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Editorial
on MS and Lyme
By,
Tom Grier
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Hello,
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.
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.
Ticks carry more than just
Lyme disease! Including:
0 -Ehrlichia;
o -Bartonella;
0 -Babesia;
o -Q- Fever;
0 -Tularemia;
o -Tick-borne Encephalitis;
0 -Mycoplasma;
o -Relapsing Fever;
0 -Rocky Mountain Spotted Fever and others.
Never WAIT and SEE about a tick bite, please! Quickly and properly treated infections are less likely to progress to later stage or chronic disease.
Sometimes tick bites are
mistaken for spider bites!
Some diseases may be spread by animal bites or scratches and from mosquitoes, fleas or lice.
There is still so much to learn about Lyme disease and related infections.
Sometimes Lyme disease and related infectious diseases are undiagnosed for years, even decades!
Watch closely for symptoms after tick bites. Some never see a tick or a bulls-eye rash.
Don't ignore tick-borne disease symptoms!
If you feel sick, ask a doctor!
SYMPTOMS may include:
0 -Tick bites;
o -Fever; Flu symptoms;
0 -All kinds of Rashes;
o -Muscle; Joint; Neck Pain;
0 -Body Aches; Weakness
o -Light /Sound Sensitivity;
0 -Bells Palsy; Nerve pain;
o -Insomnia; Poor memory
0 -Headaches; Numbness;
o -Mood disorders; Confusion;
0 -Extreme Fatigue; Exhaustion
Never let tick-borne diseases progress!
Lyme and associated diseases are often MISTAKEN FOR OTHER ILLNESSES, Including:
0 -Chronic Fatigue;
o -Fibromyalgia;
0 -Hypochondria;
o -Multiple Sclerosis;
0 -Lupus;
o -Rheumatoid Arthritis;
0 -Lou Gehrig's disease (ALS);
o -Alzheimer's and
0 -Parkinson's disease
******************
Don't be fooled about ticks and their diseases.
******************
Directly affecting humankind, worldwide:
W H A T H A P P E N E D
when the U.S. Senate addressed the Centers for Disease Control regarding Lyme disease?
Consult a good doctor!
Visit ILADS, LDF, LymeNet or LDA to find a specialist in your location.
Protect your children and your family.
Learn about ticks and their many diseases.
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- TICKS KNOW NO BOUNDARIES -
Tick-borne diseases are spreading rapidly in many countries across the world -not only in Scandinavia, UK, Hungary, Scotland, USA, France, Germany, China, and Australia.
- ONE BIG PROBLEM WITH TESTS -
There is NO 100% accurate Lyme disease test currently available to detect infection or cure. more...
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- TICKS KNOW NO BOUNDARIES -
Tick-borne diseases are spreading rapidly in many countries across the world -not only in Scandinavia, UK, Hungary, Scotland, USA, France, Germany, China, and Australia.
- ONE BIG PROBLEM WITH TESTS -
There is NO 100% accurate Lyme disease test currently available to detect infection or cure. more...
- WHERE TICKS LIVE -
Ticks can be found in and around leaf litter; grass; logs; animal fur; bird feeders; and deer, mice, squirrel, and other small animal habitats.
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Ticks travel on mice!
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Never let tick-borne
infections progress !
Tick-borne diseases can
affect any body part,
organ, and any system
of the body.
Lyme disease and Syphilis are both caused by a type of bacteria called a spirochete.
Tick-borne diseases can KILL!
Ticks travel on mice!
ALWAYS Get Ticks Tested!
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