Tuesday, 24 November 2015

What Should You Ask Your Neurologist About Neuropathy?

Today's short post from livingwithperipheralneuropathy.com (see link below) gives some useful advice as to how to get a better understanding of your neuropathic problems and that is by asking questions. Most doctors and specialists just don't have the time any more to do anything more than skim over the facts when it comes to the complexities of neuropathy. That's far from ideal and does the patient no favours at all. Therefore it's up to us to provide a list of questions and insist on some answers. By doing this you can get answers to what you really want to know. Doctors can't read minds so it's up to you to get answers to your own specific questions.

Questions to Ask your Neurologist about your Peripheral Neuropathy
By Dean S. Lewis|November 22nd, 2015

Questions to ask your neurologist

The first step to overcome a disease is to fully understand it. Of course, that does not involve being an expert in the field, not even it is essential to follow one and all research done on the subject; but understanding pretty well what it is about may lead to better solutions. Peripheral neuropathy is damage to the peripheral nerves that carry information to central nervous system (brain and spinal cord) and bring back the reply from it. It is a two-way road, to put it clearly. These nerves can transport sensory, sensitive, motor and autonomic information, so that the variability of symptoms is very wide. Moreover, peripheral neuropathy obeys to diverse causes, so prognosis and treatments may differ.

Having an excellent communication with your neurologist is essential. Though we can read a lot about peripheral neuropathy, each case is unique and unrepeatable, so understanding our particular disease is based on that communication with our neurologist. Once the diagnosis of peripheral neuropathy is done, we must establish the relationship with the neurologist, especially in the sense of clearing all our doubts.

A patient with a diagnosis of peripheral neuropathy wants to know many things. A first step is to write down all that questions as they arise. On many occasions it seems our questions are not that important and, that is a mistake. The key is not to pretend to be smart in front of our physician, but to let him solve our doubts. Do not be afraid to ask something just because it seems too simple.

Maybe sorting all those questions before your appointment and writing them down helps us a lot. For instance, we can ask about the disease that has caused peripheral neuropathy, evolution, conventional and alternative treatments, convenience of joining support groups, etc. As they say, there are no diseases but sick people. Each patient is different and would face the situation from its own angle.

Not a minor detail is to choose well the neurologist that will treat our peripheral neuropathy, not only by choosing the more knowledgeable one, but someone who can provide us a good level of information. A good doctor not only will clear up all of our doubt we have in written, but he surely will expand on those answers.

If you want to do a list of questions you can start by reading about Symptoms of Peripheral Neuropathy Here

Share with us the list of questions you have asked or you would ask your doctor and how did he handle them.


Monday, 23 November 2015

Why Aren't Neuropathy Symptoms Recognised By Doctors?

Today's post from cidpusa.org (see link below) refers to a report published by the Neuropathy Trust in which the lack of good diagnosis by home doctors and others, leads to many neuropathy patients having to wait far too long before seeing a specialist. It's a report on a U.K. situation but is almost certainly reflected worldwide. You have to ask yourself why this still happens with such alarming regularity. Doctors claim the disease is difficult to diagnose, yet the symptoms of most neuropathies are so unique, it's hard to imagine that doctors can't recognise them and move on to further investigation via a specialist. Is it because patients own accounts aren't being listened to? Or if they are, they're not taken seriously? Unfortunately the latter is all too often the case. A patient's own story of neuropathic symptoms should be enough to at least set doctors on the right track and begin the long process of testing and diagnosis but far too often it's not and in this day and age that's unacceptable.

Pain condition 'ignored' by GPs
November 2015

Doctors misunderstand or ignore a severe pain condition thought to affect more than a million people in the UK, sufferers believe.

Peripheral neuropathy (PN), a condition in which nerve disturbances cause chronic pain, often goes undiagnosed.

The survey for the Neuropathy Trust revealed a quarter of patients wait at least a year for referral to a specialist.

Doctors said the condition was often difficult to detect.

Two-thirds of patients felt their condition was not satisfactorily kept under review, leading to the feeling that they were being forgotten by doctors.

The only way I can describe the pain is like a ring of cheesewire tightening around my toes Shirley Hughes 

More than six in ten had never been given a definitive diagnosis, according to the survey of 662 members of the trust.

The condition often gives rise to severe neuropathic pain (NeP) which causes parts to the body to become super-sensitive.

NeP mainly affects the arms, hands legs and feet. It can be triggered by light pressure from clothing, air movement or temperature changes.

The pain is often described as stabbing, burning, tickling, prickling or tingling.


The survey showed almost three-quarters of people with the condition are unable to work due tostabbing, burning, tickling, prickling or tingling type pain. The trust estimates there are 1.4 million sufferers in the UK.

One of them, 70-year-old Shirley Hughes, from Runcorn, Cheshire, said the condition had a massive impact on her life.

She said: "Sometimes the pain in my feet is too much to bear. The only way I can describe the pain is like a ring of cheesewire tightening around my toes.

"I had so many plans for my retirement and these are no longer possible. I had to cancel a planned trip to Australia this summer for a family wedding."

Dr Steve Allen, a consultant in chronic pain management based at the Royal Berkshire Hospital in Reading, backed the findings of the survey.

He said: "Many patients seen in my pain clinic have waited for many months from the time that they first visited their GP to the time that they receive a definitive diagnosis and commence treatment.


"During this time their condition has often worsened, and their quality of life significantly reduced."

Co-author of a report for the Neuropathy Trust Andrew Keen, himself a sufferer of the condition, said: "Peripheral Neuropathy and Neuropathy are not new conditions. What is new is the research that is exposing them as real physical illnesses which deserve more attention than they are at present given."

He said there was an urgent need to educate GPs about peripheral neuropathy and improve fast-track patient and investigation practices. The report called for specific action by the government.

More than 100 potential causes are thought to underlie the condition, including CIDP, diabetes, cancer, and HIV.

Dr Paul Watson at the Pain Society said: "It is a difficult condition to diagnose. Often people are missed."

The solution lay in educating GPs and other frontline staff about peripheral neuropathy, he said.

He said the condition was "not very common" but that there was not enough time to see patients who need a considerable length of consultation to allow a diagnosis to be made.

Dr Watson added: "We need more resources in pain clinics."


Sunday, 22 November 2015

Juicing Cannabis Leaves To Treat Nerve Pain

Today's post is another article from naturalnews.com (see link below) and looks at the benefits of yet another part of the cannabis plant for pain relief (amongst others). This time, instead of having to smoke a joint, or other well-known cannabis uses, the juice from the crushed leaves can be used to produce CBD oil, which it's turning out, has many health benefits in itself. This article discusses how this can benefit pain sufferers and how the so-called cannabidiol (CBD) works. Further research on the internet or YouTube will unearth countless other articles along the same lines, plus tips on how to make it yourself (cheaper than buying it ready prepared). It would be wise to include your home doctor in this process, because it may become part of your overall treatment; however, that isn't always possible (or even wise, considering the law aspects) so doing your own thorough research is essential. Worth a read for neuropathy patients.

Learn about the amazing health benefits of juicing raw cannabis (marijuana) leaves
Friday, May 04, 2012 by: Ethan A. Huff, staff writer

(NaturalNews) Contrary to popular belief, the marijuana plant is a whole lot more than just a psychoactive drug that "stoners" use to get high. In raw form, marijuana leaves and buds are actually loaded with a non-psychoactive, antioxidant, anti-inflammatory, and anti-cancer nutrient compound known as cannabidiol (CBD) that is proving to be a miracle "superfood" capable of preventing and reversing a host of chronic illnesses.

Though you may not have heard much about it, the CBD found in the marijuana plant -- marijuana is technically just a vegetable, by the way -- is a highly medicinal substance with unique immune-regulating capabilities. Since the human body already contains a built-in endogenous cannabinoid system, complete with cannabinoid receptors, inputting CBD from marijuana can help normalize the body's functional systems, including cell communication and proper immune function.

The way CBDs work is that they bridge the gap of neurotransmission in the central nervous system, including in the brain, by providing a two-way system of communication that completes a positive "feedback loop," according to Dr. William Courtney, a medical marijuana expert and founder of Cannabis International. As opposed to a one-way transmission, which can promote chronic inflammation of healthy tissue, the unique two-way transmission system engaged by marijuana CBDs mimics the body's own natural two-way communications system.

So individuals whose systems are compromised by autoimmune disorders, cellular dysfunction, chronic inflammation, cancer cells, and various other illnesses can derive a wide range of health-promoting benefits simply by consuming CBDs. And one of the best ways to obtain CBDs is to juice raw marijuana leaves and buds, according to Dr. Courtney, who currently runs a clinic in Luxembourg that provides raw cannabis medicinal services to patients in need.

"CBD works on receptors, and as it turns out, we have cannabinoids in our bodies, endogenous cannabinoids, that turn out to be very effective at regulating immune functions, nerve functions, bone functions," says Dr. Ethan Russo, a Seattle, Wash.-area physician who is also a senior advisor to GW Pharmaceuticals, a British drug company that is utilizing CBDs in a new marijuana mouth spray known as Sativex.

"There's a tendency to discount claims when something appears to be good for everything, but there's a reason this is the case. The endogenous cannabinoid system acts as a modulator in fine-tuning a lot of these systems, and if something is deranged biochemically in a person's body, it may well be that a cannabinoid system can bring things back into balance."

Be sure to check out these amazing videos from Cannabis International that explain more about how raw cannabis, and specifically the CBDs found inside the plant, work to promote health and reverse disease:


Saturday, 21 November 2015

Alternative Pain Remedies

Today's post from naturalnews.com (see link below) looks once again at the alternative side of pain treatment but in this case, the focus is more on tried and tested treatments stemming from nature, which people have used over centuries before the advent of chemical pills. Of course that guarantees you nothing - especially as a neuropathy patient who is used to treatments not working in their particular case but some of these may be worth looking into. Do your research and try to talk to a professional with knowledge of the field and because of the nature of clashes with other drugs, always consult your doctor to see that you're not doing yourself any harm.

Top remedies for treating chronic pain naturally Thursday, February 14, 2013 by: Jonathan Benson, staff writer

Treating chronic pain is a complex issue because there are numerous factors that contribute to its development and persistence. Contrary to popular belief, most instances of chronic pain do not actually originate in the muscles, bones, and tissues, but rather in the nerves, which means eating foods and taking herbs that promote central nervous system health may be the best approach to getting rid of chronic pain for good. Here are 10 ways to treat chronic pain naturally without drugs:

1) Willow bark. Used for thousands of years in many different cultures to reduce fever and inflammation, willow bark is a powerful painkilling herb that is still used today to treat back pain, arthritis, headaches, and inflammatory conditions like bursitis and tendinitis. The active ingredient in willow bark, salicin, is actually the compound that was first used in the 1800s to develop aspirin. Though it may not work as quickly as aspirin, willow bark is said to provide longer-lasting benefits without the harmful side effects. (http://www.umm.edu/altmed/articles/willow-bark-000281.htm)

2) Cannabis. Aside from its psychoactive effects, the active ingredient in cannabis, tetrahydrocannabinol (THC), is a powerful analgesic with proven pain-relieving properties. Numerous studies have found that taking cannabis can help ease neurological pain without causing harmful side effects, which makes it a far more promising candidate than what conventional medicine has to offer. And even better than smoking cannabis is juicing its leaves raw, which has been shown to actually reverse chronic pain and illness. (http://www.naturalnews.com/035759_cannabis_juicing_health.html)

3) Turmeric. One of the most powerful known anti-inflammatory herbs, turmeric is virtually unparalleled in its ability to treat arthritis, gout, autoimmune disease, sciatic, and other inflammatory conditions. Systemically, turmeric helps quell disease-causing inflammation in all its forms, and may be the key to overcoming whatever pains might be ailing you.

4) Kava kava
. Pacific Islanders have long utilized kava kava, also known as "intoxicating pepper," to unwind and relax after a long day. But this natural botanical is also highly effective at reducing anxiety, easing nerves, relaxing muscles, and subdue pain. Because of its synergistic ability to promote restfulness both mentally and physically, kava kava can be extremely helpful in overcoming chronic pain, especially when such pain has a psychological component. (http://www.konakavafarm.com/articles/alternative.html)

5) Skullcap. An herb native to North America, skullcap has been used for more than 200 years to treat anxiety, nervous tension, convulsions, and pain. And Chinese skullcap, a similar but slightly different herb, has been shown to help treat allergies, infections, inflammation, headaches, and even cancer. Between the two herbs, chronic pain sufferers have a powerful weapon for naturally calming their nerves and relieving pain. (http://www.umm.edu/altmed/articles/skullcap-000273.htm)

6) Valerian. Often blended with skullcap, Valerian is another natural herb with an extensive history of use in relieving pain. Often used as a sleeping aid due to its ability to promote relaxation, Valerian is also useful for easing anxiety and psychological stress, which are often responsible for causing or exacerbating chronic pain. Valerian can also help treat depression, muscle and joint pain, headaches, and menstrual pain (http://www.umm.edu/altmed/articles/valerian-000279.htm).

7) Devil's claw.
This native African herb is so effective at relieving arthritis, lower back, knee, and hip pain that it has actually been approved as a non-prescription medicine in Germany. Devil's claw has been shown in studies to effectively relieve chronic pain in as little as 10 days of therapeutic use without causing any harmful side effects. Devil's claw can also be used in place of non-steroidal anti-inflammatory drugs (NSAIDs) like acetaminophen and ibuprofen to temporarily relieve pain. (http://www.umm.edu/altmed/articles/devils-claw-000237.htm)

8) Magnesium.
Magnesium comes up a lot as a recommendation in natural treatment protocols, and this is no accident. A powerful treatment for both muscle and nerve pain, magnesium has been shown to balance levels of a brain chemical known as NMDA that is responsible for transmitting pain throughout the nervous system. Magnesium deficiency is also a common cause and amplifier of pain, so simply supplementing with it can help significantly improve pain symptoms. (http://www.psychologytoday.com)

9) SAM-e
. A popular dietary supplement for treating osteoarthritis and depression, SAM-e, or S-Adenosyl-L-Methionine, is a compound naturally found in every human cell in the body. Recognized for its anti-inflammatory and analgesic benefits, SAM-e can help ease pain, relieve stiffness, reduce joint swelling, and even rebuild cartilage. SAM-e is also known to help treat fibromyalgia, bursitis, tendinitis, and lower back pain. (http://osteoarthritis.about.com/od/alternativetreatments/a/sam-e.htm)

10) Vitamin D.
Vitamin D deficiency is linked to a host of chronic illnesses, including chronic pain. A 2009 study found that patients deficient in vitamin D require almost twice as much pain medication as patients with adequate levels, illustrating an inverse relationship between vitamin D levels and pain. Supplementing with vitamin D and regularly exposing your skin to natural sunlight just might be the remedy you need for overcoming chronic pain. (http://www.vitamindcouncil.org/)

Sources for this article include:






Friday, 20 November 2015

See-Through Zebra Fish Reveal Nerve Regeneration

Today's post from sciencedaily.com (see link below) looks at a surprising solution to the problems researchers have had with understanding how nerves can regenerate (or not). Zebra Fish larvae are transparent, so for the first time, it's possible to watch what happens when nerves are disrupted or severed. The purpose of this is to develop genetic treatments in the future that can 'instruct' the nerve cells to seek each other out and re-join. That's a very simple version of the story of course; reading the article will tell you much more.

Zebrafish reveal how axons regenerate on a proper path
Correctly directing axons to reconnect could help in cases of trauma, degeneration 

Date:November 5, 2015 Source:University of Pennsylvania School of Medicine
This is a picture of back (green) and abdominal (magenta) peripheral nerve axons in zebrafish.
Credit: Michael Granato, PhD, Lab, Perelman School of Medicine, University of Pennsylvania

When peripheral nerves are damaged and their vital synaptic paths are disrupted, they have the ability to regenerate and reestablish lost connections. But what about when a nerve is severed completely, its original route lost? How does a regenerating axon, looking to reconnect with its proper target -- with so many possibilities and only one correct path to restore original functioning -- know which way to go? Using a transparent zebrafish model, researchers from the Perelman School of Medicine at the University of Pennsylvania, have identified key components of a mechanism that allows the nervous system to heal itself. Their work was published online this week in Neuron ahead of the print issue.

"It's been known for over one hundred years that peripheral nerves can regenerate," said senior author Michael Granato, PhD, a professor of Cell and Developmental Biology. However, the mechanics of regeneration, including the question of whether the restoration of axonal branches is random or guided in some way, have remained unresolved issues, partly because of the difficulty of observing the process in live animals. Using zebrafish, which are transparent at larval stages, Granato and his colleagues were able to literally obtain a whole new window into how axons regenerate.

"What really made the difference is the ability to visualize these nerves before and after they were completely cut," he explained. "In no other vertebrate system can you do that, so you can't really be sure what is going on. For example, in a mouse, you basically have to sacrifice the animal and look at what happened after the injury. You don't know how the situation was before, so you have to extrapolate and make assumptions."

The researchers used fluorescent proteins to label back and abdominal peripheral nerve axons to observe regeneration after nerves were transected by a laser. They found that as regenerating axonal growth cones reach a branch point at which they have to 'choose' to go one way or the other, they will explore both the correct and incorrect paths, but only the proper path will be supported by components of the extracellular matrix (ECM). The ECM is a mix of substances, including collagen, carbohydrates, and fluid, produced by cells and secreted into the environment around them. Cells are embedded in the ECM and it can affect their behavior. In the case of regenerating neuron axons, the ECM keeps axons from 'choosing' incorrect paths and tilts the balance toward the correct growth direction.

The team next investigated the ECM factors that influence this selective regeneration. "The system is heavily influenced by a genetic pathway that starts with the expression of a particular collagen in glial cells," said Granato. "The glial cells that are close to an injury site start expressing the collagen gene 4a5, which has to be modified by a particular enzyme called lh3 to be secreted into the extracellular space."

Collagen 4a5 and the axonal repellent protein Slit1 are strongly upregulated after nerve injury and form a complex. The cells in which the collagen and slit1a are upregulated are along the wrong pathway. They form a barrier because collagen will anchor slit1, present it to the axons, which have the receptor for slit1, and that makes them turn away or stop growing, thereby promoting the regeneration of axons toward their proper paths and towards their original targets. "The specificity really comes from slit1 and its receptor," Granato explained. He also noted that the same genes are conserved in other vertebrates, including humans.

These experiments are an important step in understanding peripheral nerve regeneration, establishing that it is decidedly not a random process but is controlled by particular genetic pathways. The researchers plan to delve further into the specific mechanisms at work, including the possibility that different nerve cell extensions, such as axons, may control regeneration in separate areas.

"This pathway is highly specific for only the dorsal nerve branch," Granato pointed out. "If we transect the ventral nerves, they are completely unaffected by this genetic pathway. The questions are: Where does this specificity come from? Why are some axons responding to this pathway and others are not? That's basically what's next for us; we want to find out how the specificity is achieved."

While any prospects for clinical applications are still in the future, the work points to some important new research directions. "It tells us there are pathways that we, at some point, will be able to take advantage of to really properly direct axons to regenerate nerves," Granato noted. "Even knowing that in theory one can do that, because there are genes for it, is a significant finding."

Story Source:

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

Journal Reference:
Jesse Isaacman-Beck, Valerie Schneider, Clara Franzini-Armstrong, Michael Granato. The lh3 Glycosyltransferase Directs Target-Selective Peripheral Nerve Regeneration. Neuron, 2015; DOI: 10.1016/j.neuron.2015.10.004


Thursday, 19 November 2015

Small Fibre Neuropathy - Is That What You've Got?

Today's post from ccjm.org (see link below) is one of those posts that, while long, is definitely worth reading for neuropathy sufferers. The reason being that it is so thorough and informative. So much well-explained and clear information in one article is a rare find, so it's worth promoting. Remember, although the title refers to small-fibre neuropathy, don't let this put you off if your neuropathy been given another label - the information here applies to most neuropathies and there will be many things of value for most neuropathy patients.

Small fiber neuropathy: A burning problem
Neuromuscular Disease Center, Neurological Institute, Cleveland Clinic
Director, Cleveland Clinic Cutaneous Nerve Laboratory, Neuromuscular Disease Center, Neurological Institute, Cleveland Clinic ADDRESS: Lan Zhou, MD, PhD, Neuromuscular Disease Center, Neurological Institute, S90, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail zhoul2@ccf.org.


Small fiber neuropathy is increasingly being recognized as a major cause of painful burning sensations in the feet, especially in the elderly. Although strength remains preserved throughout the course of the disease, the pain and paresthesias are often disabling. Diabetes mellitus is the most common identifiable cause of small fiber neuropathy, and impaired oral glucose tolerance and individual components of the metabolic syndrome are often associated with it. Some cases, however, are idiopathic. Skin biopsy (with an evaluation of the density of intraepidermal nerve fibers) and tests of autonomic nerve function are useful for the diagnosis. Management involves controlling pain and identifying and aggressively treating the underlying cause.
CCJM 2009 5;76(5):297-305.

Key Points
Symptoms of small fiber neuropathy typically start with burning feet and numb toes.
Causes and associated conditions can be found in over 50% of cases. These include glucose dysmetabolism, connective tissue diseases, sarcoidosis, dysthyroidism, vitamin B12 deficiency, paraproteinemia, human immunodeficiency virus infection, celiac disease, neurotoxic drug exposure, and paraneoplastic syndrome.
Findings on routine nerve conduction studies and electromyography are typically normal in this disease.
Management includes aggressively identifying and treating the underlying cause, advising lifestyle modifications, and alleviating pain.

An estimated 15 to 20 million people in the United States over age 40 have some type of peripheral neuropathy.1 In many, the impairment is purely or predominantly in small nerve fibers, and the clinical presentation consists of pain, burning, tingling, and numbness in a length-dependent or stocking-glove distribution. (“Length” refers to distance from the trunk; distal fibers are affected first.) Symptoms typically begin in the feet and slowly ascend to the distal legs, at which point the hands may also be affected (FIGURE 1).

In many of these patients, the findings on neurologic examination, nerve conduction studies, and electromyography are normal, although some may show signs of mild distal sensory loss on physical examination. The lack of objective findings on routine nerve conduction studies and electromyography may lead many physicians to attribute the symptoms to other disorders such as plantar fasciitis, vascular insufficiency, or degenerative lumbosacral spine disease.

The past 2 decades have seen the development of specialized tests that have greatly facilitated the diagnosis of small fiber neuropathy; these include skin biopsy to evaluate the density of nerve fibers in the epidermis and studies of autonomic nerve function. Common etiologies have been identified for small fiber neuropathy and can be specifically treated, which is critical for controlling progression of the disease. Pain management is becoming easier with more available options but is still quite challenging.


Small fiber neuropathy is a disorder of the peripheral nerves that primarily or exclusively affects small somatic fibers, autonomic fibers, or both, resulting in sensory changes and autonomic dysfunction when both types are involved (FIGURE 2).2

FIGURE 1. Symptoms are pain, burning, numbness, and autonomic dysfunction (lack of sweating) in the hands and feet in a stocking-glove distribution. Strength is not affected. Tendon reflexes are normal, as are nerve conduction studies.

Peripheral nerve fibers can be classified according to size, which correlates with the degree of myelination.
Large nerve fibers are heavily myelinated and include A-alpha fibers, which mediate motor strength, and A-beta fibers, which mediate vibratory and touch sensation.
Medium-sized fibers, known as A-gamma fibers, are also myelinated and carry information to muscle spindles.
Small fibers include myelinated A-delta fibers and unmyelinated C fibers, which innervate skin (somatic fibers) and involuntary muscles, including cardiac and smooth muscles (autonomic fibers). Together, they mediate pain, thermal sensation, and autonomic function.

Small fiber neuropathy results from selective impairment of small myelinated A-delta and unmyelinated C fibers.

Sensory symptoms: Pain, burning, tingling, numbness

Damage to or loss of small somatic nerve fibers results in pain, burning, tingling, or numbness that typically affects the limbs in a distal-toproximal gradient. In rare cases, small fiber neuropathy follows a non-length-dependent distribution in which symptoms may be manifested predominantly in the arms, face, or trunk.

Symptoms may be mild initially, with some patients complaining of vague discomfort in one or both feet similar to the sensation of a sock gathering at the end of a shoe. Others report a wooden quality in their feet, numbness in their toes, or a feeling as if they are walking on pebbles, sand, or golf balls. The most bothersome and fairly typical symptom is burning pain in the feet that extends proximally in a stocking-glove distribution and is often accompanied by stabbing or aching pains, electric shock-like or pins-and-needles sensations, or cramping of the feet and calves.

Symptoms are usually worse at night and often affect sleep. Some patients say that their feet have become so exquisitely tender that they cannot bear having the bed sheets touch them, and so they sleep with their feet uncovered. A small number of patients do not have pain but report a feeling of tightness and swelling in their feet (even though the feet appear normal).

Examination often reveals allodynia (perception of nonpainful stimuli as being painful), hyperalgesia (perception of painful stimuli as being more painful than expected), or reduced pinprick and thermal sensation in the affected area. Vibratory sensation can be mildly reduced at the toes. Motor strength, tendon reflexes, and proprioception, however, are preserved because they are functions of large nerve fibers.

Autonomic symptoms

When autonomic fibers are affected, patients may experience dry eyes, dry mouth, orthostatic dizziness, constipation, bladder incontinence, sexual dysfunction, trouble sweating, or red or white skin discoloration.2 Examination may show orthostatic hypotension and skin changes. The skin over the affected area may appear atrophic, dry, shiny, discolored, or mildly edematous as the result of sudomotor and vasomotor abnormalities.



Small fiber neuropathy has been associated with many medical conditions, including glucose dysmetabolism,3 connective tissue disease,4,5 dysthyroidism,6 vitamin B12 deficiency, paraproteinemia, human immunodeficiency virus (HIV) infection,7 hepatitis C virus infection, celiac disease,8 restless legs syndrome,9 neurotoxic drug exposure, hereditary diseases, and paraneoplastic syndrome. While most of these conditions cause a length-dependent small fiber neuropathy, others (Sjögren disease, celiac disease, and paraneoplastic syndrome) can cause a form of small fiber neuropathy that is not length-dependent.4,8,10

Diabetes and prediabetes

Glucose dysmetabolism, including diabetes and prediabetes with impaired oral glucose tolerance (a glucose level 140–199 mg/dL 2 hours after a 75-g oral dextrose load), is the most common identifiable associated condition, present in about one-third of patients with painful sensory neuropathy11 and in nearly half of those with otherwise idiopathic small fiber neuropathy.12–14

Research findings strongly suggest that even prediabetes is a risk factor for small fiber neuropathy, and that so-called “impaired glucose tolerance neuropathy” may represent the earliest stage of diabetic neuropathy. Several recent studies have found a high prevalence of impaired glucose tolerance in patients with sensory peripheral neuropathy,12–14 with a rate of up to 42% in cases initially thought to be idiopathic14 compared with 14% in the general population.15 Also, a dose-response relationship between the severity of hyperglycemia and the degree of neuropathy was demonstrated in one study, in which patients with impaired glucose tolerance more often had small fiber neuropathy, whereas those with diabetes more often had polyneuropathy involving both small and large fibers.14 And studies in animals and cell cultures have shown that intermittent hyperglycemia, which can be seen in patients with impaired glucose tolerance, caused sensory neuron and nerve fiber damage and increased spontaneous C-fiber firing, resulting in neuropathic pain.8,16,17

Metabolic syndrome

Insulin resistance with prediabetes and diabetes is a part of the metabolic syndrome, which also consists of hypertension, hyperlipidemia, and obesity. The individual components of the metabolic syndrome have been implicated as risk factors not only for cardiovascular and cerebrovascular disease but also for small fiber neuropathy.

One study in 548 patients with type 2 diabetes showed that those with the metabolic syndrome were twice as likely to have neuropathy as those without.18 Another study showed that in 1,200 patients with type 1 diabetes without neuropathy at baseline, hypertension, hyperlipidemia, and increased body mass index were each independently associated with a higher risk of developing neuropathy.19

A recent study of 219 patients with idiopathic distal symmetrical peripheral neuropathy and 175 diabetic patients without neuropathy found a higher prevalence of metabolic syndrome in patients with neuropathy than in normal populations. The prevalence of dyslipidemia (high levels of total and low-density lipoprotein cholesterol and triglycerides and low levels of high-density lipoprotein cholesterol), but not hypertension or obesity, was higher in patients with neuropathy than in patients with diabetes but no neuropathy.20 The findings linked dyslipidemia to neuropathy and showed the need for further studies of the potential pathogenic role of dyslipidemia in neuropathy.

Hereditary causes

Hereditary causes of small fiber neuropathy are rare and include Fabry disease, Tangier disease, hereditary sensory autonomic neuropathy, and hereditary amyloidosis.


A thorough history should be taken to obtain details regarding onset and features of neuropathy symptoms, exacerbating factors, and progression. It is also important to ascertain whether the patient has any associated conditions as mentioned above, a family history of neuropathy, risk factors for HIV or hepatitis C virus infection, or a history of neurotoxic drug exposure.

Clinical suspicion of small fiber neuropathy should be high if a patient presents with predominant small fiber symptoms and signs with preserved large fiber functions.

Nerve conduction studies and electromyography

For diagnostic testing, routine nerve conduction studies and electromyography assess the function of large nerve fibers only and are thus normal in small fiber neuropathy. These tests should still be ordered to rule out subclinical involvement of large fibers, which may affect the diagnostic evaluation, prognosis, and treatment plan. However, if the results of these tests are normal, specialized studies are needed to evaluate small fibers.

Although several tests are available to evaluate somatic and autonomic small fibers, the two that have the highest diagnostic efficiency for small fiber neuropathy and that are used most often are skin biopsy, to evaluate intraepidermal nerve fiber density, and quantitative sudomotor axon reflex testing (QSART), to assess sudomotor autonomic function.21–23

Skin biopsy

Skin biopsy is a minimally invasive procedure in which 3-mm-diameter punch biopsy specimens are taken from the distal leg, distal thigh, and proximal thigh of one lower limb. The procedure takes only 10 to 15 minutes.

Biopsy specimens are immunostained using an antibody against protein gene product 9.5, which is a panaxonal marker. Small nerve fibers in the epidermis are counted under a microscope, and intraepithelial nerve fiber densities are calculated and compared with established normative values. The diagnosis of small fiber neuropathy can be established if the intraepidermal nerve fiber density is lower than normal (FIGURE 1). Nerve fiber density may be normal in the early stage of small fiber neuropathy, but in this setting skin biopsy often shows abnormal morphologic changes in the small fibers, especially large swellings,24 and repeat biopsy in 6 to 12 months may be considered.

The diagnostic efficiency of skin biopsy is about 88%.21,23 For diagnosing small fiber neuropathy, it is more sensitive than quantitative sensory testing21,25 and more sensitive and less invasive than sural nerve biopsy.26 Intraepidermal nerve fiber density also correlates well with a variety of measures of severity of HIV distal sensory neuropathy and thus may be used to measure the severity and treatment response of small fiber neuropathy.27

Quantitative sudomotor axon reflex testing

QSART is an autonomic study that measures sweat output in response to acetylcholine, which reflects the function of postganglionic sympathetic unmyelinated sudomotor nerve fibers. Electrodes are placed on the arms and legs to record the volume of sweat produced by acetylcholine iontophoresis, in which a mild electrical stimulation on the skin allows acetylcholine to stimulate the sweat glands. The output is compared with normative values.

One prospective study showed that 67 (72.8%) of 92 patients with painful feet had abnormal results on QSART, ie, low sweat output.28 A retrospective study found that 77 (62%) of 125 patients with clinical features of distal small fiber neuropathy had a length-dependent pattern of QSART abnormalities.22 QSART abnormalities were detected in some patients without autonomic symptoms.

If these tests are not available

Skin biopsy and QSART are objective, reproducible, sensitive, and complementary in diagnosing small fiber neuropathy. One or both can be ordered, depending on whether the patient has somatic symptoms, autonomic symptoms, or both. However, these two tests are not widely available. Only a few laboratories in the country can process skin biopsy specimens to evaluate intraepidermal nerve fiber density. Nevertheless, it is easy to learn the skin punch biopsy procedure, and primary care physicians and neurologists can perform it after appropriate training. (A concern is avoiding damage to the epidermis.) They can then send specimens to one of the cutaneous nerve laboratories (but not to a routine reference laboratory).

TABLE 1 Drugs for pain control in small fiber neuropathy





Sedation, weight gain, anticholinergic effects, sexual dysfunction, arrhythmia (side effects most prominent with amitriptyline)

Amitriptyline (Elavil)

20–150 mg

Nortriptyline (Aventyl)

20–150 mg

Desipramine (Norpramin)

20–200 mg

Duloxetine (Cymbalta)

60–120 mg


Gabapentin (Neurontin)

600–3,600 mg

Sedation, dizziness, peripheral edema, weight gain

Pregabalin (Lyrica)

150–600 mg

Similar to gabapentin

Topiramate (Topamax)

25–400 mg

Weight loss, sedation, cognitive slowing, renal stones, paresthesias

Lamotrigine (Lamictal)

25–400 mg

Stevens-Johnson syndrome, rash, dizziness, nausea, sedation

Carbamazepine (Tegretol)

200–1,200 mg

Dizziness, sedation, ataxia, aplastic anemia, liver enzyme elevation

Oxcarbazepine (Trileptal)

600–2,400 mg

Dizziness, nausea, fatigue, leukopenia

Topical anesthetics

5% Lidocaine patch (Lidoderm)

Every 12 hours

Local edema, burning, erythema

0.075% Capsaicin patch

Three or four times a day


Opioids, opioid agonists

Tramadol (Ultram)

100–400 mg

Sedation, dizziness, seizures, nausea, constipation

Oxycodone (Oxycontin)

10–100 mg

Sedation, constipation, nausea; potential for addiction and abuse

A special technique, including unique fixative and cryoprotectant, is used to fix and process the biopsy specimens, because routine techniques for processing dermatologic punch biopsy specimens often result in lower intraepidermal nerve fiber densities. Therefore, it is very important to contact the laboratory regarding fixative and processing before performing a biopsy.

Key Points
Symptoms of small fiber neuropathy typically start with burning feet and numb toes.
Causes and associated conditions can be found in over 50% of cases. These include glucose dysmetabolism, connective tissue diseases, sarcoidosis, dysthyroidism, vitamin B12 deficiency, paraproteinemia, human immunodeficiency virus infection, celiac disease, neurotoxic drug exposure, and paraneoplastic syndrome.
Findings on routine nerve conduction studies and electromyography are typically normal in this disease.
Management includes aggressively identifying and treating the underlying cause, advising lifestyle modifications, and alleviating pain.

QSART requires specialized equipment and must be performed on site. In addition, the test is very sensitive to drugs that can affect sweating, such as antihistamines and antidepressants, and such drugs must be discontinued 48 hours before the study.

Basic laboratory tests to find the cause

Once the diagnosis of small fiber neuropathy is established, the next important step is to order a battery of laboratory tests to search for an underlying cause. The tests should include the following:
Complete blood cell count
Comprehensive metabolic panel
Lipid panel
Erythrocyte sedimentation rate
Thyroid-stimulating hormone level
Free thyroxine (T4) level
Antinuclear antibody
Extractable nuclear antigens
Angiotensin-converting enzyme (ACE) level
Serum and urine immunofixation tests
Vitamin B12 level
2-hour oral glucose tolerance test.

Oral glucose tolerance testing is much more sensitive than measuring the hemoglobin A1c and fasting glucose levels in detecting diabetes and prediabetes. These two conditions were detected by oral glucose tolerance testing in more than 50% of patients with otherwise idiopathic sensory-predominant peripheral neuropathy and normal hemoglobin A1c and fasting glucose levels.13,14 Therefore, every patient with small fiber neuropathy without a known history of diabetes or prediabetes should have an oral glucose tolerance test.

Special laboratory tests in special cases
If there is a history of gastrointestinal symptoms or herpetiform-like rash, then testing for gliadin antibody and tissue transglutaminase antibodies as well as small-bowel biopsy may be pursued to evaluate for celiac sprue.
Serologic tests for HIV or hepatitis C should be ordered if the patient has risk factors.
If there is a significant family history, further genetic testing should be considered.
Lip biopsy or bone marrow biopsy should be considered if clinical suspicion is high for Sjögren disease, seronegative sicca syndrome, or amyloidosis.
The serum ACE level has a low sensitivity and specificity; therefore, if sarcoid is suspected clinically, additional confirmatory testing, such as computed tomography of the chest, should be ordered despite a normal ACE value.


Treatment of small fiber neuropathy should target the underlying cause and neuropathic pain. Cause-specific treatment is a key in preventing small fiber neuropathy or slowing its progression.

Glucose control, weight control, and regular exercise

As glucose dysmetabolism is the condition most often associated with small fiber neuropathy (and since individual components of the metabolic syndrome are potential risk factors for it), tight glycemic control and lifestyle modification with diet control, weight control, and regular exercise are of paramount importance in patients with these conditions.

The Diabetic Prevention Program,29 a study in 3,234 people with prediabetes, found that diet and exercise were more effective than metformin (Glucophage) in preventing full-blown diabetes. At an average of 2.8 years of follow-up, the incidence of diabetes was 11.0 cases per 100 patient-years in a group assigned to receive placebo, compared with 7.8 in those assigned to receive metformin (31% lower), and 4.8 (58% lower) in those who were assigned to undergo a lifestyle intervention that included at least 150 minutes of physical activity per week with a weight-loss goal of 7%. Put another way, to prevent one case of diabetes over 3 years, 6.9 patients would have to undergo the lifestyle intervention program, or 13.9 would have to receive metformin. Since impaired glucose tolerance neuropathy may represent the earliest stage of diabetic neuropathy, the neuropathy at this stage may be reversible with lifestyle intervention and improvement of impaired glucose tolerance.

This concept is supported by a 3-year study in 31 people, which showed that lifestyle intervention significantly improved impaired glucose tolerance, reduced the body mass index, and lowered total serum cholesterol levels.30 Changes in these metabolic variables were accompanied by significant improvement of neuropathy as evidenced by significantly increased intraepidermal nerve fiber density, increased foot sweat volume, and decreased neuropathic pain.30

Treatment of other diseases

It has also been reported that treatment of sarcoidosis, autoimmune diseases, and celiac disease improved the symptoms of small fiber neuropathy resulting from these conditions.8,31 Therefore, it is important to identify the cause and treat it to prevent and slow the progression of small fiber neuropathy, and doing so may improve the disease in some mild cases.

Pain management

Pain management is crucial in the treatment of small fiber neuropathy, as neuropathic pain can be debilitating and can cause depression. Pain management often requires a multidisciplinary team, including a primary care physician, a neurologist, a pain specialist, and a psychiatrist. Medications include antidepressants, anticonvulsants, and topical anesthetics (TABLE 1) as well as narcotic and non-narcotic analgesics and antiarrhythmics. Nonpharmacologic management includes transcutaneous electrical nerve stimulation (TENS), heat, ice, and massage of painful areas (reviewed by Chen et al32 and Galluzzi33).

First-line choices of pain medications are the anticonvulsants gabapentin (Neurontin) and pregabalin (Lyrica), the tricyclic antidepressants amitriptyline (Elavil) and nortriptyline (Aventyl), a 5% lidocaine patch (Lidoderm), and the semisynthetic opioid analgesic tramadol (Ultram). These can be used alone or in combination.

Gabapentin is relatively well tolerated, but drowsiness can occur, especially with high starting doses. We usually start with 300 mg daily and increase it by 300 mg every week up to 1,200 mg three times a day as tolerated. Most patients need 600 to 900 mg three times a day.

Pregabalin is a newer antiepileptic drug, similar to gabapentin but less sedating. It can be started at 75 mg twice a day and gradually increased to 300 mg twice a day as needed. Weight gain and, rarely, swelling of the lower extremities may limit the use of both of these drugs.

Tricyclic antidepressants, such as amitriptyline, nortriptyline, and desipramine (Norpramin), are proven effective in controlling neuropathic pain, although no response with amitriptyline was seen in patients with painful HIV distal sensory neuropathy.34

Lidocaine patch is preferred if the painful area is small. Patients should be instructed to use the patch to cover the painful area 12 hours on and 12 hours off. If it does not provide relief within 1 week, it should be discontinued.

Tramadol is also helpful in treating neuropathic pain. It can be started at 50 mg two to four times a day as needed.

Nonsteroidal anti-inflammatory drugs and selective serotonin reuptake inhibitors are typically less effective than the other drugs mentioned.

Opioids should be reserved for refractory cases, given the potential for addiction, but they are sometimes necessary in patients with disabling pain that does not respond to other drugs.

TENS may be of benefit. The patient controls a pocket-size device that sends electrical signals to leads placed on affected areas.

Alternative therapies for small fiber neuropathy, such as meditation, yoga, and acupuncture, have yet to be studied.

It is also important to explain to patients that the typical course of small fiber neuropathy is relatively benign, as many patients worry about developing weakness and eventually not being able to walk. These concerns and fears can aggravate pain and depression, which can make treatment difficult.


Most patients with small fiber neuropathy experience a slowly progressive course, with symptoms and signs spreading proximally over time.

In one study, only 13% of 124 patients with small fiber neuropathy showed evidence of large-fiber involvement over a 2-year period. 21 None went on to develop Charcot joints, foot ulcers, weakness, or sensory ataxia, as is often seen in patients with long-standing or severe large fiber neuropathy. Neuropathic pain worsened in 30% and resolved spontaneously in 11%.21

Most patients with small fiber neuropathy require chronic pain management. Again, treatment of the underlying cause is important and can improve the prognosis.

We believe that the overall progression of small fiber neuropathy is slow. A longitudinal study with a follow-up longer than 2 years would be useful to confirm this.


As the population continues to age and as more patients develop diabetes and the metabolic syndrome, the prevalence of small fiber neuropathy will rise. Patients who present to their primary care physicians with painful, burning feet require a thorough diagnostic evaluation, which may include referral for specialized neurodiagnostic testing. Aggressive cause-specific treatment, lifestyle modification, and pain control are key elements of a team approach to managing small fiber neuropathy.


Wednesday, 18 November 2015

Some Things To Avoid For Neuropathic Pain Relief

Today's post from mainespinenerve.com (see link below) looks at a few things to try to avoid in order to bring better relief from neuropathic symptoms. You may find it somewhat simplistic and also be able to think of many other things to avoid to lighten the symptoms but maybe you haven't thought about the effect these four particular things have on the lives of a neuropathic patient. For that reason it's worth publishing. Sometimes it's the things that stare us in the face but aren't immediately obvious as links to our condition, that are those which we need to change.

Habits and Routines to Avoid for Neuropathy Pain Relief
Dr. Douglas VanderPloeg - Wednesday, November 04, 2015

Peripheral neuropathy is a widespread medical condition. A few simple adjustments to your day-to-day habits can give you relief.
Who gets PN? A look at the numbers

Peripheral neuropathy (PN) is damage to the body’s peripheral nerves, with typical symptoms incuding numbness, pain, and other sensations in the feet and hands.

The main groups of American patients suffering from peripheral neuropathy are:

• Those with diabetic peripheral neuropathy (DPN) – 20 million

• Individuals who are pre-diabetic but already experiencing PN – 21.5 million

• HIV patients who experience HIV neuropathy – up to 575,000

• Cancer patients who experience chemotherapy-induced neuropathy – 420,000.

4 habits to avoid

Here are a few habits that can increase your vulnerability to peripheral neuropathy symptoms:

#1 – Not sleeping

Failing to get enough sleep is a major problem among Americans, with the Centers for Disease Control and Prevention (CDC) referring to sleep loss as a public health epidemic. Insufficient sleep has a broad negative impact. In fact, nearly a quarter (23%) of American adults say that lack of sleep makes it difficult for them to focus.

Sleep is particularly important for peripheral neuropathy patients because so much cellular repair is conducted while we are in bed. “Important nutrients and oxygen are carried through the blood stream and delivered to our nerves – supplying them with the essentials they need to repair and recover,” explains a popular neuropathy blog.

#2 – Excessive sitting

You may know that the sedentary lifestyle of Americans, associated with ample sitting and little exercise, is a huge threat to health. In fact, more than four out of five people (86%) in the United States are seated most of the time, per a poll by Ergotron.

Sitting is particularly problematic to the nerves because it can lead to:

• Blood sugar spikes

• Nerve compression

• Hindered blood flow

#3 – Reliance on sugars and sweeteners

PN is often linked to diabetes. Maintaining a consistent level of blood glucose is critical for combatting nerve pain, particularly for diabetic patients. Sugars and sweeteners are virtually devoid of nutrients and can be disastrous for glucose management and nervous system health.

#4 – Heightened stress

Stress is a survival mechanism, but many of us now suffer from chronic stress, which means that the body remains in fight-or-flight response for an extended period of time. “In this heightened state of anxiety, the body and mind remain tense and unable to come back down to normal levels,” says the neuropathy blog. “Among other things, this leaves the body more vulnerable to pain.”

Expertise with difficult cases

Are you suffering from the pain of peripheral neuropathy? You can minimize symptoms by avoiding the bad habits above. Plus, you may benefit from treatment at our institute, where we specialize in treating PN patients who have not achieved relief elsewhere.

Dr. Douglas VanderPleog, Maine Spine and Nerve Institute

Dr. VanderPloeg has been a guest lecturer at multiple hospitals and has served on several professional boards. He is a Diplomat of both the American Board of Chiropractic Examiners and the Canadian Board of Chiropractic Examiners.


Tuesday, 17 November 2015

Cancer And Neuropathy: A Real Threat

Today's post from azneuromod.com (see link below) looks at cancer as a principle cause of neuropathy. As we live longer, more and more people are found to have cancer and by definition, are treated. By definition, that means that more and more people will unfortunately suffer nerve damage, either as a result of the cancer itself or the chemotherapy drugs used to treat it. This article goes into more detail than most concerning the various forms of cancer associated with neuropathy and is definitely worth reading. You may be lucky enough to avoid cancer in your life but then again, you may not and therefore should be aware of the possibility of nerve damage thereafter. Already having neuropathy will not exclude you from worsening symptoms if cancer is also involved. However, forewarned is forearmed and as with all these things, the quicker you know about it, the more likely any treatment will be successful.

Neuropathy in the Cancer Patient: Causes and Treatments
November 9, 2015  By webadmin@macmdaz.com

Identifying the causes of neuropathy in cancer patients can be difficult. This review looks at the common causes of neuropathy in cancer patients, as well as effective therapies—and even preventions.

Neuropathic pain is often defined as pain caused by a lesion or disease of the somatosensory nervous system. Peripheral neuropathies arise from disorders associated specifically outside the central nervous system (CNS) and within the peripheral nervous system.1 Symptoms of peripheral neuropathy include numbness, tingling, paresthesia (pins and needles sensations), sensitivity to touch, or muscle weakness. In patients with extreme symptoms, they may present with burning pain, muscle wasting, paralysis, or organ dysfunction.1

There are multiple causes of peripheral neuropathy, and in the cancer patient, identifying the culprit may be complicated by a plethora of etiologies. This review will focus on potential origins of neuropathic pain in the cancer patient, including both disease- and drug-induced peripheral neuropathy; current treatment modalities of cancer-induced peripheral neuropathy (CIPN); and how to prevent the development of peripheral neuropathy in cancer patients. According to the American Cancer Society, about 11.9 million Americans suffer from cancer pain, but it remains unclear what portion of that pain is specifically neuropathic versus somatic, visceral, or a combination. It also is equally unclear what percentage of these cases is due to disease, treatments, or both.2
Cancer-induced Peripheral Neuropathy

By virtue of the nature of the disease, cancer alone can cause neuropathy. Certain neuropathies can develop due to remote or paraneoplastic effect; invasion of the cancer or compression of the nerves; or as a side effect secondary to treatment.3 The cancers commonly associated with neuropathies are listed in Table 1. This section focuses on the role of CIPN in the cancer patient.

Paraneoplastic encephalomyelitis/sensory neuronopathy (PEN/SN) is a type of neuropathy most commonly associated with lung cancer, typically small-cell lung cancer. Unlike other types of pain syndromes, PEN/SN is not due to the effects of the tumor itself, metastasis, treatment, infection, or metabolic abnormalities. Rather, it is thought to be a result of “remote effects” of the cancer that lead to the production of antibodies or inflammatory cells against any neural antigens that the tumor may express.4 The symptoms can be acute or progressive. Patients typically present with numbness and parasthesias in the distal extremities, usually unilaterally. Eventually, this type of neuropathy may result in loss of proprioception and sensory ataxia. Oftentimes, these patients develop confusion, memory loss, depression, hallucinations, seizures, and/or cerebellar ataxia. Treating the underlying cancer does not always affect the clinical course of PEN/SN. Some patients may occasionally improve after the tumor has been treated. Other treatments such as plasmapheresis, intravenous immunoglobulin, and immunosuppressive agents have not shown any greater benefit.3,4

Tumor Infiltration
Peripheral neuropathy may develop secondary to tumor infiltration. Leukemia and lymphoma cells can infiltrate the cranial and peripheral nerves; the result can be mononeuropathy, mononeuropathy multiplex, polyradiculopathy, or plexopathy as a complication. This neuropathy is generally painful and may be an indication of newly diagnosed cancer and/or disease progression. The symptoms can be managed by treating the underlying hematological malignancy or by initiating glucocorticoids if not contraindicated.3

Lymphoma most often causes neuropathy either by infiltration or direct compression of nerves, or by a paraneoplastic process.3Most peripheral complications are due to non-Hodgkin’s lymphoma (NHL).5 Hodgkin’s lymphoma, on the other hand, rarely causes neuropathy; it generally causes immunological disorders of the peripheral nervous system such as inflammatory plexopathy or Guillain-Barré syndrome.5 Although the NHL neuropathy may manifest as a sensory or motor symptom, it is commonly seen as a sensorimotor neuropathy. The course of the neuropathy may be acute, gradually progressive, or relapsing and remitting. The neuropathy may respond to the treatment of the underlying lymphoma.5

Multiple Myeloma
Multiple myeloma (MM) is a common hematologic malignancy associated with monoclonal gammapathy. About 40% of patients with MM develop some type of peripheral neuropathy. Patients may develop painful paresthesia and loss of differentiating between pinprick and temperature sensations. The mechanism of the neuropathy is primarily due to amyloidosis with infiltration of the nerves. It is also thought to be due to the metabolic or toxic effects of the systemic consequences of renal failure.3,5

Waldenström’s Macroglobulinemia
Waldenström’s macroglobulinemia is a cancer of the B lymphocytes. It is caused by a malignant proliferation of lymphoplasmacytoid cells, which produces an overabundance of immunoglobulin M monoclonal proteins with a κ light chain—causing the blood to become hyperviscous. The mechanism of neuropathy is unknown, but it’s thought to be related to myelin-associated glycoprotein antibodies. However, a causal relationship has not been confirmed.6

Solid Tumors
The most common solid tumors associated with peripheral neuropathy include breast cancer and lung cancer as reported in case reports and in a prospective, multicenter study in radiotherapy oncology units.7,8

Bone Marrow Transplantation
Although not a neoplasm, bone marrow transplantation (BMT) is a treatment for certain malignancies, which may cause neuropathy. Peripheral neuropathy associated with BMT usually occurs concurrently with chronic graft-versus-host disease (GVHD). Chronic GVHD is a clinical syndrome that occurs in approximately 60% to 80% of long-term survivors of allogeneic hematopoietic stem cell transplantation.3 Chronic GVHD is defined as an autoimmune disorder that occurs 100 days after the allogeneic transplant. Symptoms of chronic GVHD usually include oral ulcerations; keratoconjunctivitis; xerophthalmia; hepatic failure; obstructive lung disease; involvement of the skin and soft tissues; and involvement of the neuromuscular system, CNS, and the gastrointestinal tract.9 These features are shared with a variety of autoimmune disorders, and it is possible that the etiology of this peripheral neuropathy is an immune-mediated response directed against the peripheral nerves. Patients may develop cranial neuropathies, sensorimotor polyneuropathies, multiple mononeuropathies, and severe generalized neuropathies. Symptoms may improve when the intensity of the immunosuppressive therapy for GVHD is increased.3

To read more about causes and treatments of neuropathy in cancer patients click here.


Monday, 16 November 2015

How A Nervous System Disease Can Change Your Life For Ever!

Today's excellent post from livinginalimitedworld.com/ (see link below) is the on-going story of a woman living with MS (Multiple Sclerosis - also a disease of the nervous system). It's included on this blog because it mirrors what very many people living with neuropathy also feel and describes the emotional upheavals you can feel when it becomes necessary to resort to a wheel chair. Many people living with various forms of neuropathy will be able to identify with this story, even if their own individual case may not be as dramatic or severe. It talks about realisations and acceptances, Facing the fact that your body is letting you down and there's very little you can do about it. Worth reading by everybody living with a chronic illness and afterwards, you can either count your blessings, or say that you know precisely how she feels.

Joining the dots  
Posted on November 13, 2015

Every cell in my body is no longer just tell me, they are changing, they are now screaming it, so loudly, that my head is ringing with it. It’s about six months ago that I first felt that I was in danger of being on my feet and that my wheelchair, was once more, needed in my life. At about the same time as I found that not only; were my legs muscles becoming a fan of just collapsing; every sensation my PRMS had found to play with, had also become heightened; so to where my tremors, they were increasing; my spasms were more frequent and favouring the more intense, and my mental symptoms were, well they too were more intense; everything was moving, and moving rapidly. Six months is an incredibly short time, it’s not like when we were children, when months lasted forever, now, especially now, they have become incredibly short.

When that day came that I let the words actually come out of my mouth, “I need my wheelchair”, I had this huge lump in my throat. It was all well and good, thinking it, thinking it is safe, it’s silent and no one other than you knows that thought is even there. Saying it, is like writing your own death warrant, there is no going back. Admitting it to the world is a very different thing from the world telling you. If a doctor or the MS nurse had said, “Well Pamela, I really think you are going to have to use that wheelchair”, well I would have had someone to blame, an outside observer who had diagnosed a weakness, but I just had me. I think it was the first time where I have been the only one, behind changing my life, prescribing what was needed to deal with the course of my health. I was also doing something else, using a great big piece of equipment as a foil, not to hide me, but to hide what I didn’t want to see, or even think about. It partially worked. It was a distraction. I had to buy this or that, make sure that I had the optimum space to manoeuvre in, without rearranging the entire house. Things to do, things to think about, anything but stop and admit. I could bypass everything other than my brain, it has a nasty habit of showing the world my shortcomings. Stutters, slurs and blanks, appear throughout almost every sentence I dare to try and speak. Adam, well he’s used to it, but my visit to the hospital two months ago put a spotlight on it. The consultant spotted it the second I entered the room and tried to speak.

No one but us, knows about those maddening sensations, unless, we tell them. Well, no one can see a tingle, or a lightening shock hugging our skin, not even us. Unless we jump, squeal or flinch, they are our secret. Which probably makes them one of the hardest things for those who don’t have MS to understand. Yes, we can explain, that they feel like this of that, but the average person, they only feel something similar for the briefest of seconds. They have no concept, no understanding, or any way of even imagining, what it’s like to feel them for hours, days, months or even years. Pins and needles, so what there nothing. Maybe, until you have them running across your face for a whole day. Nothing, until someone, turns those pins into knives, and those needles into spears. So numbness, well it must be a joy to someone who lives in pain, isn’t it? You might think that, but MS has a trick unique to nerve illnesses, we can feel both, in the exact same spot, at the exact same time. Internal feelings have nothing to do with the real world. If you apply moments though the danger of numbness is real. Burnt hands from an oven, fingers from a cigarette, cuts that you don’t know are there, that fester before you spot they exist. Food and drink that falls from your mouth as you don’t really know if your lips are closed or not, as you can’t even feel them, or the food. Sensations matter, be it missing ones or created ones, if they aren’t exactly or even close to what they should be, they disrupt everything, create danger and generally, make life hard.

Last week, I described a bad spasm, bad, not because of what it did on the pain scale, but because it made my health all to visible, in a not too pretty way. Not all spasms are visually dramatic, many, like those who take sheer pleasure in stopping me from breathing, constrict, just below that pain level. To find a point, in any day, where either my diaphragm or my intercostal muscles, haven’t held that position, in the last couple of years, is hard. In that same period, I can’t say that for any other part of me. 2 years ago, I went days without feeling a spasm anywhere else. That was the point when my PRMS found my intestine, but still, the rest of me, I went days. When they came, well in comparison to my torso, I really didn’t care. They were there, they were annoying, but they didn’t last, and they didn’t hurt, beyond a normal cramp, or stitch. They were mundane and forgettable. Technically, a tremor is nothing more than a fast twitch spasm, yet when it comes to dramatic effect, back then, my tremors won hands down. The spinal twitch was the best, it swung my enter body, from my toes to my head, in sharp jolts, from side to side and still does. My hands before my chemo treatment, did a complete and expert impression of late-stage Parkinsons. Post chemo, they settled to odd spells, that never lasted long and I could hold my hand out in front of me, not steady, but not flapping all over the place either.

So why the requiem, because all of this, just like the need for my wheelchair has changed too, and in just as big and as solid away as moving my chair back into my life has. My first paragraph, well it laid out the glimmer of the facts. My legs were the dangerous factor, the one part that was partially fixable by adding my chair. A wheelchair doesn’t make your legs stronger, it doesn’t stop the muscles from collapsing, and you don’t have to be standing to feel it. You might not think you are using you leg muscles when you are sitting, but you are. Sit there and totally relax your lower body and you can feel the difference. When it happen unconsciously, it affects your entire posture and body. Suddenly, you have what are in all respects two long lumps of flesh with pins in them. They are closed off, separated from reality and feel just as dead, as they would be if you tried to use them to stand. When you are in a wheelchair, believe it or not, unless you are a paraplegic you use your legs in every push. Dead legs, make every push twice as hard as they are with your legs to assist. Now add into this, the fact, that that feeling of weakness, and even deadness, is now appearing in your arms. I now, especially at the end of a day, find myself sat in a chair that I couldn’t move without, but with little of the strength or movement required, to actually achieve propulsion. My foil now feels more like a folly.

Spasms are now stronger, but that isn’t what bothers me, it is their weaker cousins that are making life tough. Doing simple things like lifting my feet so they can sit on the rests on my chair, is now literally, a hit and miss process. My muscles jump, kicking away and far too often, into the foot rest. The precision required to place in where needed is almost gone, just as it is when I’m walking. My left leg is far worse than my right, and if I had to take more than a couple of steps, would without a doubt, trip me up. Just standing can be enough, to send it off in some kind of fit, twitching and flicking itself all over the place. At it’s worst, I don’t need to even stand, it just twitches unstoppable, and those twitches in my hands, are returning. If the worsening of existing and the return of the once fixed wasn’t enough, now I also have the vanishing voice. I haven’t mentioned it for a couple of weeks, but it hasn’t gone, it just comes and goes at will. I had to mention when I was at the hospital, as it chose Monday as a good day to vanish. At least my PRMS chose that day to show itself and its latest trick.

I felt all of this growing, just as clearly as I felt my legs leaving. My concentration on making life in a wheelchair work, for me, allowed me to, not so much ignore, but more, to put aside as secondary issues, everything else. I couldn’t ignore the change in my breathing, as yes, that too appeared at the same time. Clearly, something six months ago kicked my progression into high drive. I don’t know what, I just know that my body is falling into the abyss, faster than it has done since 2 years after my diagnosis. Then, Mitoxantrone was the answer, but that was a one-off, I was told then, that I could never have it again. It does so much damage to your heart, that they don’t dare do it again. So this time, I am on my own. I know Adam has seen all of this, just as I have, he would have to be blind to not have. Like the sweetie he is, he chose to respect my lack of discussion and the blind eye, I was clearly turning on it even in here. So now, I have publically joined all the dots, brought together the fuller picture, now I just have to work on living with the results.


Sunday, 15 November 2015

Why Do Our Hands And/Or Feet Tingle?

Today's post from webmd.com (see link below) is a thorough answer to the question why our hands and feet tingle. Many people ask this question long before having heard the word neuropathy and for many people, the symptoms are temporary but equally, for millions across the world, the symptoms never go away and become progressively worse. They then have a form of neuropathy or nerve damage. This article will set you on the right path as regards opening information; after that, you need to discuss your problem with your doctor and do as much further research of your own until you have built up sufficient knowledge to be best able to live with the disease.

Tingling in Hands and Feet
WebMD Medical Reference View Article Sources
Reviewed by Varnada Karriem-Norwood, MD on September 26, 2014

Tingling hands, feet, or both is an extremely common and bothersome symptom. Such tingling can sometimes be benign and temporary. For example, it could result from pressure on nerves when your arm is crooked under your head as you fall asleep. Or it could be from pressure on nerves when you cross your legs too long. In either case, the "pins and needles" effect -- which is usually painless -- is soon relieved by removing the pressure that caused it.

In many cases, however, tingling in the hands, feet, or both can be severe, episodic, or chronic. It also can accompany other symptoms. such as pain, itching, numbness, and muscle wasting. In such cases, tingling may be a sign of nerve damage, which can result from causes as varied as traumatic injuries or repetitive stress injuries, bacterial or viral infections, toxic exposures, and systemic diseases such as diabetes.

Such nerve damage is known as peripheral neuropathy because it affects nerves distant from the brain and spinal cord, often in the hands and feet. There are more than 100 different types of peripheral neuropathy. Over time, peripheral neuropathy can worsen, resulting in decreased mobility and even disability. More than 20 million Americans, most of them older adults, are estimated to have peripheral neuropathy.

It's important to seek prompt medical evaluation for any persistent tingling in your hands, feet, or both. The earlier the underlying cause of your tingling is identified and brought under control, the less likely you are to suffer potentially lifelong consequences.

Causes of Tingling in the Hands and Feet

Diabetes is one of the most common causes of peripheral neuropathy, accounting for about 30% of cases. In diabetic neuropathy, tingling and other symptoms often first develop in both feet and go up the legs, followed by tingling and other symptoms that affect both hands and go up the arms. About two-thirds of people with diabetes have mild to severe forms of nerve damage. In many cases, these symptoms are the first signs of diabetes.

In another 30% of peripheral neuropathy cases, the cause is unknown or "idiopathic."

The remaining 40% of cases have a variety of causes such as:

Nerve entrapment syndromes. These include carpal tunnel syndrome, ulnar nerve palsy, peroneal nerve palsy, and radial nerve palsy.

Systemic diseases. These include kidney disorders, liver disease, vascular damage and blood diseases, amyloidosis, connective tissue disorders and chronic inflammation, hormonal imbalances (including hypothyroidism), and cancers and benign tumors that impinge on nerves.

Vitamin deficiencies. Vitamins E, B1, B6, B12, and niacin are essential for healthy nerve function. A B12 deficiency, for example, can lead to pernicious anemia, an important cause of peripheral neuropathy. But too much B6 also can cause tingling in the hands and feet.

Alcoholism. Alcoholics are more likely to have a thiamine or other important vitamin deficiencies because of poor dietary habits, a common cause of peripheral neuropathy. It's also possible that alcoholism itself can cause nerve damage, a condition that some researchers call alcoholic neuropathy.

Toxins. These include heavy metals such as lead, arsenic, mercury, and thallium, and some industrial and environmental chemicals. They also include certain medications -- especially chemotherapy drugs used for lung cancer -- but also some antiviral and antibiotic drugs.

Infections. These include Lyme disease, shingles (varicella-zoster), cytomegalovirus, Epstein-Barr, herpes simplex, and HIV/AIDS.

Autoimmune diseases. These include Guillain-Barre syndrome, lupus, and rheumatoid arthritis.

Inherited disorders. These include a group of disorders collectively known as Charcot-Marie-Tooth disease.

Injury. Often related to trauma, nerves can be compressed, crushed, or damaged, resulting in nerve pain. Examples include nerve compression caused by a herniated disc or dislocated bone.

Diagnosis of Tingling Hands and Feet

If you seek care for your tingling hands or feet, your health care provider will do a physical exam and take an extensive medical history addressing your symptoms, work environment, social habits (including alcohol use), toxic exposure, risk of HIV or other infectious diseases, and family history of neurological disease.

He or she also may perform additional tests such as:

Blood tests. These can include tests to detect diabetes, vitamin deficiencies, liver or kidney dysfunction, other metabolic disorders, and signs of abnormal immune system activity.
An examination of cerebrospinal fluid. This can identify antibodies associated with peripheral neuropathy.
An electromyogram (EMG), a test of the electrical activity of muscle
Nerve conduction velocity (NCV)

Other tests may include:
Computed tomography (CT)
Magnetic resonance imaging (MRI)
Nerve biopsy
Skin biopsy to look at nerve fiber endings

Treatments for Tingling Hands and Feet

Successful treatment depends on an accurate diagnosis and treatment of the underlying cause of the tingling. As long as the peripheral nerve cells have not been killed, they have the ability to regenerate.

Although no treatments are available for inherited types of peripheral neuropathy, many of the acquired types can be improved with treatment. For example, good blood sugar control in diabetes can slow the progression of diabetic neuropathy; vitamin supplementation can correct peripheral neuropathy in people with vitamin deficiencies.

General lifestyle recommendations include maintaining an optimal weight, avoiding exposure to toxins, following a doctor-supervised exercise program, eating a balanced diet, and avoiding or limiting alcohol consumption. Recommendations also include quitting smoking, which constricts blood supply to blood vessels supplying nutrients to peripheral nerves.

In some cases, tingling and other symptoms of peripheral neuropathy may be reduced with prescriptions originally developed for treating seizures and depression.