Tuesday, 1 December 2015

Pain Killer Abuse And Neuropathy Patients

Today's post from huffingtonpost.com (see link below) has a title that is a little misleading in that the article talks about pain killer/opioid abuse in general and is not specific to neuropathy patients. However, those who have had severe neuropathy for some time may well have found themselves on opioid medications to control the symptoms, mainly because nothing else works! Therefore, neuropathy patients are deemed a high risk group for medication abuse. There's no doubt that medication abuse is a huge and growing problem in many societies and there have been draconian laws put in place to try to control it. However, those laws have caused massive problems for genuine pain sufferers who need those drugs to control their pain and facilitate their daily lives. They are not addicts, they're not dealing on the black market or the internet - they just need their regular prescriptions. The fact that pharmacists are too afraid to prescribe these drugs for fear of falling foul of the law, means there is something wrong with the system and its approach.Lurid media headlines don't help they just increase people's suffering. A very interesting article.

Painkiller Abuse Hits Close To Home For A Majority Of Americans:
Jeffrey Young Health Care Reporter, The Huffington Post Posted: 11/24/2015 03:00 AM EST

  Whites, suburbanites and high-income people are the most likely to be touched by the opioid epidemic.

AP Photo/Toby Talbot 

A majority of Americans knows someone personally who has abused prescription pain medication, according to a new survey.

WASHINGTON --More than half of Americans know someone who has abused prescription painkillers or died from an overdose, or has taken these medications themselves to get high, as the opioid epidemic continues to spread, according to a new poll.

Just 6 percent of those surveyed said they had abused painkillers, such as OxyContin, but 25 percent know a close friend or family member who has. Forty-five percent are acquainted with people who have used these medications without a prescription, and 39 percent know someone who became addicted, according to a Henry J. Kaiser Family foundation survey. Sixteen percent report knowing a person who died from an overdose of pain medication, and 9 percent said they'd lost a relative or good friend to an overdose. Together, that amounts to 56 percent of Americans touched by prescription painkiller addiction, the poll shows.

In sharp contrast to the crack cocaine and heroin addictions that plagued American cities in past decades and disproportionately affected racial and ethnic minorities, abuse of pain medicine today is more common among whites, people who live in suburbs and those from high-income households, the survey shows.

In addition to rampant abuse of opioid medicines intended for patients with extreme pain, use of heroin -- derived from opium -- has soared. Drug overdoses have surpassed motor vehicle crashes as the leading cause of deaths from injury in the United States, according to the Centers for Disease Control and Prevention.

The demographics behind the crisis may explain why the political establishment is responding differently than it did to past drug addiction outbreaks. Relatively affluent, educated white voters in suburbs, small towns and rural areas have more influence with politicians. Presidential candidates campaigning in places like New Hampshire -- which has a significant drug addiction problem -- are sounding compassionate notes, not emphasizing criminal crackdowns on people who have substance use problems or blaming cultural decay.

Henry J. Kaiser Family Foundation

Democratic candidates Hillary Clinton and Bernie Sanders have emphasized expanding access to treatment for people with substance use problems in their campaign platforms. On the Republican side, candidates have highlighted personal connections to the issue, including Carly Fiorina speaking of her step-daughter's death from drug use and Chris Christie telling voters of his daughter's struggles with addiction.

President Barack Obama staged a summit on the issue last month, and has implemented policies in recent months to address the epidemic, such as increasing access to prescription drugs like buprenorphine to treat addiction and emergency medicine like naloxone that can prevent overdose deaths. State and local authorities, especially in places like Kentucky and New England states hard hit by the epidemic, also are tackling the problem.

The public believes the government has a responsibility to stem the worsening painkiller addiction problem, but is divided, 36 percent to 39 percent, over whether the federal government or states should take the lead. The results roughly fall along partisan lines, with Republicans more likely to favor state action and Democrats to support federal interventions, the Kaiser Family Foundation poll found.

Republicans were less likely to believe naloxone, or Narcan, which can prevent overdose death if administered quickly, should be available without a prescription. Sixty-three percent of respondents approve of the "good Samaritan" laws -- designed to encourage drug users to seek medical help for other users without fear of arrest -- including majorities of Democrats and Republicans.

Asked what public policies would be effective in countering painkiller abuse, treatment for addicts was the most popular answer to the survey, with 85 percent supporting this approach. Tracking painkiller prescriptions and improving physician training on appropriate use of the medicines also ranked highly.

Henry J. Kaiser Family Foundation


Monday, 30 November 2015

Is Fibromyalgia Also A Peripheral Neuropathy?

Today's post from neurologyadvisor.com (see link below) looks at a problem that bothers lots of people with or without confirmed nerve damage and that is: is this fibromyalgia: if so, is that a form of neuropathy and if not why not - it seems so clearly to be nerve related? Doctors and scientists now seem to be concluding that small fibre polyneuropathy causes many cases of fibromyalgia...but not all! The article is somewhat complex unless you have a very good understanding of medical terms but you will get the gist of what's being said. Nevertheless, the jury still seems to be out on this question - not that many fibromyalgia and/or neuropathy patients will care - their pain is still excruciating!

Fibromyalgia: A Peripheral Pain Disorder?

Chris Illiades, MD November 13, 2015

 Fibromyalgia is a common, debilitating condition that has long confounded researchers — the syndrome has had no demonstrable pathology or definitive diagnostic test. Now, new research suggests that fibromyalgia may have a neuropathic basis in some patients.

In a study published in the October issue of Seminars in Arthritis and Rheumatism, researchers found that women with fibromyalgia exhibited corneal nerve atrophy consistent with neuropathic pain. The findings suggest that some patients with fibromyalgia may actually have small fiber polyneuropathy (SFPN), a disease with potentially treatable causes.

For the study, noninvasive corneal confocal bio-microscopy was used to examine corneal small fiber nerves in 17 women with severe fibromyalgia and 17 age-matched healthy women. Fibromyalgia patients had a mean Fibromyalgia Impact Questionnaire (FIQ) score of 69.3

CLINICAL CHART: Neuropathic Pain Treatments

Compared with healthy controls, patients with fibromyalgia had significantly thinner corneal stromal nerves (mean, 5.0 ± 1.0 µm vs 6.1 ± 1.3 µm, P = .01), as well as diminished sub-basal plexus nerve density per square millimeter (85 ± 29 vs 107 ± 26, P = .02).3

All but 1 patient in the fibromyalgia group had a Leeds assessment of neuropathic symptoms and signs (LANSS) score above the 12 cut off point, suggesting a neuropathic component to their pain. Patients also had high Composite Autonomic Symptoms and Signs (COMPASS) tallies (54.6 ± 16.9), reflecting prominent autonomic nervous system dysfunction.

Further analysis revealed a link between nerve slenderness and LANSS neuropathic pain symptoms questionnaire scores (Fisher׳s exact test P = .007); similarly, an association was found between sub-basal nerve scarcity and LANSS score (Fisher׳s exact test P = .008).

“We found an association between stromal nerve slenderness and neuropathic pain symptoms,” lead author Manuel Martinez-Lavin, MD, a professor of rheumatology at the Instituto Nacional de Cardiologia Ignacio Chavez in Mexico City, Mexico, told Clinical Pain Advisor.

Although symptoms of neuropathic pain are not uncommon in fibromyalgia, the syndrome has been primarily considered to be a central nervous system (CNS) processing disorder.3,4

“Our group suspects that fibromyalgia is a neuropathic pain syndrome. We believe it is primarily a peripheral nerve disorder that causes central nervous system sensitization. We think that fibromyalgia is sympathetically maintained based on stress as a triggering event; heart rate studies suggest ongoing sympathetic hyperactivity,” Dr. Martinez-Lavin stated, noting that further studies are needed to confirm the controversial hypothesis.

Up To 50% of Fibromyalgia Cases Affected

“I would not say that small fiber polyneuropathy causes all cases of fibromyalgia. However, we now have enough confirmation from independent groups, using different research techniques, to say that SFPN is found in close to 50% of people with fibromyalgia,” Anne Louise Oaklander, MD, PhD, from Harvard Medical School in Boston, told Clinical Pain Advisor.

In a study conducted at Massachusetts General Hospital5, Dr. Oaklander and colleagues used leg skin biopsies to show that 41% of 27 patients with fibromyalgia had undiagnosed SFPN.

In contrast with the nebulous syndrome known as fibromyalgia, SFPN is a disease associated with objective evidence of pathology and pathophysiology that can be included in a differential diagnosis, Dr. Oaklander pointed out.
SFPN Linked To Other Fibromyalgia Symptoms

Although some fibromyalgia patients have symptoms of neuropathic pain, others report widespread pain, deep tenderness, insomnia, cognitive dysfunction, and fatigue.2

Research is clarifying that SFPN causes more symptoms than first thought. Abnormal small-fiber control of muscle microcirculation appears to cause deep tenderness and exercise intolerance4, while poor perfusion of the brain from neurogenic orthostatic hypotension can produce cognitive dysfunction or fibromyalgia “brain fog,” Dr. Oaklander said.

Fibromyalgia often begins after a period of physical or emotional stress. “We propose that stress causes sympathetic sprouting in dorsal root ganglions leading to changes in sodium channel gate keeping. A sodium channelopathy may be the underlying mechanism for some cases of fibromyalgia and small fiber neuropathy,” Dr. Martinez-Lavin explained.
Clinical Implications

“The major clinical implication [of the findings] is that fibromyalgia is real,” Dr. Martinez-Lavin said.

As corneal confocal microscopy is not readily available, ankle skin biopsy remains the recommended method of diagnosing SFPN. Samples taken during an office visit can be mailed to an accredited lab for testing.

“If skin biopsy reveals small fiber polyneuropathy, medical causes should be looked for because disease-modifying treatments, and even cures, may be available,” Dr. Oaklander advised, noting that symptoms may improve with management of underlying conditions, such as autoimmune disease, hepatitis, malignancy, diabetes, or prediabetes.

For patients with fibromyalgia and diagnosed SFPN, medications such as serotonin norepinephrine reuptake inhibitors (SNRIs), tricyclics, gabapentin, pregabalin, and duloxetine may be effective.1,

“If sodium channelopathy can be confirmed as a cause of fibromyalgia, new, more specific sodium channel blockers may be developed to treat fibromyalgia,” Dr. Martinez-Lavin said.

Although the role of small fiber neuropathy in fibromyalgia is still not entirely clear, researchers are now beginning to unravel details about this complex condition. A demonstrable pathology has been found in about half of patients, and a cause is being actively pursued for the other half. Once causes are identified, better treatments often follow — all of which mean a brighter future for fibromyalgia patients.

Bottom Line/Health. Fibromyalgia: New Research Helps Unravel the Mystery. http://bottomlinehealth.com/fibromyalgia-new-research-helps-unravel-the-mystery/
Pain Research Forum, Multiple Studies, One Conclusion: Some Fibromyalgia Patients Show Peripheral Nerve Pathologies, http://www.painresearchforum.org/news/33529-multiple-studies-one-conclusion-some-fibromyalgia-patients-show-peripheral-nerve
Ramirez M, Martinez-Martinez LA, Hernandez-Quintela E, et al. Seminars in Arthritis and Rheumatism, Small fiber neuropathy in women with fibromyalgia. An in vivo assessment using corneal confocal bio-microscopy. Semin Arthritis Rheum. 2015. Oct;45(2):214-9. doi:10.1016/j.semarthrit.2015.03.003.
Albrecht PJ, Hou Q, Argoff CE, Storey JR, Wymer JP, Rice FL. Excessive peptidergic sensory innervation of cutaneous arteriole-venule shunts (AVS) in the palmar glabrous skin of fibromyalgia patients: implications for widespread deep tissue pain and fatigue. Pain Med. 2013. Jun;14(6):895-915. doi:10.1111/pme.12139.
Oaklander AL, Herzog ZD, Downs HM, Klein MM. Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia. Pain. 2013. Nov;154(11):2310-6. doi:10.1016/j.pain.2013.06.001.

This article originally appeared on Clinical Pain Advisor.


Sunday, 29 November 2015

Anti-Epilepsy Drugs Control Nerve Pain

Today's post from mayoclinic.org (see link below) is very useful for those already taking anti-epilepsy drugs for their neuropathy, or those for whom that may become an option in the future. Many people are confused and more than a little alarmed as to why they're being given anti-seizure drugs for nerve damage. This article explains the reasoning behind prescribing those drugs for neuropathy. As you look through the list below, you'll probably recognise some of the drugs from your other research into the disease. The fact is, nobody is totally certain why anti-seizure drugs work for nerve pain (in some cases, not all and side-effects are an issue!) but it's clear that they block pain signals sufficiently to be effective. Worth a read.

Anti-seizure medications: Relief from nerve pain By Mayo Clinic Staff

 Anti-seizure drugs often are used to help control the type of pain caused by damaged nerves.

Anti-seizure medications were originally designed to treat people with epilepsy. But the nerve-calming qualities of some of these medications can also help quiet the burning, stabbing or shooting pain often caused by nerve damage. 

Why does it hurt?

Nerves can be damaged by many things, including injury, surgery, disease or exposure to toxins. The damaged nerves are activated inappropriately and send pain signals that don't serve a useful purpose. This type of pain can be debilitating and difficult to control.

Nerve damage
(neuropathy) can be caused by many conditions, including:
Diabetes. High blood sugar levels, common in diabetes, can damage nerves throughout your body. The first symptom generally is numbness and pain in your hands and feet (diabetic neuropathy).
Shingles. Anyone who has had chickenpox is at risk of shingles, a rash of blisters that can be painful or itchy. A condition called postherpetic neuralgia occurs if shingles pain persists after the rash disappears.
Because the risk of shingles increases with age, everyone age 50 and older should receive the varicella-zoster virus vaccine (Zostavax), which can help prevent this painful condition.

Some chemotherapy drugs can damage nerves, causing pain and numbness that generally begin in the tips of your toes and fingers (neuropathy).
Herniated disk. Nerve damage can occur if a herniated disk in your spine squeezes a nerve passing through your vertebrae too tightly.
Fibromyalgia. Fibromyalgia is a chronic condition that causes pain and tenderness throughout your body. 

How do anti-seizure drugs help?

The exact mechanism of action isn't fully understood, but anti-seizure medications appear to interfere with the overactive transmission of pain signals sent from damaged nerves.

Some anti-seizure drugs work particularly well for certain conditions. Carbamazepine (Carbatrol, Tegretol) is widely prescribed for trigeminal neuralgia, a condition that causes searing facial pain that feels like an electric shock.

It's important to note that the Food and Drug Administration has issued a warning that all anti-seizure medications are associated with a slightly increased risk of suicidal thoughts or actions. Talk to a doctor or counselor promptly if you feel depressed or suicidal.
Newer anti-seizure drugs may have fewer side effects

More recent research supports the use of the anticonvulsants gabapentin (Neurontin) or pregabalin (Lyrica) to help relieve pain caused by damaged nerves.

Both gabapentin and pregabalin are particularly effective in the treatment of postherpetic neuralgia, diabetic neuropathy and pain caused by a spinal cord injury. Pregabalin also may be used to treat fibromyalgia.

Because these drugs have few side effects and are usually well tolerated, they are often the first medications to try for neuropathic pain. You may experience side effects, such as drowsiness, dizziness, confusion or swelling in the feet and legs. These side effects are limited by starting with a low dosage and slowly increasing it.

Medications from other drug classes with distinct mechanisms of pain relief (such as antidepressants) may be used in combination with anti-seizure class medications if anti-seizure medications fail to control your pain. 

Side effects limit use of older anticonvulsants

Anti-seizure drugs have been used to treat nerve pain for many years, but their use was limited by the severity of side effects they produce.

Older anti-seizure drugs include:
Carbamazepine (Carbatrol, Tegretol)
Oxcarbazepine (Trileptal)
Phenytoin (Dilantin)
Valproic acid (Depakene)

Side effects may include:
Liver damage
Double vision
Loss of coordination

If you take an older anticonvulsant, you generally need regular follow-up visits so that your doctor can monitor for side effects. These older drugs often have more side effects than do the newer anticonvulsants, and the evidence supporting use of the older anticonvulsants for neuropathic pain is sparse at times. As a result, older drugs may be recommended only when the newer medications prove ineffective. 

Research continues

As scientists learn more about the way anti-seizure drugs work, this information will be useful in determining which drugs may work best for different types of nerve pain. Pain caused by nerve damage can be disabling, but anti-seizure drugs sometimes provide relief.


Saturday, 28 November 2015

Exercise Improves Neuropathy - A No-Brainer

Today's short post from neuropathydr.com (see link below) reinforces the message that exercise will improve your neuropathy symptoms. There are many such articles to be found here on the blog and elsewhere and the premise behind it is pretty much a 'duh!' truth but the fact remains that many people living with neuropathy will recoil in horror at the idea of putting their feet, legs and arms through yet more pain - it's so much easier to put it off until another day. We have to get the message across that it doesn't matter how much exercise (or even what sort) you do, anything is better than nothing and it will eventually improve your health and help relieve your symptoms. It's a question of getting into good habits and doing a bit each day so that eventually it becomes second nature. Do what you can, when you can and enjoy the benefits later but unfortunately, ignoring the issue will do nothing to improve your situation.

Physical Activity and The Best Neuropathy Treatment
Posted by john on November 9, 2015

Typically, inactivity will make your neuropathy worse.

So, for patients who already suffer from peripheral neuropathy, this is even more critical. So what’s the solution?

Much has been written about the effects of exercise and health in general. But what you may not know is there are good studies showing improvements in many health parameters with regular physical activity and exercise.

Not too long ago, the American College of Sports Medicine made the statement that adults should be very physically active seven days a week. Not unexpectedly, the media attacked this as totally not doable by most adults.

But the fact is, the more sedentary our lives become, the worse our health becomes. For example, we know that metabolism slows with as little as 90 minutes of continued sitting at your desk. As your metabolism slows, you become much more efficient at making fat than you do burning it. And as a regular reader of this column, you know that poor metabolism can lead to the development of neuropathy, type II diabetes, or more serious illnesses.

So this means you can boost your metabolism with a workout at the gym or a stroll in the morning—and eat properly—but sitting all day without moving will negatively impact your health.

Typically, inactivity will make your neuropathy worse. So, for patients who already suffer from peripheral neuropathy, this is even more critical. So what’s the solution?

In simple terms, it’s important to get as much physical activity as you possibly can. In times of illness, or recovering from surgery or accidents, this may simply mean getting from bed to bathroom more often. As recovery continues, it’s imperative that you push and move as much as possible.

For patients who suffer from peripheral neuropathy of the feet, using bicycles and similar low-impact equipment can be very beneficial.

But whatever you do, make sure you are doing it often enough! Even just five minutes an hour can really add up at the end of your day.

Not only will you feel better, but you will improve the chances of a better neuropathy treatment outcome!


Friday, 27 November 2015

Is Light Therapy A Realistic Option For Neuropathic Pain?

Today's post from townsendletter.com (see link below) presents the case for light therapy as a potential treatment for neuropathic pain and related problems. it does this by illustrating three study cases with different forms of neuropathy. Now the problem with light therapy is that mainstream medicine is by no means firmly in favour; some regarding it as another alternative treatment based on expensive equipment and carried out at expensive clinics. After all, if it were as effective as is claimed, the whole of mainstream neurology would be performing it across the world but that doesn't exclude the possibility that it will work for many people living with nerve pain. You have to make your own mind up and investigate further as thoroughly as possible. Talking it over with regular doctors and specialists is advised, with the expectation that they will probably not be in favour. If that's the case, then you need to ask them why. Their answers, plus your own research should give you a better perspective as to whether this may be something for you to try.

A Breakthrough in Using Light Therapy to Treat Neuropathies
by Len Saputo, MD
From the Townsend Letter November 2015

This article describes the successful treatment using light therapy of three patients with peripheral neuropathy. The etiology of neuropathy for each of these patients was different, as were the patients themselves in age, sex, and general condition. All of the patients were significantly disabled and had previously undergone extensive conventional treatment without significant relief.

I have used light therapy to treat over 2000 patients with a variety of painful health conditions since 1999, when I first met Maurice Bales, who had extensive experience with the development and manufacturing of infrared light devices, beginning in the 1970s with his work at NASA and the Lawrence Livermore Lab. Maurice trained me to treat a wide range of painful conditions that included neuropathy, neck and back pain, TMJ disorders, headaches, fractures, and sports injuries. I have found that if something hurts, chances are that treatment with light will help.

Despite its remarkable effectiveness, safety profile, and affordability, light therapy remains for the most part underappreciated and underused. This lack of utilization of light therapies is not just by mainstream medicine but also by the alternative and integrative medical communities. This situation exists despite the fact that more than 70,000 peer-reviewed articles have been published on light therapy and listed on PubMed going back to 1899. Since then light therapy has been documented to relieve pain, increase circulation, reduce inflammation, speed up wound healing by an average of 40%, increase lymphatic drainage, attract stem cells, and stimulate mitochondrial production of ATP – among other things.1-15 This sounds a bit like Star-Trek medicine!

I have selected three case histories that demonstrate the range of peripheral neuropathies that can be treated using light therapy.

Case #1: Chemotherapy-Induced Peripheral Neuropathy

J. K. is a 69-year-old female referred by her oncologist for treatment of advanced peripheral neuropathy caused by chemotherapy. She was diagnosed in 2010 with colon cancer and was treated with surgery, chemotherapy, and radiation. She felt well and remained in remission until December 2014, at which time she was found to have stage IV disease based on diagnosing metastases to her lungs. She was started on chemotherapy with Erbitux.

Her cancer responded to this treatment, but within a few months she developed progressively worsening numbness in her hands and feet. By June 2015, she had such dense numbness that she could not feel the accelerator or brake in her car and was unable to button her clothing. She became depressed because she was for the most part confined to her home. Her oncologist referred her to me for treatment of her neuropathy because it had become so severe that chemotherapy had to be discontinued.

She was treated with 11 15-minute light treatments to her feet, legs, and hands from July 29, 2015, through August 20, 2015. She regained enough sensation in her fingers and feet that she can now drive, walk normally, and button her clothing without assistance. She is now much more active socially and is back on her chemotherapy treatment. She remains in remission and is enjoying life once again.

Pre-Tx Plantar Feet

Post-Tx Plantar Feet

Pretreatment thermographic image of soles of feet show lack of circulation as blue and green colors. Posttreatment shows significantly increased circulation as red and orange.

Case #2: Trauma-Induced Neuropathy

T. S. is a 39-year-old woman who was in a tornado three years ago, when a large uprooted tree fell on her geodesic dome and crashed her to the ground. Ever since that event, she could not raise her arms above her neck; has been walking with a wide-based gait to maintain her balance; has been weak in both legs; tires easily; and developed numbness, burning pain, and tingling in her feet and lower legs.

Her podiatrist referred her to me to treat her peripheral neuropathy with light therapy.

The patient's examination revealed dense numbness extending from the bottoms of her feet to the midcalf. She had normal pedal pulses and no Babinski sign, but her knee and ankle reflexes were absent. Her lumbar spine had very significant bilateral pain to direct pressure from L3 to S1. The range of motion of her neck was restricted to 45 degrees bilaterally and there was moderate tenderness to palpation in the suboccipital portion of her neck. She also suffered from both lumbar disc disease and neuropathy.

She received seven treatments on her feet, low back, neck, and TMJ with light from July 15 through August 21, 2015. The patient reported, "Photonic stimulation has been a miracle for me. I no longer have pain when I stand or walk, and am able to straighten my knees. I walk with balance and at a normal speed, which I never imagined I would be able to do again. I am dreaming of getting a bike and returning to yoga and dance."

Posterior pre_Tx

Posterior post-Tx

Pretreatment image shows inflammation in orange and red from a posterior radiculopathy. The posttreatment image shows a reduction in inflammation and more symmetrical pattern of heat distrubution. (The white spot is an artifact of the BioPhoton treatment.)

Case #3: Diabetic Neuropathy

R. S. is a 56-year-old male with a history of type 2 diabetes, hypertension, obesity, hyperlipidemia, and being a "wine connoisseur." He was referred by his chiropractor for treatment of his neuropathy with infrared light. His symptoms began in 2008 and included numbness and mild burning nighttime pain that had been progressive and assumed to be caused by type 2 diabetes. It is noteworthy that he was being treated with glipizide, amlopidine, hydrochlorothiazide, pravastatin, and nortriptyline, all of which have an association, albeit weak, with peripheral neuropathy. Odds are that the most likely cause in this case was a combination of diabetes and alcohol.

He was treated from January 2014 through June 2015 with 31 infrared light therapy treatments to his feet. The combination of gradually reducing his alcohol consumption and employing light treatments had a major effect on improving his neuropathy symptoms. At the present time has no pain and only mild numbness in his feet. His gait is normal. In addition to using light therapy, we have successfully focused on improving his lifestyle factors including stress, insomnia, diet, exercise, weight management, and reduction in alcohol consumption. Because of his compliance we have been able to discontinue all of his medications.

Pain management has become a very sophisticated discipline that tends to be complicated and often associated with challenging side effects. Light therapy is another story, because it is simple, effective, safe, and affordable. In contrast, in mainstream clinical practice, it is typical for patients with severe pain to be treated with a polypharmacy that usually includes drugs for pain, anxiety, depression, insomnia, and a wide range of additional drugs to manage their side effects. Many people take 10 or more drugs and, not unexpectedly, simply cannot function very well. These are often those patients who come to my office!

For some neuropathies, light treatment alone is sufficient to relieve even the most severe pain. I have been able to wean more than a thousand patients off their medications. For other painful conditions, it can be helpful to use an integrative team approach that can include chiropractic, Chinese medicine, bodywork, imagery, psychotherapy, pulsed electromagnetic field therapy, and so on.

I have found that the safest and most effective way to use light therapy is to use the right device under the guidance of infrared imaging in real time. The Bales Thermal Image Processor (TIP) that we employ is a high-resolution infrared camera which is highly stable and sensitive. It allows us to use light devices that can deliver the right wavelengths with enough power that we usually get impressive clinical improvement in just a single 15-minute office visit. This approach also allows patients to observe their infrared images in real time and see for themselves the impressive changes that occur during a treatment. So patients get great clinical results not only from the effects of light itself, but also from the effects of visualizing how the treatment changes the thermal patterns on their skin.

We have learned that with certain conditions, it is critical to follow the thermal effects of light during treatment so that we visualize what we're doing and also minimize any chance of making symptoms worse. This is especially important in people with fibromyalgia and other forms of neuropathic pain such as complex regional pain syndromes, shingles, certain vascular headaches, and several other conditions.

There are hundreds of light therapy devices available, greatly varying in their respective prices, mechanisms, and efficacy. The device that I began using in 1999 was the Bales Scientific Photonic Stimulator, in conjunction with the Bales TIP camera. When its inventor, Bales, worked for NASA and the Lawrence Livermore Labs, he was developing equipment used for the space shuttle. Starting in 1985, he began to adapt his work to the medical field, creating his thermographic camera in 1990 and the Photonic Stimulator, which was approved by the FDA as a medical device to treat pain in 1997. Bales has made dozens of incremental improvements to photonic stimulators over the past two decades. What is especially noteworthy about the three cases I discuss in this article is that I used a revolutionary new model introduced only this year, now called the BioPhoton 100. This device is significantly more powerful than its predecessors, offers variable wavelengths and frequencies, is considerably smaller, and costs less.


Photonic Stimulator

Here are some of the specific differences:

Power: Output power has been increased from 0.250 watts to 8.9 watts. Output power is a very important factor for permeation depth. While lower-powered devices may benefit cells at the superficial level, they fail to penetrate deeper tissue, which is often the root problem of a chronic disease. The BioPhoton can target tissues deep within the body and penetrate the skull to reach the brain. More power equates to more photon energy being transmitted to the cells, which also reduces the duration and number of treatments.

Spectrum wavelengths: The previous model had a fixed wavelength of 850 to 880 nm, while the BioPhoton 100 has mixed-spectrum blue light at wavelengths from 450 nm and red and far-infrared light up to 940 nm. Blue light only penetrates superficial tissues but can treat cutaneous conditions such as traumatic injuries such as burns, cuts, contusions, and even infections such as MRSA.16-18 Increasing the power of blue light can deliver substantial amounts to the deeper tissues. It should be noted that blue light has greater ability than red or infrared in releasing nitric oxide to cause vasodilation.19,20 Infrared wavelengths include 850 nm and 940 nm and have the actions mentioned earlier.

Modulation (waveform) options: The BioPhoton 100 Professional model can accept external input from other devices. This provides the practitioner with the ability to replicate other frequency protocols that can be customized to meet individual treatment goals. These protocols may include square, triangular, sine, or audio waveforms at varied frequencies. It has been theorized that different waveforms are beneficial in the treatment of various diseases.

Smaller size and lower price: The size of the device has gone from 14.5² × 10² × 6² down to 5.5² × 2.5² × 2.75.² The price of the original Photonic Stimulator was $9320 (in today's dollars), while models of the BioPhoton 100 range from $2200 to $7000. These improvements make it possible for practitioners to devise a treatment protocol and then rent the device to patients to use in their homes for a specified period. This allows for daily use, which equates to faster healing, and more satisfied patients. Home treatment allows for more regular treatments at a lower cost while freeing up more time for other patients.

I believe that the BioPhoton 100 is a significant breakthrough not just in light therapy in particular but in medicine in general. We are now involved in research in conjunction with the National Institutes of Health at UCSF. Light therapy often provides superior results than do conventional treatments for a variety of illnesses and is completely noninvasive and, used correctly, free of side effects. The clinical applications of photon therapy are expanding at the speed of light!

I'm even more enthusiastic today than when I was first introduced to light therapy by Maurice Bales. It has been very rewarding to see the surprised look on the faces of so many of my patients after just a short 15-minute treatment. Because the word spreads fast when there's an effective, quick, safe, and affordable solution to managing painful conditions, I've had to devote more than half of my practice to light treatment. The vast majority of my patients come to me through word of mouth from other patients. I encourage my medical brethren to see how they might incorporate light therapy into their practices. They will not only be able to help a lot of patients who don't need to suffer, but can also make it a profitable undertaking.


Light Emitter

Len Saputo, MD, is a graduate of Duke University Medical School and board certified in internal medicine. He was in private practice in affiliation with John Muir Medical Center in the San Francisco Bay Area for more than 30 years. His approach to healing has evolved from mainstream medicine into "Health Medicine" – an integrative, holistic, person-centered, and preventive style of practice. drlen@doctorsaputo.com


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2. Irvine J, Chong SL, Amirjani N, Chan KM. Double-blind randomized controlled trial of low-level laser therapy in carpal tunnel syndrome. Muscle Nerve. 2004; 30:182–187.

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4. Ehrreich SJ, Furchgott RF. Relaxation of mammalian smooth muscles by visible and ultraviolet radiation. Nature. 1968;218:682–684.

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Thursday, 26 November 2015

Block Pain Channels And You Can Block Neuropathic Pain

Today's post from diabetes.co.uk (see link below) reveals new research which looks promising for future treatments of neuropathy. There seem to be quite a few close investigations of pain processes within the brain recently and like most others, this one has discovered that blocking a particular channel (which pain signals use), neuropathic pain can be also blocked and therefore not felt by the patient. It centres on the anterior cingulate cortex (ACC), which is the region of the brain most commonly and consistently involved in the pain processing and looks at so-called, HCN channels which carry pain signals. By blocking these in rats, pain can be 'blocked out' so to speak. Interesting development and hope for therapeutic treatments for humans in the future.

Researchers target molecular mechanisms that could relieve pain from peripheral neuropathy
Kurt Wood September 2015

A group of researchers have found molecular mechanisms that could be responsible for the pain caused by peripheral neuropathy.

The study, conducted by researchers at McGill University in Montreal, Canada, sheds new light on what was a poorly understood condition.

Peripheral neuropathy is the scientific term for nerve damage. Neuropathy can have a number of causes, including diabetes. In fact, diabetic neuropathy is one of the most common complications of diabetes. Diabetic neuropathy is caused by prolonged exposure to high blood glucose levels over a number of years.
Neuropathy, pain and the anterior cingulate cortex

This study focused on the anterior cingulate cortex (ACC), the region of the brain most commonly and consistently involved in the pain processing. The researchers made new discoveries about one type of channel (hyperpolarisation-activated cyclic nucleotide-gated channels, or HCN) that influences pain signals to the ACC.

They then tested their findings on a group of rats. By blocking HCN channels, the researchers lessened the stimulation of the ACC, which significantly reduced the pain transmitted to the rats.

The researchers hope that targeting the HCN channels will reduce the pain of neuropathy in humans, but further studies are needed to confirm that this is viable and safe.

"Our study has revealed one important mechanism linking chronic pain to abnormal activity of the ACC and it provides a cellular and molecular explanation for the overstimulation of neurons in the prefrontal cortex," said senior author Philippe Séguéla.

"This gives us new perspectives on therapeutic strategies that could target the HCN channels to help relieve chronic pain.

"Our findings open new doors to research possible treatment of these debilitating symptoms that are linked to chronic pain."

The findings were published in the Journal of Neuroscience.


Wednesday, 25 November 2015

Compression Neuropathy (I think) A Personal Story.

Today's post from ehlersdanloscontemplations.wordpress.com (see link below), is another personal story of life with one of the many forms of neuropathy. Experience has shown that readers like reading about other people's stories in this regard, so long as it's not too often and not a continuous pity-party. This article highlights the fear many people experience when they start to feel 'mysterious' neuropathic symptoms that can't easily be diagnosed. It goes on to reinforce the importance of having doctors that can not only diagnose and treat their patients but support them too. The old 'bedside manner' makes such a difference when the situation seems a little overwhelming.

Numbness, Compression Neuropathy, and Storytime
November 22, 2015 by Stephanie McManus

So, I want to tell you about the onset of a new problem I was dealing with this year. It was eventually diagnosed as compression neuropathy (in my hips). Basically, my ligaments in their looseness cause some sort of problem in my hips and impinge nerves from the base of the spine. I now lose feeling in my upper legs and up into the… bum, when I walk ‘long distances’ and then sit in a normal upright position.

The only relief I’ve found to prevent it from happening is to minimally, sit ‘normally,’ and to spend more time slightly reclined or standing or laying down. Not cool. Whenever I think, “no, I’m sure it’s fine and I’m going to vacuum and then cook and then walk the dog…” it comes back, and despite knowing what it is, I’ll admit, it disturbs me.

My neurologist at UW explained the compression, diagnosed a little vaguely as compression neuropathy, is caused by the hypermobility in my hips and repeated stretching of the ligaments followed possibly by responding muscle spasms. She did research on case studies with EDS patients with these symptoms prior to even seeing me, and she was able to narrow down the diagnosis. What?! It’s what we all hope for in a doctor, that they’ll do their ‘due diligence.’ I almost cried when she came in and knew what Ehlers-Danlos was and familiarized herself with the secondary complications we can develop. You’ll understand the tears of hope?… joy?…if you’ve been diagnosed. 

Anyway, I don’t notice a lot of this going on in my hips, because it’s normal for me and muscle spasms elsewhere feel more troublesome day-to-day. Plus, as I’m sure you’ll understand I start to tune-out sensations that interfere with ‘living life.’ You learn to survive this, and more than surviving, you eventually learn to live more often than survive. Or, always strive for it… every situation is different.

This troublesome, embarrassing, and potentially serious problem started in May of this year. I ignored it! (Don’t do that… ). In June, very ironically after a visit to the first doctor I could find after we needed to move to Washington for my husband’s job, I ended up in the ER. :sigh: My doctor was a whopping 2 hour situation to get to. I drove to Bremerton from our rental in Gig Harbor, rode on a ferry for 45 minutes, sat upright in a chair for an hour waiting for said appointment at a coffee shop, then walked a mile to the doctor’s office to then repeat this going back home.

On the ferry, of all places!, that’s when my legs up the inner thighs all the way into my lower back, and in-between, went completely numb. No feeling at all.

I called my doctor who told me to go straight to the ER. My husband was riding back on the ferry with me from his work in Seattle watching as I laid there unable to 1. panic, because there was nowhere to go or 2. talk, because I was shocked thinking it was the onset of something called cauda equina, an emergency that requires spinal surgery and can happen in EDS.

After many hours at the ER and imaging and a slightly freaked out looking doctor (that’s never a good sign), I was told they didn’t see evidence of cauda equina at this time, and I’m immensely grateful. That’s that, and you know the rest.

So, the point of my story is to illustrate you’re not alone in dealing with ‘mysterious symptoms,’ that eventually, hopefully, are figured out. Some things I deal with remain a mystery, and I’m okay with that right now, because I will keep pushing for a good team on my side when I can in-between living. We fight too hard for good care. But, it’s also important to keep fighting for good care. I got unbelievably lucky being pushed into an appointment with the top neurology clinic in the country. Lucky isn’t my normal, but look, it does happen!

A sad fact, I started experiencing this problem over a year and a half ago off and on. I’d previously been admitted to an ER in Oregon with the same symptoms. This is how I knew about the possibility of cauda equina. But, then, I had been summarily dismissed after the physician couldn’t see the problem on imaging, as if that doctor’s job was confined to diagnosis by MRI lacking any clinical insight. Well.

I’m happy I have such an intelligent and discerning doctor now. I know it will still be difficult because of the lack of awareness about EDS. I’ve continued to experience weakness in my legs and numbness, but I was told to expect it. The difference is I now have a plan and have been told when this could be a more serious problem, and how it will be handled.

Knowing you are cared for and looked over makes all the difference in the world. Right?


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.