survival and propagation.

Axl has two protein cousins, Mer and Tyro3, that can also promote metastasis. Mer and Tyro3 are also activated by Gas6.

"So one therapeutic decoy might potentially affect all three related proteins that are critical in cancer development and progression," Dranoff said.

HIV LESSONS FROM THE MISSISSIPPI BABY

The news in July that HIV had returned in a Mississippi toddler after a two-year treatment-free remission dashed the hopes of clinicians, HIV researchers and the public at large tantalized by the possibility of a cure.

But a new commentary by two leading HIV experts at Johns Hopkins argues that despite its disappointing outcome, the Mississippi case and two other recent HIV "rebounds" in adults, have yielded critical lessons about the virus' most perplexing -- and maddening -- feature: its ability to form cure-defying viral hideouts.

Writing in the Aug. 28 issue of the journal Science, HIV research duo Robert Siliciano, M.D., Ph.D., and Janet Siliciano, Ph.D., note that such "failures" are in fact stepping stones to new understanding of what "cure" may look like and new therapies that tame the virus into long-term remission.

"Heartbreaking as these three cases are clinically, they provide a dramatic illustration of the real barrier to an HIV cure and illuminate important therapeutic strategies," says Robert Siliciano. "This is not the end of the story but the beginning of a new chapter."

The 27-month off-treatment remission experienced by the Mississippi toddler is, in and of itself, a laudable therapeutic goal, the Silicianos write, and is what cure of HIV may look like in the foreseeable future. Finding ways to induce long-term remission and to closely monitor its course will be the next frontier in HIV treatment, they write.

The ability to put the virus in remission and go off treatment for months or years at a time is an important goal, because it can spare HIV-infected people from a lifetime of daily antiviral regimens, which can be difficult to tolerate and hard to follow. Failure to comply with the strict treatment protocol, which occurs often, can lead to viral mutations that make HIV resistant to drugs.

All three cases, the Silicianos write, also reaffirm that the single most important hurdle to eradicating HIV is a tiny but extremely stable pool of virus tucked away in a handful of immune cells known as memory CD4+ T cells.

Memory T cells are the immune system's combat-trained sentinels, responsible for fighting invaders they have encountered in the past. Much of the time, memory T cells lie dormant and become active only when the body is invaded by old foes they are specifically trained to recognize. HIV invades memory T cells early in the infection, and as long as the T cells lie quiet, so does HIV inside them.However, as soon as memory T cells get stirred up by an invader, the HIV DNA inside them wakes up, cranks out new virus and reignites infection. Because antiviral drugs work only against actively replicating virus, such silent viral hideouts remain out of therapy's reach. Thus, reducing the number of latently infected cells or precluding their formation altogether is an important and -- as the three recent cases suggest -- realistic strategy, the Silicianos say.

"These cases paint several clinical scenarios where a substantial reduction of viral reservoirs would allow some patients to come off treatment for prolonged yet uncertain periods of time, but they also raise the critical question of how to best monitor them for relapse so they can resume therapy swiftly when the virus rebounds," says Janet Siliciano.

In the widely reported case of the Mississippi baby, a child born to an HIV-infected mother received a full-treatment regimen of antiviral drugs within hours of birth, instead of the customary prophylactic regimen typically used in suspected but unconfirmed newborn infections. The baby's HIV infection was subsequently confirmed. The child was lost to follow-up and went off treatment but later returned to clinic. A series of standard and ultrasensitive tests failed to detect HIV in the child's blood. In total, the child remained free of HIV infection -- with undetectable viral loads and free of HIV antibodies -- for 27 months despite receiving no treatment. By contrast, most HIV-infected people experience dramatic viral rebound within a few weeks of treatment cessation.

Described as the first documented instance of HIV remission in a child, the Mississippi case suggested that very early treatment with antiretroviral drugs quashed the formation of viral reservoirs. The child was followed by a University of Mississippi pediatrician, a University of Massachusetts immunologist and a Johns Hopkins pediatric HIV expert, Deborah Persaud, M.D., who was also the lead author on case report published Nov. 7, 2013, in The New England Journal of Medicine.

In two other "remission" cases reported in 2013, HIV ultimately rebounded in two adults after months without antiviral therapy and following bone marrow transplantation for cancer. Both patients received antiviral drugs while undergoing transplantation to prevent the donors' immune cells from becoming infected with HIV. The patients' own HIV-infected immune cells were killed off by chemotherapy and by graft-versus-host disease, a common post-transplant phenomenon in which the donor's immune cells attack and destroy the recipient's organs, tissues and cells. When antiretroviral treatment was stopped, the patients went into remission for several months, but the virus came roaring back later on, according to published reports.

"Clearly, neither approach managed to eradicate all latently infected cells, and what these cases underscore is the ability of even a few such cells to rekindle infection after prolonged remission," Robert Siliciano says.

The three cases also lend urgency to the search for better ways to monitor the presence of and measure the number of such dormant HIV reservoirs, which could be used as a rough gauge of how long remission might last. Latently infected cells can evade detection by even the most sophisticated tests, which are so exquisitely sensitive that they can sniff the presence of a single HIV-infected cell. The problem is not lack of test sensitivity, the Silicianos explain, but the size of the blood sample tested. Latent HIV reservoirs exist in a few out of millions of immune cells, but a mere 2 percent of memory T cells that harbor such reservoirs are circulating in the blood at any given time. Thus, even large blood samples may not capture the few infected cells harboring dormant virus -- a feat that becomes even more challenging as the number of reservoirs is reduced.

Even though research indicates that remission duration is linked to the amount of latently infected cells, the Silicianos caution remission time is bound to vary widely from patient to patient. Its length would depend on individual biologic factors and the occurrence of other infections that might coax latently infected immune cells out of dormancy and trigger a rebound.

A few patients may never relapse, the Silicianos say, but no patient is safe from rebound as long as he or she harbors even a single latently infected T cell. The unpredictable nature of remission and rebound will therefore require frequent blood monitoring to detect the earliest signs of viral reactivation.

"It is not too soon to begin planning for this type of 'cure' scenario," the authors conclude.

Neuropathy overview from a Johannesburg Hospice

You may not automatically associate hospices with neuropathy patients; after all neuropathy, for all its painfulness, is not fatal. However, many aids patients have terrible problems with neuropathy in the last stages of their suffering and if you put that into the context of a South African hospice, it becomes more understandable.
You may be aware of much of this information but the overview it gives is thorough, clearly explained and accurate and if you're overwhelmed by the amount of information on neuropathy,you can never have enough of those!

Neuropathic Pain: A Patient Information Booklet
Hospice Association of the Witwatersrand


Introduction
Neuropathic pain ('neuralgia') is a pain that comes from nerve problems. There are various causes. It is different to the common type of pain that is due to an injury, burn, pressure, etc. Traditional painkillers such as paracetamol, anti-inflammatories, codeine, morphine, etc, may help, but often do not help very much. However, neuropathic pain is often eased by antidepressant or anti-epileptic medicines - by an action that is separate to their action on depression and epilepsy. Other pain relieving techniques are sometimes used.

What is neuropathic pain?
Pain is broadly divided into two types - nociceptive pain and neuropathic pain.

Nociceptive pain - This is the type of pain that all people have had at some point. It is caused by actual, or potential damage to tissues. For example, a cut, a burn, an injury, pressure or force from outside the body, or pressure from inside the body (for example, from a tumour) can all cause nociceptive pain. The reason we feel pain in these situations is because tiny nerve endings become activated or damaged by the injury, and this sends pain messages to the brain via nerves. Nociceptive pain tends to be described as sharp or aching. It also tends to be eased well by traditional' painkillers such as paracetamol, anti-inflammatory painkillers, codeine, morphine, etc.

Neuropathic pain - This type of pain is caused by a problem with one or more nerves themselves. There is often no 'injury' or tissue damage that triggers the pain. However, the function of the nerve is affected in a way that sends pain messages to the brain. Neuropathic pain is often described as burning, stabbing, shooting, aching, or like an 'electric-shock'. Neuropathic pain is less likely than nociceptive pain to be helped by traditional painkillers. However, other types of medicines often work well to ease the pain (see below). The rest of this leaflet is just about neuropathic pain.

What causes neuropathic pain?
Various conditions can affect nerves and may cause neuropathic pain as one of the features of the condition. These include the following:-
• Trigeminal neuralgia
• Post herpetic neuralgia (pain following shingles)
• Diabetic neuropathy—a nerve disorder that develops in some people with diabetes
• Phantom limb pain following an amputation.
• Multiple sclerosis
• Pain following chemotherapy
• HIV infection
• Alcoholism
• Cancer
• Atypical facial pain
• Various other uncommon nerve disorders
• Infiltration or compression of nerves by a tumour

Note: you can have nociceptive pain and neuropathic pain at the same time, sometimes caused by the same condition. For example, you may develop nociceptive pain and neuropathic pain from certain cancers.

More about the nature of neuropathic pain
Related to the pain there may also be:

Allodynia. This means that the pain comes on, or gets worse, with a touch or stimulus that would not normally cause pain. For example, a slight touch on the face may trigger pain if you have trigeminal neuralgia, or the pressure of the bedclothes may trigger pain if you have diabetic neuropathy.
Hyperalgesia. This means that you get severe pain from a stimulus or touch that would normally cause only slight discomfort. For example, a mild prod on the painful area may cause intense pain.

Paresthesia. This means that you get unpleasant or painful feelings even when there is nothing touching you, and no stimulus. For example, you may have painful pins and needles, or electric shock like sensations.
In addition to the pain itself, the impact that the pain has on your life may be just as important. For example, the pain may lead to disturbed sleep, anxiety and depression.

How common is neuropathic pain?
It is estimated that about 1 in 100 people in the UK have persistent (chronic) neuropathic pain. It is much more common in older people who are more prone to developing the conditions listed above.

What is the treatment for neuropathic pain?
Treatments include
Treating the underlying cause - if possible
Medicines
Physical treatments
Psychological treatments

Treating the underlying cause
If this is possible, it may help to ease the pain. For example, if you have diabetic neuropathy then good control of the diabetes may help to ease the condition. If you have cancer, if this can be treated then this may ease the pain. Note: the severity of the pain often does not correspond with the seriousness of the underlying condition. For example, postherpetic neuralgia (pain after shingles) can cause a severe pain, even though there is no rash or signs of infection remaining.

Medicines used to treat neuropathic pain

Painkillers - The usual 'traditional' painkillers may be tried at first such as paracetamol, anti-inflammatory painkillers, codeine, morphine, etc. These may help. If they do not, or only partially help, then a antidepressant or anticonvulsant medicine is usually advised.

Antidepressant medicines - An antidepressant medicine in the 'tricyclic' group is a common treatment for neuropathic pain. It is not used here to treat depression. Tricyclic antidepressants ease neuropathic pain separate to their action on depression. It is thought that they work by interfering with the way nerve impulses are transmitted. There are several tricyclic antidepressants, but amitriptyline is the one most commonly used for neuralgic pain. In many cases the pain is stopped, or greatly eased, by amitriptyline. Imipramine and nortriptyline are other tricyclic antidepressants that are sometimes used to treat neuropathic pain. A tricyclic antidepressant may ease the pain within a few days, but it may take 2-3 weeks. It can take several weeks before you get maximum benefit. Some people give up on their treatment too early. It is best to persevere for at least 4-6 weeks to see how well the antidepressant is working. Tricyclic antidepressants sometimes cause drowsiness as a side-effect. This often eases in time. To try and avoid drowsiness, a low dose is usually started at first, and then built up gradually if needed. A dry mouth is another common side-effect. Frequent sips of water may help with a dry mouth. See the leaflet that comes with the medicine packet for a full list of possible side-effects.

Anti-epileptic medicines (anticonvulsants) - An anti-epileptic medicine is an alternative to an antidepressant. For example, gabapentin, pregabalin, sodium valproate, and carbamazepine. These medicines are commonly used to treat epilepsy but they have also been found to ease nerve pain. An anti-epileptic medicine can stop nerve impulses causing pains separate to its action on preventing epileptic seizures. As with antidepressants, a low dose is usually started at first and built up gradually if needed. It may take several weeks for maximum effect as the dose is gradually increased.
Sometimes both an antidepressant and an anti-epileptic medicine are taken if either alone does not work very well. Sometimes a traditional painkiller such as codeine is combined with an antidepressant or an anti-epileptic medicine. As they work in different ways they may compliment each other and have an additive effect on easing pain better than either alone.

Capsaicin cream - This is sometimes used to ease pain if the above medicines do not help, or cannot be used because of problems or side-effects. Capsaicin is thought to work by blocking nerves from sending pain messages. Capsaicin cream is applied 3-4 times a day. It can take up to 10 days for a good pain relieving effect to occur. Capsaicin can cause an intense burning feeling when it is applied. In particular, if it is used less than 3-4 times a day, or if it is applied just after taking a hot bath or shower. However, this side-effect tends to ease off with regular use. Capsaicin cream should not be applied to broken or inflamed skin. Wash your hands immediately after applying capsaicin cream.

Other drugs - Some other medicines are sometimes used on the advice of a specialist in a pain clinic. These may be an option if the above medicines do not help. For example, ketamine injections. Ketamine is normally used as an anaesthetic, but at low doses can have a pain relieving effect.

Physical treatments
Depending on the site and cause of the pain, a specialist in a pain clinic may advise one or more physical treatments. These include -
Physiotherapy
Acupuncture
A TENS machine (Transcutaneous Electrical Nerve Stimulation)
Nerve blocks with injected local anaesthetics
Spinal cord stimulation

Psychological treatments
Pain can be made worse by stress, anxiety and depression. Also, the perception ('feeling') of pain can vary depending on how we react to our pain and circumstances. Where relevant, treatment for anxiety or depression may help. Also, treatments such as stress management, counselling, cognitive behaviour therapy, and pain management programmes sometimes have a role in helping people with chronic (persistent) neuropathic pain.

http://www.hospicepalliativecaresa.co.za/pdf/patientcarebooklet/NeuropathicPain.pdf

EXERCISE CAN PROTECT BRAIN FROM DEPRESSION

Physical exercise has many beneficial effects on human health, including the protection from stress-induced depression. However, until now the mechanisms that mediate this protective effect have been unknown. In a new study in mice, researchers at Karolinska Institutet in Sweden show that exercise training induces changes in skeletal muscle that can purge the blood of a substance that accumulates during stress, and is harmful to the brain. The study is being published in the journal Cell

In neurobiological terms, we actually still don't know what depression is. Our study represents another piece in the puzzle, since we provide an explanation for the protective biochemical changes induced by physical exercise that prevent the brain from being damaged during stress," says Mia Lindskog, researcher at the Department of Neuroscience at Karolinska Institutet.

It was known that the protein PGC-1a1 (pronounced PGC-1alpha1) increases in skeletal muscle with exercise, and mediates the beneficial muscle conditioning in connection with physical activity. In this study researchers used a genetically modified mouse with high levels of PGC-1a1 in skeletal muscle that shows many characteristics of well-trained muscles (even without exercising).

These mice, and normal control mice, were exposed to a stressful environment, such as loud noises, flashing lights and reversed circadian rhythm at irregular intervals. After five weeks of mild stress, normal mice had developed depressive behaviour, whereas the genetically modified mice (with well-trained muscle characteristics) had no depressive symptoms.

"Our initial research hypothesis was that trained muscle would produce a substance with beneficial effects on the brain. We actually found the opposite: well-trained muscle produces an enzyme that purges the body of harmful substances. So in this context the muscle's function is reminiscent of that of the kidney or the liver," says Jorge Ruas, principal investigator at the Department of Physiology and Pharmacology, Karolinska Institutet.

The researchers discovered that mice with higher levels of PGC-1a1 in muscle also had higher levels of enzymes called KAT. KATs convert a substance formed during stress (kynurenine) into kynurenic acid, a substance that is not able to pass from the blood to the brain. The exact function of kynurenine is not known, but high levels of kynurenine can be measured in patients with mental illness. In this study, the researchers demonstrated that when normal mice were given kynurenine, they displayed depressive behaviour, while mice with increased levels of PGC-1a1 in muscle were not affected. In fact, these animals never show elevated kynurenine levels in their blood since the KAT enzymes in their well-trained muscles quickly convert it to kynurenic acid, resulting in a protective mechanism.

"It's possible that this work opens up a new pharmacological principle in the treatment of depression, where attempts could be made to influence skeletal muscle function instead of targeting the brain directly. Skeletal muscle appears to have a detoxification effect that, when activated, can protect the brain from insults and related mental illness," says Jorge Ruas.

Depression is a common psychiatric disorder worldwide. The World Health Organization (WHO) estimates that more than 350 million people are affected.

Mental Health Problems From Opioids

Today's post from the ever-reliable pain-topics.org (see link below) discusses some of the potential effects of long term (and recreational) opioid use. Now many people living with neuropathy have no choice; they have to take opioids long term, to help control the pain but it is always worth knowing what they might do to you. The article looks at recent studies and assesses their accuracy. If you're concerned, discuss the issues with your prescribing doctor - he or she should be carefully monitoring you anyway, to reduce the risk of addiction and the question underlying this is whether long term opioid use actually makes us misusers (however unintentionally).

 

Pain, Depression, Anxiety in Rx-Opioid Misusers

Posted bySB. Leavitt, MA, PhD Wednesday, November 21, 2012
 Nonmedical prescription opioid use has become a substantial public health concern in North America and most other countries. Limited epidemiological data suggest an association between such Rx-opioid misuse and mental health or pain symptoms in different populations, although these correlations have not been systematically assessed, which was the purpose of a new study.

A team of Canadian researchers conducted a thorough systematic search, review, and meta-analysis to examine mental health problem symptoms and pain in general population samples reporting nonmedical Rx-opioid use [Fischer et al. 2012]. Overall, 9 qualifying epidemiological studies were identified and included in the review; 5 contributed data on the prevalence of mental health issues and 4 had data on the prevalence of pain in the target population. Most studies (8) were based on populations in the United States and the other one was centered in Ontario, Canada.

Writing in the November 2012 edition of the Journal of Pain, the researchers report that the pooled prevalence of any mental health symptoms in general population samples reporting nonmedical Rx-opioid use was 32% (95% confidence interval [CI], 24–40). Specifically, the pooled prevalence of depression was 17% (95% CI, 14–19) and the prevalence of anxiety was 16% (95% CI, 1–30). The pooled prevalence of pain in the population of interest was found to be 48% (95% CI, 37–59).

The researchers conclude that their study found evidence for disproportionately high prevalence levels of mental health problems (anxiety and depression) and pain among nonmedical Rx-opioid users in the general population. While causality cannot be established by such data, these comorbidities may influence Rx-opioid misuse and should be considered in preventive and treatment interventions.

COMMENTARY: Curiously, Fischer and colleagues do not even mention in their report the prevalence of nonmedical Rx-opioid use found in the 9 epidemiological studies they examined. However, they do include raw data in a table of study characteristics and extrapolating from those data we calculated the prevalence of Rx-opioid misuse as ranging from 1.8% to 12% (mean 5.6%; 95% CI, 3-8.2).

Judging whether 5.6% on average is an extraordinarily high and intolerable prevalence of Rx-opioid misuse requires further consideration of all factors that might be contributing to or account for the alleged aberrant behaviors. However, the wide prevalence range alone suggests that either the measurement of Rx-opioid misuse across studies was inconsistent or the populations examined were significantly different from each other.

The researchers defined “nonmedical use” or “misuse” as the use of Rx-opioids without being medically sanctioned, which may include, but is not limited to, the consumption of these medications for purposes other than prescribed, or taking nonprescribed, diverted, or illicitly obtained Rx-opioids. However, considering the high prevalence of pain, one must question how much of the putative “nonmedical use” actually was for medical purposes (pain relief), which raises questions about access to healthcare and/or the undertreatment of pain via legitimate healthcare channels.

Prevalence levels of anxiety and depression also were considered to be quite high by the researchers, but it is not known if these factors influenced Rx-opioid misuse, if they resulted from such misbehavior, or if they were largely related to unrelieved pain. These are important concerns worthy of further investigation.

Most, but not all, of the included epidemiological studies were of significant size; however, since all of them were focused in North America (primarily the U.S.), the results cannot be generalized to other populations. It is somewhat surprising that these issues have not been investigated by large-scale epidemiological surveys in the general populations of other countries.

There were some critical limitations of this review and meta-analysis by Fischer et al. that are noteworthy and question its validity. Concepts of systematic reviews and meta-analyses were discussed in a recent UPDATE here, and here are some of the concerns in the present study:
There was a significantly high degree of heterogeneity across all of the studies included in meta-analyses, even though differences between many of the studies were small and their confidence intervals were very narrow. For the 4 major analyses — any mental health symptoms, depression, anxiety, and pain — I² values (suggesting the amount of heterogeneity) were 97.3%, 94.8%, 99.8%, and 95.5%, respectively.

Also, there were extremely few studies for each of the 4 meta-analyses regarding factors of interest: 3 studies for any mental health symptoms, 2 each for depression and anxiety, and 4 for pain.

Appropriately, the researchers used random-effects modeling in the pooling of data; however, with so few studies they could not do any sensitivity analyses to determine sources of bias and reliability of results.

In sum, there were so many fundamental differences between studies — eg, population composition, definitions, assessment measures, etc. — influencing heterogeneity, and so few studies for each analysis, that it is questionable whether conducting meta-analyses of the data was appropriate. Perhaps, there have been other studies on these issues that were undiscovered by the researchers’ systematic review, although it did seem to be quite thorough. In any case, there is clearly a need for additional and more consistent research before reliable and valid conclusions can be reached on this subject of factors associated with nonmedical Rx-opioid use.

REFERENCE: Fischer B, Lusted A, Roerecke M, et al. The Prevalence of Mental Health and Pain Symptoms in General Population Samples Reporting Nonmedical Use of Prescription Opioids: A Systematic Review and Meta-Analysis. J Pain. 2012(Nov);13(11):1029-1044 [abstract here].

http://updates.pain-topics.org/2012/11/pain-depression-anxiety-in-rx-opioid.html

FROM THE NOSE TO KNEE ENGINEERED CARTILAGE REGENERATES JOINTS

Human articular cartilage defects can be treated with nasal septum cells. Researchers at the University and the University Hospital of Basel report that cells taken from the nasal septum are able to adapt to the environment of the knee joint and can thus repair articular cartilage defects. The nasal cartilage cells' ability to self-renew and adapt to the joint environment is associated with the expression of so-called HOX genes. The scientific journal Science Translational Medicine has published the research results together with the report of the first treated patients.

Cartilage lesions in joints often appear in older people as a result of degenerative processes. However, they also regularly affect younger people after injuries and accidents. Such defects are difficult to repair and often require complicated surgery and long rehabilitation times. A new treatment option has now been presented by a research team lead by Prof. Ivan Martin, professor for tissue engineering, and Prof. Marcel Jakob, Head of Traumatology, from the Department of Biomedicine at the University and the University Hospital of Basel: Nasal cartilage cells can replace cartilage cells in joints.

Cartilage cells from the nasal septum (nasal chondrocytes) have a distinct capacity to generate a new cartilage tissue after their expansion in culture. In an ongoing clinical study, the researchers have so far taken small biopsies (6 millimeters in diameter) from the nasal septum from seven out of 25 patients below the age of 55 years and then isolated the cartilage cells. They cultured and multiplied the cells and then applied them to a scaffold in order to engineer a cartilage graft the size of 30 x 40 millimeters. A few weeks later they removed the damaged cartilage tissue of the patients' knees and replaced it with the engineered and tailored tissue from the nose. In a previous clinical study conducted in cooperation with plastic surgeons and using the same method, the researchers from Basel recently already successfully reconstructed nasal wings affected by tumors.

Surprising Adaption

The scientists around first author Dr. Karoliina Pelttari were especially surprised by the fact that in the animal model with goats, the implanted nasal cartilage cells were compatible with the knee joint profile; even though, the two cell types have different origins. During the embryonic development, nasal septum cells develop from the neuroectodermal germ layer, which also forms the nervous system; their self-renewal capacity is attributed to their lack of expression of some homeobox (HOX) genes. In contrast, these HOX genes are expressed in articular cartilage cells that are formed in the mesodermal germ layer of the embryo.

"The findings from the basic research and the preclinical studies on the properties of nasal cartilage cells and the resulting engineered transplants have opened up the possibility to investigate an innovative clinical treatment of cartilage damage," says Prof. Ivan Martin about the results. It has already previously been shown that the human nasal cells' capacity to grow and form new cartilage is conserved with age. Meaning, that also older people could benefit from this new method, as well as patients with large cartilage defects. While the primary target of the ongoing clinical study at the University Hospital of Basel is to confirm the safety and feasibility of cartilage grafts engineered from nasal cells when transplanted into joint, the clinical effectiveness assessed until now is highly promising.

Lessons From A Life With Neuropathy

Today's post from painhq.org (see link below) is an honest, personal story of life with neuropathy. Reading it you may feel that this man's lifestyle has directly contributed to his condition but it's far too easy to criticise from a distance without first looking at our own lives. The story will certainly be recognisable for many neuropathy patients, proving that nothing is as black and white as it seems - sometimes, life just gets in the way. This man uses gabapentin with success but that is his case, that doesn't mean that gabapentin is necessarily the answer for you.

Life with neuropathy
2016

'Old Fart' William's Story

 

I am 72 years old and live alone in a single family bungalow in Peterborough. I eat too much, drink too much, and get too little exercise. I am a retired teacher and have lived alone since my wife died in 2000. I am a fat old fart who lives a fairly circumscribed life - only partly due to my neuropathy. Right now my sciatica is flaring up and is far more debilitating.

My peripheral neuropathy likely dates back to the early to mid ‘90s. I suffered from falling arches, and for some time I ascribed my foot and leg discomfort solely to that issue. It was only in 1997, when the numbness, burning, and occasional stabbing pain was keeping me awake, that I took the problem to my GP.

It is so long ago that I have little or no recollection of the original process of diagnosis. The story is complicated in my mind by my wife suffering a massive brain injury at that time. She was in an automobile accident in Ottawa, in the summer of 1996. She was in an Ottawa hospital until the spring of 1997, and again for several more visits during the next couple of years. She lived at home until her death in January, 2000. Naturally, at the time, my minor problem was peripheral to hers. It was while she was in the hospital (1996 – ’97) that the burning and tingling got so bad that I went to see my GP.  He referred me to a local neurologist who ran some tests and diagnosed peripheral neuropathy. By that time (1998 – ’99) the loss of feeling extended almost to my knees.

The neurologist had no answer as to the origin of the condition. I had been drinking heavily earlier in my life, but had been totally dry for ten years when the condition struck. My GP (at the time) in 1997-9 was convinced that I had diabetes. My blood sugar levels were consistently close to the threshold levels, so he took that leap and declared me diabetic; controlling it with diet and exercise.  It wasn’t until my present GP had me do a glucose test (in 2009) that the diabetes diagnosis was ruled out.

At the beginning I had “pins and needles”, burning on the soles of my feet, numbness or loss of feeling in my feet and lower legs, aching feet and legs (perhaps partly due to the falling arches) and occasional shooting pains or a feeling like a weak electric shock. I do not remember the specifics, but I am sure that the discomfort started in one foot at a time before it came to affect both feet and legs. I have a vague memory of it migrating from one foot to the other over the months.

Finding relief, also known as, gabapentin

Back in 1997 or ‘98 my GP prescribed a common medication used off-licence to treat nerve pain. I have no recollection of which one it was. I just remember him saying that no medication worked for any large percentage of the sufferers, but that particular one was the most efficacious. It might have been an anti-depressant, but the specifics escape me. I just remember that I got every side-effect listed on the fact sheet (dry mouth is one I remember), but it did nothing to ease my nerve pain.

The second medication he prescribed was gabapentin. It was a miracle cure. Within a few days the worst of the symptoms had eased, and after trying different dosages we settled on just 300mg per day. Over the years, I have had to increase the dosage as the pains and discomfort returned. I have never been free of the feeling that something in my feet and legs isn’t right. There is the constant numbness, the decrease in flexibility, and the fairly common occasional tingling sensation. It isn’t pain! For many years, the discomfort was almost forgettable as I went through my daily chores. I loaded my gabapentin into the evening to reduce any chance of pains that would get in the way of my sleep. I don’t think that I ever expected to avoid all of the discomfort of numbness and a bit of tingling. I was happy as long as I could get to sleep every night. I have never suffered from any side-effects related to the gabapentin; or none that I identified.

Currently, I am taking 1500mg of gabapentin daily. It has been my only medication since the late ‘90s, and the only change has been a gradual increase in the dosage over the past 15 or 16 years. I am told that I could probably take and tolerate higher doses and that some patients do take more than my dose.

Life with numbness

From the 1990s, I recognized that I was losing my sense of balance. I avoid ladders. I am far more sedentary than I was in middle age. I rarely travel and, if so, prefer to use my car. At present, I avoid activities which require much walking and standing. I do my own housework (such as it is), but hire people to look after the outside chores. At home, I spend far too much time sitting at the computer – as I am now! I assume that some of the inactivity and lethargy is a result of becoming a fat old fart. I stopped mowing my own lawn over 10 years ago lest I stumble on the uneven surface. For exercise, I walk on a treadmill rather than the sidewalk, as I fear tripping on the uneven surface. For a couple of years before I got a treadmill, I used to walk at 4:00 or 5:00 AM so that I could walk on the residential street which was smoother than the sidewalk.

As some of my foot muscles become dominant and others atrophy, walking becomes more problematic. I drag my heels and walk flat-footed. My feet are no longer flexible, so I describe the sensation as akin to walking with snowshoes. My feet and legs feel “heavy”. It is very tiring. I can’t walk nearly as fast, or as far as I used to. Much beyond a mile is getting to be a trial: not impossible, but not comfortable. My legs ache after any decent walk on my treadmill. Hiking or walking off road is almost impossible. An extended shopping trip can be problematic. Luckily, I detest shopping.

I can feel movement on my skin if a finger is rubbed across my foot or leg, but if touched gently without disturbing the hairs, I often can’t tell if my foot or leg is being touched at all. If I am poked I get no different sensation from a finger than from a needle. Some nerves seem to still work as occasionally I get a sharp pain from stubbing a toe, but most times my only clue that I have stubbed it is the blood welling out from under the nail.

For the past 2 or 3 years I have been noticing a gradual loss of sensation in my fingers. It is just the same numbness and tingling that affects my feet, but less severe as yet. As I do all my own cooking it presents the constant threat of burned fingers. I cook most of my food from fresh ingredients, so I find that my legs often get tired and achy from standing too long in the kitchen preparing vegetables or batch-cooking for my freezer. Perhaps it is the muscle changes in my feet and legs which cause me the most problem; not the occasional bout of neuropathy pain.

My physiotherapist comments that I have retained strength in my arms and legs, but I notice a lack of strength in my hands and a sensitivity in the skin which keeps me from opening jars or bottles. It can hurt to try to grasp an object too tightly. Accidentally hitting my hand on a piece of furniture or door jamb is often remarkably painful; far more so than used to be the case. I am more likely to drop a light object as I no longer sense, say, a sheet of paper in my hand. Simple tasks, such as doing up small buttons, becomes nearly impossible. My wardrobe reflects that new reality; few shirts with buttons and no tight collars. I struggled mightily to rewire a lamp the other day. My fingers were like useless - and senseless - lumps of clay. It is hard to manipulate thin wire with no sense of touch. Picking up small objects is a trial.

My days entail reading the newspaper, normal ablutions, essentials of housework (dusting is avoided at all costs), email contact with a couple of dozen people, internet surfing, walking on my treadmill or doing stretching exercises, watching videos from my PVR or streamed to my TV through my computer, football and occasional soccer matches watched live, daily food preparation, grocery shopping 2 or 3 times a week, occasional appointments and lunches with friends, usually weekly contests over a friend’s snooker table, weekly visits by a female friend. I drive to see my children and grandchildren every few weeks. I have pretty well ceased attending plays and concerts except for the occasional MET in HD performance. That is more due to the lack of a companion rather than the effects of my neuropathy. I have ceased travelling because of my inertia, and mostly the lack of a suitable travel companion. Neuropathy wouldn’t keep me at home were I really keen to take a particular trip. It would just affect the type of trip and the day’s activities – as it does at home. My inertia is only partly the result of my neuropathy.

What pain is like now

I have used gabapentin alone for over 15 years. I have never tried any other medication. I asked my GP about newer and better medications a year or so ago. He said I should stay with what is working rather than weaning me off it and then going through the process of trying to find something better. I was somewhat relieved.

All in all, I view myself as being rather lucky. I found gabapentin pretty early in the process and under normal conditions I can say that I am pain-free. I have discomfort, and my life is circumscribed, but I do not have the constant level of pain common to some sufferers.

My advice for anyone newly diagnosed with neuropathic pain?

• Seek out whatever medication will render the nerve pain bearable. Once you can limit the pain, everything else is reduced to the level of a really annoying nuisance. 
• Forget vanity and wear sensible shoes with proper orthotic support to keep you mobile. Work with a physiotherapist to develop a regimen of stretching exercises to help keep you as flexible as possible.
• Understand that you will have a constant struggle to maintain as much of your lifestyle as possible, to work around your new limitations, and to seek out any treatments or devices which will make life a bit easier. 
• It isn’t a death sentence so much as a constant set of hurdles which will make life a bit more difficult, but still enjoyable. It’s no walk in the park, but look around at your peers and all of a sudden neuropathy isn’t so bad. There are lots worse conditions to have to cope with.
• https://www.painhq.org/connect/personal-stories/detail/life-with-neuropathy