Rotating fms symptoms/Tried Cymbalta

Discussion in 'Fibromyalgia Main Forum' started by JohnBee, Sep 2, 2006.

  1. JohnBee

    JohnBee New Member

    We are told that Fm is not "progressive", but it certainly is bewildering that symptoms seem to change over time. Sleep deprivation and daytime fatigue are long time problems; now for the past 2 months, I have had stomach pain, nausea, and pain behind my eyes. GI Dr. advice has not helped. Does this happen to you, and is it common for FM? As an aside, have you tried Cymbalta for depression and achiness? Has it helped you, despite all the side effects? Thank you for your help. John
  2. LadyCubbieFan

    LadyCubbieFan New Member

    This dd seems to affect each person differently, mine seems to have gotten progressively worse though the years. I always have nausea when I flare which is now by the way.

    I was on Cymbalta and it did nothing for my pain and am now on Effoxer for depression. It seems to work good for me but my Dr. said it was hard to come off.

    I didn't have any side effects with the Cymbalta either come to think of it.

    Remember each med affects each of us differntly, so how it worked for me could be entirely different for someone else.

    I'm sure someone else will be who may help you more.
    Good luck.

  3. lenasvn

    lenasvn New Member

    I hope this can be of any help at all?!

    What Your Neurologist Should Know
    About FMS and CMP

    by Devin J. Starlanyl

    This information may be freely copied and distributed only if unaltered,
    with complete original content including: © Devin Starlanyl, 2002.

    Please read “What Everyone on Your Health Care Team Should Know About FMS
    and CMP” and “Headaches Due to TrPs.”

    Many fibromyalgia (FMS) symptoms can lead to a call for a neuro consult (Simms
    and Goldenberg 1988). So can myofascial trigger point (TrP) symptoms (Simons,
    Travell, Simons 1999). FMS itself is basically a neurological condition (Bradley,
    McKendree-Smith, Alarcon et al. 2002). There is, among other things, a state of
    central sensitization leading to allodynia and/or hyperasthesia. Many patients will
    come to you undiagnosed or misdiagnosed (Buskila, Neumann, Sibirski, et al.
    1997). They may also be under-medicated due to unwarranted fear of addiction
    on the part of the primary care physician. Pain further stresses the body, leading
    to further hypersensitizing of the CNS (Lebovits, Florence, Bathina et al. 1997).
    Research shows that the recent increasing medical use of opioids to treat pain
    hasn’t cause an increase “ the health consequences of opioid analgesic abuse”
    (Jornason, Ryan, Gilson et al. 2000). Pain is a perpetuating factor for both FMS
    and CMP, and as such, must be brought under control with available medicinal and
    nonmedicinal options.

    Functional MRI studies indicate that FMS is associated with augmented pain
    processing (Gracely, Petzke, Wolf et al. 2002). There may be multiple hormonal
    and autonomic imbalances in FMS, leading to profound physiological and clinical
    consequences (Adler, Manfredsdottir, Creskoff 2002). Neuorplasticity plays a
    significant role in chronic pain states (Coderre, Katz, Vaccarino, et al. 1993). The
    development of central sensitization from repeat or chronic trauma is well
    documented (Yaksh, Hua , Kalcheva et al. 1999). In FMS, this trauma may be
    physical or biochemical.

    Regional cerebral blood flow abnormalities have been documented in FMS (Mountz,
    Bradley, Modell 1995; Johansson, Risberg, Rosenhall, et al. 1995). Central
    sensitization of FMS may be maintained by peripheral stimulation, such as
    myofascial TrPs (Staud, Smitherman 2002; Borg-Stein 2002). It is vital that the
    myofascial TrPs be identified and treated promptly, because many of the
    “Fibromyalgia” symptoms are not part of fibromyalgia at all, but are part of chronic
    myofascial pain, and must be treated differently. Following the last stimulus in a
    series, the after sensations were greater, lasted longer and were more frequently
    painful in FMS (Staud, Vierck, Cannon et al 2001). Your FMS patient will hurt more
    and hurt longer from stimuli that others may not find painful at all.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 1

    FMS is associated with dysautonomia (Raj, Bruillard, Simpson. 2000). There may
    be many dysfunctional hormonal axes, and these may be difficult to pinpoint. End-
    hormone HPA axis glucocorticoids have multiple roles. They inhibit CRH, LC/NE
    and beta-endorphin systems, stimulate the mesocorticolimbic dopaminergic
    system and CRH peptidergic central nucleus of the amygdala, and inhibit the
    pituitary gonadotropin, GH and TSH secretion. They promote tissue resistance to
    a variety of hormones. They suppress 5' deiodinase, which converts T4 to T3, and
    promote Metabolic Syndrome (Tsigos, Chrousos G. 2002). Metabolic Syndrome
    itself is a common perpetuating factor for both FMS and CMP. “Chronic imbalance
    of the autonomic nervous system is a prevalent and potent risk factor for adverse
    cardiovascular events, including mortality”(Curtis, O’Keefe 2002). Please don’t
    take these patients lightly. In most cases, they will come with a history of being
    dismissed and perhaps mistreated by your medical colleagues.

    FMS is real and may be maintained by the sympathetic nervous system (Martinez-
    Lavin, Vidal, Barbosa, 2002). The stress of having an invisible and misunderstood
    medical condition, often compounded by lack of support from family, companions
    and the medical and insurance world, can add to the burdens. “The most
    aggressive challenges of the FMS concept have been from legal defenses of
    insurance carriers motivated by economic concerns. Other forms of critique have
    presented as psychiatric dogma, uninformed posturing, suspicion of malingering,
    ignorance of nociceptive physiology, and occasionally have resulted from honest
    misunderstanding” (Rau, Russell 2000).

    Fibromyalgia, a neuroendocrine illness, and chronic myofascial pain, a
    neuromuscular illness, are often confused. Many doctors lack a thorough
    knowledge of myofascial trigger points, and this often leads to inappropriate
    treatment. Raynaud’s syndrome is often present with FMS (Bennett 1991), and
    nerve, blood and lymph vessel entrapment by myofascial TrPs can compound the
    symptoms (Simons, Travell, Simons 1999). The symptoms are signs of impaired
    circulation, as well as enhanced sensitivity. There may be increased neurogenic
    inflammation (Littlejohn, Weinstein and Helme 1987), sensory dysfunction (Kosek,
    Ekholm and Hansson 1996), and altered sympathetic nerve activity (Elam,
    Johansson and Wallin 1992) in FMS. There can also be orthostatic sympathetic
    derangement (Martinez-Lavin, Hermosillo, Mendoza, et al. 1997). Multiple FMS
    symptoms may respond to central acting medications (Suzuki, Dickenson 2002),
    and the research in this area is very vigorous.

    It is important to check the whole patient, as symptoms may develop that are due
    to combinations of therapies. For instance, toxic optic neuropathy with visual
    acuity loss, dyschromatopsia, altered light adaption, and evolving bilateral
    cecocentral scotomas can develop if a patient is on a combination of Zoloft (given
    for FMS symptoms), melatonin (taken to help sleep) and is on a high protein diet
    (for Metabolic Syndrome, insulin resistance or reactive hypoglycemia) (Lehman,
    Johnson 1999). A complete history is most important in these patients.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 2

    Myofascial TrPs can mimic so many different conditions, such as visceral pain in the
    absence of visceral pathology (Gerwin, 2002). To doctors untrained in myofascial
    referred pain patterns, this may cause patients to be misdiagnosed with
    somatiform illness. Proprioception dysfunction can be associated with any
    myofascial TrPs. Some people have reported becoming dizzy to the point of falling
    just from looking at patterns of light and dark. Some patients even vomit from
    this and must avoid fabric stores and take care using escalators because of their
    tread pattern. Patterns of light and dark from trees by the side of the road can
    cause a petit-mal fugue state, depending on the lighting. It is not uncommon for
    people with myofascial TrPs to trip over their own feet, bite their tongue, or have
    disturbance of judging weight held in the hand. Some of this is due to the
    proprioception disturbances so well documented by Travell and Simons. There
    may also be a proprioceptive component in FMS. People with FMS also may have
    indications of a movement disorder and sensory disturbances (Burgunder, 1998).
    Other physicians may not know about this.

    Myofascial TrPs can cause nerve and vascular entrapments. TrPs cause
    dysfunction before they cause pain and must be suspected whenever there is pain
    at the end of decreased range of motion. They cause specific muscle weakness.
    Many TrPs can cause grip failure. Knees, ankles and hips can buckle. A list of
    common diagnoses can be found in “Travell and Simons Myofascial Pain and
    Dysfunction: The Trigger Point Manual, vol I ed 2 (Simons, Travell and Simons,
    1999, p 37). Thorough knowledge of TrPs and their individual pain patterns and
    associated symptoms are a necessity for differential diagnosis in most cases.
    There are many cases of muscle dysfunction that have persisted needlessly for
    over 20 years, because the TrPs were not diagnosed and properly treated. In
    some cases, the contractured muscles have pulled bones out of alignment, and
    degeneration of bone has resulted, not from “aging”, but from iatrogenic causes.
    Early attention to perpetuating factors and treatment of the TrPs can cause
    sometimes astounding and rapid relief.

    Carpal tunnel syndrome is a description, not a diagnosis. The cause must still be
    identified before it can be corrected. Scaleni, brachialis, brachioradialis, radial
    wrist extensors, palmaris longus, flexor carpi radialis, pronator teres, opponens
    pollicis and adductor pollicis TrPs symptoms mimic CTS (Simons, Travell and
    Simons 1999, p 688). TrPs in the subscapularis muscle can refer pain in a wrist
    band pattern. One study of over 90 cases of cumulative trauma disorders found
    that when fibrous adhesions and resulting faulty biomechanics were treated
    manually, normal function was restored, with relief of symptoms (Leahy and Mock

    III. 1992). Those researchers found that if a nerve is irritated at one point, it is
    more susceptible to compression and irritation at other points, so there may be
    many areas of nerve entrapment if detection and treatment is not timely.
    There has been some media attention (and confusion) concerning Chiari
    Malformation, spinal stenosis, FMS and CFIDS. On March 10, 2000, Barbara

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 3

    Walters interviewed some doctors who perform this surgery. During the interview,
    one neurosurgeon mentioned that even heavy coughing could cause narrowing of
    the spinal canal. It is a fact that any procedure that hyperextends the neck can
    also cause this narrowing. Medical literature shows that reductions of 1.5 mm or
    less in the diameter of the spinal canal can come from simple changes in posture,
    such as a rotation in the pelvis (Harrison, Cailliet, Harrison et al. 1999). Levator
    scapulae and scalene TrPs may be involved in cervical narrowing. It is common to
    have several areas of spinal rotation in CMP. The connection between Chiari I
    malformation and orthostatic hypotension is not well supported by research
    (Garland, Robertson 2001). Patients must be evaluated carefully, and appropriate
    and thorough noninvasive treatments tried before such surgery is even considered,
    and they should never be considered for general symptoms of FMS or CMP.

    I have heard of countless cases where vertebrae have been fused due to
    degeneration, only to have the discs above and/or below degenerate, requiring
    more spinal fusion. This can be repeated and repeated on the same patient, who
    often becomes increasingly more disabled. If muscles are contractured due to
    TrPs, they can pull bones out of alignment. Muscle function groups become
    weakened due to the presence of TrPs, and you cannot strengthen a muscle with a
    TrP. Strengthening exercises, commonly given, simply make the TrP worse. Then
    there is more chance of bulging disc and/or degeneration. Dealing with the disc or
    the vertebrae does nothing to reduce the strain from the muscles. You must deal
    with the TrPs properly, or surgery may cause even more strain, resulting in more
    contracture and future problems, as well as “failed back surgery syndrome”. TrPs
    are more likely to occur in certain muscles in the presence of cervical disc lesions
    at specific levels (Hsueh, Yu, Kuan et al. 1998). Attention to the TrPs may prevent
    the need for surgery if the soft tissue problem is caught in time. Even those
    patients requiring surgery still need attention to the TrPs, before and after surgery,
    as well as attention to perpetuating factors. This requires that doctors be trained
    in the diagnosis and proper treatment of TrPs. All too often they inject steroids,
    which may cover the problem by temporarily relieving the pain, but do nothing for
    the cause. Myofascial TrP injection training is available, as well as hands-on
    training in the diagnosis and treatment of myofascial TrPs (see ).

    Eyelid twitching can be due to myofascial TrPs. Check for periorbital TrPs, extrinsic
    eye muscle TrPs, sternocleidomastoid, the temporalis, and the trapezius TrPs for
    possible contributors. You may also find other head TrPs. Other muscles twitching
    can become bothersome. Sometimes there can be a continuous twitch of many
    muscles. In other cases, one or two muscles will fire off now and then. This may
    be intensified by mineral insufficiency and/or neurotransmitter dysregulation.
    Fasiculations and waves of twitches can be caused by low-level TrPs. This has
    been described by patients as having the nerves plugged in to twinkling Christmas
    lights. Other people have severe twitches that disrupt their functioning. These
    can become painful cramping. Check for vitamin and mineral insufficiencies as
    possible perpetuating factors.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 4

    Headaches may be modified considerably by TrP therapy (Simons, Travell, Simons
    1999; Krabak, Borg-Stein, Oas, et al. 1996; Graff-Radford, Jaeger and Reeves
    1986). There may be abnormal electromyographic results due to nerve
    entrapment by TrPs, and even abnormal EEGs, although these vary, like the
    symptoms, from hour to hour and day to day. Please use only surface EEGs.
    Remember that there is considerable pain amplification in FMS, with amplified and
    extended wind-up (Staud, Vierck, Cannon et al. 2001), so be as gentle as possible.
    An examination may boost pain levels for an extended period of time (weeks or
    longer), causing FMS flare.

    There seems to be alterations in the microstructure of sleep in FMS (Drewes,
    Kielson, Taagholt et al. 1995). Sleep restriction alters the hypothalamic-pituitaryadrenal response to stress (Meerlo, Koehl, van der Borght et al. 2002). Some
    morning stiffness may be due to the immobility of the night, as well as to the lack
    of restorative sleep. It isn’t so much the amount of sleep we get as the poor
    quality of sleep (Branco, Atalaia and Paiva 1994; Drewes, Gade, Nielsen, et al.
    1995; Horne and Shackell 1991). Sometimes diphenhydramine is enough to help
    sleep, but it does cause insomnia in a percentage of people. There may be many
    factors contributing to your patient’s lack of restorative sleep, and it is vital that
    this be addressed as soon as possible. Your patient must feel rested when he or
    she wakes up. Sleep starts can be common in FMS. Bruxism and restless legs are
    common in both FMS and CMP.

    Cognitive deficits have been well documented as part of FMS (Park, Glass, Minear
    et al. 2001). They are often called “fibrofog”, and can be more disabling and
    troubling than the pain. Difficulty distinguishing right from left and/or difficulty
    finding places or following directions is common. Short-term memory problems
    and confusional states are common. There may be difficulty with multitasking, or
    performing a number of steps in sequence. This is common in chronic pain states
    (Gritchnik, Ferrante 1991; Grigsby, Rosenberg, Busenbark 1995). Difficulty
    getting out known words, especially nouns and pronouns, is part of the “cognitive
    deficits” package we often get with FMS. In addition, TrPs in speech muscles can
    create slow, “halted” speech patterns, or garbled sounds. This in no way indicates
    a lack of intelligence. It does cause a level of frustration and misunderstanding
    that can add to the patient’s burdens. Some researchers have found that FMS
    causes slowed psychomotor speed in tasks that require sustained effort (Landro,
    Stiles and Sletvold, 1997). Also, patients may forget things they need to minimize
    symptoms, and that, plus the additional stress brought about by fibrofog, can lead
    to a flare.

    Chronic pain and injury can cause changes that lead to biochemical trauma and
    neural plasticity. These changes can take a while to develop. Many cases of FMS
    and CMP start with whiplash injury, and these effects can add to cognitive deficits.
    Whiplash can cause later deficits in attention, concentration and memory (Kischka,
    Ettlin, Heim et al. 1991). Emotional symptoms as well as brain function may be

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 5

    affected whenever the cervical spine has been injured (Radanov, Bicik, Dvorak et
    al.1999). It doesn’t take an auto accident to supply the force required to do
    damage. Some “psychological” brain-disconnects after whiplash are a
    consequence of the whiplash, and not psychological at all (Radanov, Begre,
    Sturzeneggar et al. 1996).

    Fibromyalgia and chronic myofascial pain are real, and there is a wealth of
    research available to help you diagnose them and treat them effectively. You can
    make a profound difference in the quality of life of many of these patients, and
    many can regain a measure of function that they thought was lost forever.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 6


    Adler G. K, Manfredsdottir V. F., Creskoff F.W. 2002. Neuroendocrine
    abnormalities in fibromyalgia. Curr Headache Rep 6(4):289-98.

    Bennett, R. M. 1991. Symptoms of Raynaud’s syndrome in patients with
    fibromyalgia. A study utilizing the Nielsen test, digital photopleysmography, and
    measurements of platelet alpha 2-adrenergic receptors. Arth Rheum 34(3):264–

    Borg-Stein J. 2002. Management of peripheral pain generators in fibromyalgia.
    2002. Rheum Dis Clin North Am 28(2):305-17.

    Bradley L. A., McKendree-Smith N. L. Alarcon G. S. et al. 202. Is fibromyalgia a
    neurologic disease? Curr Pain Headache Rep 6(2):106-14.

    Burgunder, J. M. 1998. Pathophysiology of akinetic movement disorders: a
    paradigm for studies in fibromyalgia? Z Rheumatol Suppl 57(2):27-30.

    Buskila, D., L. Neumann, D. Sibirski et al. 1997. Awareness of diagnostic and
    clinical features of fibromyalgia among family physicians. Fam Pract 14(3):238–

    Christensen, L. 1997. The effect of carbohydrates on affect. Nutrition 1(6):503–

    Coderre, T. J., Katz J, Vaccarino A.L. et al. 1993. Contribution of central
    neuroplasticity to pathological pain: review of clinical and experimental evidence.
    Pain 52(3): 259–285.

    Curtis B.M., O’Keefe J.H. Jr. 2002. Autonomic tone as a cardiovascular risk factor:
    the dangers of chronic fight or flight. Mayo Clin Proc 398-9; 77(1):7-9.

    Drewes, A. M., Gade M.K., Nielsen K.D. et al. 1995. Clustering of sleep
    electroencephalographic patterns in patients with the fibromyalgia syndrome. Brit
    J Rheumatol 34(12):1151–1156.

    Elam, M., Johansson G., Wallin B.G.. 1992. Do patients with primary fibromyalgia
    have an altered sympathetic nerve activity? Pain 48(3):371–375.

    Faucett, J. A. 1994. Depression in painful chronic disorders: The role of pain and
    conflict about pain. J Pain Symptom Manage 9(8):520–526.

    Garland E. M., Robertson D. Chairi I malformation as a cause of orthostatic
    intolerance symptoms: a media myth? 111(7):546-552.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 7

    Gerwin R. D. 2002. Myofascial and visceral pain syndromes: visceral-somatic pain
    representations. J Musculoskel Pain 10(1-2)”165-175.

    Park D.C., Glass J.M., Minear M. et al. 2001. Cognitive function in fibromyalgia
    patients. Arthritis Rheum 44(9):2125-33.

    Gracely R. H., Petzke F., Wolf J. M. et al. 2002. Functional magnetic resonance
    imaging evidence of augmented pain processing in fibromyalgia.

    Graff-Radford, S. B., Jaeger B, Reeves J. L. 1986. Myofascial pain may present
    clinically as occipital neuralgia. Neurosurgery 19(4):610–613.

    Grigsby, J., Rosenberg N.L., Busenbark D. 1995. Chronic pain is associated with
    deficits in information processing. Percept Mot Skills 81(2):403–410.

    Gritchnik, K. P., Ferrante F.M. 1991. The difference between acute and chronic
    pain. Mt Sinai J Med 58(3):217–220.

    Harrison, D. E., Cailliet R, Harrison D. D. et al.1999. A review of biomechanics of
    the central nervous system – Part I: spinal canal deformations resulting from
    changes in posture. J Manipulative Physiol Ther 22(4):227-34.

    Hendler N. 1984. Depression caused by chronic pain. J Clin Psychiatry 45(3 pt

    Hsueh, T. C., S. Yu, T. S. Kuan and C. Z. Hong. 1998. Association of active
    myofascial trigger points and cervical disc lesions. J Formos Med Assoc 97(3):174

    Johansson, G., Risberg J, Rosenhall U. et al. 1995. Cerebral dysfunction in
    fibromyalgia: evidence from regional cerebral blood flow measurements,
    otoneurological tests and cerebrospinal fluid analysis. Acta Psychiatr Scand

    Jornason D. E., Ryan K.M., Gilson A.M. et al. 2000. JAMA 283(13):1710-4.

    Kischka U, Ettlin T, Heim S. et al. 1991. Cerebral symptoms following whiplash
    injury. Eur Neurol 31(3):136 140.

    Kosek E., Ekholm J, Hansson P. 1996. Sensory dysfunction in fibromyalgia patients
    with implications for pathogenic mechanisms. Pain 68(2-3):375–383.

    Krabak B, Borg-Stein, J, Oas J. et al. 1996. Reduced dizziness and pain with
    treatment of cervical myofascial pain. Arch Phys Med Rehabil 77:940 (Abstract).

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 8

    Landro N. I., Stiles T.C., Sletvold H. 1997. Memory functioning in patients with
    primary fibromyalgia and depression on healthy controls. J Psychosomatic
    Research. 42(3):297 306.

    Lebovits A.H., Florence I, Bathina R. et al. 1997. Pain knowledge and attitudes of
    health care providers: practice characteristic differences. Clin J Pain 13(3):237

    Lehman N. L., Johnson L.N. 1999. Toxic optic neuropathy after concomitant use of
    melatonin, zoloft, and a high protein diet. J Neuroopthalmol 19(4):232-234.

    Littlejohn G. O., Weinstein C., and Helme R.D. 1987. Increased neurogenic
    inflammation in fibrositis syndrome. J Rheumatol 14(5):1022–1025.

    Martinez-Lavin M., Vidal M., Barbosa R. E et al. 2002. Norepinephrine-evoked pain
    in fibromyalgia. A randomized pilot study [ISRCTN70707830]. BMC Musculoskelet
    Disord 3(1):2.

    Martinez-Lavin, M., Hermosillo A.G., Mendoza C. et al. 1997. Orthostatic
    sympathetic derangement in subjects with fibromyalgia. J Rheumatol 24(4):714–

    Meerlo P, Koehl M, van der Borght K et al. 2002. Sleep restriction alters the
    hypothalamic-pituitary-adrenal response to stress. J Neuroendocrinol 14(5):397

    Mountz, J.M., Bradley L.A., Modell J.G. et al. 1995. Fibromyalgia in women.
    Abnormalities of regional cerebral blood flow in the thalamus and the caudate
    nucleus are associated with low pain threshold levels. Arthritis Rheum 38:926–

    Park D.C., Glass J.M., Minear M. et al. 2001. Cognitive function in fibromyalgia
    patients. Arthritis Rheum 44(9):2125-33.

    Radanov, B.P., Bicik I, Dvorak J. et al. 1999. Relation between neuropsychological
    and neuroimaging findings in patients with late whiplash syndrome. J Neurol
    Neurosurg Psychiatry 66(4):485-9.

    Radanov, B. P., Begre S., Sturzeneggar M. et al.1996. Course of psychological
    variables in whiplash injury — a 2 year follow up with age, gender and education
    pair matched patients. Pain 64(3):429 434.

    Raj S.R., Bruillard D., Simpson C.S. 2000. Dysautonomia among patients with
    fibromyalgia: a noninvasive assessment. J Rheumatol 27(11):2660-5.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 9

    Rau C.L., Russell I.J. 2000. Is fibromyalgia a distinct clinical syndrome? Curr Rev
    Pain 4(4):287-294.

    Simms, R. W. and Goldenberg, D. L. 1988. Symptoms mimicking neurologic
    disorders in fibromyalgia syndrome. J Rheumatol 15(8):1271–1273.

    Simons, D. G., Travell, J.G, Simons, L.S. 1999. Myofascial Pain and Dysfunction:
    The Trigger Point Manual, Volume 1, edition II: The Upper Body. Baltimore:
    Williams and Wilkins

    Staud R., Smitherman M.L. 2002. Peripheral and central sensitization in
    fibromyalgia: pathogenic role. Curr Pain Headache Rep 6:259-266.

    Staud R., Vierck C.J. Cannon R.L. et al. 2001. Abnormal sensitization and
    temporal summation of second pain (wind-up) in patients with fibromyalgia
    syndrome. Pain 91(1-2):165-75.

    Suzuki R., Dickenson A.H. 2002. Neuropharmacologic targets and agents in
    fibromyalgia. 6(4):267-73.

    Tsigos C., Chrousos G. 2002. Hypothalamic-pituitary-adrenal axis, neuroendocrine
    factors and stress. J Psychosom Res 53(4):865.

    Yaksh T. L., Hua X. Y., Kalcheva I. et al. 1999. The spinal biology in humans and
    animals of pain states generated by persistent small afferent input. Proc Natl Acad
    Sci USA 1999 96(14):7680-6.

    What Your Neurologist Should Know About FMS and CMP
    by Devin J. Starlanyl © 2002 Page 10

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