Well, the last few years she has had problems with the whole left side of her body going numb, not being able to think straight, fatigue, etc.

She is currently being treated by a Dr. for MS. She has had a few MRI's over the years that have shown white matter/lesions in her brain. She has developed more than she had from her first MRI.

She is now to the point where she has to give herself shots everyday. I'm very concerned for her - you can just see her getting worse.

I had a talk with her about the symptoms I've been having - headaches, neck pain, brain fog, Bell's Palsy, joint pains, fatigue - and these are the same symptoms she was having when they discovered Lyme disease was what was wrong with her 20 yrs. ago.

I don't know - but my gut feeling is that she is being treated for MS, when she really has Lyme. I think the Dr. took a long time before he said it was MS. The reason he finally came to that diagnosis, was because he said Lyme doesn't cause the white spots on the brain.

I don't know - but my gut feeling is that this is really lyme.

The problem is this - she thinks that it isn't Lyme now - because she was treated for it. And because of the white spots on her brain.

If anyone has had a similar experience, could you please post your story - so that I could give it to her?? I'm hoping to at least plant a seed, to let her know that people care, and that there are others out there who where misdiagnosed with MS too.

I really care about her - and I want her to get the care she needs. I may be wrong, but from what I've been reading here - it just seems to point to lyme, and right now, she doesn't seem to be getting any better.

2003...being treated for Lyme Disease. Had the herx after the first few days and still am having them.

Call it what you want. (IMO) Your sis has Lyme.How lucky for her to have had the diagnosis back then. Lots of people here didn't.

It's absolutely no surprise that one year of abx didn't "cure" it back then. Many here will tell you that the abx simply drove it into a dormant state to lay in wait.....

1) MS IS A CHRONIC CENTRAL NERVOUS SYSTEM INFECTION BY A SPIROCHETAL AGENT" by Vincent Marshall, DVM Published in "Medical Hypotheses" (1988) 25, 89-92.

Abstract: Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection somewhat similar to Lyme Disease [LD] or neurosyphilis in latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement. It does not have as yet a fully identified spirochetal etiological agent. Much clinical support for this hypothesis was published before 1954 and is based on silver stained neural lesions, animal isolation of the etiologic agent and the characteristic symptoms and pathogenesis of the disease. If this hypothesis is correct, the disease should be treatable with antibacterial agents that penetrate the CNS [antibiotics], diagnosible by immunological tests, and preventable.

Introduction
From 1909 until the mid 1950's many physicians considered multiple sclerosis (MS) to be a spirochetal infection because of its similarity to other spirochetal diseases and abundant published research implicating spirochetes in the etiology of MS. Spirochaeta myelophthora, Dr. Steiner's etiological agent is similar to the B. burgdorferi agent of Lyme disease. Research confirming a spirochetal etiology of MS flourished before the 1954 period. Spirochetes were isolated from MS patients' cerebral spinal fluid by inoculation of guinea pigs, rabbits, and monkeys. Many publications demonstrated spirochetes by silver staining of brain tissues of MS victims.
These papers were numerous before 1935 with most from MS medical research at that time being done in Germany. After the advent of Nazism many leading researchers disappeared either in the holocaust or the war, resulting in an eclipse of this work.The last papers on silver staining of MS were published in the U.S.A. in the early1950's by Dr Gabriel Steiner one of the few pre-World War II German MS researchers who survived to continue his work. In the early 1950's an unfortunate paper was published in support of this
work by an American researcher. Shortly after publishing, the author retracted the work explaining distilled water contaminated with spirochetes caused false positive cultures, but her paper was repeatedly refuted by some some researchers who tried to discreditation of the whole 50 years of accumulated reliable evidence on the spirochetal etiology of MS. In effect, "the baby was thrown out with the bathwater". About the same time, much money became available for viral research from private and governmental agencies. This money started going at first to investigate a possible etiological relationship between MS and polio, but this was shown to be a nonviable approach (Polio disappeared and MS remained). Studies were then expanded to other viruses such as scrapie, swayback, retroviruses, visna, measles, distemper and many others. One by one, these viral etiologies have largely been discredited. However, 40 years
of this emphasis on viral etiology has firmly implanted the "virus origin" of MS into the minds of the medical practitioners, teachers, and researchers who were trained during this long period. The prevalent attitude has become, "MS is a viral disease; we do not know which virus yet, but we will find it someday". Unfortunately, this resulted in a complete amnesia of the spirochetal theory during the period when antibiotics came into use. In one of his last papers (early 1950's) relating spirochetes to MS, Steiner commented that with the advent of antibiotics, MS might in the future only be of historical interest.

Evidence in Support of the Spirochetal Hypothesis:
1- The long latent period during which few or no CNS symptoms are expressed in many MS patients is also characteristic of many spirochetal diseases of man [Relapsing Fever, Neurosyphilis, Lyme disease, etc.]
2- Chronic neurological infections are characteristic of most spirochetal diseases of man and animals and often last for periods of many years
3- In MS and other spirochetal infections of man, chronic eye and neurological symptoms are commonly seen.
4- The CNS lesions in MS, Syphilis and Lyme Disease are similar in histological appearance (the perivascular locations of the lesions, the spread via the perivenous sinuses of the CNS , and the very nature of the lesions which are rich in inflammatory cells and sometimes contain spirochetes). These points toward MS being a chronic spirochetal disease of the central nervous system.
5- Neurological involvement may often occur in the early stages of many spirochetal infections of man. After an acute neurological infection (which may be clinical or subclinical), spirochetal organisms may survive sequestered away in those areas of the CNS where they are isolated from contact with the immune system, or somehow establish an equilibrium with the cell mediated immune system's protective mechanisms generated locally in the brain. In this way they can survive asymptomatically in the brain for varying periods of time. In some spirochetal infections there can be repeated episodes of neurological symptoms with short periods of remissions
in-between as this fragile equilibrium shifts in favor of, or against, the spirochete (as in Leptospirosis, Relapsing fever and Lyme Disease). In some diseases, the remission or latent period may be quite stable, lasting 15-30 years or more, as in Syphilis or Lyme disease. Chronicity, latency and periods of remission can be seen in MS and other spirochetal diseases .
6- MS is more prevalent among people with close associations with animals, the environmental reservoirs of most spirochetes. In urban areas MS has been heavily associated with contact with dogs (leptospiral urinary shedding, and ticks infected with Lyme disease spirochetes are common in dogs). High infection rates of Leptospirosis, Lyme disease and MS occur in dairy farming areas, including Minnesota, Wisconsin, New England, the Pacific Northwest, Canada, New Zealand, Australia and Western Europe (9).
7- The characteristic geographic distribution of MS seems to closely coincide with the geographic prevalence of Lyme disease. The insect vector of Lyme disease would explain the family and geographic foci seen both in Lyme disease and MS.

Comment
The routine methods used in virus research can miss spirochetes. Spirochetes require special media for culturing, special staining methods for visualization, specialized inoculation methods and selection of species for animal inoculations, and specialized microscopes. We have recently seen many examples of "newly discovered" bacterial etiological agents that were missed for many decades. Examples of this are the Legionaire's agent, Lyme disease spirochete, and bacterial agents in stomach ulcers and in Heart
Disease. The older MS research using silver staining and animal isolation is very convincing evidence of a relationship of spirochetes to MS. Silver staining (a largely lost art) has been instrumental in the discovery of both Legionaire's and Lyme disease agents and was used in much of the earlier MS spirochetal research. It is certainly worthy of further investigation now that so many wonderful techniques have been developed that were unavailable to the original researchers. The MS Society has not only been a principal source of MS research grants, but it has greatly influenced the amount of money provided and direction taken by other granting foundations and governmental agencies towards MS research. Unfortunately, the Society has never funded a single investigation of spirochetes. This area of research has been very effectively stonewalled during the entire life of the society, reflecting the opinions of its leaders and scientific advisors. The etiology of MS may still be waiting to be discovered in this era of enormously rapid advances in biological sciences only because the research has been misdirected. Few people are looking for the actual culprit because of the total lack of support, financially and otherwise, necessary to use the specialized methods required for spirochetal research. This type of research is long overdue and will be very fruitful, but it requires rethinking from those organizations that have stubbornly resisted this approach for over four decades.

Conclusions
The study of spirochetes in the etiology of MS is long overdue. A quick evaluation would be possible if researchers trained in spirochetal work were properly motivated and supported.
Antibiotics should be useful to prevent and treat MS if this hypothesis is correct. Medical practitioners and researchers might consider using antibiotics as treatments for MS patients who do not respond well to the usual supportive and immunosuppresive treatments. There are few viable alternative treatments and the risks are minimal. Antibiotics are also an indicated therapy in conjunction with immunosuppressive drug treatment to prevent secondary bacterial infections. A controlled antibiotic treatment trial would be a good project for a major clinic as one method of proving or disproving spirochetal involvement. In MS cases that are unresponsive to standard treatment or are of the unremitting continuous type, the use of antibiotic treatment would be logical both as the best alternative for the patient and as supportive treatment if immune suppression is used.(References have been deleted to save space, but are available]

2) *Department of Epidemiology and Biostatistics,
McGill University, and Centre
for Clinical Epidemiology and Community
Studies, Lady Davis Institute for
Medical Research, Montreal, Quebec, Canada; and
Institut National de la
Recherche Scientifique, Institut
Armand-Frappier, University of Quebec,
Laval, Quebec (e-mail:[email protected])

Multiple sclerosis is an inflammatory demyelinating disease in which the immune system of genetically susceptible individuals is inexplicably activated to attack the central nervous system.
Epidemiological studies strongly suggest that environmental factors are involved on a background of genetic susceptibility. (1) The possible involvement of infectious pathogens, most often viruses, has been much studied. (2,3)

Multiple sclerosis has a unique geographic distribution--temperate zones have a low prevalence and more northerly areas have a prevalence more than ten times that in warmer climates. (4) Sanitation,
climate, ultraviolet radiation, hours of sunshine, socioeconomic status, and other environmental factors have been examined with little success. (1) Much early research used case-control designs with potential recall bias. (5) More recently, seroepidemiological research has suggested the involvement of infectious pathogens in multiplesclerosis: specific antibody responses in
cerebrospinal fluid and blood, isolation of the pathogen from tissue of patients with multiple sclerosis, or in-situ or ex-vivo pathogen detection. The results have rarely been harmonious. Laboratory markers cannot be easily studied at the populationlevel because infection by some agents (eg, with human herpesvirus 6 or Chlamydia pneumoniae) does not result in identifiable clinical disease, or infection occurs in childhood and is not reliably reported by study subjects.

The convergence of epidemiology and seroepidemiology of research, however, is seen with Epstein-Barr virus. (6,7) Data from the Nurses' Health study, (8) for example, show a moderately increased risk of multiple sclerosis in nurses with a history of infectious mononucleosis (odds ratio 2.1, 95% CI 1.5-2.9). Taking only those nurses whose report of infectious mononucleosis was
confirmed by a positive heterophil-antibody-test, the risk remained (2.3,1.6-3.5). Although there was no association found between multiple sclerosis and reports of other common viral diseases
before disease onset, there was an association with mumps after 15 years of age and with late age at measles infection. Whether Epstein-Barr virus is a necessary cause requiring additional triggers to produce disease or merely a marker for a true cause is unresolved. (9)

Infection with Borrelia burgdorferi, the spirochaete responsible for Lyme disease, can involve the central nervous system and the later stages of the disease may mimic the clinical symptoms of
multiple sclerosis. (10) Seroepidemiological studies of B burgdorferi and multiple sclerosis have produced conflicting results.Chmielewska-Badora and colleagues (11) reported that ten of 26 (38%) patients with multiple sclerosis were seropositive for B burgdorferi compared with 149 of 743 (20%) patients with other neurological disorders (p=0.042). Yet others reported negative findings. (12,13) More recently, O Brorson and colleagues (14) studied the presence of the infectious agent, or at least its cystic structure, in the cerebrospinal fluid of ten patients with multiple sclerosis, in five controls who had lower back pain, and in one patient infected with B burgdorferi.
Cystic structures were found in eight of the ten with multiple sclerosis with use of immuofluorescence before culture and in all the multiple sclerosis patients by transmission
electron microscopy and acridine-orange staining. No cystic structures were found in the controls with any method. The investigators also reported a positive reaction to antispirochaetal antiserum, a similarity between the cystic structures with known cystic forms of spirochaetes, and the similarity
between the cysts found in the multiple sclerosis patients and the patient with B burgdorferi infection. These results led the team to suggest that the multiple sclerosis patients were infected with a spirochaete, most likely B burgdorferi. Whether this infection really was B burgdorferi and whether it occurred before or after the onset of multiple sclerosis cannot be determined from this study and indeed, given current methodology, it is difficult to imagine how this could be determined.

Whether infection with B burgdorferi is a cause of multiple sclerosis or whether it is merely a result of heightened susceptibility of multiple sclerosis patients to infection due to damageto the blood-brain barrier remains one of the enigmas of multiple sclerosis research. Indeed, this caveat applies to all infectious pathogens that have been associated with multiple sclerosis. Current thinking on how infections could trigger the autoimmune/immunopathological manifestations of multiple sclerosis target the following mechanisms: molecular mimicry between the pathogen and myelin
antigens, determinant spreading after injury to the central nervous system by the pathogen, and bystander inflammation caused by central nervous system infection. (3) It needs to be explained how a ubiquitous infection, such as that with Epstein-Barr virus, could be involved in the pathogenesis of multiple sclerosis. Moreover, several pathogens could be associated with
multiple sclerosis and their presence in the central nervous system may not be a necessary requirement for disease initiation or perpetuation.

(1) Granieri E, Casetta I, Tola MR, Ferrante P.
Multiple sclerosis:infectious hypothesis. Neurol Sci 2001; 22: 179-85.

(2) Alvarez-Lafuente R, Martin-Estefania C, de
Las Heras V, et al. Active human herpesvirus 6 infection in patients with
multiple sclerosis. Arch Neurol 2002; 59: 929-33.

(3) Talbot PJ, Arnold D, Antel JP.
Virus-induced autoimmune reactions in the CNS. Curr Top Microbiol Immunol 2001; 253:
247-71.

(4) Rosati G. The prevalence of multiple sclerosis in the world: an update. Neurol Sci 2001; 22: 117-39.

(5) Wolfson C, Granieri E, Lauer K. Case-control studies in multiple sclerosis. Neurology 1997; 49 (suppl 2):S5-S14.

(6) Ascherio A, Munch M. Epstein-Barr virus and multiple sclerosis. Epidemiology 2000; 11: 220-24.

(7) Marrie R, Wolfson C. Multiple sclerosis and Epstein-Barr virus. Can J Infect Dis 2002; 13: 111-18.

(8) Hernan MA, Zhang SM, Lipworth L, Olek MJ, Ascherio A. Multiple sclerosis and age at infection with common viruses. Epidemiology 2001; 12: 301-06.

(9) Wolfson C. Multiple sclerosis and antecedent infections. Epidemiology 2001; 12: 298-99.

(10) Karussis D, Weiner HL, Abramsky O. Multiple sclerosis vs Lyme disease:a case presentation to a discussant and a review of the literature. Mult Scler 1999; 5: 395-402.

(11) Chmielewska-Badora J, Cisak E, Dutkiewicz J. Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. Ann Agric Environ Med 2000; 7: 141-43.

(12) Coyle PK. Borrelia burgdorferi antibodies in multiple sclerosis patients. Neurology 1989; 39: 760-61.

(13) Schmutzhard E, Pohl P, Stanek G. Borrelia burgdorferi antibodies in patients with relapsing/remitting form and chronic progressive form of multiple sclerosis. J Neurol Neurosurg
Psychiatry 1988; 51: 1215-18.

(14) Brorson O, Brorson S-H, Henriksen T-H, Skogen PR, Schoyen R. Association between multiple sclerosis and cystic structures in cerebrospinal fluid. Infection 2001; 29: 315-19.

3) Association between multiple sclerosis and cystic structures in cerebrospinal fluid.

Brorson O, Brorson SH, Henriksen TH, Skogen PR, Schoyen R. Dept. of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway.
Abstract

BACKGROUND: The aim of the study was to search for infectious agents in the cerebrospinal fluid (CSF) of patients
with multiple sclerosis (MS).

PATIENTS AND METHODS: CSF from 10 patients with the diagnosis relapsing remitting MS and from five controls without MS were examined by transmission electron microscopy (TEM), dark field microscopy (DF), interference contrast microscopy (ICM) and
UV-microscopic examination of acridine orange staining (AO). All CSF samples from patients and controls were cultured.

RESULTS:
1.Cystic structures were observed in CSF of all ten patients by AO and TEM.
2.DF revealed 8 cyst-positive patients out of 9.
3.1 of 5 control persons had such structures in the CSF; this person had suffered from erythema migrans.
4.Spirochete or rod-like structures emerged after culturing 2 of the MS patient CSF samples and these structures could be propagated.

CONCLUSION: A significant association of CSF cysts and MS was identified in this small study among residents in a coastal area of southern Norway. The cysts could be of spirochetal origin. Our study may encourage other researchers to study larger patient groups.
PMID: 11787831 [PubMed - in process]

Many poster's here that weren't dx'ed with MS have had "white spots" show up on our MRI's and this seems to be a concern to Neurologists that we see, but, tends to not be a problem with real LLMD's for they see it often in their Lyme Disease patients.

Here's a start for you on a recent discussion on many that have had "white spots" show up on MRI's.

http://flash.lymenet.org/ubb/Forum1/HTML/020533.html

Rosemary

In 1992 had a positve blood test for Lyme, then they did another spinal tap and said this was negative, so the blood test must have been a "false-positive." I was young and stupid back then and didn't persue it.

Just last October started having pain in my left eye with movement. I knew wha was coming. Same thing happend in 1994 with my right eye. I lost the central vision in my right eye. I went to see a neurologist in November last year and had a brain MRI, this showed multiple leasions. Dr. wanted me to start treatment with daily injections of Copaxone or Avonex. I refused again. I just felt in my heart that it wasn't MS.

I had a bulls eye rash in June of 2001, and went to the doctor. I was diagnosed with Lyme and given 4 weeks of doxy.

2 months later, I was having problems with my memory, arthritis pain in my joints, and my entire right side was numb.

I went to the doctors again, and I was told (by the very same doctor who diagnosed me with lyme) that he thought I had MS and sent me to a neurologist.

When I walked in the Neurologists office, I told the doctor that from the research I had done that I thought I still had Lyme Disease, not MS. And that I thought it was too coincidental that I came down with MS, just 2 months after being diagnosed with lyme.

He agreed that lyme can go into a late stage if not treated correctly. He also found in my charts that I was put on doxy in June, but as I started to get so sick a few days into the treatment my doctor switched me to a low dose of amoxicillin.

My doctor thought I was having a reaction to the Doxy, I now know I was having a herx. So as a result, I didn't receive adequate treatment, and the neurologist thought Lyme was worth looking into.

So he did a bunch of tests, including the MRI. I did have white spots, but I was told this can happen in Lyme and MS.

The neurologist said both diseases shared so many common symptoms that he couldn't say if I had Lyme or MS. But he was leaning toward late stage lyme and put me on 6 weeks of Biaxin.

I felt better about 2 weeks into treatment. But shortly after going off the antibiotics, I was sick again.

So I was sent to an Infectious Disease doctor. There I was told, no doubt about it, that I had the first stages of MS. She wouldn't even consider my question about my still having Lyme.

She said that she couldn't give me the official diagnosed of MS until I had more lesions. She even tried to convince me that the pain I was in , couldn't be as bad as " I said " it was. She thought that if I just learned to cope better, then the pain would go away.

So I researched Lyme some more, found this site, and went to an LLMD.

I tested positive for lyme, and I started taking antibiotics. I am now about 85 - 90 % better. I shudder to think where I would be today if I had listened to that ID doctor. I reported her to the New Hampshire medical board. And every year, I mail her an anonymous Christmas card with a picture of a tick on it and Lyme Disease information.

That reminds me, I have to make up 2 new Christmas cards this year for my children's specialists..hee hee

Your sister in law may indeed have MS. But she could also have Lyme. Please urge her to see an LLMD, it could save her life.

God Bless!

~LymeBrat