Fibromyalgia and Lyme Disease Connection

Discussion in 'Fibromyalgia Main Forum' started by contentedpearl, Mar 7, 2003.

  1. contentedpearl

    contentedpearl New Member

    Here are some more medical papers about possible connections between Lyme Disease and Fibromyalgia:

    ***Audrey Stein Goldings, MD. She is a private practice neurologist in Dallas. She is a member of the Internationl Lyme and Associated Disease Society and a founding member of the Board of Directors.

    Controversies in Neuroborreliosis

    by Audrey Stein Goldings, M.D.

    Updated October, 2002

    The objectives of this article are to cover issues related to Lyme disease that are not
    even-handedly addressed in the current literature. It will:

    1. Present a practical approach for making the diagnosis of neuroborreliosis,

    2. Explore the other side of the post-Lyme syndrome (i.e. the likelihood of chronic
    ongoing infection),

    3. Discuss the relationship between MS and Lyme,

    4. Critique the current regimens published for treating neuroborreliosis, and

    5. Present my own approach which may differ from some leading authorities.

    ?Anyone who, in discussion, relies upon authority uses not his understanding but rather
    his memory.?
    ?Leonardo da Vinci, Notebooks (c. 1500)

    It is hoped this data will provide the reader with a broader understanding of
    neuroborreliosis so that he or she may better use current and evolving knowledge for
    clinical decision making.


    Because of difficulties in making the diagnosis of neuroborreliosis, the physician will
    need a familiarity with the most common forms of presentations, which will be
    emphasized. The following points will help evaluate the patient for neuroborreliosis:

    1. For most patients, systemic features of disease coexist with, or predate, neurologic

    2. Both central nervous and peripheral nervous system involvement is frequent with
    Lyme disease and typically occur together.

    3. Laboratory data may or may not confirm the diagnosis, and other disease in the
    differential diagnosis must be evaluated thoroughly in cases where diagnostic ncertainty

    4. Although history of exposure to B. burgdorferi should be sought, for various reasons,
    patients may not remember a history of a tick bite, or the pathognomonic rash
    particularly if the disease is presenting years after the exposure.

    5. Early on, personality changes, psychiatric symptoms, or cognitive manifestations may
    be the first, and occasionally the only, symptoms that the patient or family is aware of.



    ? Meningismus with normal CSF
    ? Lymphocytic Meningitis
    ? Meningoencephalomyelitis
    ? Subacute Encephalopathy (SAE)


    ? Cranial Neuropathy
    ? Painful Radiculitis
    ? Distal Neuropathy
    ? Plexopathy
    ? Myositis
    ? Polymyalgia Rheumatica


    Patients may present with headache and stiff neck without evidence of CSF
    inflammation. Since early CNS seeding has been described, as well as culture positivity
    during latent disease without concurrent CNS inflammatory changes, these symptoms
    probably indicate active infection. Stiff neck might alternatively be due to axonal
    degenerative changes of the cervical paraspinal musculature, but there should be other
    evidence of a more widespread neuropathy when this is the case.

    Lymphocytic Meningitis may appear to be indistinguishable from aseptic meningitis
    during early-disseminated disease (weeks to months after inoculation with B.
    burgdorferi). Most patients will have headaches that will fluctuate in intensity.
    Associated features may include a cranial neuropathy in about one-third. Low-grade
    encephalopathy is present in up to one-half, with mild memory concentration deficits,
    mood changes, and sleep disturbance.

    Rarely, focal parenchymal CNS lesions occur. The MRI may show punctate white matter
    lesions best seen on T2-weighted images; larger lesions occur infrequently. One brain
    biopsy showed increased numbers of microglia cells, rare spirochetes, and minimal
    inflammation. Transverse myelitis, movement disorders (extrapyramidal cerebellar,
    chorea and myoclonus), and hemiparesis can occur.

    Psychosis, mood swings (mild or bipolar), profound personality changes, depression,
    anorexia nervosa, obsessive-compulsive disorder, and panic attacks may occur. CSF may
    be normal.

    The most common chronic CNS manifestation is a SAE, characterized by memory
    problems and depression. Many patients (or their families) will complain of their
    excessive daytime sleepiness and extreme irritability. These patients generally come to
    the office disorganized (despite a supreme effort to be organized), unable to give a
    coherent history. They will bring copious notes, which are invariably in the wrong order.

    Most patients will complain of fatigue, and about one-half have headaches. Coincident
    polyneuropathy is very common with spinal or radicular pain, or distal paresthesias.
    Quantifiable deficits in memory, learning and retrieval, attention and concentration,
    perceptual-motor skills, and problem solving are common. MMPI testing generally shows
    a stable psychological pattern without significant psychopathology, similar to other
    medically ill patients.



    Confirmation by CSF CULTURE is seldom practical because the organism is very
    fastidious, present in small numbers, takes a long time to grow out, and may undergo
    changes to forms which cannot be cultured easily.

    CSF ANTIBODY TITERS may be present but are inconsistent and therefore their
    absence does not rule out CNS infection. The MRI is seldom abnormal and the findings,
    when present, are not specific for Lyme.
    CSF PCR (test for spirochetal DNA) is a useful tool, but at present, because the capture
    of DNA is inconsistent, a few questions still need to be addressed.

    Looking for evidence of an intrathecal immune response may be helpful, but it is not
    specific. As a rule, oligoclonal bands and an elevated IgG index are not present in North
    American Lyme disease and their presence should suggest other diseases.

    Cranial neuropathy, painful radiculitis, distal neuropathy, and plexopathy are seen and
    generally reflect different clinical presentations of mononeuritis multiplex
    (polyneuropathy). Bell?s Palsy occurs in almost 11% of all Lyme patients and is bilateral
    in up to 1/3. Therefore, a bilateral Bell?s Palsy is very suspicious for Lyme in an endemic
    area. Painful radiculitis or cranial neuropathy can be seen with meningitis but also with
    normal CSF due to axonal neuropathy. Myositis may occur with Lyme as well as
    polymyalgia rheumatica. Symptoms of chronic involvement of the peripheral nervous
    system in a series of patients with chronic neurologic manifestations of Lyme disease
    developed a median of 16 months after the onset of infection, while CNS involvement
    began a median of 26 months after the onset of disease.

    Electrophysiological testing may show evidence of a mild peripheral neuropathy. Axonal
    degeneration and perivascular inflammatory infiltrates are noted on pathological



    Most typically, patients present with SAE, most often combined with polyneuropathy.
    Brief episodes of arthritis, primarily involving the knees, generally predate the symptoms
    and may persist after onset of neurological abnormalities. The TRIAD OF SAE,

    Since serologies may be contradictory or negative, the physician will have to settle for
    treating if clinical suspicion is strong enough and assess whether the patient has
    ?possible? or ?probable? neuroborreliosis. Vigilant attempts to rule out other disorders
    should be undertaken. Screening should be done for collagen vascular disease, other
    infections, cancer, metabolic or endocrinological disturbances, etc. when a definite
    diagnosis cannot be made.



    Many patients are sent home with antidepressants, muscle relaxers, but no antibiotics
    from doctors? offices because they have symptoms of fibromyalgia. Pictures similar, or
    identical, to fibromyalgia may be part of the constellation of symptoms of Lyme; it may
    occur more rarely as an isolated symptom, or surface after what would otherwise be
    considered successful treatment.

    Symptoms of fibromyalgia due to Lyme disease have not been cured with short-term oral
    or intravenous antibiotics, so some argue fibromyalgia is not due to active infection. I
    would question whether those particular antibiotic regimens were adequate to eliminate
    the infection, rather than assume the patient has developed ?Post-Lyme Syndrome?
    (some yet to be defined immunologically triggered disorder).

    Bujak et al. evaluated patients a mean of almost five years after treatment. 15% of these
    patients had symptoms of fatigue and arthralgia. Almost one-half met criteria for
    fibromyalgia or chronic fatigue syndrome. Fibromyalgia is thought to be a variant of the
    chronic fatigue syndrome. Of note, nearly all patients continued to complain of memory
    loss or concentration difficulties. One quarter had objective evidence of cognitive
    impairment, and 15% manifested depression.


    All physicians experienced with treating Lyme disease have had patients who present
    with a recurrence of flu-like symptoms, months to years after they have completed the
    usual antibiotic course of therapy, oral or intravenous, and re-exposure had not occurred.

    These patients describe their flu-like symptoms as identical to their early-disseminated
    stage of Lyme disease. The flu-like symptoms may reoccur following what appears to be
    a trivial stressor, such as an uncomplicated viral URI. Patients may be able to ?contain?
    their symptoms without specific antimicrobial therapy, but many will have to resume
    antibiotics. These patients complain of having to go to bed due to excessive fatigue or
    hypersomnolence. They cannot think straight, their muscles and joints ache, and they
    may have a low-grade fever. Do these symptoms sound like a ?fibromyalgia-like
    syndrome? or ?acute fatigue syndrome?? Prior medical experience suggests reactivation
    of infection. Despite what may appear to have been a previous ?cure,? relapse of
    symptoms in this context would appear to be due to failure to eradicate the infection and
    with reactivation after a period of dormancy.

    Reoccurrence of symptoms due to
    immunologically triggered disease, INDEPENDENT of persistent infection seems
    FIBROMYALGIA, AND CHRONIC FATIGUE BLUR. It seems more logical to
    postulate that fibromyalgia and chronic fatigue syndrome, when seen with Lyme disease,
    may be attenuated forms of chronic manifestations of earlier flu-like symptoms
    associated with early dissemination.



    Lyme may present as a MS-like illness, but on many occasions the pathology is not
    actually in the CNS. Since chronic Lyme symptoms often are predominantly shifting,
    vague, behavioral-psychological, psychiatric, and, as mentioned, neurological, they are
    likely to conjure up the diagnosis of MS in patients and physician alike. However, the
    existence of pathology outside the CNS should rule out the diagnosis of MS. Some of the
    vague symptoms that can be mistaken for MS include those that are better attributed to
    peripheral nervous system damage, as part of the mononeuritis multiplex that may occur.

    This might cause numbness, tingling, facial weakness, diplopia, etc. The diagnosis of MS
    cannot be made in the absence of CNS symptoms and signs. MRI and CSF findings
    would also help support the diagnosis of MS. In addition, a significant CSF pleocytosis
    may occur with Lyme disease, which should not be present with MS.


    Patients can have CNS lesions in the brain or spinal cord with Lyme disease. The
    European literature includes many more cases than the American for encephalomyelitis,
    strokes, etc. In those cases where there is focal involvement of the brain or spinal cord, it
    may be more difficult to distinguish neuroborreliosis from MS. Again, a brisk CSF
    pleocytosis would help diagnose Lyme and the specific aforementioned test for CNS
    Lyme antibodies. Simultaneous appearance of peripheral nervous system abnormalities
    or arthritis should suggest the diagnosis of Lyme.


    There are some patients who have a clear-cut preexisting history of MS before the onset
    of Lyme disease. The Lyme appears to accelerate their clinical course. For others, it
    appears to be the initiating infection that triggers the MS. These patients are most likely
    genetically predisposed to MS and the Lyme bacteria exerts its major effect by ?turning
    on? immunologically directed CNS injury. It is not uncommon to get a history of the
    onset of an exacerbation of MS related to infections, so Lyme exacerbating MS would be
    expected. HLA Class II molecules determine the intensity of the immune response to
    pathogenic foreign or self-antigens. With MS, the HLA-DR4 DQw8 haplotype has been
    associated with chronic progressive MS and the HLA-DR2 DQw6 haplotype has been
    associated with susceptibility to both chronic progressive and relapsing or remitting MS.
    It is possible that in genetically predisposed patients of certain HLA types that infection
    by Lyme bacteria would cause a high production of cytokines that would mediate the
    demyelination and destruction of oligodendrocytes.

    Most recently, researchers are studying positive outcomes when antibiotics that are most
    useful in treating Lyme disease are used to treat ?MS.?


    First, read the fine print.
    It is interesting to note that recommendations for treatment in the medical literature may
    carry provisos in small print that can easily be overlooked but are instrumental to
    understanding how important individualization of therapy is at the current time. For
    instance, in the past and in small print Dr. Alan Steere has written, ?treatment failures
    have occurred in all these regimens, and retreatment may be necessary; the duration of
    therapy is based on clinical response, and the appropriate duration of therapy with late
    neurological abnormalities may be longer than two weeks.?

    A more recent article written
    by Rahn and Malawista states ?these guidelines are to be modified by new findings. It
    should always be applied with close attention to the clinical course of individual
    patients.? Dr. Katzel surveyed several Lyme Borreliosis conferences, including
    international ones. He finds a trend towards the use of antibiotics for longer periods than
    previously described and lack of standardization of care worldwide. 50% of physicians
    responding considered using antibiotics for time periods greater than one year in
    symptomatic seropositive patients, with almost as many extending therapy up to one and
    a half years when necessary.


    Studies have shown that Lyme bacteria can be an intracellular pathogen and may evade
    the normal host immune response. The causative spirochete, B. burgdorferi, for instance,
    may persist within fibroblasts and survive at least 14 days of exposure to ceftriaxone. In
    addition, B. burgdorferi has been cultured from CSF more than a half year after a
    standard regimen of IV antibiotics, according to Preac-Mursic. Logigian and Steere
    looked at patients with chronic neuroborreliosis, evaluating them six months after two
    weeks of IV ceftriaxone. Over one-half of the patients had already been treated with
    therapy that was thought appropriate for their stage of illness, yet the illness progressed.
    The majority of patients studied had subacute encephalopathy and polyneuropathy. Most
    had persistent fatigue, and almost one-half had headaches. One-third of these patients had
    to stop working or had to go part-time, underscoring the disability that may be seen with
    Lyme disease on an individual and societal level. After therapy, two-thirds of patients
    improved markedly, but seldom completely. Twenty-two percent improved but then
    relapsed, and fifteen percent had no change in their condition.

    This study suggests that additional antibiotics greatly helped the majority with
    neuroborreliosis but they were insufficient to cause long lasting remission in those
    patients who subsequently relapsed. Persistent residual or irreversible disease may
    explain the fifteen percent who had no change in their condition.

    For those clinicians who have had extensive experience with chronic neuroborreliosis,
    more recent recommendations suggesting that a regime of only 20 to 28 days or even 6
    weeks of intravenous antibiotics is sufficient for cure proved contrary to clinical
    experience. That brief dosing does not appear to prevent relapse or improve long-term
    outcome dramatically in many cases. Perhaps, as recent information has instructed, that
    is because the immune system does not begin to repair itself until the beginning of the
    fourth month of antibiotic treatment. A trial of prolonged use of oral antibiotics seems
    more reasonable in many cases, given these circumstances.

    Antibiotics used for chronic neuroborreliosis should be able to penetrate the blood-brain
    barrier, express activity against intracellular organisms, and assure good intraphagocytic
    penetration. It is anticipated that the microbe during late disease has achieved maximal
    adaptation to its host environment. Also, because of the long generation time of the
    organism, lengthier therapy is warranted.


    If a patient has meningitis or appears acutely ill, particularly with possible arrhythmia,
    admit him or her to the hospital for intravenous antibiotics and observation.

    however, in patients with stable late disease, oral antibiotics can be tried first. The
    majority of patients will have some improvement or gradual resolution of
    encephalopathic symptoms with a better energy level. After a six-week trial of
    appropriate antibiotics, the patient is re-evaluated. If there is no Herxheimer response or
    some clinical improvement during this interval, it is worrisome, and the physician needs
    to be concerned about: 1) misdiagnosis, 2) noncompliance, and/or 3) permanent end
    organ damage. These possibilities should be addressed with the patient before proceeding
    with intravenous antibiotics since they may not be maximally beneficial either
    Over the long haul, whether intravenous antibiotics are used for two weeks or longer,
    with chronic refractory disease, ultimately other methods are necessary. A lengthier use
    of oral antibiotics seems more logical than intravenous antibiotics for some patients.
    Unfortunately, there are no current tests that adequately measure disease activity with
    neuroborreliosis in all patients.
    We are sorely in need of a test similar to the CSF VDRL for syphilis that would give us a
    measure of disease activity. Culture negativity or disappearance of a specific immune
    response in the serum or CSF has not been useful at this time to establish cure. CSF
    antibodies may persist for years after otherwise successful treatment. Particularly in the
    CNS, judging response of therapy is problematic because pathological changes may
    incompletely or, at least, very slowly reverse. Any clinical improvement would be
    expected to occur in a delayed fashion after therapy is given. Likewise, one would expect
    neuropathy related to axonal degeneration to remit slowly and/or incompletely. Formal
    neuropsychiatric testing is of value in documenting pathology and following the patient.

    It also helps delineate what the patient can and cannot do. It also can help to define the
    disease for the patient, family, insurer, and the employer. The patient needs to be told
    that his or her symptoms should remit slowly and incompletely, when on antibiotic
    treatment. This is particularly important when the symptoms have been chronic.


    The premise of this approach to diagnosing and treating neuroborreliosis needs to be

    1. There is no current laboratory test that makes or breaks the diagnosis of
    neuroborreliosis. It is a clinical diagnosis substantiated by laboratory data when possible.
    Fortunately, the majority of cases are fairly uniform in their lack of uniformity, and other
    diagnoses are easily ruled out. In situations where the physician simply cannot achieve
    diagnostic certainty, he or she should notify the patient that the diagnosis is ?possible? or
    ?probable? neuroborreliosis. This has been done previously with MS (i.e., possible,
    probable, and definite MS), another disease where laboratory testing does not make the
    diagnosis in and of itself.

    2. There is no perfect current laboratory test to monitor success of therapy, and this is
    critically needed. Until better testing is available, assessing progress, or lack thereof, will
    largely be determined with clinical acumen.

    3. The infection is difficult to eradicate and may require long-term treatment. The
    spirochete, particularly in later stages, becomes well adapted to survival within its host
    environment. There are some patients that we may not be able to cure, but will be able to
    palliate with currently available antibiotics.

    4. Although immunopathogenic factors may play a crucial role in disease presentation,
    the presence of chronic infection appears necessary to perpetuate the process and play a
    causative role in persistence of immunologically triggered symptoms.

    5. There is no Diagnostic and Statistic Psychiatry Manual (DSM IV) category for
    ?antibiotic seeking behavior.? It is common for physicians who are unable to explain
    patients? symptoms or effect their cure to ascribe a psychiatric cause to their malady.
    This is easily done with Lyme since objective findings may be subtle or non-existent.

    Because neuropsychiatric symptoms may pre-dominate, it is easy in some patients to
    attribute their symptoms to depression or secondary gain. These patients do not in any
    other way seek other medication that would be associated with habituation or addiction
    (i.e., pain medicine).

    Many patients suffer unfairly at the hands of physicians who refuse to make the diagnosis
    because blood tests are either contradictory or negative. ?Lyme bashing,? for instance,
    referring to Lyme disease as ?yuppie flu,? is demeaning. The ?just say no? attitude of
    certain physicians towards Lyme patients who request retreatment with antibiotics should
    not be condoned in the face of continuing experience with this potentially chronically
    disabling infectious disease.

    ***Audrey Stein Goldings, MD is a private practice neurologist in Dallas, is member of
    Internationl Lyme and Associated Diseases Society and a founding member of the Board
    of Directors.

    If you were diagnosed with Fibromyalgia or Chronic Fatigue..

    Please read this article by Dr. Donta...

    Lyme Disease as a Model of Chronic Fatigue Syndrome Sam Donta, M.D.;

    Boston University Medical Center The CFS Research Review 2002; 3: 2, 1-4

    With the discovery of the causative agent of Lyme disease, a new chapter has been
    opened in the understanding of chronic fatigue syndrome (CFS) and other multi-symptom
    disorders. Lyme disease, caused by spirochetal bacteria transmitted by the bite of an
    Ixodes (deer) tick, is now known to be one cause of chronic fatigue disorder that cannot
    be readily distinguished from CFS, nor from what is termed fibromyalgia. These
    disorders have similar major symptomatology consisting of fatigue and neurocognitive
    dysfunction, along with numerous other symptoms that probably relate to altered
    neurological function. Musculoskeletal symptomatology may be more frequent in
    fibromyalgia and in some patients with chronic Lyme disease than in CFS, but the
    definition of CFS also encompasses myalgias and arthralgias as part of the disorder.

    Causative agents In Lyme disease, following the bite of an infected deer tick, the Borrelia
    burgdorferi bacteria may spread locally and cause a variety of skin rashes, the most
    typical being an expanding circular rash with a clearing area and center resembling a
    bull's eye. Half of the rashes, however, are not typical, causing diagnostic problems for
    physicians. Patients who are infected may not develop or see the rash, and may not
    develop any future symptoms, remaining asymptomatic.

    Some asymptomatic patients, however, may reactivate their infection following various
    stressors such as trauma, surgery, pregnancy, an intercurrent illness, taking an antibiotic
    for an unrelated reason, severe psychological stress or having received the Lyme vaccine.
    Similar triggers such as trauma and other stresses are known to precipitate CFS and
    fibromyalgia. It is likely that there are a number of other causes of CFS and fibromyalgia
    in addition to chronic Lyme disease.

    Epstein-Barr virus (EBV), the major cause of infectious mononucleosis, continues to be
    debated as a cause of CFS. It is uncertain whether EBV can cause symptoms other than
    fatigue, such as myalgias and arthralgias that are not seen during acute or reactivated
    EBV infection in patients who are being immunosuppressed, but it remains possible that
    EBV could cause one type of chronic fatigue disorder.

    Some more recently recognized species of Mycoplasma (Mycoplasma fermentans,
    Mycoplasma genitalium) have been implicated in chronic fatigue and other multi-system
    disorders, including CFS itself, fibromyalgia and Gulf War Illness. These same bacteria
    have also been implicated as causative agents of rheumatoid arthritis, based on
    PCR-DNA evidence in patients with these disorders in which 50 percent are found to
    have the DNA of the Mycoplasma in circulating white blood cells, compared to 5-10
    percent of a normal population. Whether the presence of this DNA represents past
    exposure or ongoing infection remains to be resolved. No longitudinal studies have yet
    been performed in patients with CFS to determine whether the finding of Mycoplasma
    DNA persists over months or years or whether such patients have any evidence of other
    infection such as Lyme disease or infection with Chlamydia species.

    Gender effects The effects of gender and host on susceptibility and expression of Lyme
    disease, CFS and other multi-symptom diseases are also in need of further study. In all
    these disorders, women appear to be more affected than men, usually at about 2:1 ratios.
    It seems notable that neural cells contain estrogen and progesterone receptors, and that
    herpes viruses can utilize estrogen receptors to gain access to the reservoir in the cell
    nucleus. Treatment of chronic Lyme disease also seems to be gender-dependent to some
    degree, with men generally having more speedy and complete recoveries compared to
    women. Gender relationships are known for a number of infectious diseases, so it would
    not be surprising that such a relationship exists for chronic Lyme disease, CFS and other
    multi-symptom disorders.

    Disease targets

    In Lyme disease, the nervous system seems to be the primary target for the bacteria
    causing the disease. Patients with the disease express many neurologic symptoms such as
    pain, paresthesias including numbness, tingling, crawling and itching sensations, as well
    as cognitive difficulties and mood changes. Even the joint pains and occasional
    arthritis(joint pain is much more frequent than actual swelling of joints) appear to be
    neuropathic in origin, as anti-inflammatory agents such as ibuprofen and other
    nonsteroidal anti-inflammatory agents have little if any effect on the pain.

    Experimental evidence from animal models, primarily dogs and non-human primates,
    also affirm the localization of B. burgdorferi DNA to the nervous system. The
    mechanisms underlying the pathophysiology of the disease remain to be defined, but
    could involve inflammatory responses, autoimmune responses or toxin-associated
    disruption of neural function. Any inflammatory responses appear to be weak, and there
    is no compelling evidence that Lyme disease is a result of immunopathologic
    mechanisms. The target(s) for other causes of CFS remain to be defined. Without any
    animal models, it becomes more difficult to study its pathogenesis and pathophysiology.

    Nontheless, the central nervous system would appear to be a logical target for other
    pathogens or other pathophysiologic processes. Any changes in immunologic function
    would not appear to be sufficient to explain the various symptoms, and are likely to be
    secondary to other pathogenetic processes.


    The diagnosis of Lyme disease is primarily based on clinical grounds. Just as with CFS,
    the combination of symptoms over months and years, in the absence of an obvious
    alternative diagnosis, is sufficient to make a presumptive clinical diagnosis. The
    diagnosis of Lyme disease is made easier if a typical rash is present during the early
    phase of infection. After that, it is difficult to distinguish the flu-like illness that can
    occur a few weeks later, or can recur over a number of months. Some patients develop
    severe headaches and an aseptic meningitis, which frequently is diagnosed instead as
    "viral" meningitis.

    If a Bell's palsy occurs, causing drooping of one side of the face, the possibility of Lyme
    disease should occur to the physician. If an unprovoked arthritis occurs, causing swelling
    of a single joint, especially the knee, but sometimes more than one joint, then the
    possibility of Lyme disease should also be given high consideration. But it is the chronic
    phase of the disease that causes most of the problems for physicians and patients,
    because of the lack of "objective" signs and the presence of so many symptoms that it
    causes some doctors to invoke psychologic reasons for the patients' symptoms.

    Many such patients receive a diagnosis of CTFS or fibromyalgia, when they may have
    underlying Lyme disease as the cause of their symptoms. The laboratory has been helpful
    is some patients with Lyme disease, especially those with arthritis, in whom there are
    stronger antibody responses than in those with the chronic, multisymptom form of the
    disease. The criteria for the laboratory diagnosis has been patterned after the arthritic
    form of the disease, and not the chronic for; thus, there are many physicians who are
    misinformed about the test's lack of value in chronic disease.

    The Lyme Western Blot is helpful when it shows reactions against specific proteins of B.
    burgdorferi, but can be negative in 25-30 percent of patients who otherwise have chronic
    Lyme disease. PCR-DNA tests for Lyme in blood, urine and spinal fluid are rarely
    positive, most likely because the bacteria and their DNA are not present in those body
    fluids, but inside nerve cells. The MRI exam of the brain in about 10 percent of patients
    with chronic Lyme disease can show some white spots in various areas, similar to those
    seen in multiple sclerosis, a neurologic disease of unknown cause that has some
    overlapping symptoms with Lyme disease, such as the paresthesias. It is unclear how
    many patients who have Lyme disease as a cause of CFS have these findings.

    The brain SPECT scan, a variation of a PET scan, shows some changes in blood flow to
    various parts of the brain, primarily the temporal (cognitive processing) and frontal
    (mood) lobes in about 75 percent of patients with chronic Lyme disease. Patients with
    CFS have also been reported to have some brain SPECT scan changes, frequently
    involving the occipital lobe. No comparative studies have been made among patients
    with chronic Lyme disease, CFS and fibromyalgia.

    The mechanisms underlying these changes remain to be defined, but may be due to a
    mild vasculitis or to a signaling problem within the nerve network of the brain in those
    specific areas. It is promising, though, that these changes are reversible in most patients
    treated with antibiotics that appear to be effective in treating the chronic Lyme disease.
    Treatment Treatment of chronic Lyme disease, CFS, fibromyalgia, and other chronic
    multi-symptom disorders has been primarily symptom-based. Although some of these
    treatments (e.g., amitryptiline, other sleep medications, antidepressants, pain
    medications) can offer some relief, they rarely lead to resolution of the chronic

    In chronic Lyme disease, there continues to be controversy whether antibiotics can be of
    value. In our studies, intracellular-type antibiotics such as tetracycline or the combination
    of one of the erythromycin-type antibiotics (e.g., clarithromycin - Biaxin, azithromycin-
    Zithromax) and hydroxycholoquine ( a drug which changes the pH inside cells to be less
    acid, thus allowing the erythromycin-type antibiotics to be effective) given over a number
    of months (6-18 months, sometimes longer) has resulted in substantial improvement and
    cures in most patients with chronic Lyme disease.

    Similar results have been noted in some patients with CFS of unknown cause, supporting
    the hypothesis that some patients with CFS have an underlying infection responsive to
    those antibiotics. Antibiotic trials in CFS have been limited to one month, a duration
    inadequate to more properly evaluate the potential of certain antibiotics to exert a
    positive effect on the disease. Additional studies, examining both potential etiologic
    agents of CFS and treatment trials should lead to a better understanding of both the cause
    and treatment of patients with CFS.

    Selected readings Asch ES et al. "Lyme disease: an infectious and postinfectious
    syndrome". J Rhjeum, 1994; 21:454061. Brouqui P et al. "Eucaryotic cells protect B.
    burgdorferi from the action of penicillin and ceftriaxone but not from the action of
    doxycycline and erythromycin." Antimicrob Agents Chemother, 1996; 40:1552-4 Choppa
    PC et al. "Multiplex PCR for the detection of Mycoplasma fermentans, M. Hominis, and
    M. penetrans in cell cultures and blood samples of patients with chronic fatigue
    syndrome." Mol Cell Probes, 1998; 12:301-8 Donta ST. "Treatment of chronic Lyme
    disease with macrolide antibiotics." In: Program and abstracts of the VIIIth International
    Conf. on Lyme Borreliosis, June 20-24, 1999; Munich, Germany. Abstract P193. Donta
    ST "Reactivation of Lyme disease following OspA vaccine." Int J Antimicrobial Agents,
    2001; 17:S116-7. Donta ST. "The existence of chronic Lyme disease." Current Treatment
    Options in Infectious Diseases, 2001; 3:261-2. Georgilis K et al. "Fibroblasts protect the
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    ___________________________________________________________- The CFS
    Research Review is published quarterly by The CFIDS Association of America, PO Box
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  2. Fibromiester

    Fibromiester New Member

    A Must-Read !
  3. contentedpearl

    contentedpearl New Member

    Hi Sonny,
    I use aromatherapy for my brain fog and it helps a lot. I use a massage oil with a few different essential oils diluted in it and I rub it on my forehead, neck, and scalp, and it helps a lot. You can find the formula I use at You may want to find a doctor who is open to doing long term antibiotic therapy. Infectious disease doctors are generally quite unhelpful. Minocycline seems to be the antibiotic that helps my neurological and mental symptoms the most.