Difference-Maker
Unlike FMS, SFPN has identifiable pathology, physiology, and causes, and thus is definitionally a disease. Oaklander et. Al.
Oaklander’s findings could benefit many
Dr. Anne Oaklander MD, PhD, is making a difference – maybe a very big difference in the lives of many. Making a difference runs actually runs in her family. Her mother, the neurologist Louise Rapin, was one of the seminal figures advancing the concept of autism spectrum disorder.
Oaklander is director of the Nerve Unit in the Massachusetts General Department of Neurology and an associate professor of Neurology at Harvard Medical School. The first to break the news that small fiber neuropathy (SFN) is found in fibromyalgia, her 2013 paper “Objective evidence that small–fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia” started off a blizzard of work (at least for fibromyalgia) on the subject. Since 2013, thirteen papers have examined SFPN in fibromyalgia – an unusually high number of research papers for this very poorly funded disease.
Now Oaklander is presenting evidence that not only is SFN found in FM, ME/CFS and other diseases, but that it can be treated as well. If she’s right she may be the first to crack a major subset of patients across an entire range of mysterious diseases. She doesn’t think these patients have ME/CFS or FM at all; they have something called small fiber polyneuropathy (SFPN).
Making the Invisible Visible
The problem for SFPN sufferers – and ME/CFS and FM – has been that the diseases are invisible. There’s no way to tell from the outside that the small nerve fibers in your skin or elsewhere have been damaged or destroyed.
If you have SFPN you’ll probably complain of a range of unconnected, seemingly vague symptoms. Small nerve fiber problems can be driving you nuts – causing you to experience weird sensations, numbness, pain, problems standing, racing heart, gut issues – while you will look fine. When your strength and reflex and other tests turn out normal your doctor will probably think you are nuts and act accordingly.
The reason these small nerve fibers could be causing so much havoc is that they do so much. Dr. Oaklander lead off her 2015 Immunotherapy paper by calling attention to just how strange the small, unmyelinated C and thinly myelinated D nerve fibers she’s studying are. These primitive nerve fibers engage in an astonishing array of activities. Not only do they transmit pain and sensory signals, they also release substances that trigger edema, vasodilation, modulate immune responses (including mast cell activity), and affect autonomic nervous system functioning. In turn, they are also affected by the immune system.
When small nerve fibers are damaged, you have small fiber polyneuropathy (SFPN). In contrast to the small nerve neuropathy found in the skin, SFPN affects peripheral nerves across the body causing potentially a staggering array of symptoms from pain to tachycardia, orthostatic intolerance (problems standing), headache, exercise intolerance (due to circulatory insufficiency), gut issues, cognitive problems and more.
That large array of potential symptoms suggests SFPN could be causing every ME/CFS and FM symptom in the book.
A Diagnosis Waiting to Happen?
“The difference between FMS and SFPN labels is not merely semantic – SFPN is an established disease with considerable information established about pathogenesis whereas FMS is an aggregate of symptoms without prior evidence of a biological basis. Oaklander et. al.
Many doctors are aware of small nerve fiber neuropathy – It’s common in diabetes, chemotherapy and infections and exposure to toxins can cause it as well – but my guess is that few are aware of SFPN. It’s not as if they haven’t been unwittingly exposed to it: idiopathic SFN, which is often likely to be SFPN, is not uncommon; fully 30-50% of small nerve fiber problems arise without an understood cause.
The patients who get it, many of whom are women, are often greeted with a psychiatric diagnosis, blank looks by doctors or rounds of opioids which probably won’t block the pain for long, or if they do, will likely have no effect on the actual problem.
After being disbelieved for years or even decades, many patients, Dr. Oaklander said, “break and cry with relief at having something real to finally point to”.
“It’s pretty routine that I have patients who break down and cry when they get an answer for the first time to something that’s been disabling them for years or decades.”
Dr. Oaklander doesn’t know how many people have SFPN but she knows it’s not a small number; if it’s not hundreds of millions of people, it’s going to be at least tens of millions. She’s sure that it commonly occurs in diseases like fibromyalgia, chronic fatigue syndrome (ME/CFS) and irritable bowel syndrome (IBS).
“This is not just some rare, esoteric disease that Harvard eggheads are investigating. It is common. People—including kids and teens—are sick, but they don’t know what they have and their doctors don’t know, either.” Anne Oaklander
SFPN is usually diagnosed via a small skin biopsy – a truly objective test – that many doctors probably don’t know about. Other tests can pick it up – a corneal microscopy test can, for instance, non-invasively and quickly determine if issues with the small nerve fibers in the eye exist. The Sudoscan sweat gland test, questionnaires and others may be helpful as well.
The field is new enough that the diagnostic protocols for some of these tests are being forged as we speak. Dr. Oaklander is assessing the efficacy of all of these tests in a large 5-year, NIH funded study.
Treatment
Oaklander has been thinking about treating these small nerve fiber problems for quite some time. In her 2015 paper “Immunotherapy Prospects for Painful Small-fiber Sensory Neuropathies and Ganglionopathies” she proposed that the vast interplay between the small nerve fibers and the immune system suggest that immunotherapies will probably work better than opioid drugs.
Because SFPN is very underdiagnosed it’s hardly ever treated properly. That’s a big mistake, Dr. Oaklander thinks: her latest study suggests that a treatment is available that may help many. Dr. Oaklander put her intuition to the test in a retrospective study that examined the medical records of 55 patients treated at Massachusetts General Hospital (MGH) for autoimmune small-fiber polyneuropathy (SFPN).
The study – which news reports back in November referred to but which has not apparently been published yet – found that treatment with intravenous immunoglobulin (IVIG; 2 grams/kilogram every four weeks) provided symptom relief and improved nerve function for 75% of patients.
One person on high doses of oxycodone reported that her pain disappeared within five days. “I didn’t know how I was going to live with that level of pain,” she said, adding that it returns every time she stops treatment.
Dr. Oaklander called the results “wildly surprising” and “paradigm-changing” in that the study presented the first strong evidence that SFPN is an autoimmune condition.
“This is a proof-of-concept finding that dampening the body’s immune system may be safe and effective for treating apparently autoimmune SFPN, a condition that most patients don’t even know they have.”
The really exciting news is that IVIG may be able, in some patients, to actually restore the nerves to normal functioning. Sixteen percent of her patients were able to wean themselves off the drug without their symptoms returning.
“This is the first treatment that has the potential to actually improve the nerve damage, not just block symptoms with drugs such as opioids that don’t address its cause.” Dr. Anne Oaklander
Oaklander urged insurance companies to take note of the success and to “consider covering three-month trials in appropriately diagnosed patients.”
Autoimmune Disease?
The implications of the study are pretty clear. If IVIG is helping, it’s because the people in the study had an autoimmune or inflammatory disorder. IVIG, which is composed of immunoglobulins, is often used to treat these types of disorders.
Autoimmunity would not be a surprise. Oaklander’s first SFPN study indicated high rates of autoimmune disorders occurred in the families of those afflicted. Since autoimmune disorders of different sorts tend to cluster in families, that result suggested an autoimmune process of some sort was probably blowing out the small nerve fibers in her patients.
SFPN wouldn’t be the first neurological disease to be caused by an immune response. Other autoimmune diseases, such as Guillain-Barre Syndrome, Sjogren’s Syndrome and rheumatoid arthritis can attack nerve fibers in the body as well.
It’s important to note that Oaklander’s study was a proof of concept study, not a phase III trial. A proof of concept study is the first step to a Phase III trial. It demonstrates that a treatment might be effective and appears to be safe. A randomized, controlled trial is hopefully next.
The downside of IVIG is that it is extremely expensive ($10,000/month) and hard to get insurance companies to pay for. Dr. Oaklander is reportedly exploring less expensive and easier to manage immunotherapies.
Big Questions Ahead
The biggest question ahead for fibromyalgia and ME/CFS patient is not how common the small fiber neuropathy is but how far it extends. If its simply found in the skin it’s importance is limited. If it extends further into the body – watch out.
A recent study suggested that small nerve fiber problems could be impacting the lungs in fibromyalgia. The study found that FM patients total lung volume was fine, but every measure of lung functioning (carbon monoxide transfer factor, carbon monoxide diffusion capacity, alveolar capillary membrane volume and pulmonary capillary blood volume) was significantly reduced.
Oaklander’s hypothesis could make sense out of the seeming chaos in FM and ME/CFS
Further analyses found that the reduction in lung diffusing capacity was probably due to a significant reduction in lung capillary lung volume; i.e. the microvascular volume of the FM patients lungs had declined. That, in turn, implicated the cardiac autonomic nerves. .
Bigger studies are clearly needed. This field is still evolving. The diagnostic protocols, especially for younger people, are being reworked. It’s not clear, at least to me, how SFPN damage in other areas can be assessed. It’s also not clear how much the SFPN patients in the study were helped or what other less expensive treatments might be helpful.
This field of inquiry, however, is moving forward fairly quickly and obviously has chance to make a major impact. The idea of a process affecting small nerve fibers across the body is nothing if not intriguing. For me, I’m particularly interested because only in the context of small fiber neuropathy has one of my most aggravating symptom – burning sensations in the skin particularly after exercise – ever been mentioned.
Dynamic Duo?
Dr. Oaklander is working with Dr. Systrom, the pulmonologist at Brigham and Women’s Hospital in Boston, who produced groundbreaking work on the cause of the exertional intolerance in ME/CFS and other diseases. A donor initiated grant to the Solve ME/CFS Initiative (SMCI) is allowing Dr. Systrom, for the first time, to focus specifically on ME/CFS.
The Oaklander/Systrom partnership seems ripe with possibilities. Both researchers believe an autoimmune or inflammatory process is likely behind the exertional intolerance and other issues in their patients. Both believe the skin is just the starting place in these patients; what’s happening there is also happening in other places, including the autonomic nerves that surround and regulate the activity of the blood vessels in our bodies.
Dr. Systrom can objectively identify people who can’t exercise. Dr. Oaklander can identify people with SFPN. Both are searching for the molecular roots of the problem.
This is duo has come completely out of left field. Neither of these researchers have been associated with ME/CFS before and both are backing into both ME/CFS and fibromyalgia in the best way possible. Both simply applied their testing protocols to people in pain and/or who are unable to exercise and found physiological issues. A lot of those people turned out to have ME/CFS and/or FM. Both are respected leaders in their fields. It’s a wonderful progression.
Please push a little money Health Rising’s way.
BIG (Little) Donation Drive Update – Ensure that you’ll be kept up on the latest findings by supporting Health Rising with a small recurring donation or one-time donation. (Where else, really, do you get blogs like this?) [Find out how to support Health Rising here.](https://www.healthrising.org/blog/2017/12/08/health-risings-big-little-2017-fundraising-drive/) or just use the Donate or Subscribe (recurring donations) on the right hand side of the page. Thanks to the 86 people who have brought Health Rising 40% of our way to our goal!
The rituximab trial (Fluge & Mella) was aimed at B-cell autoimmunity. Rituximab apparently didn’t work for the majority of patients (study hasn’t been published). A positive result here would be good but how do we know that the treatment (IVIG) is working?
According to the reports it significantly improved the symptoms of about 75% of the people in the retrospective study. How much significantly is I don’t know. Some people it apparently made well.
Hasn’t the immunoglobulin angle been explored already for ME? The doctor (Dr. Dubois in Atlanta 1987) who gave me my initial diagnosis of CFS told me that blood transfusions help the condition but don’t last – Similar to what is stated in this article.
It’s definitely been tried. For some patients it works; for others it doesn’t. I just talked to someone who was doing quite well on it. Dr. Tae Park has reported using it with success as well but it doesn’t work for everyone. I’m not sure just how effective it was in that study. It’s clear that in general it helped but I’m not sure how much.
I don’t at all think IVIG is the be and end all of treatments – except for very occasionally when apparently it is. I think it probably needs to be combined with other treatments to have optimal effectiveness.
I’m actually more interested in the idea of these small nerves all over our bodies getting damaged or killed off. I would love it if they could pin that down. That makes total sense to me.:)
I wish these studies would include a questionnaire of all patients, about their daily routine – I strongly believe that there will be a common correlating factor for the subset that improves or recovers.
It seems to me that just about anything that targets something in the vicious circle of FM effects, at any point in the vicious circle, causes an improvement or recovery provided the patients concerned are also doing something else that targets something else in the vicious circle. I pick “the right amount and kind of exercise” as the most important one that will show up with most people who improved under whatever drug or therapy being trialed. Those who do not improve, will most likely be too inactive, but some (going by my experience) may be overdoing it. Patients in the fortuitous mid-range “zone” for activity and exercise will be the “improvers”.
There may be other factors that result in a beneficial combination – diet, stress levels, supplementation, hands-on therapies, etc. Medical researchers need to get interested in these non-pharmacological aspects.
I think we’re going to start seeing researchers connecting real time data on activity, exercise, sleep etc. using wearables. It could tell a lot, I agree.
I have some dysimmune markers and aspects of my medical history that caused an immunologist to recommend a course of IVIg therapy for 3 months several years ago, in the aftermath of my small fiber nerve injury. It did nothing for the pain at all. Prednisone did a little. Opioids to date have done the most, save ketamine and lidocaine infusions, whose effects last precious little time.
I have extensive small fiber neuropathy with many of the vascular signs and symptoms referred to by Drs Rice and Oaklander. This was from a course of Ciprofloxacin. Since then, I have not been the same, mentally or physically, and it seems these effects, with which I live every day, will be permanent.
The pain syndrome over time seemed to morph into a fibromyalgia.
Low dose naltrexone is next up for bids. Sure hope it works.
Am also looking forward to Nav 1.7 sodium channel blocker drug availability in the coming years. Hopefully they will work and not cause the same kind of unacceptable side-effects as the anti-convulsants.
I think a lot of people with SFN and FMS have probably been poisoned by fluoroquinolone antibiotics.
Dr Beatrice Golomb is doing a large-scale study on the wide range of “adverse reactions” these drugs cause.
Remember that nerve injury causes many of the phenomena Dr Rice refers to, which is but one pain mechanism going on in these types of syndromes, which are much like CRPS.
This is a question for Kelly Lee in the thread below. She mentioned small nerve damage from Ciproflaxin. Is that common? I have taken Cipro several times while traveling to India. I am interested in finding out more about this.
Does anyone have information on this as a side effect of Ciproflaxin?
I have been denied IVIG by my insurance. I have Fibromyalgia ( my mom has it too) so my SFPN probably led to that dx. I have possible inflammatory issues. I fatigued when exercising wich led to FM diagnosis. I have adult asthma, food, indoor, outdoor allergies. If I do an activity my fatigue is described as my battery has run out. im in bed for days or weeks. Im getting fat bc lack of exercise bc of exhertion. I use to have lots of energy tons now its gone. I started with toe amd finger tip numbness now I cant feel to type or text. I miss my old self before shoulder surgery in 2013 when all these symptoms of CFS and many others began. Help!
Has dokter oaklander allready have the 5 year grant for research or is she/he asking for it?
My brain is to bad, so if anybody could help me please?
Is it already a good idea to get a small fiber biotie?
thanks!
No problem! Dr. Oaklander is in the middle of one five- grant assessing small nerve fiber issues in younger people. She’s also determining which tests and questionnaires work best.
She is also applying to the NIH for a grant to study the effects of IVIG in people with SFPN. Let’s cross our fingers for that…
I still think SFPN, along with measurable CNS dysfunction, is a symptom – nice to have as proof that we have a “disease”, but not where the cure will be found.
One of the things that is angering me more and more, is the dismissive attitude that those who have influence over research funding, have towards the palpable lumps and corrugations that FM patients have in their muscles – which have been as evident all along as “The Emperor’s New Clothes” to hands-on therapists (massage etc) and any FM patient who goes to them.
I just had a long discussion with Dr John Quintner on this point. I agree that his focus is valuable – the genetic predisposition to getting FM in the first place is probably a defective “stress response” gene – and a cure may well be found in that direction of research. But why do mainstream doctors and researchers regard “palpability” as “unscientific” and anything evident by that means as irrelevant until there is “scientific diagnosis that proves their existence” as something distinct from normal healthy tissue?
http://www.fmperplex.com/2017/12/01/behold-the-mighty-trigger-point
I argue that biomechanical processes could cause myofascial adhesions which then lead via these palpable deformations, and very real pain from them, to an overloaded CNS and even to the SFPN. Numerous other symptoms of FM are explicable also from the simple hypothesis that micro flows and nerve pathways are trapped in distorted, taut fascia.
I am not convinced that CNS dysfunction could be the prior cause of these deformations, it makes much more sense that it is the other way around. How about SFPN – could this, coming first, lead to the development of these lumps and corrugations?
I too believe in a wide multi-disciplinary approach. “Anecdotal” (due to lack of sufficient research) success such as yours and other patients does support that view. That comes with it’s mirror image: if a multi-disciplinary approach does increase chances for success, it also does increase likelihood that the disease itself is a compound “being”.
That we do not talk about a single disease or cause, but one were multiple causes are present and where things that started out as a consequence of the “prime” cause evolve into a strong driver for the disease itself. For example wide-spread fascia damage could have been a very strong initiator of your FM, but the cascade of co-morbidities it caused can be a very strong disease by itself and further entrench both fascia problems and its consequence. “Just” solving fascia problems by itself is then akin to a single-disciplinary approach and tackling combined fascia/other tissue damage problems, nerve problems, auto-immunity problems,… may be both what is needed and what you somehow do.
I do understand that you very much dislike the fact that such an important part is not looked into. “Encircling” the disease is a slow process where many obvious things are not done as long as there is a lack of both knowledge and research budget unfortunately…
Yes, I see your point. Possibly the best term for my success is a “lifestyle strategy”. If I were to go back to “living like a normal person” and my FM worsened again, obviously there is a cause that is not cured.
But there are numerous conditions people suffer, for which alternative medicine offers help, including “de-toxing” and supplementation and “organic” living and so on. Most people and doctors mock this because their standard is normal healthy people who do not “over react” to tiny amounts of common toxins, routine stressors, routine surgery, common foods, etc. Maybe the cure to all these problems will be found in the area of gene research – if as John Quintner hypothesises, all people with FM have a faulty gene that affects stress reactions, then switching that off would probably greatly reduce people’s vulnerability to the other factors such as toxins, “normal foods”, anaerobic exercise, etc
Phil- I just wanted to second your intuition.
The edges of my lower traps are like two ropes and I’ve never had a doctor take an interest in that (and I’ve told more than one). I suspect that if you figure out why those are like that you’ll have a solid hunch about what I’ve got. My upper traps, on the other hand, are extremely hyper-active.
I’ve had a lot of work done on both by PTs (ART massage, dry needling, etc.) and the lower bands don’t seem to be trigger point-based (no twitch from the dry needling).
Cort, can you recommend a medical / scientific journal that I can write to, posing my questions?
Five year studies are not going to help some of us and, once again, the dismal truth is that many of us will go on to the next phase with fibromyalgia. I half expect to be in pain when I’m dead.
But thanks for reporting, Cort.
So sorry to all of us who are suffering.
I have been searching for answers for over a decade and have seen top specialists in this field. I have been told I have idiopathic SNFPN. Just for clarification, damage to small nerves confirmed by biopsy but large nerves intact.- no known cause can be identified.
I eat a very clean diet, have a a low normal BMI, do not drink alcohol or smoke, take alpha lipoic acid and other vitamins, antioxidants etc., walk for exercise.
I do however have a stressful job which requires that I get little sleep during the week and some significant stress in other aspects of my life. I was told there is nothing else that can be done to help me.
I do try to meditate nightly as well.
I hope that better options will be available soon. It is a difficult life with all of the pain and numbness as well as the GI symptoms which are awful. Peace to all.
I always disliked the idea that auto-immunity could play an important role in ME/FM, especially if it involved auto-immunity against nerves or even worse brain cells.
It’s not that I find auto-immunity to be so unlikely but that I disliked the idea that auto-immunity is often hard to treat and damage to nerves and brain was supposed to be unreversible leaving us with no sight for a cure; only a stop in further decline.
Recently however the brain has been show to have more capacity for renewal than was thought for ages and now it seems damage to the nerves could be far more repairable than expected.
Having a potentially objective test for those affected, having a potentially very large amount of patients that could benefit, having some auto-immunity drugs being usable for multiple auto-immunity related diseases and having the potential for making part of the patients productive citizens of society once more adds up to this: it could turn to be a multi-billion market for big pharma.
If chances of commercial success were good enough that would open the doors to billions of research dollars and better chance for some real progress. Once that would happen, big pharmas lobbying and advertising budget would dwarf both current advocating and research budget. They quickly would pick up work such as Corts recent endeavor to show the true economical cost of this disease to both patients and society. So it would turn out to be big pharmas budgets, patients justified outcry and governments need to increase healthy workforce in an aging population against insurers pitiful attempt to save a penny. Take that insurers!
Maybe I’m just a dreamer?
You never know!
OH MY GO_!!Cud this Japanese study on a thing called ME/CFS BE the answer to what I’ve been suffering from 4 about 12+ yrs?? The detailed explan. of symptoms R spot on.Hav tried numerous anti-dep. & on & off 4 yrs use Rx amphet. to help me do shopping household chores etc. But this is NOT GOOD!! Cud this brain damage have been caused by a tonic seizure a year or so B4 this started? Article or Jap. Study did not mention poss. Causes of poss. Brain damage. Please help me!!! Reply,ok,??
Then what kind of immunotherapies would work for ME/CFS patients? Plz recommend me some treatments
other than IVIG. because I have found some result of this IVIG trial which reports the effect is not certain.
The biologics have produced a number of candidates which are hands off until researchers can prove ME/CFS is an immune illness.
There’s also Ampligen which for some patients can be transformative. There’s always hope that its parent company will find the money for a trial. The Simmaron Research Foundation is beginning a study that could shed a lot of light on what Ampligen is doing when it works. A blog is coming up on that.
I have ME/CFS and Fibro. I also have a partial IgA deficiency as does my daughter. This is very interesting I wonder if it could help me but I doubt anyone would offer this in Minneapolis/St Paul for awhile
Cort,
You mentioned that Dr.Systrom has a new paper coming out soon. Are there any specifics on what this paper is about — I have read his past paper on CPET (which are not specifically about CFS). What is his new paper about?
I have no clue! I’m pretty sure that he hasn’t wrapped up his SMCI study.A friend told me it was happening. I asked Systrom if it was relevant to ME/CFS, and if it was if we could talk. He said yes….
Very interesting indeed! My two adult kids have had a long journey with “POTS/CFS” and while improved a great deal still struggle. Previously very active daughter had been bedridden for months at 12/13 when a dr gave her an inpatient course of IVIG. While there were no immediate obvious effects, several weeks later she began having the first small signs of some improvement. She has always said she felt the IVIG played a big role in setting things in motion for progress. She and son also had some abnormalities on sweat testing at one point that pointed to possible SFN. And did I mention a VERY strong family history of autoimmune disease on both sides of our family? I am very excited about this research, needless to say!
Interesting! I imagine that IVIG will need to supplemented with other treatments to reach its maximum effects.
And another person with autoimmune diseases in the family. That’s such an intriguing topic.’ I’m amazed that we don;t have more information on prevalence of autoimmunity in families with ME/CFS. Some family studies are underway though.
Was your daughter only given one course of IVIG? What were the other things that helped your daughter and son get better?
I wonder how many readers were absolutely thrilled to read this. I know I was—until I came down to earth and considered how many more years I may have to wait for an outcome that might help me (I’m increasingly bedridden, with limited use of my hands due to SFN). Still, I’m hugely grateful for the news. I don’t quite understand “If it’s simply found in the skin its importance is limited.” Do you mean to say that it assumes a more critical status only if tied to lung & cardiovascular impacts that directly endanger the life of the patient? Just wondering.
Yes, I would think if the SFN found in the skin is also found in the small nerves in the gut or near the spinal cord or in the lungs or wherever they are – the problems they could cause would increase exponentially. They could account for virtually every symptom in ME/CFS and FM.
I had success overcoming CFS using Inosine which helps to regrow nerves. B cells also are depleted of purine in a chronic infection and inosine restores their function. Using Arginine/Ornithine and DMAE increases its effectiveness.
Thanks for sharing that Doug. I encourage you to tell your story in Health Rising’s Recovery/Recovering story section here – https://www.healthrising.org/forums/recovery-stories/categories/alternative-health.166/
Doug,
Can you be more specific about what you used? How much and how long? what brand?
where would one go to get skin biopsy to diagnose small fiber neuropathy. im very ill and dont know where to turn anymore
Hi Carol. I think its a pretty standard test. I imagine that you just need to get your doctor to order it. Perhaps if you show him/her how your symptoms match up with the list of symptoms in the questionnaire mentioned in the blog that will work. Good luck!
I just had a skin biopsy done at MUSC in Charleston SC (November 26, 2018. From what I understand their is not many places that offer this procedure. It took me over a year to land a doctor who is listening to me. Dr. Westerkam, Lexington Medical Center, West Columbia, SC, a brain and spine doctor.
You need a neurologist who believes in small fiber neuropathy. Most will start with EMG nerve tests to test the larger nerves. Dont let them stop there! If you have all the symptoms press for the nerve biopsy for small fiber neuropathy. They simply numb 2 areas of your lower legs and take a skin sample. A lab looks at the nerves from there. It is still an iffy science and some dont agree it is a thing. I had mine done at Barrows Neurology/Muscle clinic in Phoenix, AZ.
My fam doctor sent me to a neurologist for my skin biopsy. It took 3 wks for the diagnosis to come back.
I do not have Fibro, but have been told I have neuropathy. The large nerve test came back normal. Today I had the small nerve test no results yet. But I have every symptom mentioned with small nerve neuro with one exception I am freezing especially my feet, no hot spots. I am now seeing a pulmonologist, never thinking it could be related. Any my biggest question is every time temperature issues are mentioned it is always hot spots, my feet feel like I’ve been playing in ice cold puddles in my socks and cannot warm or dry them. Any answers?
Good luck Marla! Please let us know how your test results turned out and what the doctor recommends. My guess is that either cold or hot could be nerve problems.
What kind of Dr do I go to who will be familiar with small cell neuropathy??
I have always felt my fibro and small fibro neuropathy were autoimmune related. My family tree has so many autoimmune diseases it was inevitable. My first problem started with my Hashimoto’s hypothyroid diagnosis. Five years later, I was diagnosed with fibro, then SFN. My only prayer is that I am pain-free in the after life, or whatever happens to me after this horrible body of mine dies. No one should have to live with this level of pain. Nothing really helps. I take high doses Lyrica, and wear a morphine patch …and still have so many days of lying on a heating pad in pain. My legs feel like they are covered in 3rd degree burns 24/7. It’s enough to drive most people mad. My life’s activities revolve around my pain.
How do you get in on an IVIG trial? I suffer horrendously: Fibro,SFN,CF, and possible Lupus, reaction to Cipro, reaction to Lupron – burning pain in legs, pelvis, bladder hell, muscle hell
Been to neurologists, urologists, rheumatologists – I have a collection of diagnoses but no pain relief. I am super sensitive to all medications. No one will believe me that steroid injections help. I am a mom and need to be there for my kids, not bedridden. Live in AZ. Help please. Military insurance.
Hi, Did you get help? I also have neuropathy (seems to be SFPN) but is undiagnosed due to awful neurologist. I also react to meds with neuropathy flares in response to most meds and supplements. I’m interested if you found any help anywhere?
I am curious is the thought if you cure fibromyalgia you might sold SFPN, or cure SFPN and might cure fibro?
I suffer terribly from severe burning 24/7 body wide from Cipro. Positive for SFN. What can be done? It is hell. Something affordable and effective needs to become available.
Would like to add to this excellent discussion that I believe that my severe SFPN was caused or exacerbated by statin drugs which I took for many years. The causal relationship of statins to peripheral neuropathy is well documented in a number of case and population studies. The latest iteration of the MGH recommended tests for evaluating SFPN states that a recent article has proven that statinsdo notcause SFPN. I hope that this error will be corrected as the article defined neuropathy by the presence of an abnormal nerve conduction study which would apply to large fiber disorders. The full reference will be found at the lower right section of the MGH sheet. The study is by Warendorf JK in Neurology 2019: Statins do not increase risk of polyneuropathy. (I also believe that the methodology of the trial and the literature review are both flowed and that statins do indeed cause polyneuropathy).
My neuropathy started after taking statins and metformin (I’m not diabetic and was taking for other prescribed reasons). I react to most meds now with worsening neuropathy flares.