Before a patient is diagnosed with fibromyalgia the following blood work must have been ordered and values must be in the normal range: complete blood count (CBC), chemistry screen to evaluate liver and kidney function, sed rate, ANA titer, muscle enzymes, CRP, salivary or serum hormone levels including cortisol, progesterone, DHEA and testosterone, IgF_1, TSH, T3, T4, anti-thyroid antibodies. A vestibular screening examination should be performed to rule out endolymphatic disorders.

If the patient reports symptom onset following spine trauma, a trial of treatment can be done to determine if the pain can be reduced. However the patient is entitled to more than one diagnosis and may have pain from fibromyalgia and one of the above conditions.

Different etiologies of fibromyalgia

In a clinical setting, fibromyalgia patients seem to sort into eight fairly clear although often overlapping etiologies. These are clinical distinctions based on patient histories and response to treatment developed during 12 years of treating hundreds of fibromyalgia and myofascial pain patients.

• Stress: One type of FMS seems to be associated with prolonged emotional or physical stress and physiologic sequelae of prolonged elevated cortisol

Figure 8.1 • The algometer allows delivery of a calibrated amount of pressure to assess pain sensitivity. The ACR criteria require that the patient report pain at 11 of 18 pressure points in response to 4 pounds per square inch pressure. There is also some mention of “the amount of pressure required to produce blanching of the examiner’s thumb nail bed” which leaves room for considerable ambiguity. The algometer allows more precise and reproducible pressure.

and other stress hormones and the subsequent adrenal depletion (Maes 1998, Adler 1999). The section below describing the physiologic effects of severe prolonged stress explains the mechanism by which stress can create fibromyalgia (Dessein 1999).

• IgG food sensitivities: FMS can be associated with “leaky gut” and IgG food or environmental allergies. Mast cell overload from elevated IgG complexes causes the release of histamine causing “brain fog” and fatigue and stimulating class C pain fibers to create widespread aching.

• Toxicity: This etiology of FMS is associated with one-time acute or long-term chronic exposure to organic chemicals, heavy metals or pesticides that change nerve membrane firing characteristics creating generalized body pain, cognitive dysfunction and fatigue. Liver enzymes, especially GGT, may be elevated. GGT is so frequently positive that many labs no longer include it in a standard chemistry screen. It is the most sensitive marker for liver inflammation and must be ordered specifically. History questions regarding previous places of employment and residence, previous job descriptions such as hair dresser, landscape maintenance, printer, or painter will reveal exposures to organic chemicals (Baker 1997).

• Genetic: This type has a genetic link, seems to run in families and may be associated with food sensitivities, especially gluten, or may represent an increased need for enzyme substrate in the liver detoxification or serotonin pathways.

Figure 8.2 • When the tender points are evaluated with an algometer the number recorded on the diagram represents the number of pounds per square inch pressure that caused pain. Dating the record allows tender point evaluation to track progress.

Figure 8.3 • When large numbers of IgG antigen–antibody complexes are ingested by macrophages histamine is released into circulation. Histamine stimulates class C pain fibers causing widespread diffuse aching and stimulates immune system responses leading to fatigue and cognitive dysfunction and a diagnosis of fibromyalgia.

• Viral: This type occurs after immunizations or viral illness. The symptoms may be from immune response to the virus or from nervous system response to the mercury preservatives in the immunizations.

• Vestibular injuries: This condition is not truly fibromyalgia but it is associated with the sleep disturbances and cognitive difficulties resulting from a vestibular injury or brain trauma. The sleep deprivation creates neuroendocrine stress eventually resulting in fibromyalgia. The patient will present with symptoms characteristic of FMS and the vestibular etiology has to be teased out during the history.

• Peri-menopause and trigger points: This type of FMS is associated with poorly managed menopause. Estrogen reductions cause sleep disturbance due to hot flashes and relative progesterone deficiency causes fatigue. Myofascial trigger points cause regional pain which can be in all four quadrants leading to central sensitization and a diagnosis of fibromyalgia. The solution for this etiology of fibromyalgia is proper hormone management and trigger point therapy using FSM (see Chapter 7) (McMakin 1998, 2004).

• Spine trauma: This type of fibromyalgia occurs after whiplash injuries, cervical or thoracic spine trauma, or after surgery and can be caused by any trauma that involves spinal flexion/rotation, spinal compression or ballistic segmental movement during a fall or impact (Bohlman 1979, Mendel 1989). The post-surgical cases are thought to occur when the neck is hyper-extended during intubation and constitute a cervical injury. Approximately 24–30% of fibromyalgia patients associate the onset of their condition with physical trauma although privately some clinicians have proposed the percentage to be closer to 50%. As a group they are the only FMS patients who complain specifically of pain in the hands and feet or describe their pain as burning.

All fibromyalgia patients, regardless of the etiology of their condition, have the same neuroendocrine and central sensitization features described in the fibromyalgia research but each etiology responds to different treatment strategies (Bennett 1999, Crofford 1998, Neeck & Reidel 1999). The model for the different types of fibromyalgia was developed when it was discovered that fibromyalgia could be successfully resolved when the treatment strategy addressed the specific cause or etiology of the pain or dysfunction.

Fibromyalgia associated with spinal trauma (cervical trauma fibromyalgia or CTF) represents a distinct etiology from fibromyalgia associated with other causes. The other types of fibromyalgia can be improved or cured without the use of FSM, although FSM helps accelerate the process. Fibromyalgia from spine trauma appears to respond only to FSM treatment and probably represents the 30% of non-responding fibromyalgia patients found in most fibromyalgia therapeutic studies.

Fibromyalgia from spine trauma – typical presentation and history

Treating fibromyalgia from spine trauma (CTF) is fairly easy; recognizing it can be more problematic because patients do not always associate their pain with the physical trauma but may attribute it to the emotional stress that accompanied the physical event. The patient who described her FMS as being due to the “emotional stress” of her divorce failed to recall falling off of a chair and hitting her head on the wall while painting the kitchen ceiling during her divorce until after treatment for CTF alleviated her pain and persistent questioning jogged her memory.

The pain diagram and symptom complaint describes aching burning midscapular pain, shoulder, neck, arm and hand pain that begins soon after the trauma and persists to varying degrees from the time of the injury to the date of presentation. Mid-scapular pain may represent referred pain from an injured cervical disc (Cloward 1959, Bogduk 1988). After some period of time, usually 1–6 months post-injury, the pain generalizes to the whole body, particularly down the thoracic and lumbar paraspinals, the gluteals and down both legs into the feet. The pain will be described as burning, aching, stabbing and sharp.

The patients generally rate the pain as varying between a 4 and a 9/10 on a visual analog scale. Most describe their hands and feet as feeling cold, burning or aching since the accident or injury. CTF patients have a characteristic affective response to the pain; it is particularly bothersome. Most have chronic headaches that can be quite severe. Many have been on narcotics, Neurontin or Lyrica for some time.

Imaging

MRI studies usually show a disc bulge or a contained herniation at C5–6 or C6–7 and less often at C4–5. In many cases the films have been read as normal by the original radiologist since degenerative changes and

Figure 8.4 • The pain diagram for fibromyalgia associated with cervical spine trauma (CTF) differs from other fibromyalgia pain diagrams. As a group, CTF patients are the only fibromyalgia patients who describe their pain as burning and stabbing and report aching and burning in the hands and feet. This pain diagram is characteristic and predictive of a CTF diagnosis. It is virtually identical to pain diagrams characteristic of central pain except that central pain patients usually also report pain in the head and face (see Chapter 10).

small disc bulges are considered “normal” in a patient population. Many pain-free patients have disc bulges that do not produce symptoms. When the films were re-examined by a consulting radiologist specializing in spinal imaging the revised report described a central bulge or contained herniation.

The clinician is encouraged to review the films personally and not rely on the report when assessing fibromyalgia patients. The findings on the film must be correlated with the clinical assessment and physical examination as there is no way to tell from imaging alone whether a disc is causing symptoms.

Weight bearing flexion–extension MRI studies have recently become available in some facilities and will occasionally reveal a disc bulge that looks small in neutral but then extrudes in either flexion or extension causing spinal cord compression and myelopathic changes in the cord. The risk to the spinal cord requires a surgical referral for these patients.

Plain film x-rays cannot assess disc injuries but may reveal anterolisthesis or retrolisthesis near the abnormal segment. Flexion–extension lateral cervical spine x-rays may show increased translation, at the level of disc injury documented on the MRI.

In a very rare case the imaging may be completely normal but the mechanism of injury may involve force vectors that stretch the spinal cord and cause direct injuries to the spinal cord vasculature or neuronal tracts.

Figure 8.5 • This microscopic examination done at autopsy shows contained herniation and end plate fractures in a disc whose postmortem imaging was read as normal (reproduced with permission from Taylor & Twomey 1993). The patients in this study died from causes other than spine trauma during motor vehicle accidents.

Physical examination

The patellar reflex will be hyperactive, very brisk with a larger than normal amplitude. This is the hallmark diagnostic physical examination finding for fibromyalgia associated with spine trauma. In many cases, striking the patellar tendon on one side causes not only the hyperactive patellar reflex but also causes the adductors on the opposite leg to contract. In most cases the upper extremity and Achilles reflexes will be normal. Fibromyalgia that is not due to spinal trauma will demonstrate normal or even reduced patellar reflexes.

The sensory examination invariably shows hyperesthesia in one or more upper extremity dermatomes, usually C3, C4 or C5, and occasionally in a lower extremity dermatome.

Muscle strength will be normal in most cases. These patients are not generally surgical candidates although some may be. Cervical compression, performed by applying axial pressure to the spine by pressing on the top of the head, will produce neck pain and an increase in shoulder pain in most cases.

Measurement of the 18 ACR defined tender points by algometer show at least the required 11 out of 18 necessary for a fibromyalgia diagnosis unless the patient was on narcotic medication that reduced sensitivity. Many of these patients will report pain with as little as 1–2 pounds per square inch of pressure.

Figure 8.6 • CTF patients have specific dermatomal hyperesthesia in addition to the allodynia characteristic of all fibromyalgia patients. This patient had hyperesthesia to sharp in the right C3, C4, C5 and C6 dermatomes. C7, C8, T1 and all of the lumbar nerve roots had normal sensation.

How spine trauma leads to fibromyalgia

How could cervical spine trauma cause fibromyalgia and central pain sensitization? Trauma creates cracks in the disc annulus or the cartilaginous end plate and exposes the spinal fluid and spinal cord to the material in the disc nucleus. The disc nucleus contains neurotoxic concentrations of phospholipase A₂ (PLA₂) shown to cause nerve destruction in dogs, pigs and rabbits. PLA₂ has been shown to be so inflammatory and neuro-toxic that it destroys nearby nerves in a dose related response (McCarron 1987, Olmarker 1993, 1995, Ozaktay 1995, 1998, Cavanaugh 1997, Chen 1997, Marshall 1997).

The damage to the discs shown by Taylor & Twomey (1993) occurs in the postero-lateral portion of the disc which is directly adjacent to the antero-lateral portion of the spinal cord. The paleospinothalamic tract is the outermost of the two tracts in the lateral column of antero-lateral cord and carries diffuse deep pain information up the spine to the thalamus, caudate nucleus and the cortex (Lombard 1983). This tract is the one closest to the portion of the disc most likely to be damaged (Netter 1991).

The anatomic proximity of the cracks in the discs and endplates could expose this tract to very high neurotoxic levels of PLA₂.

If inflammation progressed to create damage in the paleospinothalamic nerves it would effectively create a chemical deafferentation of the pain pathways in the spinal cord. Inflammatory chemicals reduce the firing of nerves and slow or stop nerve conduction.

Trauma can cause direct mechanical disruption of the antero-lateral pathways and the spinal cord leading to deafferentation of these axonal pathways according to Taylor & Twomey (1993). Deafferentation in the antero-lateral ascending pain pathways in the spinal cord would produce what is essentially thalamic or central pain. Disruption of pain pathways in the spinal cord leads to central pain:

“Central pain can arise not only from pathologic lesions in the thalamus but also from neurosurgical lesions placed anywhere along the nociceptive pathway from the spinal cord and brain stem to the thalamus and cortex. … The sensations are unpleasant and abnormal, often unlike anything the patients had ever felt before: spontaneous aching and shooting pain, numbness, cold, heaviness, burning and other unsettling sensations that even the most articulate patients find difficult to describe. Central pain is particularly distressing emotionally.”

(Kandel & Schwartz 1985)

Fibromyalgia patients with a cervical trauma etiology use exactly the same pain descriptors, word for word, as central or thalamic pain patients. Patients with fibromyalgia that is not caused by cervical trauma do not have the same severity, quality or location of pain that cervical trauma patients describe. Their pain is diffuse and achy but it lacks the disturbing affective neuropathic intensity seen in the cervical-trauma mediated fibromyalgia patients. Post-traumatic fibromyalgia patients are the only group who complain of aching in their hands and feet and the only group that responds to the treatment protocol for inflammation in the spinal cord.

Treating fibromyalgia associated with spine trauma

Medical science accepts as a given that fibromyalgia is an incurable condition and the randomized controlled studies done so far have had that view as a starting point. Controlled trials by their nature can study only one intervention as it affects one or more symptoms. Since fibromyalgia is a collection of multiple symptoms affecting numerous systems each affected by multiple influences, the possibility that any one intervention will produce remission of all symptoms or cure the condition is extremely remote, especially if one starts with the presumption that the condition is incurable. The clinical strategies that have created recovery for so many patients operate within a framework in which recovery, while not inevitable, is thought possible because it has been observed to be so (Teitelbaum 2001). It is left to the reader to decide which viewpoint is most productive.

The treatment protocol in this chapter was developed by trial and error in 1999 and found to be effective in eliminating pain in over 200 FMS patients with spinal trauma onset. Pain has been reduced from an average of 7.4/10 to 1.4/10 in every patient with hyperactive patellar reflexes, dermatomal hyperesthesia, a history of trauma and pain in the hands and feet. Reducing the pain is relatively easy; achieving recovery is more involved because of the neuroendocrine and metabolic disturbances (McMakin 2005).

Pain is only part of the fibromyalgia diagnosis and symptom picture. Once the pain can be alleviated the patient still has the metabolic abnormalities characteristic of fibromyalgia. The neuroendocrine dysfunction in fibromyalgia patients is almost as disabling as the pain and it may be associated with alterations in central hormone function, primarily mediated corticotrophin releasing hormone or corticotrophin releasing factor (CRF or CRH).

Neeck & Reidel (1999) proposed, and it seems a reasonable hypothesis, that the pain itself serves as a chronic stressor elevating CRH in the hypothalamus. CRH in turn modifies levels of LHRH (luteinizing hormone releasing hormone), TSH (thyroid stimulating hormone), and GHRH (growth hormone releasing hormone) centrally contributing to disruptions in circulating hormones. Progesterone, growth hormone, thyroid hormone levels and thyroid receptor sensitivity are all affected. Chronic moderate neuropathic pain would be sufficient to cause the elevations in CRH found in fibromyalgia and the alterations in central pain processing common to fibromyalgia patients (Bennett 1999).

By the time the patient has been in moderate to severe pain for 1–2 years the symptoms generalize to include the classic neuroendocrine abnormalities seen in fibromyalgia caused by any etiology (Crofford, Demitrack 1996, Crofford, Engleberg, Demitrack 1996, Crofford 1998, Neeck & Reidel 1999). Understanding the neuroendocrine abnormalities is helpful when diagnosing fibromyalgia but it becomes crucial when attempting to resolve or cure it.

Understanding stress and neuroendocrine dysfunction

The key problematic central neuroendocrine hormone in fibromyalgia is corticotrophin releasing hormone or corticotrophin releasing factor (CRF or CRH). The stress response has its own evolutionary survival logic. When the body comes under attack it does not respond differently if the level 8/10 pain is caused by a tiger dragging you into the woods or by a disc bulge causing full body neuropathic pain. Certain stress responses go into effect mediated primarily by CRF/CRH and cortisol to keep the body alive until the attack is over. CRF stimulates the adrenals to increase cortisol levels and it acts centrally to modulate central regulatory hormones.

All repair systems and long-term physiologic processes are put “on hold” until the threat either kills you or resolves (Sapolsky 1994). This survival strategy is perfect for short-term attacks by tigers but creates problems when the stress persists in the form of moderate to severe pain lasting years.

Stress and thyroid

CRF suppresses thyroid stimulating hormone (TSH) centrally (Neeck & Reidel 1999). Primitive survival logic dictates that the stress hormones are stimulating enough and additional thyroid hormone would be hyper-stimulatory. Elevated cortisol from the adrenal glands suppresses the peripheral conversion of the T4 storage form of thyroid hormone into the T3 active form of the hormone. Many fibromyalgia patients present as if they are clinically hypothyroid complaining of weight gain, constipation, dry skin, hair loss, fatigue and feeling cold. The patient becomes functionally hypothyroid because T4 cannot convert efficiently into T3 but TSH is almost always found to be in the normal or upper end of normal range when tested. TSH cannot rise in response to the relative peripheral insufficiency because it is suppressed centrally by CRF.

Stress and gonadal hormones

CRF suppresses FSH (follicle stimulating hormone) and LH (luteinizing hormone) centrally (Sapolsky 1994). The long-term projects of ovulation, sperm production, copulation and pregnancy are put on hold until the threat is gone. In women FSH and LH promote maturation of the corpus luteum and its increased production of progesterone to balance the estrogen produced by the ovaries during the post-ovulatory portion of the menstrual cycle. If production of progesterone by the corpus luteum is insufficient to balance estrogen the patient experiences the symptoms of premenstrual syndrome (PMS) caused by estrogen dominance. The patient complains of fatigue, irritability, water retention, sleep problems and emotional lability. These complaints are common to fibromyalgia patients.

Stress and growth hormone

CRF suppresses growth hormone releasing factor (GHRH) centrally interfering with growth hormone secretion (Bennett 1997). In an adult, growth hormone facilitates amino acid transport across the cell membrane to enhance tissue repair. Growth hormone in an adult is released during stage IV sleep and in a burst about 1 hour after vigorous exercise. Fibromyalgia patients do not experience stage IV sleep and they do not have the normal burst following exercise due to CRF suppression. Without adequate levels of growth hormone the normal exercises and activities of life and the minor tissue damage that follows are not easily repaired. This explains why fibromyalgia patients experience days or weeks of muscle pain after simple exercise or exertion.