of Cort Johnson
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).
A major question facing SFN researchers in fibromyalgia is how important the small nerve fiber problems are to fibromyalgia. 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 – by measuring axon diameter in nine different areas 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.
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. (Natelson has found a similarly curiously pattern in ME/CFS: ME/CFS patients without mood disorders display more neurological abnormalities than those 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 affected 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 Alzheimer’s 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 disease, 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.
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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 as 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
There was no sense in this study that the nerve loss was damaging FM patients; the amount of the fiber loss was subclinical, i.e., not enough to produce symptoms. Ritchie Shoemaker M.D., however, believes that neurotoxins have affected the visual acuity of people with ME/CFS and developed an online Visual Contrast Sensitivity (VCS) test which he believes picks that up.
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, being able to differentiate fibromyalgia from other pain states which are not “neurodegenerative” 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 the aberrant nerve fiber findings in the skin and eyes of FM patients could indicate other nerves may be affected in the muscosal areas of the body.
The tie that binds in all these FM studies are problems with the small unmyelinated nerves. Because peripheral neuropathies found in diseases like Guillian-Barre Syndrome do not affect the corneal nerves, the authors asserted that the thinning they found in FM had a central nervous system sensitization. Corneal thinning in diabetes, however – a disease which is not associated with central nervous sensitization – indicates that corneal thinning can occur in other ways.
Whether the same nerve degenerative processes are causing problems in both the cornea and the retina of the eyes as well as the skin in FM is unclear. In fact, the cause of any of the nerve damage is unknown. What is clear, thus far, is that the further researchers have probed, the more they have found.
Evidence of damage to the unmyelinated small nerves in fibromyalgia continues to mount. Several studies have 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 asserted that FM is a neurodegenerative disease, as well.
Other neuro-imaging tests have found abnormalities in FM but are expensive. The ease, cost-effectiveness and non-invasive nature of the tests 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.
About the Author: ProHealth is pleased to share information from Cort Johnson. Cort has had myalgic encephalomyelitis /chronic fatigue syndrome for over 30 years. The founder of Phoenix Rising and Health Rising, he has contributed hundreds of blogs on chronic fatigue syndrome, fibromyalgia and their allied disorders over the past 10 years. Find more of Cort’s and other bloggers’ work at Health Rising.