Editorial by Thomas M. Grier, M.S. ©
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.
These 3 patients received two months of oral antibiotics and responded more favortably than any others in the treatment group of 26 with eventualy 50 % or better recoveries including in two the the three a return to working, an increase in activity, less depression, a better quality of life and the ability to handle their own affairs with less family help.
We also had five patients with partial recoveries that never seroconverted leading us to believe antibiotics were useful in some M.S. patients even when Lyme could not be diagnosed by serologies or urine antigen. These partial recoveries in two months were more subjective as patients responded by questionaire rather than objective measurements of things like walking ability, stamina, cognitive testing etc.
Finally we had a treatment failure patient who after three months of antibiotics had no noticeable response to therapy either positive or negative.
Like all the patients they were phoned one year later for the one year follow-up of the study. To our complete surprise Judy had returned to working full time as a rural mail deliverer in Northern Minnesota after several years of total disability. She herself attributed this to staying on amoxicillin 1000 mg TID voluntarily for an entire year after the study had officially ended because in her words: “It was so cheap and I had no side effects, I just thought why not? What have I got to lose?”
Because of Judy, we had to consider that in 1995-96 our antibiotic treatment protocols of eight weeks and a follow-up of another four weeks with Lyme testing was insufficient to make a true assessment of diagnosis or overall potential patient improvement attainable by antibiotics. *( The L.E.A.M.S. study was partially funded by Critical Care America Home Health Care who had nothing to do with study design, protocols, treatment, or interpretation. Their nursing staff did all the patient evaluations, questionnaires and assessments. All patients either received oral doxycycline, Biaxin, or amoxicillin. All testing was done through IGENEX of Palo Alto and North American Labs)
Results 3 of 26 MS patients were shown to have Lyme disease and seroconverted between 4 and 8 weeks of treatment on IgM Western blot or about 11 % of our selected M.S. population in a Lyme endemic area (Pine County, St. Louis County, Aitken County, and Cass County Minnesota) had true Lyme disease and most probably not M.S.
An additional 5 of the 26 patients had partial favorable response to antibiotics at eight weeks with things like better stamina, better memory, increased labido, decreased joint and muscle pain, decreased heart palpitations etc. So it could be said in round figures that in this selected population of M.S. patients that had three or more major Lyme symptoms 10% had significant recoveries and another 20 % had partial improvement from an eight week course of antibiotics. This is very similar to the results that Dr Patricia Coyle MD PhD got in her study presented in an abstract at the SanFrancisco International Lyme Conference in 1998.
Abstract #D646 – P.K. Coyle, et al, Multiple Sclerosis vs. Lyme disease a diagnostic dilemma. Forty-seven patients were identified as possible MS patients. Many had brain lesions on their MRIs, consistent with MS 61%. CSF was consistant with MS in 46 % of the patients. The final breakdown of the 47 patients was: 21 had true MS, 15 had Lyme disease and not M.S., and 7 had findings consistant with both LD and MS. Thirteen patients of the 15 patients (27%) whose CSF findings were
consistent with LD responded to antibiotic therapy.
47 % or 22 of the 47 patients had CSF evidence of possible Lyme disease, but not everyone responded to antibiotic therapy despite evidence of Lyme involvement in the CSF.
The unpublished data from Dr, Coyle suggests that either two weeks of antibiotics was not sufficient to affect any significant change in MS symptoms in some patients with positive Lyme disease tests, or that some patients positive for Lyme remain symptomatic for MS despite treatment, or the LD tests did not detect true active infection in these non responsive patients. From our study I believe patients need to be treated much longer, more aggressively and assessed every six months for at least a year to determine the true effects of antibiotic therapy on MS symptoms.
As a result of my talk in Houghton MI, many M.S. patients sought out antibiotics either from their doctors or on their own.
As a result of several positive patient outcomes from these patients seeking out antibiotic therapy for M.S., I was informed that members of the support group wrote the M.S. society and asked them to be more supportive of better educating M.S. patients about the possibility of misdiagnosis of M.S. when patients may actually have neurological Lyme disease, and that the use of antibiotics in M.S. patients may be beneficial despite the lack of any positive Lyme test.
The result was that a few days later a representative contacted the group leader and tried to discourage any pursuit of a Lyme diagnosis. The reasons being that it distracted from the acceptance of M.S. and often required the use of experimental and potentially dangerous antibiotic regimens. The intent seemed to be to purposely discourage any direction that led to either a true cause of illness and or a successful treatment of a potentially and often debillitating illness.
M.S. is after all a chronic condition that is actually nothing more than a collection of symptoms and pathology that has no known etiology and may in fact have several initiators and causes.
My conclusion after 12 years of having dealt with M.S. and Lyme patients is that M.S. patients are willing to seek out more aggressive treatments than the medical community is willing to prescribe. I feel that the issue here is equal parts medical-legal liability issues, and a lack of understanding the microbiology by physicians of the Borrelia family of bacteria that causes Relapsing Fever and Lyme Disease.
As for organizations that collect funds for the study of M.S., I think the original altruistic benevolent intentions of the founders of these groups has long since been abandoned for the pursuit of economic security. In other words I these organizations feel that it is not profitable to find a definitive cause and cure for M.S.
I happen to disagree with this policy of avoiding spirochete research because I think Lyme is just one element that causes an M.S.-like pathology. A recognized breakthrough such as Borrelia induced lesions could be used to generate a greater interest and generate more income if handled properly by the people in charge of public relations. Lyme could be a good working model to better understand the pathology of M.S. But it requires mor monies and an open mind of the medical researchers.
What has really happened is that both the medical community and the research organizations have boxed themselves in by medical liability issues, and a fear of losing research monies. Until the medical community feels it has the room and freedom to prescribe antibiotics for M.S. and that the M.S. society sees that Lyme is a potential working model for M.S. pathology, Lyme patients will be handicapped by both a lack of treatment and a lack of good research.
As for using Lyme tests to make the determination if an M.S. patient should receive antibiotics, I think there is no Lyme test short of an autopsy at this time or the near future that can detect spirochetes trapped in the central nervous system. The serology tests can detect Lyme-antibodies for a short window of opportunity, but a long established infections will for many reasons too complicated to address here will eventually result in a loss in antibody production. The infection will seek out and establish deep tissue immune sequestered sites. These infections will be chronic, longstanding and as difficult to treat as they are to detect, but that does not mean a patient should be denied the right to seek a course of therapy especially when the alternative is a lifetime of morbidity and disability.