Or...Search This Site
Home
Symptoms
Live Discussion
Diagnosis
Treatment
World-wide Support Finder
Library
Research
Lymelinks
Contact
Pets & Lyme
DONATIONS
Drug Info
Medical Dictionary
Board of Directors
Click on the graphic to vote for this site as a
Starting Point
Hot Site.
-
-
No Warranties or Representations
The data and information presented in this web site are presented in good faith and believed to be accurate. Any and all liability for the content or any omissions including any inaccuracies, errors, or misstatements in such data or information is expressly disclaimed. The web site is compiled for the sole purpose of informing community members of resources and information pertaining to Lyme Borreliosis Disease and its coinfections. The Canadian Lyme Disease Foundation, Directors and members are not liable for any direct or indirect damages or any damages whatsoever resulting from loss of use, data or profits, whether in an action of contract, negligence or other tortious action arising out of or in connection with the use or performance of information available from this website.
Consult a qualified Lyme ( Borreliosis ) Disease literate doctor for medical advice if Lyme Disease is suspect.
en français
For Physicians
Ticks
Coinfections
Prevention
Our Stories
Click Here to order our
free Lyme Disease Flyer
,
Here for our
free Lyme Disease Poster
..documents may be copied (to distribute)
but edit only for alignment.
Editorial on MS and Lyme
By, Tom Grier
In 1996 I gave a talk on neurological Lyme disease to the Upper Peninsula Michigan Health Department.
A large part of that talk was about quinolinic acid, a neuro-toxin that is produced in both Lyme patients and M.S. patients as a result of macrophage activation in the CNS. (Quinolinic Acid production and myelin destruction is a very specialized form of inflammation in the brain that does not involve lymphocytes as part of the inflammation process. Inflammation in the peripheral system is quite different and involves many more elements including lymphocytes, neutrophils, lymphokines, histamines, vasoactive amines, fibrinogen, bradykinin, prostaglandin synthesis, and other cascade events not often seen in the M.S. or Lyme patient’s brain.)
(In acute advanced neuro-Lyme and M.S. the levels of Quinolinic Acid are at similar levels in both patients and about 40x the normal levels. Quin-Acid is the cause of dementia in AIDS patients where levels can exceed 200-400 x normal and result in a comatose state.)
Attending the Michigan conference that I spoke at, was a Lyme patient who asked me to give a less technical talk to the Houghton/Hancock Lyme disease support group. Attending that informal meeting of Lyme patients was an M.S. patient from the local M.S. support group who then asked me to give a talk discussing in more detail the similarities of M.S. and Lyme disease. (At that time John arrived in a wheelchair legally blind: in six months he would be on crutches and in a year walking on his own with corrected vision improved to the point where he was driving again! This was all after six months of doxycycline.)
I was only too happy to talk with the M.S. patients outside their official meeting about Lyme because I had been misdiagnosed with probable M.S. from the Fall of 1989 to the Spring of 1992 when it was finally determined that I actually had become disabled by Lyme encephalitis.
I responded slowly to antibiotics and made about a 75 % recovery and now work close to 40 hours a week again but often I require crash and recover days for rest.
In my talk to the Houghton/Hancock M.S. patients, I covered many similarities to Lyme and the inadequacies of Lyme testing. (I recently wrote a 100 page booklet on Lyme testing soon to be printed.) Some interesting correlations as most M.S./ Lyme patients are well aware of, are such things as: M.S. occurs mostly in temperate climates in the same latitudes where the Ixodes ticks that carry Lyme disease thrive. M.S. often seems to be clustered in areas where Lyme is frequent, M.S. often manifests in young adults most active and exposed to tick infested areas. In every Lyme Support Group I ever attended there was always at least one patient or more who had been misdiagnosed with M.S.
But what many people were unaware of were the four Lyme disease animal-models that showed the reasons for Lyme disease’s tropism for the CNS and the mechanism of entry through the Blood Brain Barrier . I discussed these animal models, the mechanism of Borrelia burgdorferi initiating tissue-plasminogen to perforate the endothelial cells of the blood vessels which causes temporary leaks from the blood vessels into the brain of : bacteria, albumin, and immune cells into the CNS for up to 14 days post infected tick bite.(The immune system usually does not have an active presence in the brain and lymphocytes are kept out by the BBB.)
Then I presented over a dozen pre World-War II spirochete studies suggesting spirochetes as a primary cause of M.S. I displayed a slide of an isolated spirochete from an M.S. lesion in 1922 by Dr Gabriel Steiner doing work in Germany (We named Steiner Silver Stain after him.) This slide was then compared to another spirochete Steiner isolated from a human M.S. lesion in 1952. That was then compared to several spirochetes isolated from M.S. patients in the 1990s. The thing to note was that spirochetes which have no business being in the CNS were being isolated from M.S. lesions and not from healthy control subjects.
During this time I was the executive director of the on going L.E.A.M.S. study (The Lyme Endemic Area Multiple Sclerosis Study* ) In this study we enrolled 26 M.S. patients that were seronegative for Lyme disease but had a M.S. diagnosis but also had at least three major Lyme symptoms in three different systems such as: joint pain/arthritis, fibromyalgia, chronic fatigue, heart palpitations/ arrhythmias, fevers, sweats, A.C.A. or E.M. rash, and many more considerations. In short we found three patients that seroconverted and tested positive for Lyme disease on IgM Western Blots.
TOP