Wednesday, June 29, 2011

How does fibromyalgia affect my musculoskeletal system?

This was such a good question asked of me as Share Care fibromyalgia expert, I just had to blog here for my fellow bloggers and followers.

Times are changing, but we aren't quite there yet. The preliminary diagnostic criterion intends to do away with the tender point model, which has become the hallmark for diagnosing FM.

Fibromyalgia is a central sensitization problem thought to be brought on by a dysfunction of the HPA (hypothalamus-pituitary-adrenal) axis and other central nervous system (CNS) disruptions. The criteria considers the effects CNS sensitization, and comorbid conditions, migraine, IBS, irritable bladder, cognitive deficit, RLS, disordered sleep etc.

However, it does not address the co morbidity of chronic myofascial pain, a peripheral nerve to muscle disease that causes myofascial trigger points (MTrPs). Trigger points are knotted up muscle fibers in a taut (tight) band of muscle. They are EASILY felt unless behind bone or other muscles, or the band of muscle affected is too tight. It is an objective piece of evidence to indicate the presence of FM when other comorbid conditions are present, research suggests possibly all FM patients have them. This is not new to me, but many patients with FM and is why myofascial pain is included in our book, Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome, and Myofascial Pain: The Mind-Body Connection by Celeste Cooper, RN and Jeff Miller, PhD. These MTrPs are peripheral pain generators that lend to sensitization, and keep the FM brain in wind-up.

M = Myofascial
TrP = Trigger point, synonymous with
MTrP = Myofascial trigger point
FM = Fibromyalgia
CMP = Chronic myofascial pain

Doctors that diagnose FM need comprehensive, non-confusing guidelines to diagnose & provide helpful treatments. Exercising a muscle riddled with MTrPs, will only make the pain and dysfunction worse, leading both the patient and the physician down a road of misguided conception.

A similar article, Letter to the Editor, from me will be published in the July issue of the Journal of the American Academy of Pain Management.

“Initially we struggle to accept, backsliding from time to time, but we maintain forward momentum, coping, defining and defending our new life.”

In healing,
Celeste Cooper, RN / Author, Freelancer, Advocate

Think adversity?-See opportunity!

~ • ~ • ~ • ~ • ~ • ~

Learn more about Celeste’s books here. Subscribe to posts by using the information in the upper right hand corner or use the share buttons to share with others.


Basford JR, An KN. New techniques for the quantification of fibromyalgia and myofascial pain. Curr Pain Headache Rep. 2009 Oct;13(5):376-8. Mayo Clinic, SW, Rochester, MN 55905

Cakit BD, Taskin S, Nacir B, Unlu I, Genc H, Erdem HR. Comorbidity of fibromyalgia and cervical myofascial pain syndrome.Clin Rheumatol. 2010 Apr;29(4):405-11.

Ge HY.Prevalence of myofascial trigger points in fibromyalgia: the overlap of two common problems.Curr Pain Headache Rep. 2010 Oct;14(5):339-45.

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D.G. Simons, J.Travell, and L. S. Simons, Myofascial Pain and Dysfunction: The Trigger Point Manual, 2nd ed. (Baltimore: Williams and Wilkins, 1999.)

Starlanyl and Copeland, Fibromyalgia & Chronic Myofascial Pain Syndrome: A
Survival Manual, 44.

Thursday, June 23, 2011

We’re Hunting Wabbits: Labels, Research and Doctors

This is a blog I resurrected from the archives because I felt it needed a face lift.

Questions from one of my FM/CFID/CMP friends.“I am on a hunt for the right diagnosis.”

My friend has genuine and valid concerns for understanding why the labels/names have changed over the years and what it really means, why the doctors that treat us seem to have less information than we do, and how to sort through the cross over symptoms of FM, CFID, now known as CFS/ME, and CMP.

My response:Ah, yes. It is the research, and we are moving in the right direction. Newer research shows that possibly all people with fibro also have chronic myofascial pain (CMP) from trigger points (TrPs). CMP is also known as MPS, (myofascial pain syndrome). Why do Devin Starlanyl and I switch terms? MPS suggests a syndrome and we know now that TrPs are caused by excessive release of acetylcholine (a chemical messenger between the brain and the peripheral nervous system) at the nerve to muscle junction, moving it out of the syndrome classification and into a disease classification. What we don’t know about chronic myofascial pain (CMP) from myofascial trigger points is why in some people TrPs keep recurring, when in the patient with acute injury TrPs can be treated and they remain gone unless a re-injury occurs. I hypothesis that this could be because of poor cellular healing in FM, and the excessive release of pro-inflammatory cytokins in the absence of inflammation and cellular injury, which in turn creates a hypoxic state (not enough cellular oxygen), and creates an ion channelopathy, and the domino effect begins, and repeats itself over and over again. This is where CMP comes in. It is believed to be and research is beginning to support that people with FM also have chronic myofascial trigger points, yielding chronic myofascial pain. I speak to this frequently, and a great deal of research into this went into the book, which was published in 2010, and the research continues to bear fruit in this direction.

Trigger Point (TrP) or Myofascial Trigger Point(MTrP): A hypersensitive bundle of muscle fiber in a taut band of muscle that causes dysfunction of the muscle involved, pain, and a referral pattern that is consistent among all patients for that specific trigger point. Anywhere there is muscle, a trigger point can occur.

Why is research yielding this? We know more now about CMP than we did when the FM model erected (a tool for selecting FM patients in some of the first studies, it was not meant to be a diagnostic tool, but evolved into one). I kept wondering why all my pain docs thought FM was part of the TrP component, when the tender point model has never suggested the presence of myofascial trigger points. Could it be that they were there all along but we didn’t take the time or know how to assess or feel for the knotted up muscle fibers? Possibly, the taut band of muscle was too tight in these participants to feel the trigger point (TrP). I suspect, that those with FM diagnosis without TrPs (if that turns out to be true, replication studies are needed) may have been misdiagnosed, OR there is a subset of FM patients that has both FM and CMP. With better participant screening we will be seeing better study results. We do know that people can and do have myofascial trigger points but do not have FM.

In FM/CMP complex it is the dysfunctional HPA axis that (central sensitization) that bombards the periphery (nerve to muscle) with the wrong messages, or possibly the message for pain relief from the trigger point (in response to the excessive release of the neurotransmitter chemical acetylcholine) never reaching the brain.

In research, things take time and funding is needed. Despite all of the recent controversy, I still suspect that XMRV related viruses will be in a subset of CFS/ME, (chronic fatigue syndrome/myalgic encephalomyelitis) patients like neutrally mediated hypotension (NMH) and postural orthostatic tachycardia (POTS).

There are many cross over symptoms between FM and CFS/ME. You should be able to sift through and determine which are attributable to you. If you are having difficulty because it seems you have them all, it is possible you have all three, FM, CFS/ME, and CMP, as I do. Research may also yield that there is more than a casual connection to FM and ME/CFS and other neuroendocrineimmune (NEI) disorders. Though not published the WPI did find XMRV in their samples of FM patients. As we know it now though FM and CFS/ME are similar they are different, and the differences in the science are discussed in the book.

The WPI study and other studies suggesting a biological marker for CFS/ME, have not only stimulated the research, the term CFS is no more. Scientists and the CFSAC (an action committee on CFS/ME that reports directly to the Secretary of Health in the administrative branch of the US government), now agree there is a biological cause and the need for the name change. For those of us who have dealt with this and screamed out for a name change this inspires hope.

See my blog Hope for ME/CFS a Possible Biological Marker

Symptomatology and quality of life.

How are your symptoms affecting your life? And, have you found a doctor that listens to and takes your symptoms seriously? In their defense, this is new science. Some filters down to their individual specialty journals, and not. I doubt many subscribe to Science, as this is for scientists mostly. Docs are clinically minded. A GOOD doctor wants to learn, but all are intimidated by patients and mention of the internet. It is in the way you approach them. If your doc isn’t willing to be part of your care (it should be a trusting collaborative relationship), try to find a new one. Ask, why do pharmaceuticals have an edge? The answer is they contact doctors and educate them about their new cutting edge product.

Suggest to your doctor, “You are probably already aware of this, but I was not, and wanted to share this article with you.”

I think if we were educating them regularly about FM, CFID and CMP they would know more about it. That is why I wrotea letter to the editor of The American Academy of Pain Management, which will be published in July issue. Don't expect your doctor to sort through it all as we are all still learning. Have patience if he/she seems interested in learning. If not, GET A NEW DOCTOR!

Things are changing. This is an exciting time for us. Push and support research.
“Bestowed on me is strength from those who exemplify the possibilities of hope, not only believing in the right thing, but putting a megaphone to their voice and action behind it” Harmony and Hope,  Celeste

Share Care Expert
Website http://TheseThree.comTwitter!/FibroCFSWarrior
Author: Integrative Therpies for Fibromyalgia, Chronic Fatigue Syndrome and Myofascial Pain: The Mind-Body Connection (co-author Jeff Miller, PhD
Available at book stores with direct links at: Sharecare, this blog and my website


M. Calis, C. Gokce, F. Ates, S. Ulker, H. B. Izgi, H. Demir, M. Kirnap, S.Sofuoglu, A. C. Durak, A. Tutus, and F. Kelestimur, “Investigation of the hypothalamo-pituitary-adrenal axis (HPA) by 1 microg ACTH test and metyrapone test in patients with primary fibromyalgia syndrome,” Journal of EndocrinologyInvestment 27, no. 1 (2004): 42–46.

Ge HY, Wang Y, Danneskiold-Samsøe B, Graven-Nielsen T, Arendt-Nielsen L. The Predetermined Sites of Examination for Tender Points in Fibromyalgia Syndrome Are Frequently Associated With Myofascial Trigger Points. J Pain. 2009 Nov 13. [Epub ahead of print]

R. Gerwin, “Trigger points: a comprehensive hypothesis of trigger point formation,” Journal of Musculoskeletal Pain 15, no. 13 (2007): 12.

Green PG, Alvarez P, Gear RW, Mendoza D, Levine JD. Further Validation of a Model of Fibromyalgia Syndrome in the Rat. J Pain. 2011 Apr 8. [Epub ahead of print]

C. Z. Hong and D. G. Simons, “Pathophysiologic and electrophysiologic mechanisms of myofascial trigger points,” Archives of Physical Medicine and Rehabilitation 79, no. 7 (1998): 863–72.

Kim SK, Kim KS, Lee YS, Park SH, Choe JY. Arterial stiffness and proinflammatory cytokines in fibromyalgia syndrome. Clin Exp Rheumatol. 2010 Nov-Dec;28(6 Suppl 63):S71-7. Epub 2010 Dec 22.

Lombardi VC, Ruscetti FW, Das Gupta J, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, Mikovits JA. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Science. 2009 Oct 23;326(5952):585-9. Epub 2009 Oct 8.

J. L. Newton, O. Okonkwo, K. Sutcliffe, A. Seth, J. Shin, and D. E. Jones, “Symptoms
of autonomic dysfunction in chronic fatigue syndrome,” Q JM 100, no. 8
(2007): 519–26.

S. Pay, M. Calguneri, Z. Caliskaner, A. Dinc, S. Apras, I. Ertenli, S. Kiraz, and V. Cobankara, “Evaluation of vascular injury with proinflammatory cytokines, thrombomodulin and fibronectin in patients with primary fibromyalgia,” Nagoya Journal of Medical Science 63, no. 3–4 (2000): 115–22.

Reyes Del Paso GA, Garrido S, Pulgar A, Martín-Vázquez M, Duschek S. Aberrances in autonomic cardiovascular regulation in fibromyalgia syndrome and their relevance for clinical pain reports. Psychosom Med. 2010 Jun;72(5):462-70. Epub 2010 May 13.

P. C. Rowe, “Neurally Mediated Hypotension and CFS.” 1998 Clinical and Scientific
Meeting, (accessed August 2003).

Schutzer SE, Angel TE, Liu T, Schepmoes AA, Clauss TR, et al. (2011) Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. PLoS ONE 6(2): e17287. doi:10.1371/journal.pone.0017287

Silverman MN, Heim CM, Nater UM, Marques AH, Sternberg EM. Neuroendocrine and immune contributors to fatigue. PM R. 2010 May;2(5):338-46.

About XMRV – Whittemore-Peterson Institute

Wednesday, June 22, 2011

The Cat's Out of the Bag-ShareCare Expert

I have accepted the invitation to be a fibromyalgia expert at a new online health and wellness interactive social QA platform created by Dr. Mehmet Oz, Jeff Arnold, Harpo Studios (Oprah) and Discovery Communications.

We answer your questions, such as:

“What are the physical effects of fibromyalgia?”
"Do sleep disorders cause fibromyalgia?"
"Is fibromaylgia curable?"
"What factors make fibromyalgia worse?"
"What is fibro fog?"

And any question you want to ask. In all my years of teaching I learned that when one person has a question someone else has the same one. Be the first to raise your hand.

Other experts include, but are not limited to:

•Renowned physicians, nurses, and health authors from around the country
•Top wellness, fitness, and wellbeing experts (including Dr. Michael Roizen, Bob
Greene, Deepak Chopra, Dr. Dean Ornish, Kelly Travers and many more)
•Leading health organizations including American Cancer Society, American Heart
Association, AARP, American Red Cross and American Diabetes Association.
•Nationally recognized hospitals including Johns Hopkins Medicine, New York
Presbyterian, Cleveland Clinic and The Mt. Sinai Medical Center

Come visit me at

Saturday, June 18, 2011

The Untold Story of your Thyroid, FM and CFS/ME

Why is it important to understand how these conditions can relate to those of us with fibromyalgia (FM) and/or chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)? The answer is, research is consistently pointing to an association of hypometabolism, hypothyroidism, Hashimoto's, and thyroid resistance, particularly in fibromyalgia, but also ME/CFS. This research has been ongoing for at least a decade now, and it is important that we pay attention to what the results are showing. The participants in these studies are representative of us and what we go through every day.

Following are some brief overviews and resources for learning more.


The thyroid gland is a butterfly-shaped organ located in the front of the neck, just over the windpipe. It produces iodine-containing hormones, such as thyroxin. Thyroxin regulates the rate at which body cells use energy and produce heat. When these hormones are low, a person is said to have hypothyroidism.

There are several types of hypothyroidism, (discussed here) but the symptoms are generally the same; physical and mental sluggishness, fatigue, dry skin, weight gain, hair loss, cold sensitivity, muscle cramps, constipation, irritability, and in more serious cases, enlargement of the tongue and/or thickening of the skin.
End excerpt (Cooper & Miller, pg 93-94).

According the the National Institute of Health at
The most common cause of hypothyroidism is inflammation of the thyroid gland, which damages the gland's cells. Autoimmune or Hashimoto's thyroiditis (insert, discussed later). Some women develop hypothyroidism after pregnancy (often referred to as "postpartum thyroiditis").

Other common causes of hypothyroidism include:
•Congenital (birth) defects
•Radiation treatments to the neck to treat different cancers, which may also damage the thyroid gland
•Radioactive iodine used to treat an overactive thyroid (hyperthyroidism)
•Surgical removal of part or all of the thyroid gland, done to treat other thyroid problems
•Viral thyroiditis, which may cause hyperthyroidism and is often followed by temporary or permanent hypothyroidism

Certain drugs can cause hypothyroidism, including:
•Drugs used for hyperthyroidism (overactive thyroid), such as propylthiouracil (PTU) and methimazole
•Radiation to the brain
•Sheehan syndrome, a condition that may occur in a woman who bleeds severely during pregnancy or childbirth and causes destruction of the pituitary gland

Risk factors include:
•Age over 50 years
•Being female

More recent research, suggests that Hashimoto's may be a risk factor for fibromyalgia. I am in hopes that the NIH, will be able update their information as the science evolves.

A great book with a holistic approach on hypothyroidism or Hashimoto’s is Living Well With Hypothyroidism: What your Doctor Doesn’t Tell You that you need to Know by Mary Solomon.

You can find information and patient comments on physicians around the country at her website;


Dr. Jacob Teitelbaum is one of her physician consultants and author of From Fatigued to Fantastic. He has energy systems that include high vitamin B Complex and other treatments. Find out about him and what he has to say at:

LAB Values have changed
This is probably one of the best kept secrets of all time, yet a factor that can have a great impact on your quality of life if you have undiagnosed thyroid problems.

The old antiquated thyroid assessment scale of 0.5 to 5.0 for the thyroid stimulating hormone -- TSH was changed by specialists in the field in 2003. All labs and physicians should be assessing the thyroid by:

TSH of 0.3 to 3.0

This means in a normal individual (remember in FM and CFS/ME the HPA Axis is out of kilter) a TSH of <0.3 would indicate hyperthyroidism and a TSH of >3.0 would indicate hypothyroidism. At any rate, either requires further investigation, thyroid scans to actually check the function and ultra sounds to see if there could be a tumor that needs to be removed are indicated, but frequently missed with disastrous results for anyone with thyroid disease, but particularly the FM and ME/CFS patient.

The wretchedness of this story is that it STILL is not recognized in most labs, and doctors are either unaware of the changed parameters or chose to ignore them.

Read “The Tragic and Invisible Epidemic of Thyroid Disease” at Vitality 10

HYPOMETABOLISM–Thyroid Resistance ©

Hypometabolism is not the same as hypothyroidism. In this case the thyroid is working appropriately, but the body isn’t utilizing the thyroid hormones. Like reactive hypoglycemia, thyroid hormone levels are normal but they are resisted in the peripheral tissue; this is thyroid resistance. As suggested in chapter 1 of our book, some FM and CFID (ME/CFS) patients have hypometabolism.

The role of thyroid resistance in the fibromyalgia patient is being investigated, and thyroid autoimmunity has been associated with FM severity (Bazzichi, et al. 2007). It may also contribute to the development of myofascial trigger points (Starlanyl and Copeland, 2001).

Thyroid resistance has also been considered as a metabolic factor in chronic fatigue syndrome, as well as fibromyalgia. (Garrison and Breeding, 2003)

End of excerpt (Cooper and Miller, pg 94-95.)

Dr. John C. Lowe is a fibromyalgia, thyroid, and metabolism researcher. As Director of Research for the Fibromyalgia Research Foundation, he has spearheaded the scientific study of two related topics: the metabolic causes of fibromyalgia, and the relief of fibromyalgia symptoms through the treatment approach he developed and named "metabolic rehabilitation." Read more at:

IMHO, I am not sure that treating hypometabolism will END fibromyalgia, or CFS/ME. Though having my own Hashimoto's treated with thyroid hormone has helped with the life altering fatigue, it has not helped my pain, insomnia, migraines, and other centrally mediated co-morbid conditions or the peripheral pain generators from myofascial trigger points. However, I do believe hypothyroidism has a more than casual connection to fibromyalgia. And, it is possible that some diagnosed with chronic fatigue syndrome, may not have a viral connection, but a metabolic one if they have undiagnosed thyroid disease. As in my case, one cannot rely solely on a TSH. The proper tests must be done for a proper diagnosis.

Knowing if you have hypothyroidism or hypometabolism, and treating it will certainly help control this co-existing condition. As we talk about in the book, this is extremely important and gives one a sense of empowerment over fibromyalgia and chronic fatigue syndrome.

You can read about Dr. John Lowe’s theory on hypometabolism in an article written by Mary Shomon at:

HASHIMOTO'S THYROIDITIS—Autoimmune Thyroiditis ©

Hashimoto’s thyroiditis is a condition known to coexist—although not exclusively—in a certain subgroup of CFID patients. It is a type of autoimmune thyroid disease, meaning the body’s immune system attacks and destroys the thyroid gland. Its characteristics are inflammation of the thyroid gland, fatigue, depression, cold sensitivity, weight gain, muscle weakness, thickening of the skin, constipation, dry or brittle hair, muscle cramps, increased menstrual flow, and goiter. Some patients may not have any symptoms.
End excerpt (Cooper and Miller, pg 95).

As we now know, Hashimoto's has been significantly linked to fibromyalgia, in the latest Bazzichi, et al study (Nov 2010). This is not the first study and should be receiving the recognition it deserves by those who treat fibromyalgia.

Kristin Thorson, is a patient, advocate and editor of Fibromyalgia Network.!/FibroNetwork She also runs the nonprofit organization, http;// which funds important FM research and the board has several well known physicians.

As do all of her articles, the January 2011 edition of Network News article, “Thyroid Malfunction Dragging you Down?: Symptoms, Tests and Treatments" caught my eye.

I suggest you take her article and the studies cited her, and a copy of my blog with you to your doctor if you are having unusual symptoms consistent with those mentioned here. Preface your remarks with, you probably already know this, but I found it quite interesting, and thought I would like to share it with you so we can get to the bottom of my symptoms. Get that TSH, free T4, free T3, TPO and TG. Take them actual journal articles and articles supported by research. If they are not interested, find a new doctor.

“As I walk this path, I understand the privilege of intersections, these interruptions enrich my life.” --Celeste

You can find my letter of gratitude to the authors in my blog, Thyroid Autoimmunity and Fibromyalgia, Letter to the author, (Laura Bazzichi, lead author of studies).
I hope you will read it. It is important to recognize people for their unending dedication to helping others.

Resources other than those previously linked:

Bazzichi L, Rossi A, Zirafa C, Monzani F, Tognini S, Dardano A, Santini F, Tonacchera M, De Servi M, Giacomelli C, De Feo F, Doveri M, Massimetti G, Bombardieri S. “Thyroid autoimmunity may represent a predisposition for the development of fibromyalgia?” Rheumatology International, Nov 18, 2010., by Division of Rheumatology, Department of Internal Medicine, University of Pisa, Pisa, Italy.

L. Bazzichi, A. Rossi, T. Giuliano, F. De Feo, C. Giacomelli, A. Consensi, A. Ciapparelli, G. Consoli, L. Dell’osso, and S. Bombardieri, “Association between thyroid autoimmunity and fibromyalgic disease severity,” Clinical Rheumatology 26, no. 12 (2007): 2115–20.

Cooper C and Miller J. Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome, and Myofascial Pain: The Mind-Body Connection. Healing Arts Press: Vermont, 2010.

R. L. Garrison and P. C. Breeding, “A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone,” Medical Hypotheses 61, no. 2 (2003): 182–89.

Network News. (2011, January) “Thyroid Malfunction Dragging you Down?: Symptoms, Tests and Treatments.”

Mary Shomon. Living Well with Hypothyroidism: What Your Doctor Doesn't Tell You... That You Need to Know (Collins; 1st edition, March 2000)

Devin. J. Starlanyl and Mary. E. Copeland, Fibromyalgia & Chronic Myofascial Pain Syndrome: A Survival Manual (Oakland, Calif.: New Harbinger Publications, Inc., 2001), 44.

Wednesday, June 15, 2011

Bespeak or Begrudge: finding and affording the shingles vaccine

People with fibromyalgia (FM) and chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)often have impaired or ineffective immune systems. This, along with some medications and treatments, a history of certain types of cancer, and stress and fatigue puts us at a higher risk of developing shingles.

Shingles also known as herpes zoster is a viral infection from varicella-zoster virus that causes painful rash/blisters on the skin following a nerve tract. If you have had chicken pox the virus can lay dormant until it erupts later in life as shingles. Early treatment with an anti-viral drug may decrease the risk of reoccurrence.

See the latest reports and information.

Shingles Vaccine from US Today: Your Life Health.
“Shingles vaccine can protect you but it can be hard to find.”

More on the vaccine from the CDC, standout comment, if you have had shingles, the vaccine may help prevent recurrence.

Post Herpatic Neuropathy (PHN) = The residual effect of shingles, where nerve pain, neuralgia, last long after a shingles outbreak has cleared up. It can last months or a lifetime.

Treatment currently includes: antidepressants, anticonvulsants (gabapentin like drugs), topical lidocaine or capsaicin cream, opioid analgesics and TENS units.

Having had shingles, the US Today article left me with an unanswered question. “Does the vaccine help long term effects that can occur, post herpatic neuropathy?”

According to the FDA, the vaccine, Zostavax, will not help PHN.

An important question was raised after I posted this blog. “Should known immunocompromised patients receive the vaccine?” This is something I think each individual should discuss with their doctor, following is why.

Vaccinating the already immune compromised, from the National Foundation for Infectious Diseases:
“Immunocompromised people are more likely to have serious illness with complications as a result of chickenpox. The best way to prevent infection in such people is by immunizing their susceptible family members and their other close contacts. However, some immunocompromised people are eligible for vaccination.”

Harmony and Hope, Celeste,

Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome, and Myofascial Pain: The Mind-Body Connection (co-author, Jeff Miller, PhD).

You can find out more about me, the book, how to order the book, and other helpful information and links at

Wednesday, June 8, 2011

My critique of “Diagnosing fibromyalgia: Moving away from tender points”

When I got up this morning, the last thing on my mind was writing an advocacy piece, let alone a blog, however, following my own philosophy of “seize the moment” I found my mind would not let me set it aside.

In an effort to raise awareness of centralization in FM from the peripheral input of pain by myofascial trigger points, the following letter when out to doctors who have been kind enough to communicate with me on this issue from both sides of the fence. A Bcc went out to other advocates to provide opportunities for them to carry this forward.

First and foremost, a huge THANKS to Marla Silverman at PANDORA for bringing this to my attention and for giving me the privilege of commenting.

Following is my letter, which is pretty much my comment to Marla’s request with a few clarifications. After this letter is the full abstract for “Diagnosing fibromyalgia: Moving away from tender points.”
RE: Diagnosing fibromyalgia: Moving away from tender points
The Journal of Musculoskeletal Medicine. Vol. 27 No. 4

Hello Dr. Gerwin, Dr. Bennett, Dr. Russell and Dr. Whiteside

Marla Silverman, President of the Patient Alliance for NeuroEndocrineimmune Disorders Organization for Research and Advocacy has asked me to comment on the noted article in the Journal of Musculoskeletal Medicine. I thought you all might be interested in what I had to say:

It is refreshing to see continued acknowledgement of the science by noting this [FM] is a diagnosis of inclusion. No doubt the aspects reviewed in 2010 were a precursor to the New Proposed Diagnostic Criteria for Fibromyalgia. The Proposed criteria do look at inclusion versus exclusion by noting the comorbid conditions with FM and the centralization of pain. My beef and the beef of others is that they are not including the assessment of myofascial trigger points. If we know this is the main complaint in FM, and science shows repeatedly that MTrPs are peripheral pain generators to the centralization of FM, why wouldn't we acknowledge their presence so they can be appropriately treated?

Exercising a muscle with active or latent trigger points (TrPs) will lead to further dysfunction and shortening [of muscle] and development of TrPs in compensating muscles unless the TrPs are treated prior to exercise. It is one of those double edged swords.

Exercise, stretching and aerobic (there is believed to be a cellular hypoxia related to TrPs) conditions muscles and helps prevent TrPs. The problem is, with FM, TrPs are not the same as in the average person who sustains an injury. It appears that the injury occurs at a very basic cellular and metabolic level, hence the release of pro-inflammatory cytokines in the absence of injury and no inflammation measured in FM, and the presence of elevated sensory preceptors in FM as indicated in a recent study [“the FM-only group had significantly higher baseline quantities of mRNA for sensory receptors P2X4 and TRPV1 and for the cytokine IL10.” Based on the group’s earlier work in mice, they hypothesize that these markers represent increased signal for muscle metabolites that would lead to widespread increases in muscle pain and secondary hyperalgesia in skin throughout the body. Light, et al., 2011].

Side Note:
This study was collaboratively funded by the American Fibromyalgia Syndrome Association (Associated periodical “Fibromyalgia Network News”)
CFIDS Association of America,
And the National Institutes of Health

To me and to others who have studied this extensively, such as Devin Starlanyl, Dr. Gerwin, Dr. Bennett, Dr. Hong, Dr. Ge Hy, etc. this all seems pretty basic, but continues to be overlooked.

The article will help raise awareness to the centralization of FM and that certain conditions are common in FM because of brain defects or defects in the messaging system, but it is a very minor start in educating about the aspects of FM. It does take a multimodal approach, but part of that is myofascial therapy, which again, has been omitted.

I found it strange that the authors commented that opioids have been shown to be of little benefit, when there are other studies that show the contrary, and they say that the SSRIs and SNRIs are indicated, as well as Lyrica and Neurontin like drugs, when the evidence of their success in treatment of FM has been very underwhelming. Of course, the benefit of medications of any of these classes would depend on other co-existing conditions.

My biggest concern, as you know is that MANY with FM have migraine and treat them with triptans, which are contraindicated with the SNRIs or SSRIs or combo drugs such as Cymbalta. This MUST be considered for patient safety.

Patient education is imperative, I certainly agree with that, but so is physician education. Everybody needs to be on the same page. The patient should feel free to roam the internet to educate themselves and not be put down for doing so. We are in an entirely different age than we were even 10 years ago. Many patients and patient advocates have saved lives by being entirely informed.

This was the most important bullet of the entire article.
•We refer the patient for sleep study, if indicated; physical therapy; or aquatic therapy. Most patients can motivate themselves for pool therapy. Refer the patient for sleep medicine if that is indicated by the results of the sleep questionnaire.

These days if the doctor asks for a myofascial assessment, the physical therapist will be specialized in this and be able to report back to the physician on the presence of myofascial trigger points, about dysfunction, range of motion of the muscles involved, etc. When this starts to happen, doctors will set up and take note. Dr. Robert Bennett once told me that in all of his years in clinical treatment of FM, he never had one patient that didn't have myofascial trigger points, and Dr. John Whiteside has told me the same. Of course they know how to assess for them, this is paramount.

There you have it, my take. Hope that helps, and TY for valuing my opinion.

Harmony and Hope, Celeste

Light AR, Bateman L, Jo D, Hughen RW, VanHaitsma TA, White AL, Light KC. Gene expression alterations at baseline following moderate exercise in patients with chronic fatigue syndrome and fibromyalgia syndrome. Journal of Internal Medicine.2011 May 26. doi: 10.1111/j.1365-2796.2011.02405.x.

Diagnosing fibromyalgia: Moving away from tender pointsEvaluation now emphasizes “areas of pain” and seeing the “whole patient”
Dr Khasnis is a fellow and Dr Wilke is a staff member in the department of rheumatic and immunologic disease at the Cleveland Clinic in Ohio.

Since the American College of Rheumatology definition of fibromyalgia syndrome (FMS) was set in 1990, multiple studies have lent support to relying less heavily on tender points. Patients may indicate “areas of pain,” and the diagnostic process includes other common symptoms. The Symptom Intensity Scale provides an objective measure of pain and fatigue. Recognition of FMS may be aided by the presence of other conditions. FMS should be a diagnosis of inclusion rather than exclusion. Multimodal management of FMS starts with patient education, and exercise is a keystone of treatment. Sleep optimization is an important issue. Depression deserves investigation, recognition, and optimal management. Pain management in patients with FMS often is challenging. A combination of patient education and nonpharmacological and pharmacological measures is key to management. (J Musculoskel Med. 2010;27:155-162)

Full article can be viewed at Fibrotalk Blog,

Saturday, June 4, 2011

Points That Need More Than Pondering: Defining Myofascial Trigger Points

What is a Myofascial Trigger Point (MTrP), and why does it matter, especially in fibromyalgia?

Myofascial trigger points can mimic many things and cause pain, dysfunction, and shortening of the muscle affected by this knotted up muscle fiber in a taut band of muscle. Such things as paresthesias (numbness and tingling that can be local or radiate in a specific pattern), burning, and pain can result from a MTrP, which is entrapping a nerve. Circulation/temp changes can occur if a MTrP is located next to a blood vessel, and swelling can develop if the MTrP is located next to a blood or lymph vessel). (Helpful treatments are links following).

The following book excerpts are protected by copyright, you must ask permission from Healing Arts Press to reuse this content.

Common Abbreviations©

MPS: myofascial pain syndrome
CMP: chronic myofascial pain
MTP: myofascial trigger point
TrP: trigger point

Myofascial Trigger Point©
A myofascial trigger point (TrP) is a self-sustaining, irritable area in the muscle that can be felt as a nodule in a taut band. This irritated spot causes the muscle to gradually shorten, interfering with the motion function of the muscle and causing weakness and pain. Trigger points differ from tender points in that generally they refer pain to other parts of the body and can usually be felt with the hand (palpated) unless the muscle is too rigid from intense muscle involvement, or the trigger point is in a deep muscle or under bone. The tender points of FM or myalgias associated with CFID do not restrict motion or cause localized muscle weakness. If they do, the patient should also be evaluated for the presence of CMP. Trigger points in CMP are well defined and often radiating—the pain radiates out to other parts of the body.

Active Trigger Point©
An active TrP is a myofascial trigger point that causes pain at rest. It is always tender, causes shortening of the muscle, weakens the muscle, and causes patient complaints of referred pain on direct compression. An active trigger point can elicit a visible local twitch response when adequately stimulated by compression or needle insertion. It can produce referred motor and autonomic phenomena, generally occurring in the TrP referral zone. An active TrP can also cause the referral zone to become tender.

Secondary Trigger Point©
A secondary TrP is one that develops in a second compensating muscle. A compensating muscle is one that is trying to make up for the malfunction of the muscle affected by primary trigger points. In other words, when a primary trigger point causes muscle dysfunction, the opposing muscles become stressed. These opposing muscles become overloaded because they are attempting to carry the entire load of the muscle work needed to perform a task. When staring at a computer screen your head starts to drift forward after a while, particularly if you spend hours there. You may have primary TrPs in muscles on the front of your neck, which may or may not be making their presence known. As your head starts drifting forward, putting less stress on the primary TrPs because of the slackening, the muscles on the backside of your neck are being stretched and stressed in an effort to keep your face from falling onto your keyboard. The sustained overstretching of these muscles causes secondary trigger points to develop in the muscles on the back of your neck. (This is an important reason to pay attention to posture as an aggravating factor, to be discussed in chapter 4.)

Satellite Trigger Point©
Chronic myofascial pain (CMP) from myofascial trigger points is a peripheral nerve to muscle problem. Acetylcholine (a neurotransmitter, a chemical that carries information from the peripheral nervous system to the central nervous system) has been found in excessive amounts. Fibromyalgia, CFID/ME, migraine, IBS, irritable bladder and several other common co-existing conditions have a strong central nervous system component. When any of these co-exist with chronic myofascial pain (CMP) from myofascial trigger points (TrPs), the peripheral message of painful trigger points to the brain keeps the brain in a hypersensitive state," causing a “wind up” phenomenon at the HPA-axis (dysfunctional in FM and thought to be dysfunction in CFID) is off an running.

End Comments:
Chronic myofascial pain (CMP) from myofascial trigger points is a peripheral nerve to muscle problem. Acetylcholine (a neurotransmitter, a chemical that carries information from the peripheral nervous system to the central nervous system) has been found in excessive amounts where nerve meets muscle. Biopsies show a histological difference in MTrP fiber and even differences between an active and latent MTrP. Because of development of new technology examiners can now easily locate MTrPs for treatment.

Fibromyalgia, CFID/ME, migraine, IBS, irritable bladder and several other common co-existing conditions have a strong central nervous system component. When any of these co-exist with chronic myofascial pain (CMP) from myofascial trigger points (TrPs), the peripheral message of painful trigger points to the brain keeps the brain in a hypersensitive state," causing a “wind up” phenomenon at the HPA-axis (dysfunctional in FM and thought to be dysfunction in CFID) is off an running.

Myofascial trigger points can mimic sciatica, pelvic floor pain, or costochondritis. They can also cause painful intercourse, impotence, vulvodynia, cavitational necrosis, TMJ/TMD, restless leg syndrome, PMS, and much more. They can be one of the main factors in migraine headaches, chronic sinusitis and a host of other conditions. They are NOT to be taken lightly, especially now with abounding and repeated research over more than a decade showing us that they are a main component in the pain of FM.

Myofascial Release

Active Release Therapy (ART)

National Association of Myofascial Trigger Point Therapists

Recommended reading for self treatment:
Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome and Myofascial Pain: The Mind-Body Connection by Celeste Cooper, RN and Jeff Miller, PhD. Healing Arts Press: Vermont, 2010. (Forward by Devin Starlanyl, author, researcher, endorsed by Dr. John Whiteside, myofascial and holistic specialist physician, Australia, and Bill Douglas, Best Selling author, teacher, and founder of many stress management programs with global recognition.)

Healing Arts Press (Publisher) (On Sale)

Amazon in Kindle)

Barnes and Nobel,%20Chronic%20Fatigue%20Syndrome,%20and%20Myofascial%20Pain:%20The%20Mind-Body

The Trigger Point Therapy Workbook, 2nd ed. By Clair Davies, NCTMB with Amber Davies, NCTMB. New Harbinger: Oakland, 2004. (Forward by Dr. David Simons)


Barnes and Nobel

I hope you found this information helpful.

"Though our bodies are weak our determination is unbreakable, standing tall, standing strong, standing united, committing to a cure."


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