Optic Nerve Thinning Suggests Fibromyalgia is “Neurodegenerative” Disease
by Cort Johnson | Sep 9, 2016 

“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. 

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)

Small losses in optic nerve density suggested FM is a neurodegenerative disease

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. 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.


The Study

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 Satue1,2  This 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.


Results

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 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 direclty 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 losswas 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 a online Visual Contrast Sensitivity (VCS) test which he believes picks that up.


Because the retinal or optic nerves come from brain tissue the study found evidence of central nervous system nerve damage


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 which 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
no
t considered part of  the central nervous system.  Dr. Martinez-Lavin suggested that the aberrant nerve fiber findings in the skin and eyes of FM patient could indicate other nerves may be affected in the mucosal areas of the body.

Eye 
Opening Finding: Small Fiber Neuropathy Found in Fibromyalgia Patients Eyes


The tie that binds in all these FM studies are problems with the small unmyelinated nerves . Because peripheral neuropathies found in di
seases 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 in unknown. What is clear, thus far, is that the further researchers have probed the more they have found.

Conclusion

Evidence of damage to the unmyelinated small nerves in fibromyalgia continues to mount. After 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 these test used in this study suggested they could be used as a diagnostic tool to differentiate FM patients from other patients with pain. The


Temperature Sensitivity in Fibromyalgia & Chronic Fatigue Syndrome
Why Cold & Hot Hurt When They Shouldn't


By Adrienne Dellwo - Reviewed by a board-certified physician.
Updated April 15, 2016


When you're exposed to heat, does it feel like you're burning up? Does it seem impossible for you to cool off? Or maybe it's cold that bothers you, chilling you to the bone, leaving you unable to warm up.

Or are you one of those people with fibromyalgia (FMS) and chronic fatigue syndrome (ME/CFS) who is cold all the time, or hot all the time, or alternately hot or cold while out of sync with the environment?

If any of those scenarios sounds familiar to you, you may have a symptom called temperature sensitivity.

We don't yet know exactly what causes this symptom, but we do have some compelling research. Much of it suggests abnormalities in the autonomic nervous system, which deals with homeostasis and our bodies' reactions to environmental changes, including the "fight or flight" reaction.

With that established, researchers are now able to look deeper into that system to figure out what exactly is going wrong, and they're finding some interesting things.


                                                   Temperature Sensitivity in Fibromyalgia


​In FMS, some research shows abnormal body temperatures, an inability to adapt to changes in temperature, and a lower pain threshold to both heat and cold stimuli -- meaning that it takes less extreme temperatures to make you feel pain. For example, sunlight shining through a car window onto your arm may cause burning pain in you but only mild discomfort in someone else.

One study (Albrecht) suggests a reason for our temperature sensitivity, and it's one based on a series of discoveries.

The first step involved people who may be the exact opposite of fibromites -- those who can't feel pain at all. It's a rare condition that they're born with. Doctors observed that these people can feel temperature, which was confusing.

Why would the same nerves that could feel one type of stimuli (temperature) not be able to feel another (pain)?

That question led them to a discovery: it's not the same nerves at all. In fact, we have an entirely separate system of nerves that senses temperature. These nerves are on our blood vessels and scientists used to think they just dealt with blood flow.

So it turns out that these special nerves don't just adjust blood flow, they detect temperature. They then became a logical target for FMS research, since we're known to have both blood flow abnormalities and temperature sensitivity.

Sure enough, researchers found that FMS participants in their study had extra temperature-sensing structures on those nerves. The structures are called AV shunts, and they're in your hands, feet and face. Their job is to adjust blood flow in response to temperature changes. You know how when it's really cold out, your cheeks get rosy and your fingers get all puffy and red? That's because the AV shunts are letting in more blood, trying to keep your extremities warm.

This is the first study looking at how this system is involved in our illness so we can't say for sure whether it's accurate. However, it is an interesting direction for more research, and an explanation that appears to make a lot of sense.


 ​​Migraine, ME/CFS and Fibromyalgia – Low Oxygen, High Lactate Disorders?
 

Are migraine, fibromyalgia and ME/CFS connected at the hip?





Migraine effects 12% of the population (!) or about 40 million people. Two studies suggest as many as 75% of people with chronic fatigue syndrome experience migraines and that most migraines in ME/CFS are undiagnosed.  A  recent large fibromyalgia study suggested that 55% of FM patients may meet the criteria for migraines. WebMD, which has very little to say otherwise about chronic fatigue syndrome, states ME/CFS is one of five disorders with high migraine rates.
If those studies are accurate, ME/CFS and FM may have more in common with migraine than with each other. That’s an astonishing possibility given that migraines were hardly talked about with respect to either disease five or ten years ago.

Migraines, Chronic Fatigue Syndrome and Fibromyalgia:  

That makes a recent migraine study highlighting hypoxia (low blood oxygen levels) and increased lactate  – two intriguing possibilities in ME/CFS and FM –  all the more interesting.

A recent blog suggested that increased lactate levels in the brains of ME/CFS patients could set the stage for increased fatigue. Several studies, in fact, suggest that increased lactate levels exist in the brain, muscles and perhaps guts of both chronic fatigue syndrome and fibromyalgia patients.

What is causing these lactate accumulations is unclear but one of the possibilities is hypoxia or low oxygen levels. When oxygen levels are low cells turn to glucose to produce energy via a process called glycolysis. This process produces pyruvate which, in turn is converted into lactate and released into the bloodstream.  As that happens hydrogen ions also build up causing acidosis.

The Migraine, Hypoxia, Lactate Connection :

A recent study exposed people who experience migraines to hypoxic conditions to see if they would trigger a migraine.  They found that low oxygen conditions did, in fact, trigger a migraine in about half the women with a history of migraines but not in the healthy controls.

The ability of low oxygen conditions to trigger migraines in such a high percentage of women was astonishing. Why? Because until this study showed up it’s been difficult to intentionally trigger a migraine in the lab. The oxygen levels the researchers subjected their subjects to was quite low but it did suggest that hypoxia may play a role in triggering migraines.

How was it doing that? It’s long been known that small dilations of the blood vessels in the brain occur during a migraine. These researchers showed that hypoxia did indeed cause those arteries to dilate – but in both the healthy controls and the migraineurs. Since the amount of dilation was no larger in the migraineurs than in the healthy controls it wasn’t clear that enlarged blood vessels were behind the migraines. Nor were levels of glutamate, an excitatory neurochemical long been believed to play a role in migraine, increased.

Lactate:


Lactate levels mushroomed in the migraine patients after hypoxia.

Instead, lactate levels significantly increased in the migraine patients brains and blood. Why the migraineurs responded to low oxygen levels by producing higher levels of lactate than the healthy controls was unclear, but it was clear the lactate increases were associated with a migraine and/or the occurrence of unusual visual disturbances.

Some of those visual disturbances may be familiar to people with ME/CFS or FM; they included black spots, “worms” (floaters?), difficulty focusing and blurred vision. (Those visual disturbances technically fulfilled two criteria for migraine. Three of the four people with visual disturbances also experienced a migraine-like headache.)

The high levels of lactate were also sustained for several hours after the hypoxic challenge ended. That suggested that mitochondrial problems may come into play.  A 1998 study, in fact, found increased plasma lactate levels after exercise in migraine, and numerous other studies have shown decreased ATP production in the visual cortex of migraineurs as well.

Conclusions :

What do we know? We know that migraine is common in ME/CFS and FM and vice versa, and that hypoxia and lactate accumulations and mitochondrial problems may be involved in each of these diseases.

We also know that as with ME/CFS and FM, women are primarily effected by migraines, and migraines and ME/CFS symptoms are often substantially reduced during pregnancy.  People with severe ME/CFS, in particular, often have significant problems with stimuli – as do migraineurs –  and migraineurs and ME/CFS/FM patients also often seek out low stimuli environments during attacks or crashes.

The connections between the three diseases appear to be growing :

We know exercise during a migraine is usually impossible. People with migraines often experience ME/CFS-like symptoms of fatigue and cognitive issues for several days following their migraine attack.

In fact, in a 2015 paper Rayhan and Baraniuk proposed ME/CFS/FM patients may exist in a kind of chronic migraine-like state. Given the considerable symptom overlap migraine has with ME/CFS (visual disturbances, sensitivity to light/sound, weakness, pins and needles, speech problems, nausea, vomiting, increased urination, etc) they could very well be right.













Yes, there is a test to diagnose fibromyalgia. Not many doctors use it, and it’s not approved by the American College of Rheumatology, but some insurance companies are now paying for it.


MORE INSURANCE COMPANIES NOW PAYING FOR FM/A FIBROMYALGIA TEST :

The story below on the FM/a fibromyalgia test first appeared on NationalPainReport.com. It is being republished here with permission from the editor. (Note: I have no financial interest in EpicGenetics or the FM/a fibromyalgia test.) 


Medicare and some private insurers, including Blue Cross

Blue Shield, UnitedHealthcare and Aetna, are now paying

for the FM/a fibromyalgia test on a case-by-case basis.

EpicGenetics, the company that developed the test, offers free

assistance to determine if your insurance will cover the test.

Do you have a family member, friend or physician who doubts you have fibromyalgia? Well, there’s a little-known test you may not have heard of that could finally prove you’re really sick.

In 2013, Los Angeles-based biomedical company EpicGenetics made international headlines when it introduced FM/a, the first ever fibromyalgia test.

While FM/a hasn’t caught on in most doctors’ offices, more insurance companies are now paying for the test. FM/a is covered by most Medicare plans. Private insurers, such as Blue Cross Blue Shield, UnitedHealthcare and Aetna, also are starting to pay for the test on a case-by-case basis.

The test’s steep price tag – $794 – has been a deterrent for patients, many of whom are already living on fixed incomes because they’re unable to work due to poor health.

EpicGenetics is trying to make it easier for patients to afford the test by providing free assistance with insurance processing.The company’s insurance processing department contacts insurance companies on the patients’ behalf to find out if the test is covered and what the cost would be to the patient.

(A six-installment, no interest payment plan is available for people who are uninsured or whose insurance won’t cover the test.)

Dr. Bruce Gillis, EpicGenetics’ CEO, says the No. 1 reason patients get the test is to prove to family members and others that they are really sick.


He believes physician bias is the main reason why the test is not more widely used.

“The majority of physicians do not believe that fibromyalgia is real, so they haven’t kept up with the advances that have occurred, including reading something as simple as WebMD, which tells everyone the test exists,” he says. “In under 10 seconds, a Google search reveals the test.”


Many physicians don’t consider fibromyalgia to be a disease; they believe it’s a collection of symptoms and lump it into the “syndrome” category.

And then there’s another group of physicians who don’t believe fibromyalgia exists at all. Patients are routinely told they’re “depressed” or “getting older” – or worst still, the pain, fatigue, brain fog and other debilitating symptoms are all in their heads.

The legitimacy of fibromyalgia has been complicated for decades because of the lack of a diagnostic test to prove its existence. It’s typically a diagnosis of exclusion – meaning illnesses with similar symptoms have been ruled out through extensive (i.e. often expensive) medical testing.

According to EpicGenetics, patients can spend between $10,000 and $42,500 on diagnostic tests leading up to their fibromyalgia diagnosis. That’s a lot of money, and that’s another reason why physicians haven’t embraced the FM/a test, Gillis says.


“Many rheumatologists prefer to offer patients rule-out tests, which they can perform in their office labs, thereby making for a financial incentive to follow that route,” he explains.

How the FM/a fibromyalgia test works :


A licensed healthcare professional must order the test for the patient. The test requires a simple blood draw, and results are available within five to seven days. It has a sensitivity of 93 percent – equivalent to the blood test for HIV. (No test has a sensitivity of 100 percent.)

Gillis admits he used to be one of those physicians who doubted the existence of fibromyalgia, but the results of EpicGenetics’ research studies have made him a believer.


EpicGenetics focuses on developing diagnostic tests where none currently exist. When Gillis was asked to look at fibromyalgia, he and researchers from the University of Illinois College of Medicine in Chicago theorized that fibromyalgia’s mishmash of symptoms might be caused by amalfunctioning immune system.

The first study looked at a series of immune system biomarkers in 17 patients with fibromyalgia and 17 healthy people, and the results were striking. Researchers found several biomarker abnormalities among the fibromyalgia patients, leading Gillis to conclude fibro symptoms are somehow associated with a suppressed immune system.


“We believe (the term) fibromyalgia is a misnomer,” he says. “These people aren’t suffering with anything that’s affecting the muscles, per say. What they are suffering with is their immune system cannot product normal quantities of protective proteins. …There are cells in the immune system called peripheral blood mononuclear cells. They are not producing normal quantities of the protective proteins called chemokines and cytokines.”

The test focuses on four chemokines and cytokines found at reduced levels in fibromyalgia patients, according to Gillis.


Two subsequent studies, one of which compared fibromyalgia patients to those with rheumatoid arthritis and lupus, supported the results of the initial study, Gillis says.

“These people with fibromyalgia have immune system dysfunction,” he says. “These people are really sick. It’s not in their head. … Why aren’t the drug companies knocking down our door to develop a treatment?”

EpicGenetics’ research and the FM/a test aren’t without critics. The American College of Rheumatology does not recognize FM/a as a valid test.

Fibromyalgia expert Dr. Daniel Clauw has said EpicGenetics’ studies contradict other research, which has shown normal or elevated cytokine levels in fibromyalgia sufferers. Researcher and rheumatologist Dr. Fred Wolfe called one of EpicGenetics’studies “junk science,” saying it didn’t meet minimal scientific standards.

But in 2012, the American Association for Clinical Chemistry gave EpicGenetics an award for outstanding research in clinical and diagnostic immunology for its fibromyalgia research, says Gillis.

EpicGenetics isn’t letting the doubters keep them from moving forward. In the future, Gillis said the company would like to study the DNA of fibromyalgia sufferers to see if a genetic component can be identified. Proceeds from the FM/a test are being funneled toward that effort.


Click here for more information on the FM/a fibromyalgia test.  Info from : fedupwithfatigue.com













 












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​                   Scientists Find New, Non-Addictive Opioid Painkiller Compound

Posted on 2016 

By National Pain Report


The quest for a non-addictive opioid analgesic that doesn’t cause respiratory problems with increased doses has been a target of scientists for decades.

Did someone find something new?

In today’s edition of the online edition of the Proceedings of the National Academy of Sciences, researchers from Wake Forest Baptist Medical Center published findings on a new pain-killing compound (called BU08028) is not addictive and does not have adverse respiratory side effects like other opioids.

“Based on our research, this compound has almost zero abuse potential and provides safe and effective pain relief,” Mei-Chuan Ko, Ph.D., lead author of the study and professor of physiology and pharmacology at Wake Forest Baptist said. “This is a breakthrough for opioid medicinal chemistry that we hope in the future will translate into new and safer, non-addictive pain medications.”

The study included 12 primates, and targeted a combination of classical mu opioid peptide (MOP) and non-classical nociceptin-orphanin FQ peptide (NOP) opioid receptors. Ko and his colleagues examined behavioral, physiological and pharmacologic factors and demonstrated that BU08028 blocked the detection of pain without the side effects of respiratory depression, itching or adverse cardiovascular events.  With respect to pain relief for the primates, it lasted up to 30 hours and repeated administration of the compound did not cause physical dependence.

“To our knowledge, this is the only opioid-related analgesic with such a long duration of action in non-human primates,” Ko added. “We will investigate whether other NOP/Mop receptor-related compounds have similar safety and tolerability profiles like BU08028, and initiate investigational new drug-enabling studies for one of the compounds for FDA's approval." While this breakthrough is impressive, the drug's introduction is still years away. Studies on humans may start in
less than two years.                                                                                                                                          

                         Antiviral Combo May be Next Blockbuster Fibromyalgia Drug


Posted on 2016 in Pain Medication

By Donna Gregory Burch
Skip Pridgen, MD


A general surgeon with a small practice in Tuscaloosa, Alabama, Dr. William “Skip” Pridgen admits he’s an unlikely creator for the next blockbuster fibromyalgia drug.

But the U.S. Food and Drug Administration (FDA) has fast tracked Pridgen’s novel pairing of famciclovir (Famvir), a common antiviral, with celecoxib (Celebrex), an anti-inflammatory arthritis drug, for a phase III trial next year. Based on data from a 2014 phase II trial, the combo known as IMC-1 could give some stiff competition to Lyrica and Cymbalta, two of the most profitable drugs prescribed for fibromyalgia.

Like so many discoveries, Pridgen’s was accidental. He’d been treating patients with chronic gastrointestinal conditions for years and started to notice a pattern: Their symptoms would wax and wane over time, increasing whenever patients would become overly stressed. Pridgen’s mother is a virologist, and the pair speculated the stressors could be activating a virus, which in turn aggravated gastrointestinal and other symptoms. He’s concluded the HSV1 virus, commonly associated with cold sores, may be a culprit in fibromyalgia.

“Many herpes viruses are known to significantly upregulate COX enzymes in the body, which in turn are important for efficient viral replication,” he explained in a media release. “In theory, physical or emotional stress in patients can reactivate the virus and result in perpetuation of the symptoms of fibromyalgia. Effectively suppressing latent viruses may significantly improve the pain and related symptoms of fibromyalgia.”

But almost everyone on the planet has been exposed to the HSV1 virus. So, why do some people develop fibromyalgia while others do not?

“There’s a group of people who are genetically damaged in a way,” Pridgen explained. “There’s something that’s wrong with the immune system such that most people can force the virus to go into dormancy. These patients can’t.”

Pridgen thinks the virus remains active in the gastrointestinal tract and possibly in the sinuses and pelvic region as well.

“The body thinks there’s an ongoing war 24/7; everything gets amplified,” he said.

(This story gives a more technical synopsis of Pridgen’s theory about the connection between HSV1 and fibromyalgia.

Years ago, Pridgen began testing his HSV1 theory by offering antiviral medications to fibromyalgia patients whose symptoms alternated over time, and they reported some minor improvements in functioning. These same patients often complained about their chronic pain, and he began giving samples of Celebrex, an anti-inflammatory commonly prescribed for arthritis, to see if it might help.

He noticed those who received the combination of an antiviral and Celebrex dramatically improved over time. They not only reported a decrease in their gastrointestinal issues, but they also had less pain, fatigue, headaches and other symptoms commonly associated with fibromyalgia. Pridgen realized he might be onto something, and so did his patients. Word of mouth spread, and more fibromyalgia patients began coming to his practice.

“It really was just the planets aligning for me,” he says. “I knew each drug alone didn’t do a whole lot, but when given together, they did something remarkable.”

In 2014, Pridgen’s biotech company, Innovative Med Concepts, released data from its phase II trial involving 143 fibromyalgia patients treated at 12 U.S. clinics. The patients either took IMC-1 or a placebo for 16 weeks.

“We had pain reduction levels that rivaled or were comparable to other fibromyalgia drugs,” Pridgen said. “It wasn’t just that we reduced their pain. In all the measures we looked at [including fatigue, anxiety, headaches, TMJ, etc.], we seem to have an impact overall.

“We’re radically different [from other fibromyalgia drugs],” Pridgen continued. “Instead of just trying to reduce pain perception, we think we’ve discovered what is at the root cause [of fibromyalgia].”

Carol Duffy, associate professor of biological sciences at University of Alabama at Tuscaloosa, began partnering with Pridgen on his research in 2011. She believes IMC-1 works because it’s hitting HSV1 on two fronts: Famciclovir keeps the virus from replicating, and celecoxib stops reactivation and replication.

“When he gives them the meds, those fibro-like symptoms of widespread pain [and] fatigue, seem to go away, but it takes a while. It usually takes two months of being on the meds. … I think it’s much better than narcotics as far as treating symptoms. I feel like it’s treating it further up the line than narcotics.”

Annie George, a 22-year-old college student from Boston, is one of Pridgen’s success stories. She was diagnosed with fibromyalgia in high school and has tried numerous pharmaceutical treatments over the years. None of them helped, and most caused bad side effects.

When she first started seeing Pridgen in 2014, she was struggling to complete her undergraduate degree in engineering. She’d landed in the hospital several times with unexplained fevers, severe stomach pain and other symptoms. Her fatigue was so debilitating that she’d get up in the morning, take a shower, eat breakfast and then have to take a nap before she could attend classes. After a two-hour class, she’d come home and sleep for 12 hours, only to wake up exhausted again.

“I basically gave up all hope of living a normal life, of wanting to be a doctor, of wanting to be an independent person,” George said.

George and her mother flew to Tuscaloosa to meet with Pridgen after reading about his promising drug combo. She’s been on IMC-1 for about a year now, and it’s changed her life.

“Within two months, I started noticing a very big difference,” she said. “I could go to class and not get a fever. I could be out of the house for eight hours straight, which I hadn’t done since high school. I could do more, and the pain is just a lot less.”

She’s pain free most days, and her fatigue is nearly gone. George is working on her master’s degree and applying to medical school.

“It’s a day and night difference,” she said. “I’m not even the same person. I’m actually a normal 22-year-old girl.”

Like every fibromyalgia treatment, IMC-1 doesn’t work for everyone. Phase II results showed 37.9 percent of patients reported a 50 percent or greater reduction in pain after 16 weeks of treatment. That’s slightly better than Cymbalta, the most effective of the three FDA-approved fibromyalgia drugs.

Side effects were low, with more patients from the placebo group dropping out of the trial due to adverse reactions than those taking IMC-1.

Pridgen expects even better results from next year’s phase III trial because it will use the dosage he’s been perfecting in his practice for the past six years. Phase II used a lower, less effective dose.

Phase III may enroll up to 1200 patients at around 60 sites, some of which could be international. Several major pharmaceutical companies have already expressed interest in IMC-1, and a new drug could be on the market within three years.

Pridgen thinks the combo might also benefit patients with ME/CFS and irritable bowel syndrome, and trials are tentatively planned for those conditions.

​​​The Fibromyalgia Ci​rcle of Hope