“The RNFL is an ideal structure (no other central nervous system tract has this unique arrangement) for visualizing the processes of neurodegeneration, neuroprotection and, potentially, even neuro-repair. The authors
We know that fibromyalgia is a central nervous system disorder; the question is whether we can do away with the “central” part and call it simply a nervous system disorder. It’s clear that somewhere around 40% of people with FM also have small nerve fiber damage (SFN). That neuropathy describes not only the disappearance of some of the small nerves in the skin and eyes but the thinning of the remaining ones in the skin. That last finding is so unusual that it’s been suggested that the small nerve fiber problems found in FM be called something else entirely ( small nerve pathology)
How important the small nerve fiber problems are to fibromyalgia, however, is unclear. Daniel Clauw, a prominent FM researcher, believes the SFN is probably incidental and has little to do with the core pathology of the disease. Others believe that the process causing the loss and thinning of the unmyelinated fibers in FM probably plays a core role in the disease.
This Spanish study examined nerve thickness in a new part of the body – the retina of the eye. Until now nerve studies have focused on the peripheral nerves found in the body. Because this part of the eye is considered to be part of the central nervous system, this study was the first to examined potential small nerve problems in that area.
Fibromyalgia Is Correlated with Retinal Nerve Fiber Layer Thinning Elena Garcia-Martin1,2*, Javier Garcia-Campayo2,3, Marta Puebla-Guedea2,3, Francisco J. Ascaso2,4, Miguel Roca5, Fernando Gutierrez-Ruiz1,2, Elisa Vilades1,2, Vicente Polo1,2, Jose M. Larrosa1,2, Luis E. Pablo1,2, Maria Satue1,2This study measured axon diameter in nine different areas of the eye.
With 116 age and sex-matched patients and a 144 controls it was a nice-sized study. It aimed to determine if retinal nerve fiber thinning had occurred in three sections of the eye, and if it had, if disease duration, severity, etc. were associated with it. (They subdivided the FM participants into people with severe and “mild” FM.) They used several different kinds of optical coherence tomography (OCT) in the study.
The study found that even patients with “mild” FM displayed “subclinical” thinning of the retinal nerves in the nasal and temporal sectors of the eye. The degree of thinning was not significantly greater in people with longer duration or more severe FM, but was greater in the “biologic FM” subset; i.e., people with FM who did not display anxiety or mood disorders, than in FM patients with mood disorders.
Noting that the retinal and optic nerves in the eye derive from brain tissue during development, and thus are considered part of the central nervous system, the authors suggested that their findings suggested that the eyes of FM patients could function as windows into whatever central nervous system problems present.
A Biomarker of Neurodegeneration?
The unmyelinated nerves in the temporal quadrant of the eye – the most effected section of the eye in FM – are amongst the first nerves to show damage in neurodegenerative diseases. Axonal loss in the eyes is correlated with the extent of disability found in neurodegenerative diseases such as multiple sclerosis, and Parkinson’s and Alzheimer’s disease. Because the nerve fiber thinning occurs early in Alzheimers and MS progresses, retinal nerve fiber density tests have been suggested as early disease biomarkers.
The study findings buttressed the idea that FM is a neurodegenerative; i.e. a nerve damaging disease – placing it in the same general category as Alzheimer’s, Parkinson’s, multiple sclerosis and others. The author asserted the findings indicate that FM is a neurological disease which produces “neuropsychological” symptoms.
The idea that FM is a neurodegenerative disease is not a new one. Something after all has to be causing the nerves in the pain inhibiting pathways of the central nervous system to more or less give up the ghost, and plenty of evidence suggests that nerve damage is present in the skin and corneas of significant numbers of people with FM. This may be the first study, though, to present physical evidence that FM is neurodegenerative in the same way that Alzheimer’s or Parkinson’s disease; i..e that central nervous system nerves are being directly compromised to some degree.
Reduced nerve fiber thickness in obstructive sleep apnea is believed due to reduced blood flows and the resulting low levels of oxygen in the fibers. That’s an interesting finding given that this same group last year found reduced blood perfusion in the optic nerves of FM patients.
Dry eyes are more common in FM, and altered visual perception has been found in ME/CFS patients as well.
Subclinical Losses Mean No Loss of Eyesight
The amount of the fiber loss was subclinical; i.e., not enough to produce symptoms or loss of vision.
The authors suggested that because OCT scans are quick, cheap and non-invasive that they could easily become part of the diagnostic criteria for the disease. Given the high degree of FM misdiagnosis reported, that would be a major step forward.
This isn’t the first study to use the eyes to try to understand fibromyalgia or chronic fatigue syndrome (ME/CFS). An earlier SFN study using a different technique found significant reductions in nerve fiber density in the thin outer layer or cornea of the eye. Because this part of the eye is not believed to derive from brain tissue it’s not considered part of the central nervous system. Dr. Martinez-Lavin suggested that that finding meant nerves may be affected in the muscosal areas (mouth, gut) of the body as well.
Whether similar nerve degenerative processes are causing problems in the cornea and retina and skin of FM patients is unclear. What is clear, thus far, is that the further researchers have probed the more nerve problems they have found.
Evidence of damage to the unmyelinated small nerves in fibromyalgia continues to mount. Several studies had found nerve loss or reduced nerve size in the peripheral nervous system (the skin and corneas of FM patients), but this was the first study to find evidence of small nerve fiber thinning in the central nervous system. Because a similar process occurs in neurodegenerative illnesses such as Alzheimer’s and Parkinson’s disease the authors of the study asserted that FM is a “neurodegenerative” disease.
The ease, cost-effectiveness and non-invasive nature of the test used in this study suggested they could be used as a diagnostic tool to differentiate FM patients from other patients with pain. The subclinical nature of the nerve fiber losses indicated that they were not likely to affect eyesight.
The question I ask, is “what is the small nerve fibre damage a consequence OF”?
As you note, Cort, corneal thinning can be caused by another well-known condition. How many conditions exist, that might cause small nerve fibre damage; is FM just one among several?
At least when it is diabetes, the underlying condition is a recognized and well-researched one and there are known protocols for treatment. FM needs to be as recognized and well-researched; it seems all we are doing is discovering more and more symptoms. At least the evidence is substantial, that the pain and other dysfunctions are not “all in the mind”.
I still suspect that the “damage” in FM is the result of the muscle-exertion waste-byproduct clearance system being impaired in some way. But this itself may be a pathway, not a cause – the flow system (vascular, lymph, etc) may be shutting down in the face of toxins including byproducts of infection.
Much of the problems in the muscles is because of myofascia ground substance losing its lubricant property and becoming sticky, which obviously can be a consequence of waste products lingering too long. One wonders if there is an immune response to a toxin, would the toxin do more damage than what happens to muscle fibre and nerve fibre with the system flows shut down?
I do think the improvement I have experienced and am still experiencing, is a sign that the initial vicious circle of decline can be reversed into a virtuous circle of recovery. Will small nerve fibre be “repairing”, I wonder? If small nerve fibre dysfunction was “the cause” rather than one result of the overall condition, then it would be very hard to get the improvement I have got.
Phillip Hayward can you tell us what you’ve done in order to see improvement with fibro symptoms? Would be greatly appreciated. And how you found this treatment and if it was on your own or help of a doctor specialized in treating fibro patients. Thanks Susan fibro patient
I wanted to ask this very same question. Thank you, Susan and Philip.
I have fibromyalgia and I have had surgery for a detached retina in my right eye, 2 lots of laser surgery in this eye and a cataract removed. I have had a cateract removed and laser surgery in my left eye. I am only 47 and had only needed distance glasses until I got fibro. My mum has dementia and is completely blind with detached retinas. I live in Glasgow Scotland , uk
I had a detached retina in my left eye that was surgically repaired and lasered & one year later I had a cateract removed from the same eye and a Toric lens put in. My right eye has been good. I believe I have had Fibro most of my life as I have had symptoms as far back as I can remember.
I have had four detached retinas (no, I do not have four eyes, LOL), and two laser treatments to prevent detachment. I have ME/CFS. I was first diagnosed with FM, then ME/CFS and now have been dx’d with Ehlers-Danlos Syndrome (EDS). Do most people with FM have EDS, too?
I’m wondering if most people with FM have had detached retinas and how many other people have and if they were otherwise healthy or not.
I have not been Dxd with EDS but I have not been tested for it either. I have been Dxd with FM and CFS and small fiber neuropathy.
“It’s clear that somewhere around 40% of people with FM also have small nerve fiber damage (SFN). ” There have only been a handful of studies, each with only a few dozen participants. To say that 40% of those with fibromyalgia have SFN is misleading. My concern, and I know it is jaded, is that all with fibro will be branded with SFN, a convenient way of getting all on Lyrica, Grails or Neurontin.
Fair enough…It’s about time a list was made anyway. Here are the studies thus far
Most of the studies are small but there are now nine of them – and the findings have been consistent. It would be good to have some really large ones, for sure. Hopefully those are in the works.
I am 65 and had laser surgery in my early twenties on both of my eyes due to lots of holes & tears.
I share your concern, Rodger, see my longer comment above. The medical system loves to find a symptom and then prescribe a drug to suppress it, and say they have done all they need to.
Would that be the right approach for people with SFN as the result of, say, diabetes????
I say there is something underlying in FM, that everything else is a consequence “OF”, and that is what proper medical research and discovery of cures should be all about.
Even the diagnosis I got more than 20 years ago, of FM, was nothing more than “you have sensitive spots in enough of the 18 recognised places”. The fact that someone with FM can be shown to have SFN might be no further progress towards the best actual treatment of the condition.
The naturopath Gary Moller says that almost everyone with FM who comes to him, shows up in a hair mineral analysis test, to have a high level of some toxic element. In my case it was cadmium. Many others have an undiagnosed infection, often dental.
I think that FM is triggered by a combination of factors that someone unluckily experiences simultaneously. Genetic predisposition will be one of them. Environmental toxicity, stress, an accident, disease, operation, trauma, whatever. Reversing the vicious circle of symptoms triggered in the first place, requires a multi-disciplinary approach. I do not think there will ever be a single miracle drug that cures FM on its own. What is important is stress reduction; detoxing (diet etc); exercise to promote flushing but strictly at below the intensity that it causes damage to get worse; intelligent mineral supplementation to address imbalances and shortages; intelligent gradual re-mobilising of muscles with stretching and therapies.
Intelligent treatment of, say, cerebral palsy, is extremely multi-disciplinary, and I say FM is a “real condition” like CP. CP sufferers are not self-occupied cranks because they do hydrotherapy and patterning exercises and so on; neither are we.
How did you stop yours Roger?
Sorry, Fibro brain… I meant Phil
What percentage of healthy people have a thinning optic nerve?
I don’t know. They did about 20 measurements with different instruments and found that in every case the nerve fiber density was reduced in the FM patients. In about 10 of they were able to stay statistically that the difference was significant. Since this was a pretty big study – over 100 FM patients and 100 controls I imagine that it’s pretty accurate.
Small fiber neuropathy is found in many diseases ranging from Parkinson’s to diabetes to Ehlers Danlos Syndrome.
“…patients without mood disorders display more neurological abnormalities than those with mood disorders…”
This is incredibly interesting. What if this is because the patients without mood disorders are more motivated, and exert themselves more, and cause themselves more damage as a result? FM, and CFS, might be particularly cruel conditions in that the harder you honestly try, the more damage you do yourself. I strongly believe this in my own case. Discovering that low intensity exertion was the key, was vital – I spent 20 years getting bursts of initiative, doing “fitness”, and each time after a few months I had lost more basic functionality than ever. Squatting was always impossible during 20 years, but when I got worse through throwing myself into exercise programs, I was struggling to even stand up from a seated position, in fact even lowering myself onto a chair in the first place was agonizing.
Picking up some pointers from this blog, led me to focus on exercise in large quantities but at low intensity, and that is when everything turned around. Before, I was always walking too fast, or lane-swimming too fast, or pushing too big a load on the exercise machines.
But paradoxically, avoiding the muscle-strengthening activities has not led to a reduction in strength, rather the opposite. Devin Starlanyl points out relating to FM dysfunction, that muscle “range of movement” is critical. Gaining “muscle range of movement”, I believe has given me more actual strength even though I am not doing any “strength building” exercise at all, I am actually avoiding it! With FM, the myofascia dysfunction means that muscle strengthening activities merely create more and worse trigger points in the muscles, and increase the “stuck” zones between adjacent muscles and muscle strands.
Interesting! The importance of increasing muscle range of movement fits in very well with Rowe’s studies which find it much reduced in adolescent ME/CFS.
I had bilaterial careracts at age 40, it was overlooked for years cause it went from very dark like my eye color to than green witch kind of glowed in the dark when light hit it witch scared off doctors until they both became absolute and a doctor that didn’t see them before tackled the surgery, I have had double vision throught out these years and still do, sometimes it’s more than double but doule is always present, however the highest, magnifying glasses correct the double vision if the print is large enough, for me to read. (have ME/CFS from water damaged home exposures) and do have depression issues but usually only get depressed over dealing with the pain of severe fibromyalgia and ya sometimes just because I want my life back. I think first it has to be realized weither any of us suffer true depression or weither theres exposures that affect certain areas of our brain that can alter our moods because I know I can have exposures that not only send my brain to lalaland pretty quick but also can cause mood changes. I have pretty severe hypersensitivities , allergic and non-allergic. was diagnosed with MCS some years ago.
Thanks for this information Cort. I am happy, but also a little surprised, to see that “The subclinical nature of the nerve fiber losses indicated that they were not likely to affect eyesight.” It’s encouraging to know there may be another diagnostic tool available. Something about the FM and/or ME/CFS, however, does seem to affect my eyesight and I know a number of patients with the same issues. It is very difficult to get a prescription for glasses I can see clearly with all the time. Last year I saw three different doctors (opthomologists and optometrists) within a span of a few months and all three gave me totally different prescriptions for glasses, none of which I could see perfectly clearly with. My vision seems to change frequently depending upon how bad my FM and ME/CFS symptoms are on any given day. It continues to be a mystery.
Your comment is interesting to me, as I’ve had similar issues. About 20 years ago I was one of the early Lasik patients. I believe my pre-op exam revealed thin corneas, but they did the surgery anyway. My vision was fantastic for about 7 years, but began declining and I soon required glasses again, and the prescriptions were never quite right. I initially chalked this up to altitude changes (I live at 8500 ft but would often travel to sea level, and my vision changes seemed to follow a similar pattern), but it’s proven to be more complicated than that.
Recently I was officially diagnosed with keratoconus (a thinning disorder of the cornea that causes visual distortion), and wear scleral contact lenses to correct for it. You may wish to look into that for yourself.
While I lack most EDS symptoms, I do wonder if this keratoconus is due to a collagen dysfunction, and might also explain my historically poor wound-healing, and is ultimately rooted in whatever syndrome has plagued me for the last 35 years.
Thank you. I’ll check into that. Interestingly, I too have a problem with slow wound healing. Six weeks ago I had a squamous cell carcinoma removed from the top of my foot and was told it would take about three weeks to heal. It’s still not totally healed, although it is getting there.
Yes, Philip. Over exertion and repetitive strength building exercise increase the over-contracted painful muscles and trigger point addition and activation. On the other hand, movement which aims to stretch, oxygenate and move muscles in moderate and varied ways can help maintain or even increase strength without aggravating muscles to a destructive level. Dance teachers from my distant past used to say that a (properly) stretched muscle is stronger than a contracted one. Hard, contracted muscles are not only painful, they are weak.
I think you may be right about waste products in the system causing more trouble, maybe degeneration.
Increasing oxygenation and circulation are better than exertion-based exercise and regular strength training, I believe. In fact, the latter become destructive.
I have ME/CFS, Myofascial Pain Syndrome and SFN.
Thanks, Cecelia. I would add that attempting to stretch the muscles while in the full grip of FM, is not by itself going to result in progress towards fixing the problem. I liken this, to trying to stretch rubber bands that have been soaked in some kind of glue or hardener. You need to start by dissolving the hardener. Detoxing with diet and supplementation, and doing whatever low intensity exercise you can handle so as to get some flushing out going on, needs to be the priority. Stretching can gradually be increased according to the ability to do it, period! This is definitely my experience.
Interesting that you mention a dance teacher; as I have become more and more flexible with my multi-disciplinary protocol, I have looked for the right kind of programs to properly target more and more of my muscle groups, and I have found one run by a lifetime career ballet instructor. She is an absolute guru of muscle group mobilization – exactly what I need. Now I am getting my whole core and torso mobilized, I have felt my spine adjusting as though it is getting a chiropractic manipulation, but I am doing this myself. Just by getting deep-layer muscles working again, that have not been working for 20 years.
That is terrific, Philip! I know how it takes strategy and commitment to unravel the strands of this problem and get things on the right track. I am glad you found an old dance teacher. Some of the very experienced dancers really understand the body.
I would add to what I wrote about stretching before–i.e., how stretching comes before strengthening–that when my muscles are like rocks and aching a lot, what I do is to lie on a hard roller until a spot starts to respond and open a bit, then move the roller to the next spot, and on, around my whole back and butt, then push it down into those areas of the neck. I happen to use a “Ma Roller”. Some use tennis balls, but what I like about the roller is that it can get either one spot, or both paraspinal muscles at the same time. I can watch a video at the same time this passive self massage is going on. The work around my back might take 45 minutes, but it gives me both temporary relief and renews a much better starting place for regular stretching and movement.
I know this whole subject would be a terrific bore to a normal person, and it is to that part of my mind, but for people like us, there’s a lot we need to do for our bodies which they are no longer doing for themselves (so to speak).
Yes Philip Hayward, I would also like to know. Please
Very interesting read I have fbiro sleep apnoea and diabetes among various other things my right eye has deteriorated rapidly I have seen various consultants I have ghosting double vision and blurred vision can’t see much even with glasses I have been diagnosed with mild cateracs age related degeneration and a stigma I’m terrified about loosing my vision and feeling I’m going that way I’m not sure this diagnosis is correct I feel something more serious is going on as I can barely see
I have blurring issues too, and ya, things change along with how I fell, also suffered vertigo for several years and still once in a while but not as severe, I still cant read very small writeing like a phone book and even with my magnifiers on and a hand held one. if a tv is to small all words are brurred and because that’s not close up my glasses are not any help.
Gray matter abnormalities associated with fibromyalgia: a meta-analysis of voxel-based morphometric studies
In fibromyalgia patients compared with healthy controls, regional GM decreases were consistently found in the bilateral anterior cingulate/paracingulate cortex/medial prefrontal cortex, the bilateral posterior cingulate/paracingulate cortex, the left parahippocampal gyrus/fusiform cortex, and the right parahippocampal gyrus/hippocampus. Regional GM increases were consistently found in the left cerebellum
Altered Dynamic of EEG Oscillations in Fibromyalgia Patients at Rest
Fibromyalgia has central nervous system origins
Fibromyalgia Is Associated with Decreased Connectivity Between Pain- and Sensorimotor Brain Areas
2016 Revisions to the 2010/2011 Fibromyalgia Diagnostic Criteria☆
Fibromyalgia has a larger impact on physical health than on psychological health, yet both are markedly affected: The al-Ándalus project
Overall, fibromyalgia women showed a worse status in pain, fatigue, health-related quality of life, depression, and anxiety than controls (P < 0.01). In general, the observed associations presented very large effect sizes (Cohen׳s d from ~1 to ~5.5). No differences between fibromyalgia and controls were observed in cognitive and memory performance, except for delayed recall, but the observed effect size was low (~0.25). The effect size observed for the global physical component (~3.3) was larger than that for the global psychological component (~1.3), all P < 0.001.
Our results reinforce the understanding of fibromyalgia as a polysymptomatic distress condition with pain as its main symptom. Our findings support that fibromyalgia seems to have a greater impact on physical than on psychological outcomes, though both are largely affected.
thought this was interesting because if I remember right endocannibinoids were listed in the woman's list in the hibernation article by Naviaux
J Neuroinflammation. 2016 Sep 2;13(1):231. doi: 10.1186/s12974-016-0682-8.
Interaction between interleukin-1β and type-1 cannabinoid receptor is involved in anxiety-like behavior in experimental autoimmune encephalomyelitis.
Gentile A1,2, Fresegna D1,2, Musella A1,2, Sepman H1,2, Bullitta S1,2, De Vito F1,2, Fantozzi R3, Usiello A4,5, Maccarrone M1,6, Mercuri NB1,2, Lutz B7, Mandolesi G8, Centonze D2,3.
Mood disorders, including anxiety and depression, are frequently diagnosed in multiple sclerosis (MS) patients, even independently of the disabling symptoms associated with the disease. Anatomical, biochemical, and pharmacological evidence indicates that type-1 cannabinoid receptor (CB1R) is implicated in the control of emotional behavior and is modulated during inflammatory neurodegenerative diseases such as MS and experimental autoimmune encephalomyelitis (EAE).
We investigated whether CB1R could exert a role in anxiety-like behavior in mice with EAE. We performed behavioral, pharmacological, and electrophysiological experiments to explore the link between central inflammation, mood, and CB1R function in EAE.
We observed that EAE-induced anxiety was associated with the downregulation of CB1R-mediated control of striatal GABA synaptic transmission and was exacerbated in mice lacking CB1R (CB1R-KO mice). Central blockade of interleukin-1β (IL-1β) reversed the anxiety-like phenotype of EAE mice, an effect associated with the concomitant rescue of dopamine (DA)-regulated spontaneous behavior, and DA-CB1R neurotransmission, leading to the rescue of striatal CB1R sensitivity.
Overall, results of the present investigation indicate that synaptic dysfunction linked to CB1R is involved in EAE-related anxiety and motivation-based behavior and contribute to clarify the complex neurobiological mechanisms underlying mood disorders associated to MS.
Anxiety; Experimental autoimmune encephalomyelitis; Interleukin-1β; Striatum; Type-1 cannabinoid receptor
PMID: 27589957 PMCID: PMC5009553 DOI: 10.1186/s12974-016-0682-8
[PubMed – in process] Free PMC Article
seems to me that Fibromyalgia is a brain injury and the more severe >mTBI, and some TBI, GWI Vet’s that were previously dioagnosed with PTSD were recently diagnosed as TBI/PTSD and the cause was chemical exposure. GWI as in the long looked at GWI (PTSD,MCS,CFS,FM,IBG) I WAS DIAGNOSED WITH PTSD after my exposure, people close to me includeing my daughter, a nurse agrees with me that this was TBI, my eyes were affected badly, I’ve been diagnosed with ME/CFS, FM (SEVERAL TIMES) MCS, IBS, reactive airways,hypersensitivies,TILT, CHRONIC SINUSITIS/RHINOSINUSITIS WITH POLOPS AND CYSTS, ANAPHYLAXIS TO MOLD EXTRACTS,highly allergic to molds and airways reactive to voc’s gases fumes,oils, ect. < this may be why some of us cant tolerate alcohol, because whats in our airways and alcohol fumes/gases don't mix to well and is probably pretty toxic to the brain, that's what I think anyways.
That is an interesting hypothesis; the toxins or infection cause brain damage that end up impairing our physical functioning? I have been hypothesizing the opposite: the toxins or infection led (with me) to hydration issues, myofascia lubrication loss, muscle issues, and then the feedbacks of chronic pain and muscles not responding to brain signals, cause the brain damage.
I think it is true that prisoners (political, war-time etc) who are tortured / sleep-deprived etc show brain damage. Same with soldiers in highly stressful posts (eg urban warfare against guerillas). There is the combination of stress and toxins, again. I think FM is triggered by combinations of factors that unfortunately coincide.
there may be some different ways to get to the same outcomes, aspergillus has been shown to cause mast cell degranulation on contact, , mast cell contents than cause a second poisoning effect, mast cells are very involved in mold and chemical/toxin exposures, and pretty sure I have a MCAD disorder and mast cells are involved in fibromyalgia and hypersensitivity , and the hypersensitivities basicly rule my world and I’ve done the research. Dr. Theohorides has put out a new article on Fibromyalgia, he is the man when it comes to mast cells and I related very much to autism, so much so that I’ve followed research on it. I think Dr. Theohorides knows what he is talking about
I have a difficult time believing that you are not born with fibromyalgia. I was born with it. My two year old daughter was born with it. There is no infection for her, no trauma. Just ….so weak at times she can’t walk up stairs. Even when it is warm outside she wants a jacket. When the sun starts to rise it’s, “too bright, too bright”. She complains of pain in her knees every night. Her poop switches from constipation to diarrhea often in the same setting. She rarely sleeps and is awakened by the slightest noise. Unfortunately this is all too familiar.
I had meningitis to top of the second very bad exposure, the CSF ran out my ears and nose, I let it run on my hand and saw the white streaks of infection, I just don’t know what kind of infection it was really , no doubt several opertunestic invaders hany.
from where I’m setting, Fibromyalgia points straight to airways and environmental exposures like chemicals and voc’s and irritants and even allergens and pathogens, and fibro brain involvement point to the sinuses and lungs and yep in inhalation exposures dermal absorbtion and ingestion also matter. and the stomach and bowel are a continuation of the airways and are also involved and I can have a bad exposure and can affect my stomach and bowels and brain that way too, my neck gets so stiff sometimes I cant turn my head and have pretty chronic pain on the left side of my neck, I live with ice packs and cold towels to fight brain inflammation and washing sinuses has also been a life saver. once I desided to try a steroid nasal spray a ENT had gave me, one shot up my nose set every nerve in my face on fire and it quickly spread to every nerve in my whole body, it was horrable for about a week. that’s when I knew fibromyalgia was the sinus and lung to brain because it happens within seconds. so seems fibromyalgia could be in a way the beginning while CFS could be the result, if anyone can understand what I’m saying. with a exposure injury leads to infection.
I’d like to see someone that has a clue about the eye damages, who might that be?
also have been diagnosed with optic neuritis, inflammation, yes it gets bad in my eyes
and I actually have a pretty good idea of what kind of infection it was because for years afterwards I would sometime caugh and there would be little tiny mold spores, I looked them up online and that’s what they were so I’m figuring the infection was in the mucosa, haven’t coughed any up for years now tho so I think I beat it but I remain very ill.
Dr. Theoharides – What do mast cells “Mast Cell Activation Disorder” have to do with pain, fatigue, allergies and even autism
J Pharmacol Exp Ther. 2016 Mar;356(3):664-72. doi: 10.1124/jpet.115.230060. Epub 2016 Jan 13.
Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells.
Tsilioni I1, Russell IJ1, Stewart JM1, Gleason RM1, Theoharides TC2.
Fibromyalgia syndrome (FMS) is a chronic, idiopathic condition of widespread musculoskeletal pain affecting more women than men. Even though clinical studies have provided evidence of altered central pain pathways, the lack of definitive pathogenesis or reliable objective markers has hampered development of effective treatments. Here we report that the neuropeptides corticotropin-releasing hormone (CRH), substance P (SP), and SP-structurally-related hemokinin-1 (HK-1) were significantly (P = 0.026, P < 0.0001, and P = 0.002, respectively) elevated (0.82 ± 0.57 ng/ml, 0.39 ± 0.18 ng/ml, and 7.98 ± 3.12 ng/ml, respectively) in the serum of patients with FMS compared with healthy controls (0.49 ± 0.26 ng/ml, 0.12 ± 0.1 ng/ml, and 5.71 ± 1.08 ng/ml, respectively). Moreover, SP and HK-1 levels were positively correlated (Pearson r = 0.45, P = 0.002) in FMS. The serum concentrations of the inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF) were also significantly (P = 0.029 and P = 0.006, respectively) higher (2.97 ± 2.35 pg/ml and 0.92 ± 0.31 pg/ml, respectively) in the FMS group compared with healthy subjects (1.79 ± 0.62 pg/ml and 0.69 ± 0.16 pg/ml, respectively). In contrast, serum IL-31 and IL-33 levels were significantly lower (P = 0.0001 and P = 0.044, respectively) in the FMS patients (849.5 ± 1005 pg/ml and 923.2 ± 1284 pg/ml, respectively) in comparison with healthy controls (1281 ± 806.4 pg/ml and 3149 ± 4073 pg/ml, respectively). FMS serum levels of neurotensin were not different from controls. We had previously shown that CRH and SP stimulate IL-6 and TNF release from mast cells (MCs). Our current results indicate that neuropeptides could stimulate MCs to secrete inflammatory cytokines that contribute importantly to the symptoms of FMS. Treatment directed at preventing the secretion or antagonizing these elevated neuroimmune markers, both centrally and peripherally, may prove to be useful in the management of FMS.
Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.
PMID: 26763911 PMCID: PMC4767394 [Available on 2017-03-01] DOI: 10.1124/jpet.115.230060
I don’t really know what to make of all of this. This post peaked my interest because I have an article in my 23andMe folder titled, “Thinner changes of the retinal nerve fiber layer in patients with mild cognitive impairment and Alzheimer’s disease.” (http://bmcneurol.biomedcentral.com/articles/10.1186/s12883-015-0268-6)
I decided to do a quick search of my top five 23andMe elevated health risks and guess what…
1) Age Related Macular Degeneration – “Retinal Nerve Fiber Layer Thinning in Advanced Age Related Macular Degeneration” – http://iovs.arvojournals.org/article.aspx?articleid=2387783
2) Type 2 Diabetes – “Retinal Nerve Fiber Layer Loss in Patients With Type 2 Diabetes and Diabetic Neuropath” – http://care.diabetesjournals.org/content/39/5/e69
3) Alzheimer’s Disease – see above.
Some focus on retinal nerve fibers and some on optic nerve fibers.
Of note is the fact that in one article I read Dr. Sanjay Gupta stated, “The optic nerve, which is behind the eye, is actually part of the brain. In fact, it’s the only part of the brain you can see from the outside.”
It seems to me that issues with the retinal or optic nerve fibers might be indicative of a lot of illnesses.
just read a article that pointed to oxidative stress as possible cause of ARMD. as we age our natural defence mechanisms don’t protect us as well as they use to, 🙁
mine are already shot to heck, and I’m 55 🙁
This is fascinating to me from the standpoint of examining the eyes, non invasive window to what is going on throughout the body. I’ve just come from a week of observation/testing/treatment at POTS Care. They use eye exams to determine many things including vascular issues. They found in me indications of inflammatory POTS & possible vascular fibrosis… Maybe the eyes will become the standard way of diagnosing some of our issues.
2016, Allergen-encoded signals that control allergic responses, fungi, indoor exposure
MICROBES AND ALLERGIC DISEASE
Viruses, bacteria, fungi, helminths, and protozoa all exhibit protease activity and can each contribute other unique signals that contribute to allergic and asthmatic phenotypes, either positively or negatively. Recent advances have helped to elucidate the specific mechanisms of these microbial influences.
I think this is major finding here.
Airway epithelial NF-κB activation promotes the ability to overcome inhalational antigen tolerance
There is valuable information on the optic nerve at upright-health.com. Search the site for optic neuritis. One article, “Optic Neuritis and its Occurance with Chiari Malformation and MS” is particularly helpful. Dr. Flanagan’s book, The Downside of Upright Posture : the Anatomical Causes of Alzheimer’s, Parkinson’s, and Multiple Sclerosis, helped me understand my multiple health issues.
Right after the injury to my upper neck I had extreme visual problems- vision was like a fractured TV screen. Three years later I had a huge retinal tear. Now, just black spots and blurry vision when my neck is really out – like after dental visits.
Also, look at Diana Driscoll’s info on the eye under media at this site.
Understanding structure and function of the upper neck and lower skull ( and key circulatory routes) is critical to any progress with FM and CFS.
I have Fibromyalgia and have Optic Atrophy and the Drs.think i was born with the OA. I also have Vitreous Floaters for about over 10 yrs.but the eye Dr. never said i have a detached retina.She said if i see white lights flashing or like a shower to contact her right away. I have 2 tiny cataracts and my eye Dr.said I’m too young for cataracts. I am 54 yrs. old. I also have memory problems. I just wonder if i have more than FM and maybe misdiagnosed to being MS or Lupus. I also have Chronic Kidney Disease, Carpal Tunnel.
pretty sure my spinal cord on the left side at the base of my brain is damaged, a lot of pain in this area.
I simply would like to know what type of Doctor is the best today for diagnosis and treatment of Fibromyalgia? I was diagnosed in 1992 by a Rheumatologist, but it seems to me that today, perhaps a Neurologist may be better. Please advise.
I would honestly just focus on trying to find someone – a rheumatologist or neurologist or GP who knows about and is interested in the disease.
Since we’re talking about eyes and fibromyalgia…Have any of you noticed that you don’t cry “normally” any more. I might tear up, but I can’t actually cry.
I wonder if any of the scans I’ve had to get for plaquenil reveal any of this or if its not specific enough. Plaquenil requires several opthamology tests a year to make sure permanant retinal toxicity is not occuring from the drug (a rare side effect). One of the tests they do is like an MRI of the retina.
My fibromyalgia was diagnosed in 1998 but most doctors believe I had it long before this time. Looking back, my mother had the same symptoms I have but who knew back in the late 80s, early 90s. My mothers vision improved as she aged. She passed at 78 but had very little eye issues. I on the other hand I am the one person in the family with very poor vision, Started wearing glasses in 8th grade and distance just became progressively worse. But it can be corrected to 20/20 so far. With many tests, i dont have any other issues. No detached retina, no floaters, just poor eyesight (blue eyes are the worst I tell you!)
This topic interests me. I lost vision 12 years ago due to optic neuritis. I was diagnosed with Lupus then. After cortisone treatments my sight was regained. I now am diagnosed with a hodgepodge of immune disorders. I wonder if my initial problem was fibromyalgia from the beginning. I have problems with light sensitivity, migraines and brain fog, but not joint issues. Thank you for this article.
I’m diagnosed with FM and live in Sweden. Most doctors here dont take this seriusly . My eye sight has dekresed by nearly 40% on one eye and more than 60% on the other in just a few month. I have no inflamation on the optic nerve but i have frekvent eye migrens. Has any one else lost that mutch visibility in short time?
My son has been diagnosed with a pale optic nerve. Should I worry? I have suffered myself from chronic neck pain since w009. I am 46 years old now. I do notice that in a bad flare of my neck pain that my eyes take on a mind of their own twitching and such….I have not been diagnosed with FM but myofacial pain by my GP. I have had nerve blocks, Occipital nerve injections, etc.