Fibromyalgia is not a disease – it's a condition. It’s a pain sensitization condition [1], where pain causes sleep disturbance, causing increased pain sensitivity, causing further sleep disturbance, causing increased pain sensitivity, etc. It acts as a positive feedback loop, and to correct the Fibromyalgia condition, one must break the loop.

Sensitivity increases to other irritants as well, such as smoke and weather changes, and causes irritable cough, irritable bladder, irritable bowel and food sensitivities, etc. The assessment and diagnosis of Fibromyalgia is made through the use of standardized criteria [2].

SOME HISTORY

Back in the 1970's, Dr. Hugh Smythe and Dr. Harvey Moldofsky did a number of studies which showed that people with Fibromyalgia had disturbances of stage 4 non-REM sleep [3]. A follow-up study [4] showed that intentionally disturbing stage 4 non-REM sleep in otherwise healthy subjects induced Fibromyalgia symptoms.

At the time, the cause was unknown but some blood work indicated altered serotonin levels [5], suggesting that low doses of antidepressants such as amitriptyline might help promote restorative sleep. As a result of that work, amitriptyline has become the gold-standard treatment for Fibromyalgia. However, much has been learned since that time and current knowledge suggests that altered serotonin levels are a symptom rather than cause. Indeed, the more modern selective serotonin re-uptake inhibitors (SSRIs) have proven less effective than non-selective tricyclic compounds such as amitriptyline.

Many have incorrectly viewed Fibromyalgia to be a psychological problem, either because of a lack of any other plausible explanation [6], or due to the inappropriate use [7] of a test protocol that was never intended for chronic pain syndromes [8]. This has done a great disservice to Fibromyalgia sufferers, and many physicians still cling to these outdated views.

A summary of the evolution of understanding of the syndrome up to the year 1986 is available [9]. A slightly more recent summary up to the year 1989 is also available [10].

PAIN AND REFERRED PAIN

Often, people who develop Fibromyalgia report that it started after some pain-causing injury (e.g., car accident with whiplash [11], gut infection, lower back injury, viral or bacterial infection), and long after the original injury has healed, the condition remains and worsens over time. Indeed, one study showed that 40 % of Fibromyalgia patients reported a neck injury at the onset of symptoms, and 31 % reported a lower back injury at the onset of symptoms [21]. Another study [11] showed that Fibromyalgia is 13 times more likely to result from neck injury than from a lower extremity injury such as a broken leg. However, as stated above, a painless but sleep disturbing episode can also initiate the condition [4, 12].

Pain plays a pivotal role in Fibromyalgia. More accurately, “referred pain” [13-16] is key to understanding the condition. If you have an injury deep in the body, the brain does not know how to tell you where it is located since the brain has no “body image” that includes this region, and so it "refers" the pain to other areas where there is no pathology. Our brain's "body image" is developed over years of stimulus and therefore only includes regions of the body that regularly experience sensation [9].

If you place your hand on a hot plate, your body will increase the pain sensation in your hand until you pull it away. If you keep your hand there, the pain sensation will continue to increase. It increases the pain in those areas so you'll remove the injuring action. Eventually, over longer periods of time, the body starts producing increased substance P (neurotransmitter detectable in spinal fluid) [17-19], the brain starts making new pain connections, and increased numbers of nerve receptors appear. There is measurable evidence of hypothalamic-pituitary-adrenal system changes as well [20], such as reduced growth hormone.

Because the pain in Fibromyalgia is referred from deep structures, it confounds the patient and doctor, and examination or biopsy of the area experiencing pain is invariably negative (i.e., finds nothing wrong) [21].

Remarkably, not only is pain referred from these deep sites, but various reflex responses also appear in the areas of referred pain [21]:

“Persistent pain of any origin gives rise to protective reflex changes. These include muscle spasm, inhibition of voluntary movement, increased blood flow, and cutaneous or deep hyperalgesia. Because neural localization may be wildly inaccurate when pain is of deep origin, these reflex effects may be found in areas far removed from the original site of pathologic change.”

Thus, pinching the skin in areas of referred pain tend to cause a reactive hyperemia (excessive reddening of the skin), brushing teeth can cause excessive bleeding of the gums, otherwise minor stimulation (weather changes, caffeine, etc.) can cause increased susceptibility to migraine headaches, and regions of referred pain often contain muscles in spasm.

THE HUMAN SPINE

To fully understand why Fibromyalgia is sustained with no apparent chronic injury, one must know a bit about the spine.

There are two very vulnerable points along the human spine:

1) lumbar vertebrae 4 and 5 (labeled L4-5) and L5-S1 (L5 and sacral vertebra 1) in the lower lumbar spine, and

2) cervical vertebrae (“segments”) 5 and 6 (labeled C5-6) and C6-7 in the cervical spine of the neck [22, 26-27].

Lower lumbar spine (back) [21]

Humans have evolved to walk upright, but at the cost of having the lower lumbar spine locked in hyperextension (flexion occurs when leaning forward, extension occurs when leaning backward). Lower back pain is extremely common because of this vulnerability. The result is large crushing forces on disks and bone, and nerve irritation. Walking in a straight upright position ensures a lumbar spine locked in hyperextension. Lying on your back on a flat bed also puts the lumbar spine into locked hyperextension. Sitting causes the abdominal muscles to relax, allowing the vertebrae to slide with respect to each other leading to further injury. Driving in a car is even worse since the vehicle’s motion promotes this sliding action. Truck drivers are notorious for lower back pain as a result.

The pain from this injury is necessarily referred, since the brain has no “body image” that includes this area of the lumbar spine, and thus pain is felt in healthy regions in a variety of forms. These include: lower back, thighs, tops of feet, genitals, irritable bladder, and irritable bowel, etc. The pain can be burning, tingling, aching, and numbness, but the cause is the same and these are called, “pain equivalents” [23]. The nerve bundles that go to the lower spine, also go to these regions (e.g., intestines, bladder), so the referred pain occurs in areas where the common nerve bundles are routed. If you press on these nerves, you feel intense pain. These locations of accessible nerves are the same in everybody, and in fact, are the “tender points” often discussed. They are very useful as a diagnostic tool in identifying the location of the actual injury. Absence of pathology in the painful locations and tenderness at these nerve locations clearly identifies the location of the true injury. Some people with Fibromyalgia develop areas of skin sensitivity (also a form of referred pain), as well as generalized skin sensitivity (due to pain amplification from nonrestorative sleep).

Cervical spine (neck) [23-28]

When people sleep, their neck muscles relax, the neck sags, and vertebrae lock since the neck forms an unsupported bridge from the head to the shoulders. This relaxation response of muscles is illustrated when you consider a person’s head nodding as they fall asleep while sitting. Again, the crushing forces of locked vertebrae and tight ligaments lead to referred pain. This pain appears in the neck, shoulders, jaw, elbows, palms of the hand, etc. Temporomandibular joint (TMJ) disorder often results from this injury. But again, since the pain is referred to healthy regions of the body, the source is almost always misdiagnosed. The results of this cervical injury have been described [23] thus,

“The patterns of referred symptoms from the cervical spine are complex and variable, even in the same patient. The arm and hand develop from the cervical segments, and any of the structures of the arm or controlling the arm can be the target for referred symptoms. Interscapular pain is common, because the muscles that control the position of the scapula are functionally and neurologically part of the arm. Anterior chest pain and tenderness are common, because the pectoralis major and minor muscles control the shoulder and share its nerve supply. Patients complaining of breast (anterior chest) heaviness and discomfort will often be found to have significant tenderness deep to the breast, in the origin of the pectoralis minor muscle, and not in the breast itself. The breast, derived from skin, has thoracic innervation, as do the ribs and pleura. Only the muscles have cervical innervation, and the finding of referred tenderness at characteristic sites within the muscles argues strongly for a cervical origin of the symptoms, and against disease of the breast, ribs, pleura, or viscera.”

Also,

“The neck muscles function as extraocular muscles and are closely integrated with all the apparatus of balance.”

More implications of the cervical injury are documented [25],

”Further, the patterns are segmental, but not confined to a single segment, or even a group of adjacent cervical segments. Frontal headache, and jaw pain implicate the trigeminal nerve, trapezius pain and tenderness involve the spinal accessory nerve, and imbalance involves even more complex principles. We are dealing with the neurophysiology and neuroanatomy of eye-hand coordination, and the spinal cord in the mid and low cervical is central to the high-speed integration of all of these functional elements.”

Supporting the notion of cervical origin for upper-body symptoms is the fact that the tenderness associated with this cervical injury is completely resolved in cases where the neck is fused, either due to late spondylitis or surgical fusion of the cervical spine [23, 31].

DIAGNOSTIC TESTS

To check for the lower lumbar spine injury, one pinches the fatpads three inches above and below the knee line on the inside of the leg [21, 30] [view image]. More specifically, the deep subcutaneous fat overlying the tendons of the medial hamstrings 3 to 6 cm proximal to the joint line, and also the deep subcutaneous fat overlying the insertion of these tendons, slightly more posterior and distal to the joint line. A healthy subject can withstand a significant squeezing pressure, while a person with Fibromyalgia and the lower lumbar problem will jump (increased sensitivity) upon the slightest pressure to this referred tender point. Control points also exist where pressure should cause no discomfort in all subjects [21, 30].

To check for the cervical spine injury, one pokes a finger into the front of the neck behind the collar bone about one-and-a-half inches to the left and right of center (the location of the injury) [23, 31] [view image], or more specifically, the anterior aspects of the intertransverse ligaments between C5 and C7, reached by pressing the thumb behind the lower sternomastoid muscle. The patient is skeptical because, without poking, the pain is felt in the shoulders and back of the neck. However, massage of those areas tends to feel good, while poking the test point (site of injury) is unpleasant. Massaging a broken leg is unpleasant and the fact that massaging painful Fibromyalgia shoulders feels good is clear indication that the pain there is referred.

There is a further test point for the cervical injury as well [21]. A referred tenderness can be found distal to the lateral epicondyle - the "tennis elbow" site. It is, "...a narrow line of tenderness, which may begin at the epicondyle and extend up to 10 cm distally, usually maximal between 2 and 5 cm along this line. It is closely related to the lateral intermuscular septum. If the examiner palpates the nontender flexor muscles with the patient's forearm supine and then slowly rotates the forearm into pronation, the patient will react sharply as the septum passes under the thumb and then relax again as the pressure moves to the extensor aspect. Clearly, the tender structure is attached to radius rather than lateral epicondyle, and lies deep, close to the attachment of the septum to bone."

The location and routing of nerve bundles through the lower lumbar spine and cervical spine can be seen in a good atlas of anatomy [29].

Interestingly, a strong argument can be made that the syndrome historically called, “growing pains” is actually a manifestation of exactly these cervical and lumbar injuries.

THE SPINE-FIBROMYALGIA CONNECTION

The reason for such emphasis on these two areas of the spine is this: once stage 4 sleep has been disturbed (due to an initial injury, for example), pain sensitivity is increased, and since these two areas of the spine are constantly injured/irritated in most people (unknown to them), they become the source of pain which sustains, and eventually worsens, the condition of Fibromyalgia through further sleep disturbance [12, 21]. These two regions are injured in most healthy people and they don’t know it because the pain, if any, is referred to healthy locations, or their normal pain sensitivity is such that they are asymptomatic.

The two sources of pain amplification have been described thus [9]:

"The factors determining pain amplification may be segmental in effect, as in the referred pain syndromes, or centrally determined, as in the nonrestorative sleep syndromes."

So to break the cycle and resolve the condition, one must correct the actions injuring these areas of the spine. The solutions are simple, yet challenging.

SOLUTIONS

During the night, one solution is to sleep on the back with two or three pillows under the knees such that the lower lumbar spine is not locked in hyperextension. Furthermore, a small roll of soft material should be placed under the neck to support it during sleep. A simple solution is a thin pillow rolled up at one end such that the roll is placed under the neck [view image]. In general, the head should be low (thus a thin pillow). The neck must be supported from C5 to C7, and not just C5-6, otherwise the injury remains at C6-7 [24, 26-27]. One cannot deviate from this position during the night and allow the back or neck vertebrae to lock, even for short periods of time, or the improvement will be undone.

Sleeping on the side requires the use of a special shaped pillow [view image] or cervical ruffs [view image] that extend into the front-side of the neck to support the lower cervical spine, otherwise the neck sags causing injury. Sleeping on the side with a pillow between the knees alleviates the back problem, but if the neck issue is not addressed, no progress will be made in the Fibromyalgia condition. Most people sleep on their sides and therefore need to use a shaped pillow or ruffs, but attention to the exact location for support is essential [23, 26-27].

During the day, if walking is necessary, it should be done in the “power-walk” position, leaning forward with gut sucked-in. This is counter-intuitive, since we've been taught all our lives that we should stand up straight. No exercises should be undertaken with legs straight. Often people say that “light” exercise is recommended for patients with Fibromyalgia. It is now known that heavy exercise is even better [32], as long as the spine is not locked in hyperextension (when running, for example, most people’s lumbar spine is locked in hyperextension). Indeed, in the experiments of stage 4 sleep deprivation [4], all the healthy subjects who didn’t exercise developed Fibromyalgia symptoms, while a few of the subjects who were physically very fit, did not develop any symptoms of Fibromyalgia at all, even though they were denied stage 4 sleep.

So, intense but lumbar-friendly exercises are an important part of the solution. Exercises that strengthen the abdominal muscles [32-34] are also essential because these muscles prevent the lower spine from collapsing into the sway-back position.

WHAT TO EXPECT

Progress can be measured by the squeeze test of the inner thigh fatpads and poking test of the cervical neck, as discussed above. However, the constant pain, aching, and sleep disturbance will continue for a long time after the diagnostic points show improvement. In fact, unlike the treatment for most other conditions or diseases, it is not uncommon for Fibromyalgia symptoms to continue to worsen until final resolution, because sleep disturbance continues until the back and neck pain intensity drops below the threshold for causing sleep disturbance. Typically, the diagnostic points take at least six months to one year to become non-tender.

However, the pain will remain after the injury has healed and diagnostic points have become non-tender. If you have a serious injury to, say, your hand, and it gets infected, hurts for weeks and is then amputated, you will feel that pain in that non-existent hand for six months to a year after it's gone. The brain forms connections and remembers this pain. This also, will preclude or at least interfere with, stage 4 sleep. As a result, even the most diligent patient who adheres exactly to instructions, cannot expect improvement for at least six months to one year after the diagnostic points have become non-tender. Thus, the entire process can take up to two years. One must follow these instructions on a purely intellectual basis because positive results won’t appear for a long period of time, and it's hard to believe the injury is not where the pain is felt (referred pain). Dogged, unwavering persistence is required.

Alcohol and caffeine should be avoided at all costs, since these drugs affect areas of the brain already perturbed by the Fibromyalgia condition.

MEDICATION?

Dr. Smythe now recommends the use of no drugs at all [35], save perhaps Tylenol before bed (although it is of very limited benefit). A recent study [36] has shown that tricyclics such as amitriptyline are helpful for symptoms of Fibromyalgia, but only for a short period of time. After six months, these drugs are only as effective as placebo. The natural tendency is, of course, to double the dosage. This is a mistake because, inevitably, the new dosage also becomes ineffective, and discontinuation of the drug involves withdrawal. Use of these drugs therefore tends to delay progress towards restoration of correct sleeping patterns.

FINAL THOUGHTS

Solving Fibromyalgia (pain sensitization) is contingent upon there being no other untreated condition, such as rheumatoid arthritis, gut infection, broken bones, etc. However, back and shoulder pain, amplified by Fibromyalgia, will be lessened significantly by correcting the lower lumbar and cervical spine problems, so they should be addressed regardless.

There are several papers that summarize all these principles [9, 21, 23, 26-27, 30]. Reference 21 is somewhat out-of-date in the sense that it still recommends the use of SRIs, since it precedes Reference 34.

The Globe and Mail newspaper published an article (HTML) briefly touching on the concepts given above.

REFERENCES

1. Smythe, H.A., 'Fibrositis' as a Disorder of Pain Modulation, Clinics in Rheumatic Diseases, 1979; 5(3):823-832

2. Wolfe F, Smythe HA, Yunus MB, et al, The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia, Report of the Multicenter Criteria Committee, Arthritis & Rheumatism, 1990; 33(2):160-172

3. Moldofsky H, Scarisbrick P, England R, Smythe HA, Musculoskeletal Symptoms and Non-REM Sleep Disturbance in Patients with "Fibrositis Syndrome" and Healthy Subjects, Psychosomatic Medicine, 1975; 37:341-351

4. Moldofsky H, Scarisbrick P, Induction of Neurasthenic Musculoskeletal Pain Syndrome by Selective Sleep Stage Deprivation, Psychosomatic Medicine, 1976; 38:35-44

5. Harvey Moldofsky, Jerry J. Warsh, Plasma Tryptophan and Musculoskeletal Pain in Non-Articular Rheumatism ("Fibrositis Syndrome"), Pain, 1978; 5:65-71

6. Ellman P, Shaw D, The “Chronic Rheumatic” and His Pains. Psychosomatic Aspects of Chronic Non-Articular Rheumatism, Annals of the Rheumatic Diseases, 1950; 9:341-357

7. Payne, T.C., et al., Fibromyalgia and Psychologic Disturbance, Arthritis & Rheumatism, 1982; 25:213-217

8. Smythe, H.A., Problems with the MMPI (Editorial), Journal of Rheumatology, 1984; 11(4):417-418

9. Hugh Smythe, Tender Points: Evolution of Concepts of the Fibrositis/Fibromyalgia Syndrome, American Journal of Medicine, Vol. 81 (supplement 3A), September 29, 1986, pp. 2-6

10. Hugh Smythe, Fibrositis Syndrome: A Historical Perspective, Journal of Rheumatology, 1989; Supplement 19(16):2-6

11. Buskila D, Neumann L, Vaisberg G, Alkalay D, Wolfe F, Increased Rates of Fibromyalgia Following Cervical Spine Injury, Arthritis and Rheumatism, 1997; 40(3):446-452

12. Smythe HA, Studies of Sleep in Fibromyalgia; Techniques, Clinical Significance, and Future Directions, British Journal of Rheumatology, 1995; 34:897-899

13. Kellgren J.H., Observations on Referred Pain Arising From Muscle, Clinical Science, 1938; 3:175-190

14. Kellgren J.H., On the Distribution of Pain Arising from Deep Somatic Structures with Charts of Segmental Pain Areas, Clinical Science, 1939; 4:35-46

15. Lewis T., Kellgren J.H., Observations Relating to Referred Pain, Visceromotor Reflexes and Other Associated Phenomena, Clinical Science, 1939; 4:47-71

16. Kellgren JH, Deep Pain Sensibility, The Lancet, 1949; 1:943-949

17. Russell IJ, Orr MD, Littman B, Vipraio GA, Alboukrek D, Michalek JE, Lopez Y, MacKillip F, Elevated Cerebrospinal Fluid Levels of Substance P in Patients with the Fibromyalgia Syndrome, Arthritis & Rheumatism, 1994; 37:1593-1601

18. Russell IJ, Fletcher EM, Vipraio GA, Lopez Y, Orr MA, Cerebrospinal fluid (CSF) Substance P (SP) in Fibromyalgia (FMS): Changes in CSF SP Over Time Parallel Changes in Clinical Activity, Arthritis & Rheumatism, 1998; 41 Supplement 9: S256, abstract: 1340

19. Bradley L, Alarcón GS, Sotolongo A, Weigent DA, Alberts KR, Blalock JE, et al., Cerebrospinal fluid (CSF) Levels of Substance P (SP) are Abnormal in Patients with Fibromyalgia (FM) Regardless of Traumatic or Insidious Pain Onset, Arthritis & Rheumatism, 1998; 41 Supplement 9: S256, abstract 1341

20. Griep EN, Boersma JW, Lentjes Eef GWM, Prins APA, van der Korst JK, de Kloet ER, Function of the Hypothalamic-Pituitary-Adrenal Axis in Patients with Fibromyalgia and Low Back Pain, Journal of Rheumatology 1998; 25:1374-1381

21. Hugh A. Smythe, “Nonarticular Rheumatism and Psychogenic Musculoskeletal Syndromes”, in Arthritis and Allied Conditions A Textbook of Rheumatology, 11th Ed., Daniel J. McCarty editor, Lea & Febiger, 1989, pp. 1241-1254

22. Hayashi H, Okada K, Hamada M, Tada K, Ueno R, Etiologic Factors of Myelopathy, A Radiographic Evaluation of the Aging Changes in the Cervical Spine, Clinical Orthopaedics, 1987; 214:200-209

23. Hugh A. Smythe, “Cervical Spine Syndromes”, in Arthritis and Allied Conditions A Textbook of Rheumatology, 11th Ed., Daniel J. McCarty editor, Lea & Febiger, 1989, pp.1413-1421

24. Hugh A. Smythe, The C6-7 Syndrome – Clinical Features and Treatment Response, Journal of Rheumatology, 1994; 21(8):1520-1526

25. Hugh A. Smythe, Rheumatologists and neck pain, Scandinavian Journal of Rheumatology, 2000; 29:8-12

26. Hugh Smythe, The “Repetitive Strain Injury Syndrome” is Referred Pain from the Neck (Editorial), Journal of Rheumatology, 1988; 15(11):1604-1608

27. Hugh A. Smythe, The “Repetitive Strain Injury Syndrome” is Referred Pain From the Neck (Reply), Journal of Rheumatology, 1989; 16(7):1007

28. Hugh Smythe, Links Between Fibromyalgia and Myofascial Pain Syndromes (Editorial), Journal of Rheumatology, 1992; 19(6):842-843

29. Frank H. Netter, Atlas of Human Anatomy, Second Edition, Icon Learning Systems, 1997, ISBN 0-914168-80-0

30. Hugh A. Smythe, Robert P. Sheon, Fibrositis/Fibromyalgia: A Difference of Opinion, Bulletin on the Rheumatic Diseases, Volume 39, No. 3, 1990

31. Hugh Smythe, Referred Pain and Tender Points, American Journal of Medicine, Vol. 81 (supplement 3A), September 29, 1986, pp. 90-92

32. Hugh A. Smythe, Musculoskeletal Q&A: Exercise Must Be Strenuous to Ease Fibromyalgia Pain, Journal of Musculoskeletal Medicine, 1991; 8(7):13

33. Helewa A, Goldsmith CH, Lee P, Smythe HA, Forwell L, Does Strengthening the Abdominal Muscles Prevent Low Back Pain – A Randomized Controlled Trial, Journal of Rheumatology, 1999; 26(8):1808-1815

34. Helewa A, Goldsmith CH, Lee P, Smythe HA, Forwell L, Does Strengthening the Abdominal Muscles Prevent Low Back Pain – A Randomized Controlled Trial (Reply), Journal of Rheumatology, 2000; 27(9):2287-2288

35. Smythe, H.A., Does Modification of Sleep Patterns Cure Fibrositis?, British Journal of Rheumatology, 1988; 27(6):449

36. Simon Carette, Mary J. Bell, Hohn Reynolds, Boulos Haraoui, et. al, Comparison of Amitriptyline, Cyclobenzaprine, and Placebo in The Treatment of Fibromyalgia - A Randomized, Double-Blind Clinical Trial, Arthritis & Rheumatism, 1994; 37(1):32-40

This page last updated November 19, 2003