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Saturday, 1 November 2014

Late and chronic LymeDisease: symptoms overlap, CFS and Fibromyalgia- Tinnitus

By Sam Donta,M.D.

INTRODUCTION

Following the introduction of Borrelia burgdorferi into the skin
by an infected tick, the organisms begin to spread both locally
and systemically. Several days typically elapse before the
appearance of the first sign of infection, i.e., erythema
chronicum migrans (ECM), or other less typical rashes (29).

The rash occurs in fewer than 50% of patients with Lyme Disease
(8,10), but the true incidence of Lyme Disease in the absence
of a rash is unknown.

The occurence of multiple rashes is indicative of systemic spread
of the organisms. Multiple rashes usually do not occur until 2-4 weeks following the initial tick bite. This is the same time
period during which the organisms are being disseminated to their
target tissues and cells. The incidence of multiple rashes was
initially reported to occur in as many as 50% of cases, but has
been much less common in the last two decades, probably because
of frequent use of antibiotics.

Approximately 4-6 weeks following the tick bite, the first
systemic symptoms (other than multiple rashes) occur in some
patients, usually in the form of "flu" (15). These symptoms
include sore throat, severe headaches and neck aches, and severe
fatigue. Rhinitis, sinusitis, and cough are not usually present,
distinguishing this "flu" from other influenza-like illnesses.
While the Lyme-flu symptoms can spontaneously resolve, patients can experience recurrent "flu".

Soon after the onset of Lyme-flu, fatigue, arthralgias and/or
myalgias may begin. The arthralgias appear to primarily involve
the large joints (i.e., knees, elbows, hips, shoulders), although
smaller joints (e.g., wrists, hands, fingers, toes) may be
involved(29). Some patients may have actual arthritis, often oligoarticular, more frequently in men than in women. Earlier estimates were that 50-75% of patients who developed late Lyme Disease had arthritis, but more recent analyses suggest that the incidence of actual arthritis in patients with late or chronic disease is closer to 25% (33).

Neck stiffness is common. The pains are described as severe, jumping from joint to joint, and may be present for only short periods of time. Pain in the teeth or in the temporal-mandibular joints is not uncommon. Rib and
chest pains occur frequently, leading some patients to seek care
in emergency rooms and urgent care centers for evaluation of
possible cardiac disease. Frequently as well are paresthesias such
as burning, numbness and tingling, and itching. Some patients
experience crawling sensations, vibrations, or electric shock-like
sensations. Rarely is there any actual palsy of the affected areas, making this much more of a neurosensory, rather than a motor, disease.

In addition to paresthesias, purely neurological symptoms and signs include headaches, an aseptic meningitis, facial nerve (Bell's)
palsy, and encephalitis or encephalopathy that may be manifested by cognitive dysfunction, especially short-term memory loss, and
psychiatric symptoms such as panic, anxiety, or depression (14).
The aseptic meningitis and Bell's palsy tend to occur within the
first few months following the tick bite, but may also occur as
part of reactivation disease (9).

Other symptoms may include fevers (usually low grade, but may be high), sweats (which may be severe), visual dysfunction (described
primarily as blurriness, but can include optic neuritis or uveitis),
tinnitus, sensitivity to sounds, or hearing loss. Shortness of
breath, palpitations and/or tachycardia, abdominal pains, diarrhea or irritable bowel, testicular or pelvic pain, urinary frequency
or urgency, dysequilibrium, and tremors are also common symptoms.
Some of the dysautonomia symptoms can be disabling.

Rarer symptoms may relate to panniculitis and hepatitis. Rarely as well are
congenital and intrautero infection; when this occurs, it appears
to be similar to toxoplasmosis and rubella, i.e., a primary infection
during the first trimester. The occurrence of optic neuritis or
uveitis raises other possibilities such as multiple sclerosis, but
can be part of Lyme Disease.

The course of the disease can best be described as persistent, but
with periods of worsening symptoms, often cyclical every few weeks
or monthly. Especially disconcerting are persistent symptoms such
as headaches and fatigue that can be exhausting. Some patients are more symptomatic than are others, which may reflect genetically- determined differences in responsiveness or extent of infection.

The disease does not appear to be progressive or destructive, as
with cancer, nor is it fatal, but can be very debilitating.

The incidence of asymptomatic infection has not been adequately
delineated. There appear to be substantial numbers of patients
who remain asymptomatic, but reactivate their disease a number of
months or years later, following trauma, pregnancy, a medical
illness for which an antibiotic is prescribed, or other stresses,
including psychological stresses (9). The Lyme OspA vaccine has
appeared to reactivate Lyme Disease in a number of individuals who
knew, but some who did not know, they had prior Lyme Disease (11).
The mechanisms responsible for the reactivation of the disease
have not been defined, but may include both molecular mimicry and
underlying infection.

PATHOGENESIS

The pathogenesis of Lyme Disease remains to be defined. From the
available studies, it would appear that the organisms are trophic
for either the endothelial cells of the blood vessels that serve
the nervous system or for the glial or neural cells themselves
(4,24,26,31). Accumulating evidence supports the hypothesis of
a persistent infection as the cause of the persisting or relapsing
symptoms (26,31). Whether molecular mimicry is involved in the
pathogenesis of some of the symptoms remains more speculative (18).

Although arthritis can occur in Lyme Disease, the organisms can
only rarely be found in synovial tissue. And as many of the
arthralgias that occur in the disease do not respond well to
antiinflammatory agents, the disease is more of an infectious
neuropathy than an actual invasion of synovial or bursal tissues.

DIAGNOSIS

The diagnosis rests heavily on the clinical symptomatology.
When there are clinical signs, e.g., rash, aseptic meningitis,
optic neuritis, arthritis, an appropriate differential
diagnosis must be pursued. On a clinical basis, "chronic
fatigue syndrome" or "fibromyalgia" cannot be readily
distinguished from chronic Lyme Disease. Indeed, accumulating
experience suggests that Lyme Disease may be a frequent cause
of fibromyalgia or chronic fatigue (8,12).

Other microbes have been proposed as causative agents of multisymptom disorders that are being termed chronic fatigue and fibromyalgia, especially
more recently recognized mycoplasma species such as M.fermentans
and M.genitalium, but definitive proof of cause and effect has
not yet been established (6, 23).

There has been an attempt to separate "late" Lyme Disease
from "chronic" Lyme Disease, the former being manifested by
objective signs of arthritis or neurological disease (32).
Some have denied the existence of chronic disease, inferring
that these patients suffer from psychiatric disorders; some
have used the term "chronic" to mean post-treatment disease
("post-Lyme"), assuming that the infection has been treated,
and the remaining symptoms are in the same realm as those
patients who have "fibromyalgia" or "chronic fatigue" (27, 30).

These assertions are speculative and remain unproven. That
chronic Lyme Disease actually exists, and is likely the most
common form of the disease, is supported by epidemiologic
studies demonstrating that 30-50-% of treated and untreated
patients go on to develop a multisymptom disorder typical of,
and indistinguishable from, fibromyalgia and chronic fatigue
(1, 28). As with other multisymptom disorders, chronic Lyme
Disease is a clinical syndrome consisting of fatigue,
arthralgias and myalgias,and other nervous system dysfunction(7).

Furthermore, the results of treatment studies appear to support
the hypothesis that persistent infection is responsible for the
chronic symptoms. It is likely that Lyme Disease will serve as
a useful model for other chronic multisymptom disorders. Whether
the pathogenesis of "late" Lyme Disease differs from that of
the chronic form of the disease remains to be established.

Routine laboratory tests are usually normal in Lyme Disease.
The ESR is most often normal, distinguishing it from some of
the inflammatory disorders such as rheumatoid arthritis or
lupus. Culture of the borrelia is possible early in the
disease, usually from biopsies of the erythema migrans rash;
however, most laboratories are not capable of culturing the
organisms.

The only currently available useful laboratory tests are the
immunologically-based ELISA and Western blot assays. The
recommendation was made in 1994 to have a two-tiered testing
system in which the Western Blot would only be done on ELISA- positive samples (5). The recommendation was based primarily on
the results obtained from patients with arthritis (13), did not
take into account the chronic form of the disease, and was made
despite the lack of consistent reproducibility of results between
various laboratories (2, 16).

The ELISA has been shown to be an unreliable test in many patients with Lyme Disease, both in early infection and later disease (8, 10). Part of the reason for the lack of sensitivity of the ELISA is the use of whole organisms, resulting in a high amount of background absorbance.

After correction for the high background, only a small percentage of
positives can be detected. Because Western blots separate the
proteins of the borrelia, specific reactions can be visualized,
and more accurate interpretations of the results made. Over 75%
of patients with chronic Lyme Disease are negative by ELISA,
while positive by Western blot (8, 10). Patients with
oligoarticular arthritis may be more likely to have robust IgG
responses and positive ELISA tests and IgG Western Blots (13).

By Western blot analyses, the first immunologic reactions in
Lyme Disease are to the 41kd flagellar protein, and the 23kd
OspC protein. Typically, at the time of the ECM rash, there will
be an IgM reaction against the 23kd and 41kd proteins, and no IgG
reactions. Within the next few weeks, the IgM reactions persist,
sometimes accompanied by less specific reactions against 60kd and
66kd proteins, and IgG reactions are now visible against the 23kd
and 41kd proteins. Thus, in the presence of an appropriate
clinical picture, the immunoreactivity against the 23kd and 41kd
proteins appear to be diagnostic of Lyme Disease.

Whereas the 41kd protein is not unique to B. burgdorferi, the 23kd
protein appears to be unique. Also apparently unique proteins of
B.burgdorferi are the 31kd (Osp A) and 34kd (Osp B) outer membrane proteins, and the 35kd, 37kd, 39kd, and 83/93kd proteins. Reactions
to the 31kd proteins are not usually seen until after a year or more following the onset of disease. Not all patients with symptoms for
more than one year, however, display reactions to the outer membrane
proteins.

Most symptomatic patients have specific reactions on IgM
Western blots (8,10). With resolution of the symptoms, the IgM
reactions disappear or attenuate. IgG reactivity may continue
to be present with resolution of symptoms, but it typically also
disappears or attenuates with successful therapy. There are some
patients (20%) who have symptoms, but whose Western blots are
negative (8,10). If the borrelial organisms remain intracellular,
with no extracellular reemergence once established, this could
explain the absence of additional or persistent immune responses.

PCR (Polymerase Chain Reaction) is a highly sensitive means to
detect microbial DNA or RNA, and it was hoped that this technique
would find an important role in the diagnosis of Lyme Disease.
Thus far, however, despite the specificity of this method,
borrelial DNA or RNA has not been reliably detected in the blood,
urine, or spinal fluid of patients with early or later forms of
Lyme Disease, findings again supportive of an intracellular
reservoir for the borrelia.

It should be possible to develop a better, highly specific ELISA
for Lyme Disease, using recombinant 41kd, 23kd, 31kd and/or 34kd
(and perhaps other B.burgdorferi-specific) proteins. Currently,
however, the Western blot assay is the most reliable immunologic
test.

TREATMENT

In vitro, B. burgdorferi is sensitive to several antibiotics
(20,25). This assumption is complicated, however, because of
the long incubation times needed to determine minimum
inhibitory concentrations (MIC), as the borrelia have doubling
times of 20-24 hrs. With these limitations, the results of a
few studies show minimum bactericidal concentrations (MBC) to
penicillin of 8ug/ml, ampicillin: 2ug/ml, tetracycline: 1-2ug/ml,
doxycycline: 2ug/ml, ceftriaxone: 0.5ug/ml, cefotaxime: 0.5ug/ml,
cefuroxime: 1-2ug/ml, cefixime: 8ug/ml,erythromycin: 0.5ug/ml,
clarithromycin: 0.5ug/ml, azithromycin: 0.5ug/ml,
and ciprofloxacin: 4ug/ml.

At the time of the first rash, any one of several antibiotics
appear to be effective, if given for 2 weeks, according to several
published studies. However, a number of patients so treated
developed subsequent symptoms of arthralgias, fatigue, and
paresthesias, with positive Western blots, who were then
successfully treated with longer courses of antibiotics (8, 10).
The recommendation at this time, therefore, is that tetracycline,
doxycycline, or amoxicillin be used for 1 month if ECM is the
only symptom of Lyme Disease.

Once any other symptoms appear, the treatment of Lyme Disease
for only 2-4 weeks is associated with frequent failures and
relapses (8, 10). Our initial experience suggested that a 3 month course of tetracycline was associated with a higher success rate(8).

In patients with symptoms present for more than six months, the
treatment course may need to be more prolonged, or a retreatment
course of varying length may be needed. In patients with symptoms
for more than a year, 12-18 months may be needed for complete resolution of symptoms. The rationale for a longer treatment course is based on extensive observations (8,10), plus the analogy to the longer treatment courses required for tuberculosis, leprosy, Q fever, and certain fungal diseases.

With Lyme Disease, the slow growth rate and metabolic activity of the borrelia would seem to correlate with the need for longer treatment periods.

Once treatment is initiated for patients beyond the earliest
signs of infection, their symptoms frequently increase during
the first several days, or even for the first several weeks of
therapy. For patients with preexisting symptoms of more than a
few months, relief of any of their symptoms may not occur until
after 4-6 weeks of therapy (8, 10). Typically, there are short
periods of relief, followed by relapsing or migrating symptoms;
with continued therapy there are longer symptom-free periods.
Some arthralgias may require 3 months or more to resolve, and
fatigue may be the last symptom to disappear.

The preference for tetracycline evolved because of the large
number of failures that were noted in patients who had been
on ampicillin and doxycycline. Patients generally had some
response to doxycycline, but it was uaually not complete, nor
long-lasting. Tetracycline may be more effective than
doxycycline simply because of the greater dose, i.e., 100mg
of doxycycline twice daily is not equivalent to 500mg of
tetracycline three times daily; also, doxycycline is highly
protein-bound, compared to tetracycline, which could limit the
availability of free drug to diffuse into tissues and cells.

Some physicians use doxycycline at doses of 300-400mg daily to
try to achieve a successful result. A strict comparison
between doxycycline and tetracycline has not yet been
made. Minocycline has also been used by some physicians, with
varying success, but faces the same issues of dosage and
protein binding.

Of the beta lactams used for the treatment of Lyme Disease, the
most efficacious appears to be ceftriaxone. In limited comparitive trials, cefotaxime appears to be equally efficacious, and high-dose
IV penicillin may also be effective.

In early Lyme Disease, oral amoxicillin is as effective as doxycycline. In later disease, many failures are noted, despite the use of up to 3 grams of amoxicillin daily, with probenicid. Cefixime would also not appear to be
effective therapy. Cefuroxime axetil has been evaluated only in
the treatment of early Lyme Disease, and appears comparable to
doxycycline. Limited reports of its use in later Lyme Disease have
not shown it to be efficacious.

The role of the newer macrolides in the treatment of Lyme
Disease needs further assessment. Erythromycin has been regarded
as ineffective, despite its good in vitro sensitivities.
Azithromycin has been reported to be less effective in the
treatment of early Lyme Disease than amoxicillin (21). Some
physicians use clarithromycin and azithromycin in higher dosages
and for longer periods of time, but there have been no reports of
greater success with these drugs than with the tetracyclines or
beta-lactams. In our experience, all macrolides are effective
when combined with a lysosomotropic agent, especially
hydroxychloroquine(see below)(10).

In evaluating the possible factors, it would appear that
antibiotics that can achieve intracellular concentrations and activity are the most efficacious drugs. The results of studies in Klempner's laboratory using a tissue culture model of borrelia infection demonstrated that ceftriaxone was incapable of eradicating intracellular organisms (17); similar experiments in Raoult's laboratory using an endothelial cell model
demonstrated that tetracycline and erythromycin were effective,
but beta lactam antibiotics were not (3). These results are in line with our experience that the tetracyclines and macrolides achieve the greatest success.

In contrast to beta lactams, antibiotics of the tetracycline and macrolide classes are capable of good intracellular penetration. Experience with the macrolide antibiotics has been disappointing, however, when compared with
its in vitro activities against the Lyme borreliae, and with the established efficacy of macrolides against other intracellular parasites such as chlamydia, legionella, mycobacterium-avium intracellulare, and toxoplasma. If, though, the Lyme borreliae reside in intracellular vesicles that are acidic, the macrolides' activity would be sharply decreased at the lower pH.

This is in contrast to the tetracyclines, which are active at acid pH; even
so, the activity of doxycycline was shown to be further increased by increasing the pH. In a tissue culture model of ehrlichia infection, the use of lysosomotropic agents such as amantidine, NH4Cl, and chloroquine increased the killing of intracellular organisms by doxycycline (22).

Based on those studies, and the hypothesis that late Lyme Disease symptoms are due to persisting intracellular infection, we have been successfully treating patients using the combination of a macrolide and hydroxychloroquine (10).

As regards "CNS" disease, there is no evidence that ceftriaxone
is more successful than either the tetracyclines or the combination of macrolide and hydroxychloroquine; if our presumption that the pathogenesis of the disease involves the localization of the borrelia to the endothelial cells of the blood vessels serving the nervous system or to glial or neural
cells is correct, then one would not need to have a drug that can cross the blood-brain barrier to be effective. Indeed, the tetracyclines can cross the blood-brain barrier to some extent, and were used when initially introduced into clinical medicine for the treatment of meningitis, with some success.

Macrolide antibiotics do not cross the blood-brain barrier, but have been
effective in treating other CNS infections (e.g., toxoplasmosis), and in our experience have been effective in reversing the neuropsychiatric symptoms and signs (eg SPECT scans) of Lyme Disease (10). With regard to the issue of bactericidal vs bacteristatic effects, any such effect in vivo has not been demonstrated.

Finally, there have been no reports showing any change in antibiotic resistance patterns during the course of treatment. Ultimately, the determination of efficacy of therapy depends on the clinical response.

FUTURE DIRECTIONS

The diagnosis and treatment of Lyme Disease have been
hampered by less than adequate diagnostic tests and inadequate
comparisons of antibiotic regimens. Specific antigen-based
ELISA tests should result in greater specificity, but
sensitivity of any tests based on measurements of the host
immune response might still be of limited value if the borrelia
remain intracellular. Most useful would be the development of
tests that can determine the presence and extent of any residual
borreliosis. In the therapy of Lyme Disease, double-blind,
placebo-controlled and comparitive trials are needed to answer
the questions relating to duration and class of antibiotic
therapy.

The apparent failure of a regimen of one month of
IV ceftriaxone, followed by two months or oral doxycyline,
to improve the outcomes of patients with chronic Lyme Disease
(19) was not surprising, based on prior observations that neither
regimen used for a limited duration was capable of yielding
patient improvement (8,10,33). Additional trials are needed to
evaluate whether longer durations of treatment, using tetracycline
itself, or the novel combination of macrolide and lysosomotropic
agent, would be proven effective treatments.

REFERENCES

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2. Bakken LL, Case KL, Callister SM, et al. Performance of 45
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3. Brouqui P, Bodiga S, and Raoult D. Eucaryotic cells protect
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6. Choppa PC, Vojdani A, Tagle C, et al. Multiplex PCR for the
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7. Donta ST. Lyme Disease: A clinical challenge. J Spirochet and
Tick Dis 2:50-51, 1995.

8. Donta ST. Tetracycline therapy of chronic Lyme Disease. Clin
Infect Dis 25: S52-56, 1997.

9. Donta ST: Reactivation of latent Lyme Disease. X Annual LDF
International Conference on Lyme Borreliosis, National Institutes of Health, April 1997.

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Borreliosis; June 20-24, 1999; Munich, Germany. Abstract P193.

11. Donta ST: Reactivation of Lyme Disease following OspA vaccine.
Int J Antimicrob Agents 17:S116-7, 2001.

12. Donta ST: The existence of chronic Lyme Disease. Current
Treatment Options in Infectious Diseases 3:261-2, 2001.

13. Dressler F, Whalen JA, Reinhardt BN and Steere AC. Western
blotting in the serodiagnosis of Lyme disease. J Infect Dis
167:392-400, 1993.

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Am J Psych 141:1571-83, 1994.

15. Feder HM Jr, Gerber M, and Krause PJ. Early Lyme disease: a
flu-like illness without erythema migrans. Pediatrics 91:456-9, 1993.

16. Fister RD, Weymouth LA, McLaughlin JC, et al. Comparative
evaluation of three products for the detection of Borrelia burgdorferi
antibody in human serum. J Clin Microbiol 37:2834-7, 1989.

17. Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect
the Lyme Disease spirochete, Borrelia burgdorferi, from ceftriaxone
in vitro. J Infect Dis166:440-4, 1992.

18. Gross DM, Forsthuber T, Tary-Lehman M, et al. Identification of
LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis.
Science 281:703-6, 1998.

19. Klempner MS, Hu LT, Evans J, et al. Two controlled trials of
antibiotic treatment in patients with persistent symptoms and a
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20. Levin JM, Nelson JA, Segretti J, et al. In vitro susceptibilities
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21. Luft BJ, Dattwyler RJ, Johnson RC, et al. Azithromycin compared
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24. Pachner AR, Delaney E, O'Neill T, and Major E. Inoculation of nonhuman primates with the N40 strain of Borrelia burgdorferi leads
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Neurology 45:165-72, 1995.

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nervous system. J Infect Dis 178:722-32, 1998.

27. Seltzer EG, Gerber MA, Carter ML, et al. Long-term outcomes of
persons with Lyme disease. JAMA 283:609-616, 2000.

28. Shadick NA, Phillips CB, Logigian EL, et al. The long-term
clinical outcomes of Lyme Disease. Ann Intern Med 121:560-7, 1994.

29. Steere AC, Malawista SE, Hardin JA, et al. Erythema chronicum
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30. Steere AC. Lyme Disease. NEJM 345:115-25, 2001.

31. Straubinger RK. PCR-based quantification of Borrelia burgdorferi
organisms in canine tissues over a 500-day postinfection period.
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32. Wormser G, Nadelman RB, Dattwyler RJ, et al. Practice guidelines
for the treatment of Lyme disease. Clin Infect Dis 31(S1):S1-S14, 2001.

33. Ziska MH, Donta ST, and Demarest FC. Physician preferences in
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Sam T. Donta, M.D.
Professor of Medicine,

Divisions of Infectious Disease and BioMolecular Medicine Director, Lyme Disease Unit Boston University Medical Center, Boston, Massachusetts

Corresponding author for proof and reprints:

Sam T Donta M.D.

Boston Medical Center

650 Albany Street, 8th floor

Boston MA 02118

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I think this artical is very good
Posted by: cazoome Jun 23, 2009	Was this review helpful? 280
this artical is very good
Reply

Late & Chronic Lyme Disease
Posted by: Graham Mustow Mar 16, 2010	190
Wow, finally I have some answers, I had Lymes Disease in 1992. My symptoms come and go even now. Excellent, Thank You.

Lyme
Posted by: racjaa Jul 23, 2009	Was this review helpful? 238
excellant article, Lyme disease does not always go away after initial treatment. Many doctors will not even treat patients after initial antibiotics course. It is great to read that studies support increased antibiotic treatment for those who have long term Lyme symptoms
Reply

Best report available
Posted by: ddrsi Apr 1, 2010	Was this review helpful? 203
This article could not be any more informative!! Long term symptoms, are right on, and the treatment discussion leaves the reader confident with the knowledge of the options. Anyone with long term symptons, knows how hard it is to describe their experiences to physicians. Thank you for writing this article
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This article is an advocate for Chronic Lyme Patients
Posted by: rosterspot Apr 26, 2010	Was this review helpful? 208
Having been recently diagnosed after a year of Lyme symptoms, I hope more patients and doctors find this information. The pathology of Lyme disease is very misunderstood by everyone but this article does a great job of explaining it.
Reply

Really?
Posted by: Classique Jul 11, 2010	Was this review helpful? 181
My symptoms of Lyme Disease lasted over 18 months before I was diagnosed. Attributing the aches and pains and other problems with getting older. I was diagnosed and was put on a course of tetracycline for 30 days and it relieved my symptoms in the first week. Now though, I have reoccurring problems that I attribute to the Lymes. But going back to a health professional is something that I dread for the very reasons in the article. Will it be the Lyme's Disease? If after tests show a negative to it where does one go from there. Hopefully the medical experts will come up with a more postitive test for this reoccurring problem.
Reply

Lyme Disease and RA
Posted by: Ann-RA Sep 25, 2010	Was this review helpful? 170
Very informative and helpful. Was told that my Rheumatoid Arthritis may have been caused by Lyme Disease. Glad to find some information relating to that poosibility and will talk to my rheumatologist about testing me. But will dr agree that there may be a link? Looks like the Western blot assay may be the test to have done? Is there more info about the link between the two diseases?
Reply

Fibromyalgia or Post-Lyme Disease?
Posted by: USAMaid Oct 16, 2010	Was this review helpful? 188
Since 1995 I have been treated for fibromyalgia. None of the drugs worked, so I discontinued all four years ago. Coincidentally I had a diverticulitis flare-up and was kept overnight in the ER and put on IV with broad-based antibiotic Unisyn. Amazingly, for two weeks after that IV, I had no pain anywhere in my body. I began to doubt the fibromyalgia at that point. Since pain responded to antibiotics, I began to think Lyme Disease. I am an avid gardener and live adjacent to a wetlands and nature preserve, so deer ticks would certainly be present. A year or so ago, my doctor told me he saw faint Lyme bands in my bloodwork, so what we have here is a missed Lyme diagnosis. I have pain all over my body, cannot sit for more than half an hour without barely being able to walk upon arising, have tinnitus in my left ear, have crawling sensations across my neck and shoulders and have all-over itching at night. I actually keep a natural bristle brush by my bedside and scratch my body before going to bed at night. I own a retail store, so am on my feet six days a week. I've heard about Dr. Donta and would very much like to have him see me. After Christmas I will have more free time and will definitely make an appointment. The article was a treasure trove of information on every level. There is no doubt he knows his subject matter inside and out. I would give anything to be able to power walk again. I can barely walk without pain in my hips and the outsides of my thighs. This article gave me hope for the first time in 15 years.
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Extremely informative
Posted by: Mariette Nov 5, 2010	Was this review helpful? 161
Just fabulous. I have been diagnosed with chronic lyme disease as of October 27, 2010 It is a long story which I have started to write. So many years of miss diagnosis,such as fybromyalgia, heart arithmya with no cause, depression because of my extreme fatigue, not counting the series of specialist that came up with nothing. Only one of them validated that something was terribly wrong but just could not diagnose it. How? you may ask did it get diagnosed... by a passing comment of one of my lifelong girl friend. Asked for the test and voila... years later I have hope for my future. This article is the best so far. I have taken notes and will refer to it in my writing. I am working on establishing a blog in order to perhaps help others hope in this voyage that can be lonesome. Humm! you may want to look for words from a teacher such as ¨Sick of being sick¨.
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I was looking for a gift for my friend suffering
Posted by: Matthew_McCabe Jan 11, 2012	Was this review helpful? 118
I was looking for a gift for my friend suffering from CFS, and somehow stumbled upon this page with such an extensive collection of

Lyme, Tinnitus, Atlas - this is very interesting

Helping Ourselves
Diane J. Marie, patient advocate

Tinnitus--Ringing Between The Ears

Before I figured-out that I had chronic Lyme disease, I worked at bettering my tinnitus. I found that often tinnitus is metabolic mayhem, a result of the mess of disease, hormone levels too high or too low and hundreds of cellular co-factors in flux, often due to multiple conditions. Five factors improved exasperating noise between my ears.

1.] I learned about getting optimized treatment for my hypothyroidism. Being low thyroid means the thyroid gland in the neck isn't making enough thyroid hormone. The pituitary in our brain screams that our body needs more and that screaming can be measured with a TSH test.

I take both Levoxyl (thyroid hormone T4) and also Armour Thyroid (containing both T3 and T4) compounded for time-release by a compounding pharmacist. T4 is stored in our body; T3 acts quickly and needs to be made available slowly, by time-release.

With Armour, the Sun rises in my head! Though it’s a mighty foggy Lyme Sun. T3, in the form of Armour (or Cytomel) does wonders for the workings of my brain, trying to recover from Lyme. Most doctors boo-hoo this, but it’s like Lyme—when treatment helps you, you go with it!

Thyroid hormone affects every cell in our body, from the top of our head clear down to our big right toe. T4 locks-in to cells, converting to T3--little logs for our metabolic fire. Can that process be interrupted by Lyme cell damage? Lyme lives in and damages many of our cells. Can cells with enough T4 locking in for conversion to T3 help us fight Lyme better?

Too much, and we’re hyperthyroid: we’re nervous, jittery, our heart thumps, blood pressure goes up, headaches increase and more. Each low thyroid patient needs to find brands and dosages that work best, for them. Problems with T3 working at the cellular level are frustrating, because it’s off the scope of conventional medicine, which denies its existence.

Most doctors don’t know we have cells. Knowing this is crucial for Lyme recovery because if we lack T3, or it’s not bioavailable, our immune system won’t function well. We Lyme folks need our immune system to function well in order to work in partnership with antibiotics.

Disturbing Tinnitus is also a symptom of hypothyroidism. Infections are another symptom—and boy do we have a Lyme infection/coinfections!

Signs and symptoms are many: fatigue / exhaustion, feeling cold when others do not (more apparent in northerly climates,) digestive problems and constipation are beginning troubles, though they may be masked by Lyme or meds.

After that: foggy head, sleep apnea, insomnia, tinnitus, infections, carpel tunnel, dry hair, hair loss, weight gain, high cholesterol and lipids, high or low blood pressure, bradycardia (slow heart rate,) depression and much more.

For enormous help, see Living Well With Hypothyroidism, 2005 Edition, by Mary J. Shomon. Her website http://www.thyroid-info.com offers tremendous search help and ties into her about.com site. At her “Top Docs” page you may find a local doctor to help you. Maybe your insurance will pay for that doc.

Having any disease when we have hypothyroidism, and getting it treated and then optimized makes everything work better! I’ve also found that having Lyme disease and hypothyroidism means continually evolving thyroid care, such as med dosage.

In the general population, hypothyroidism is so common it’s pathetic—epidemic. Thyroid issues are many. Along with other body-wide help, optimizing hypothyroidism lessened my tinnitus!

2.] Still, my head rang between my ears. I’d lie in bed appalled at the noise, unable to pass into sleep night after night ‘til the early hours, making more stress, frustration and pain.

I’d had insomnia for over 4 decades.

Fatigued to Fantastic Revitalizing Sleep Formula by Enzymatic Therapy helped me fall asleep and put me into 4th stage healing sleep, the sleep to help heal anything. It’s a beautiful formula on the face of the Earth, balancing valerian and passionflower with other ingredients. The way to know if you’ve found the right dose is when you feel better in the morning. Deep sleep made my tinnitus better the following night, night after night.

When herxheimer pain prevents me from falling asleep I also use a small dose (1 mL) of Source Naturals Melatonin, liquid or spray (capsules don’t work.) Be sparing with melatonin doses. It’s a powerful hormone.

3.] I’d been to a very good physical therapist with love in her heart, who helped me raise my right shoulder blade with exercise. I became a little more balanced. She used ultrasound (heat) at the back of my neck, huge heating pads, craniosacral therapy and neck traction. Muscle pain and range of motion improved a bit.

I told her my worst symptom was constant, severe head pain. She thought I had myofascial trouble. That wasn’t a therapy they offered, yet she arranged for a fellow therapist, to try. This therapist, also with love in her heart, performed a maneuver on me that lessened my head pain! After "things settled in my head" my tinntus lessened a bit.

I had a painful partly-locked shoulder caused by trigger points—knots of metabolic waste in my muscle fascia causing referred pain (on top of Lyme pain in my muscles, though I didn’t know it.)

The Trigger Point Therapy Workbook, by Claire and Amber Davies, is eloquent and precise--the best book to explain what myfascial trigger points mean and what needs to be done. I stopped counting at 62 trigger points everywhere. When I studied the book carefully, I got rid of some trigger points, some pain and gained a bit better range of motion.

However, it was apparent I needed the best therapist in town. Armed with knowledge from studying the book, I knew what questions to ask as I interviewed crooks around town (though the Davies’ method can differ.)

Four months later, I found him, with love in his heart and expertise! After several sessions he’d unlocked my shoulder more, lessened my severe, constant head pain—thank you very much--and improved my range of motion. He'd made ringing between my ears a little better. Hurray! Still, we knew something else was very wrong.

I had yet to arrive at my Eureka! moment of discovery, that I had chronic Lyme.

Please note: Many with severe hypothyroidism can develop trigger points in unexpected places. When meds don’t include T3, then when you get myofascial therapy, trigger points will come right back.

Many with muscle pain have, or also have, trigger points, when they don’t have hypothyroidism--even taking multiple painkillers, not knowing it’s a myofascial problem.

If you think you might have trigger points—don't stretch. For example, don't reach up to a microwave, or back into a car trunk, because like dominoes, trigger points then get worse. Stretching exercise that increases pain may be trigger point trouble. Be picky about choosing your therapist.

Trigger points differ from “tender points” of fibromyalgia. A really good myofascial therapist can also help with fibromyalgia. When all else fails, some people get regular hypodermic injections behind their ear for tinnitus or headaches. See the Davies’ book for a discussion.

4.] My myofascial therapist suggested I see an atlas orthogonal chiropractor, as my right foot was one full inch shorter than my left! I thought, “That can't be good.”

I was very much helped by a special doctor with love in her heart. She uses a relatively new therapy, a high-tech one, which I think we’re all going to hear more about. She uses a percussion wave to make gentle, major chiropractic adjustments of C1 and C2.

For a year-and-a-half I’d been shuffling along with my head hanging out to the right and down (and dragging along my right-side severe muscle pain.) It hurt, was disgusting and frustrating. My head was out of alignment with my spine. I just knew my head wasn’t screwed on right! One of the causes is muscle atrophy. In my case, the muscles couldn’t hold the head in place. Lyme certainly can cause muscle atrophy.

Lie flat on a bed, shoes on or off and have someone check: if a leg is shorter even by a little--see an atlas orthogonal therapist, for proper assessment. For the list of doctors see http://www.atlasorthogonality.com.

Regular chiropractors may help you--some may make it worse. Every time you have a conventional chiropractic adjustment, you’re joints are damaged a bit.

Lying on a table, my special chiropractor moved my head a particular way according to what x-rays showed and did the quick percussion wave treatment, realigning my head. She helped me sit up. I put two "even" feet to the floor--and was stunned. Silence ... Silence! I'd forgotten the sound of silence.
I went back and forth between my myofascial therapist who also “worked” my atrophied muscles and the atlas orthogonist, who sometimes needed to realign my head, followed by lying on her roller table to help adjust my entire spine. It’s feels like being on a ship at sea, rolling with big waves.

Now I walk upright, balanced. This helped everything. Untreated, this condition can cause pain, stress, frustration, digestive problems, a weakened immune system, and more.

Your local atlas orthogonal chiropractor may provide a dandy referral to a good myofascial therapist.

All of these methods brought true healing, before Lyme treatment. Books I’ve mentioned may be found at public libraries.

5.] Tinnitus is a symptom of Lyme disease. My hearing also wavered for a year. A year and seven months after the BAM of Bell’s palsy caused by Lyme, I had my Eureka! moment, realizing I had chronic Lyme. Now, after a year of prolonged, high dose, multiple Lyme antibiotics (and more to come) I can't remember the last time I had ringing between my ears. Thank goodness!

On the Internet are many references to tinnitus, most being metabolic mayhem always present in disease, as is inflammation. Whether you’ve been able to win your fight for getting prolonged antibiotics, or not--so far--I encourage you to tend to also optimizing conditions you have as a result of Lyme, or had before you got Lyme.

For example, is your GI tract humming or hurting? What can be done to better it? Perhaps a gastroenterologist could help. Surf the Internet and check library and bookstore shelves.

Tinnitus can be an accumulation of causes. You could discover other trouble you never had a name for. Caring for those conditions optimally improves Lyme recovery.

Here are other causes of tinnitus: wax/dirt build up in the ear canal (use off-the-shelf liquid remedies,) ear or sinus infections, allergic reactions, specific foods rich in salicylates, aspartame, too much caffeine, noise exposure, noise-induced hearing loss, meds interfering with other meds (check the pharmacy information,) vascular anomalies (a pulsing sound; pulsatile tinnitus, pulsatile tinnitus with Lyme) high blood cholesterol, intracranial hypertension, head injuries, dental procedures, mercury fillings, lead poisoning, TMJ (temporo-mandibular joint.)

Some drugs can cause it: Aleve, Ibuprofen, aspirin, antidepressants, quinine, oral contraceptives, vancomycin, erythromycin (this begs the question: clarithromycin?)

Also, B12 deficiency (relieved with shots of B12,) any neurological infections, potentially any metabolic disorders, autoimmune diseases, chemotherapy and more. Hyperacusis information may help.

Also, structural defects of the inner ear or from the ear to the brain may cause noise. Tinnitus can accompany ostosclerosis, Meniere’s syndrome, auditory nerve lesions and growths/tumors.

Tinnitus can accompany Lyme hearing loss, Lyme sound sensitivity and Lyme stress (for instance, being sensitive to the noise of hearing more than one conversation at a time and having difficulty with Lyme multitasking to understand what’s being said--is stressful.)

Bell’s palsy, Lyme encephalopathy and fibromyalgia can cause tinnitus. Your awareness of your tinnitus can be stress-related.

Having a herxheimer can make tinnitus worse or exacerbate it.

Many of us have to fight for Lyme treatment, housing and more, causing more stress. When no doctor cared, I did what I could to care for myself and to search for other causes. That brought less stress because I was helping myself.

Reducing stress helps in a big way. For example, I drew a line in the sand by telling everybody what’s going on inside your head, in no uncertain terms and how they can help. Taking nice Lyme naps helped.

For children see, http://www.pediatrics.aappublications.o ... /108/2/477, “Optic Neuropathy in children with Lyme disease.”

Stay on the path of finding your own answers, no matter how hideous our disease is.

All discussions in this column are for information only and should not be interpreted as medical or other professional advice. Each person is unique and all readers should carefully consider their own personal situation before pursuing any course of action.

Daise: Posts: 140; Joined: Thu 1 Nov 2007 4:47

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Breakthrough Science for sufferers of Miniere's Disease, tinnitus, Vertigo and Dizziness by Dr. Donald Leibel

Breakthrough

Science For
Sufferers of Meniere’s Disease,
Tinnitus, Vertigo and Dizziness

     By Dr. Donald Liebell

    There’s new hope for Meniere’s Disease, a condition which affects the inner ear—resulting in symptoms such as: ringing in the ears (tinnitus), dizziness, vertigo, balance trouble, ear pressure, and hearing loss (usually in one ear): Meniere’s disease has a vast history, with few substantial solutions provided since it was first reported by Dr. Prosper Meniere in 1861. It may begin with just one of the above symptoms and progress gradually with others. No exact cause of Meniere’s disease has been established or agreed upon. It has been theorized that it’s related to an increase in pressure and volume of a fluid that exists outside the cells, called endolymph.
    Other factors that have been suggested include aspirin use, alcohol and smoking, as well as viral infection. There is no specific medical test for Meniere’s disease. The diagnosis is typically made as a result of other conditions and causes being ruled out.

    Fortunately, a handful of doctors around the world have been successful in treating patients afflicted with this condition through specialized, non-surgical treatment. Our "secret"... Examination and Treatment of the Upper Neck (Not Just the Ear). For more than 50 years, doctors who specialize in the upper neck (cervical spine) have found it most certainly can be involved in Meniere’s. More importantly, through precise structural correction of upper neck imbalances, considerable success with patients suffering Meniere’s disease has been achieved. Sadly, this aspect of diagnosis for this condition has been largely ignored by the American “mainstream” health care system.   However, a recent medical research paper in the International Tiniitus Journal (2007, Vol. 13, No. 2. pp. 132-137) has revealed some critical support to our viewpoint:

    ”Unquestionably, the upper cervical spine [top of the neck], the Temporomandibular joints [TMJ or jaw joint], the Eustachian tube, and the autonomic nervous system can contribute to the global symptom complex of Meniere’s disease… Clinical practice also shows that treating disorders of the upper cervical spine and temporomandibular joints can lessen Ménière’s disease symptoms, suggesting a relationship.”

       - Burkhard Franz and Colin Anderson, Department of Anatomy and Cell Biology, University of Melbourne, and Tinnitus Research and Balance Clinic, Victoria, Australia - The Potential Role of Joint Injury and Eustachian Tube Dysfunction in the Genesis of Secondary Ménière’s Disease

    The researchers indicated that the neck (and the TMJ) could be related to Meniere’s disease through nerve and/or blood vessel connections… and that expert treatment of the upper neck has been successful in treating patients with Meniere’s symptoms.

    CRANIO, The Journal of Craniomandibular Practice also published research revealing that the majority of patients in their Meniere’s study had neck problems:

“Symptoms of cervical spine disorders, such as head and neck/shoulder pain, were all significantly more frequent in the patient group than in the control group. Most of the patients (75%) reported a strong association between head neck movements in the atlanto-occipital and atlanto-axial joints [top of the neck] and triggered attacks of vertigo… The study shows a much higher prevalence of signs and symptoms of cervical spine disorders in patients diagnosed with Meniere's disease compared with control subjects from the general population.

        - Cranio. 1998 Jul;16(3):194-202. Cervical signs and symptoms in patients with Meniere's disease: a controlled study. Bjorne A, Berven A, Agerberg G. Clinic of Periodontology, Lasarettet, Ystad, Sweden.

    In 2008, the Journal of Vertebral Subluxation Research published a stunning study of ten patients who all experienced significant improvement in their Meniere’s condition following non-surgical upper cervical corrective care. In fact most had a complete recovery. All patients had their neck examined and x-rayed, revealing misalignment of the upper two bones (atlas and axis, or C1-C2 vertebrae). The misalignments were causing interference to normal nervous system function.

    Even more stunning were the results of a research study, published in the same journal with 60 cases of chronic vertigo. 100% of cases either improved or completely reversed their condition. 56 of the patients recalled a history of trauma, but all had a neck imbalance, which was treated by precision upper cervical correction. All participants had been diagnosed by their physicians with various forms of vertigo, including Meniere’s, positional vertigo and migraine associated vertigo.

    J. Vertebral Subluxation Res. Nov. 8, 2006   Sixty Patients With Chronic Vertigo Undergoing Upper Cervical Chiropractic Care to Correct Vertebral Subluxation: A Retrospective Analysis. Dr. Erin Elster

    As supportive evidence piles up, it’s clear that anybody who suffers from Meniere’s or any form of dizziness, vertigo or migraines should be examined by an upper cervical specialist. In my practice I successfully utilize Bio-Energetic Medicine, in addition to the Atlas Orthogonal procedure.
Click HERE to Learn More About the Upper Neck (Atlas Vertebra)
Click HERE to Learn About Upper Neck (Atlas Orthogonal) Treatment
Click HERE to Learn About Cold Laser Therapy
Click HERE to Learn About Auricular Therapy (Needle-Free Ear Acupuncture)



NeckSecret@gmail.com        Ask Me Questions

Although I receive lots of questions daily, I do respond to all of them (in the order received), usually within 48 hours. Please understand that my answers are for general information only. I cannot provide specific medical advice via email; that can only be provided through proper evaluation in my office.  For appointments, please call my office.

   Your email address or other information is confidential; I will never share it with anyone, nor will it be used for any form of solicitation.   I look forward to your questions!

                                         - Dr. Donald Liebell

Dr. Flanagan - The Upright Doctor's Book: The Downside to Upright Posture

The Upright Doctor's Book: The Downside of Upright Posture

The Upright Doctor's book is a true story of more than twenty years of investigative research that begins in the Department of Anthropology at the American Museum of Natural History in New York, where Dr. Michael Flanagan tells how a chance investigation started him on his journey. Dr. Flanagan's research into the fluid mechanics of the brain - including the unique design of the sutures and base of the human skull - led to the discovery of a clear and unmistakable link between upright posture of Homo sapiens and neurodegenerative diseases seen in aging adults. This "link" is the cervical spine - especially the upper cervical spine and base of the skull - which contains key circulatory routes for blood and cerebrospinal fluid flow entering and exiting the brain.
In a style that is accessible to the lay reader, as well as the scientist, Flanagan explains why his discovery offers important new information and hope for the many millions of patients, family members, physicians, and scientists who are devoted to understanding the causes of - and finding cures for - neurodegenerative diseases of the brain and spinal cord.

A book purchased through this website entitles you to a complimentary consultation regarding your case or a discussion with Dr. Flanagan on site topics. You will receive the email address once your purchase been made. Scroll down for details and to make a purchase of Upright Doctor's Book.

Here's What Others Have to Say About Upright Doctor's Book

Comments
"You did an outstanding job. Like you, we believe that venous drainage plays an important role in the regulation of intracranial pressure."
Dr. Noam Alperin, Department of Radiology, University of Miami, research scientist with special interests in upright MRI, Chiari malformations, normal pressure hydrocephalus and idiopathic intracranial hypertension.

"Your book is a grand achievement, discussing complex concepts in a way an average person can understand - all around a story that keeps you reading until the end." Dr. Charles Woodfield of the NUCCA National Upper Cervical Research Foundation.

"… nicely written and makes easy reading of very complex material ... I get a sense that I am reading something very important - work that might be an eye opener to how we treat these diseases of the brain ... I don't read much these days - but I will read and re-read this several times ... a book I truly believe is about to make a contribution in a very big way." Martin Gomberg M.A. (physical anthropology) V.P. A&E TV network.

"I am really pleased with your book. The information in the book has had a great impact on my approach when working with patients suffering from multiple sclerosis..."Franz Bossenbroek, craniosacral therapist

"...interesting and very informative...greatly useful for my practice...an extremely important book for the NUCCA doctor to read and study..." Steven N MacDonald D.C. - board certified NUCCA doctor, Pacific Grove, CA.

“I found it very interesting and I am sure it will promote further discussion and further investigation ... Congratulations on this marvelous contribution to science and clinical applications.” Ted Carrick, DC, PhD., chiropractic neurologist

"Great book...I love the storytelling and the way you make a complex subject easy to understand." David Shores D.C.

" ... great book ... " In 2009, JAMA published a review on “The Chiari Conundrum”, that focused … on the possible interrelationships between the structural and functional anatomy depicted by Upright MRI of the cervico-occipital junction … I had been collecting a series of MRI findings on patients with the seemingly unrelated , varied and disparate, neurological maladies of migraine headaches, NPH, MS, Parkinson’s and Alzheimer disease, when a single thread of connection became apparent; CSF flow disturbance … I did a cursory investigation of the literature and proposed “The unifying concept of CSF – Cerebellar Ectopia” … This initial “gathering” of my thoughts is obviously naive compared to your level of experience, originality, understanding and explanation of the theory …
... The articles on your website demonstrate clearly that you have the most complete understanding and explanation of this concept ...
David Harshfield M.D., M.S., radiologist - College of Integrative Medicine

Michael Flanagan's book "The Downside of Upright Posture," is the first text that provided me with a sound framework for why many patients with upper cervical subluxations and neurodegenerative disease respond well to upper cervical chiropractic care. I believe that the implications for his work can affect the way our health care system manages difficult to treat diseases like traumatic brain injuries and chronic neurological disorders.
This book should be required reading in all chiropractic colleges.
Jonathan Chung, D.C. NUCCA Chiropractor and Member of the Upper Cervical Research Foundation

Dr. Flanagan's book is the the most important piece of literature, written to date, validating Upper Cervical Chiropractic's success with certain conditions. His explanation of the fluid dynamics of the brain helps bring into clear focus B.J Palmer's Brain Congestion theory. It is a must read for all chiropractors.
John Hilpisch, D.C Past President of the Blair Upper Cervical Society

Outstanding read! Compelling for considering optimal brain health for all of us. I bought 6 copies and had to order more. We plan to include Dr Flanagan's research as part of our upper cervical Diplomate program.
Julie Mayer Hunt DC DICCP FICA ( hon) Orthospinology president , Upper Cervical Council curriculum administrator and ICA's 2014 chiropractor of the year

Book Reviews
Grounding breaking research, incredible information, December 3, 2010.
D. Driscol, O.D.
This is an amazing book, written by a Doctor who was 20 years ahead of his time on the subject of neurodegenerative conditions--including multiple sclerosis, Parkinson's and Alzheimer's disease.
Dr. Flanagan is one of those rare individuals with the intellectural curiosity often lacking in the overworked, rushed medical field. He studied the extremely complicated dynamics of CSF flow and how, when not optimal, it could lead to many brain disorders for which causes and effective treatments remain elusive. The medical field is just now embracing his ideas, and as both a doctor and a patient, I am thrilled to see it (for example, please see how CCSVI is becoming widely utilized--this is the tip of the iceberg). Personally, I must recommend this book for any patient with Ehlers Danlos, who suffers with autonomic dysfunction also.
Dr. Flanagan is changing lives. He changed mine. I can't recommend this book highly enough.

Brilliant thesis with hope for many with neurodegenerative diseases, February 2, 2011.
Barbara E., R.N.
An unusually inquisitive mind and many years studying skulls in the Museum of Natural History in New York have culminated in a book that may help to change the way we think about multiple sclerosis, Alzheimer's and Parkinson's diseases. Dr. Michael Flanagan has laid out a logical and comprehensible thesis that demonstrates how inherited, acquired and degenerative disorders of the spine, especially the upper cervical spine and base of the skull may predispose humans to blockage of the venous drainage system of the brain resulting in chronic edema, ischemia and normal pressure hydrocephalus (NPH).
...The conditions in turn intiate a cascade of neurodegenerative processes, such as the glutamate cascade and subsequent diseases such as multiple sclerosis, Alzheimer's and Parkinson's. This is a life-changing book for anyone seeking answers to some neurodegenerative processes. I give it a full 5-star rating for its contribution to a developing body of knowledge. ...It has been an enormous help to me.

What a fantastic book! Peter S., computer programer, multiple sclerosis and ccsvi patient.

Book Review by Daniel Sosnoski, editor-in-chief, Chiropractic Economics magazine
Among the many things we take for granted, our ability to walk and run upright ranks foremost. Unlike every other mammal, humans alone spend their lives balancing on two legs. This gives us an advantage over other animals in several respects, but it also comes at a heavy cost.
The price we pay for our unique style of gait is the subject of Dr. Michael Flanagan's text. "The Downside of Upright Posture". Writing almost in the style of a mystery author, Flanagan leads the reader along the story of his own questioning and research, and shows how he reached his startling conclusions - that the structure of the cervical spine and base of the skull that allow us to stand and walk also facilitate the onset of neurodegenerative diseases like Alzheimer's, Parkinson's and multiple sclerosis.
...Any reader with an interest in the diagnosis and treatment of neurodegenerative disorders should find ample material of interest in the book's 211 pages, which include 20 full-color plates that clarify the discussions of physiology and descriptions of human anatomy. The book culminates in a dramatic turn of events in which Flanagan needs to employ the hard-won knowledge he's gained.
...The text should be of interest to the chiropractor, the student of biology and neurological medicine, and general readers with curiosity about physiology and human development.

Canadian Chiropractor magazine
July 28, 2010
...In this book, Dr. Flanagan makes a compelling case for an anatomical cause of these three neurodegenerative diseases. He tells the story of how he stumbled upon an apparent connection, due to upright posture, between the design of the human skull, spine and circulatory system of the brain and a predisposition to neurodegenerative conditions. Over the course of two decades, he investigated this connection until it became clear that there was an unmistakable link between upright posture and the neurodegenerative diseases seen in aging adults.
Having already published multiple articles on his findings throughout his career, Dr. Flanagan takes a more comprehensive approach in The Downside of Upright Posture...

I found your website while trying to do searches on Ehlers-Danlos, and was blown away. The Downside of Upright Posture is, in my humble layman's opinion, brilliant, as are you. Having studied anthropology back in college, I really admire the thorough comparative research you put into your ideas on upright posture, and the ways that you narrated your tales (it's not often that we get a great sweeping look at how scientists make their insights and wrestle with their ideas).