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» LymeNet Flash » Questions and Discussion » Medical Questions » What is muscle twitching actually from?

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Author Topic: What is muscle twitching actually from?
lalyme
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I have Lyme and Bart and was on Levaquin for 3 months. It was great. It made the twtching almost dissappear. I then started Doxy after that and have been on that one month and the twitching started up again. LLMD put me on Ripampin and the doxy now. Have been on hat combo for about a week, 300 milligrams ramping up to 600 of Rifampin and am on 400 of Doxy. My twitching seems worse and in parts of my body it has never been in. What is happening? Thank you so much. Don't know what I would do without you people.
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bettyg
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quote:
Originally posted by lalyme:
I have Lyme and Bart and was on Levaquin for 3 months. It was great. It made the twtching almost dissappear.

I then started Doxy after that and have been on that one month and the twitching started up again.

LLMD put me on Ripampin and the doxy now.

Have been on hat combo for about a week, 300 milligrams ramping up to 600 of Rifampin and am on 400 of Doxy.

My twitching seems worse and in parts of my body it has never been in. What is happening?

Thank you so much. Don't know what I would do without you people.

I'm unable to help you but bringing you back up for answers.

I had twitching before where I had to hang onto the walls. pain MD put me on baclofen 10, 3 times daily; been on it since 99. It eventually left me! Bettyg [Big Grin]

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minoucat
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The short answer is, I don't know.

My speculation is that you may be experiencing increased die off on the new regimen, and that you are experiencing some encephalopahthy (leading to myoclonus) as part of your herx. Rifampin in particular has excellent penetration into brain tissue, far more than levaquin.

Are you having other herx indicators? And have you had any MRI/Spect scans that might indicate anything?

Myoclonus is frequently associated with neurotoxins of all kinds.

They hubby's myoclonus, which was never severe, resolved pretty much completely after the bulk of his tx.

Always a good idea to check with the doc. If this is herx related, de-toxers like CSM, chlorella, etc. might help. There are some pharmaceuticals for relieving the myoclonus if it's getting to be a big problem.

Good luck.

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RECIDITE, PLEBES! Gero rem imperialem!
(Stand aside plebians! I am on imperial business.)



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lalyme
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Thanks. Yes Minou,
Had an MRI and it showed lesions. Tiny ones that my LLMD said were typical of Lyme even though a terible Neuro duck Misdiagnosed me with MS. I guess I just get scared that I am regressing and not getting better. I have all sorts of flaring symptoms, dizziness, muscle aches, but these seemed to come before the Rifampin. More like in the 3rd and 4th week of Doxy. I think that Neuro duck also did a real number on me and at my bad times , I always think "maybe he was right", which after two great LLMD's telling me I don't have MS you'd think that I would believe, but somehow the fear creeps in. I just want to believe I am getting better.

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minoucat
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4th week of doxy is classic for increased herx sx. So it sounds as if you're on target.

The good news is that the levaquin/rifampin combo was excellent for me for bart (took 5 months of bart tx to get rid of it, but afterwards I was much improved even though I still had Bb).

Have faith! Be of good cheer! You're suffering but it's a goooood thing! (and it builds character at no extra charge)

--------------------
*********************

RECIDITE, PLEBES! Gero rem imperialem!
(Stand aside plebians! I am on imperial business.)



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lalyme
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Wow! Minou. You have a great attitude. How do you do it? How long have you had Lyme?
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Areneli
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I assume that twitching is caused by Bb toxin that messes up synapses with acetylocholine.


I believe that twiching could be a manifestaton of herx as well.

Bugs die > more toxin > more problems with acetylocholine > more twitching

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break the chains
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"Magnesium deficiency is very often present and quite severe. Hyperreflexia, muscle twitches, myocardial irritability, and recurrent tight muscle spasms are clues to this deficiency."
ADVANCED TOPICS IN LYME DISEASE
DIAGNOSTIC HINTS AND TREATMENT GUIDELINES FOR LYME AND OTHER TICK BORNE ILLNESSES
JOSEPH J. BURRASCANO JR., M.D.


I get muscle twitching when Im not taking my magnesium. Also they are not nearly as bad now that I am off abx.

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lalyme
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Again, thanks everyone. I gues it just gets VERY discouraging when the twitching went nearly away while on Levaquin only to start up again with a vengence. Hopefully rifampin will help.
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treepatrol
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And dont forget about Bb eating the mylene covering on nerves like short circutting speaker wires on your stereo lots of static same as mucles not getting clear signals.

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madhattan
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Yes, but I thought that was actually a misconception about Bb chomping on myelin. I was told that it is the neurotoxins that Bb releases that act as irritants to the nerve tissue and causes inflammation. After all my nerve pain, if my myelin was all screwed up, I think my EMG would show something. But that's just one doctor's opinion. It seems like there is so much conflicting information out there.
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Areneli
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You are right, madhattan. Myelin is normally not damaged by Bb although sometimes it may. Than MRI will show some changes as well.
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cutie
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I have this twitching/myoclonus and it's one of my worst symptoms! It got so bad when I was taking doxy, and that was only at 200 mg/day! It was horrible.

I'm off abx right now and it's gotten better but when i get back on them who knows. I also had an EMG and an MRI - both were normal.

Does your twitching get worse when you're tired or have exerted yourself? Like lifting heavy things? Mine gets way worse when I'm tired.

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Cutie

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cutie
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bumping up...

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Cutie

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Areneli
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8 months of Tetracykline 2 g/day or Doxycyline 600 mg/day and I don't twitch at all.
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treepatrol
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quote:
Originally posted by madhattan:
Yes, but I thought that was actually a misconception about Bb chomping on myelin. I was told that it is the neurotoxins that Bb releases that act as irritants to the nerve tissue and causes inflammation. After all my nerve pain, if my myelin was all screwed up, I think my EMG would show something. But that's just one doctor's opinion. It seems like there is so much conflicting information out there.

17. Mario Philipp and the Bb-infected monkeys- The non-Human model of nerve damage from undertreated Lyme disease This, the attack on the nerves by Borrelia burgdorferi, is examined in autopsy of Bb infected monkeys, a model for human neuroborreliosis, which demonstrates the kind of nerve damage that can happen when people have Lyme disease. The IDSA Guidelines specify that a person has to have "objective" signs of neurological effects.


That means: YOU HAVE TO HAVE *NERVE DAMAGE* , ALREADY, BEFORE THE IDSA SAYS YOU CAN BE RETREATED "TITLE: Chronic lyme disease in the rhesus monkey AUTHORS: Roberts ED; Bohm RP Jr; Cogswell FB; Lanners HN; Lowrie RC Jr; Povinelli L; Piesman J; Philipp MT AUTHOR AFFILIATION: Department of Pathology, Tulane Regional Primate Research Center, Tulane University Medical Center, Covington, Louisiana.


SOURCE: Lab Invest 1995 Feb;72{2}:146-60 CITATION IDS: PMID: 7853849 UI: 95156954 COMMENT: Comment in: Lab Invest 1995 Feb;72{2}:127-30 ABSTRACT: BACKGROUND: We have previously reported the clinical, pathologic, and immunologic features of "early" Borrelia burgdorferi infection in rhesus monkeys {3}.


We have now evaluated these features during the chronic phase of Lyme disease in this animal model.

EXPERIMENTAL DESIGN: Clinical signs, and pathologic changes at the gross and microscopic levels, were investigated 6 months post-infection in several organ systems of five rhesus macaques {Macaca mulatta}, which were infected with Borrelia burgdorferi by allowing infected Ixodes scapularis nymphal ticks to feed on them.


A sixth animal was used as an uninfected control. Borrelia antigens recognized by serum antibody were identified longitudinally by Western blot analysis, and C1q-binding immune complexes were quantified.


Localization of the spirochete in the tissues was achieved by immunohistochemistry and in vitro culture. The species of spirocheta cultured was confirmed by the polymerase chain reaction. RESULTS: Chronic arthritis was observed in five out of five animals.


The knee and elbow joints were the most consistently affected. Articular cartilage necrosis and/or degenerative arthropathy were the most severe joint structural changes. Synovial cell hyperplasia and a mononuclear/lymphocyte infiltrate were commonly seen. Nerve lesions were also observed, including nerve sheath fibrosis and focal demyelinization of the spinal cord. Peripheral neuropathy was observed in five out of five animals and could be correlated in the most severely affected monkey with the presence of higher levels of circulating immune complexes.


Differences in disease severity did not correlate with differences in the antigens recognized on Western blot analysis.

CONCLUSIONS: B. burgdorferi infection in rhesus macaques mirrors several aspects of both the early and chronic phases of the disease in humans.


This animal model will facilitate the study of the pathogenesis of Lyme arthritis and neuroborreliosis...


"It has been our experience at Tulane Primate Research Center that functional deficits due to joint disease in nonhuman primates do not occur until very significant pathologic changes exist... "Nerve changes.


A detailed survey of the central nervous system lesions was carried out, which included 50 sampling sites. The lesions observed are listed in Table 4. Sensory ganglia of the dorsal root and trigeminal ganglia of animals J 831 and K 216 had individual neurons that immunostained positive with anti-Bb 7.5kD lipoprotein mAb {fig 16}. These neurons were swollen and were undergoing chromatolysis.


The dorsal root ganglia of the thoracic and cervical regions were especially affected. Nerve sheath fibrosis within the spinal cord was limited to the thoracic segment in animal J 831. Positive staining with anti-Bb mAb, accompanied by vacuolization of peripheral nerves, was observed in three of four animals.


This change occurred as a radiculoneuropathy of the thoracic segment and peripheral nerves {Fig 17}. Animal L 131 had five peripheral nerves affected. When the same nerves were stained for fat, focal vacuolization was observed {Figs 18 and 19}.


Focal demyelination of the cervical cord was limited to J 831. Lymphocyte infiltration of the affected nerves was mild in extent and confined to perivascular spaces. In animals L 131 and K 383, Bb could be demonstrated by immunostaining {Fig 20}.


" The pathogenesis of Lyme disease neuropathies is poorly understood...Sensory ganglia involvement has previously been described in human borreliosis {27-28}.


In our study, many of the ganglia positive for Bb by immunstaining were undergoing necrosis. This staining was seen in two out of five animals and was not accompanied by a cellular infiltrate. " Nerve tissues with perivascular lymphocyte infiltrate were present in three out of five animals.


This was the only lesions where extracellular Bb could be demonstrated. Peripheral cutaneous nerves were prominantly affected in the early phase of borreliosis of rhesus macaques{20, 28-29}.

Changes of the nercous system include the full range of changes observed in neuroborreliosis, which suggests a variety of disease mechanisms, including sensitization or mimicry as suggested by the vacuolization of peripheral nerves and cytokine-mediated destruction of nerves as a result of the infiltrating lymphocytes..."

Conclusion: {IDSA Guidelines} Do not retreat until objective signs of neuroborreliosis are seen. Therefore: Determine objective evidence of loss of nerve function before wasting healthcare resources? Nerves are expendible? According to the Infectious Diseases Society of America and the American Lyme Disease Foundation

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Do unto others as you would have them do unto you.
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treepatrol
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Some more::

LYME AND MS HAVING THE SAME ETIOLOGY

Subject:
MS/Lyme literature



JOURNAL REFERENCES


html-edited by Joachim Gruber
Due to several reqeusts for posting and hundreds of snail mail requests around the country, I am posting the listing of research I have accummulated on the net so that more people will have access to information re:


Lyme and MS having the same etiology perhaps and providing hands-on info for those whose interest lies in thise area so that they may access this list for future use. I accummulated this list in 1992 and so there are many more that follow I am sure. Feel free to make addendums


This should give one a good start anyway. Please attach my name on the research for credit purposes.


This has been sent to the National MS Society in NY and they have discredited its profound implications as being not worthy of bacteriologic research into the etiology of Lyme disease which I found to be a very sad commentary on the mindset of their organization.

Note: These articles do not all insist that Lyme and MS are the same but keep in mind that MS means "multiple sclerosis". Multiple sclerosis simply put means "many lesions".

It is simply a DESCRIPTIVE NAME of a disease which causes the nerves to lose their myelin sheath and in particular
to show lesions on the brain on MRI which Lyme does as well.


My readings and research have indicated that the brain lesions, the spinal fluid findings and the actual clinical manifestations of Lyme and MS cannot be distiguished one from the other, perhaps simply due to a strain variance of Lyme.


We know that Lyme causes an immunologic dysfunction including a component of autoimmune activity possibly causing this neuro-damage in the form of MS activity.


The bottom line -and most disturbing thing- to me is that the MS society refuses to put out money for intensive research even after Dr. Vincent Marshall's exhaustive research from the 80's showing spirochetes on the axons of nerves of MS patient autopsies in Europe. When viruses became popular, they threw the baby out with the bathwater and now research funding is geared toward viruses and immunologic work; bacterial taking a second seat.


The worst of all, there is no etiology to MS or other autoimmune diseases and there seems to be clinical response of polymyalgia rheumatica, MS, polymyositis, rheumatoid disease, Alzheimers, ADD, chronic fatigue syndrome, fibromyalgia and other diseases such as lupus {we see them feeling better} when given antibiotic therapy.


This is most frightening when the antibiotic therapy is taken away from them by their rheumatologists and ignored by their internists. The very key that may unlock the door to these illnesses and the publications that implicated ALS and other life-threatening diseases are being ignored as having an infectious underpinning.


Personally, I find this inexcusable and find antibiotic over 3 months IV to be much less damaging than methotrexate, Cytoxin, prednisone high dose etc. over the long haul for these patients.


Please do attach my name when using this listing, as I want to maintain the research rights to this time-taking work. Thanks to everyone for your interest and support through the years.


When looking up some of these journal articles, one will have to use a medical school or sophisticated library which contains most journals so that they can more easily access them in one trip.


For those pondering the MS diagnosis, perhaps this will make a better case for the parallel between the two diseases. Rarely do we pick up an article on neurologic Lyme (neuroborreliosis) in which we do not see demyelinating syndrome as part of the disucssion {brain lesions}.


Also remember that syphilis caused demyelination and we are but a cousin to this dreaded infection.


The one thing good that did come of this research was the posting of the MS Society of Lyme on their web page as being a demyelinating disease.

This post is also intended for ALS patients and perhaps even Guillain-Barre patients as well.


1. MRI Reveals Pathology in Neuro Lyme Disease. "Diagnostic Imaging-MRI Insights".


2. "Biopsy-confirmed CNS Lyme Disease: MR Appearance at l.5T" American Journal of Neuroradiology-11:482-484.


3. Allen Steere, MD. et al. "The Long Term Course of Lyme Arthritis in Children" The New England Journal of Medicine. Vo. 325No. 4, Jly 18, 1991.


4. Stephen L. Schechter, MD. "Lyme Disease Associated with Optic Neuropathy" The American Journal of Medicine. July 1986. v. 81, 143-145


5. H. Kohler, Dept. Clinical Neurology and Neurophysiology, University of Freiburg, West Germany. "Letter to the Editor". Borrelia encephalomyelitis." The Lancet. July 5, 1986, p35.


6. "Kyke Award: GD-DTPA-Enhanced MR Imaging of Experimental Bacterial Meningitis: Evaluation and Comparison with CT. American Journal of Neuroradiology. 9:1045-1050; Nov./Dec. 1988.


7. Derek Gay et al. "Multiple Sclerosis Associated with Sinusitis: Case-controlled study in General Practive. {Ed. note: Recent research in showing 99% Lyme patients have active sinusitis as presenting symptoms which often go undetected {unpublished results from personal research on symptomatology}}. The Lancet. Saturday 12 April 1986. 815-819.


8. Eric L. Logigian, MD; Allen Steere, MS et al. "Chronic Neurologic Manifestations of Lyme Disease. "The New England Journal of Medicine" 323:21;1438-1444, 1990.


9. Derek Gay , "Hypothesis" Is Mutiple Sclerosis caused by an Oral Spirochete? The Lancet. July 12. 1986. pp. 75-77.


10. Fernandez et al. "Lyme Disease of the CNS: MR Imaging: Findings in 14 cases. American Journal of Neuroradiology. 11; May/Jyne, 1990.


11. John Halpersin, MD et al. "Immunologic Reactivity Against Borrelia burgdorferi In Patients with Motor Neuron Disease." Archives of Neurology 47:586-594. May 1990.


12. Will Kohlhepp. et al. "Extrapyramidal Features in Central Lyme Borreliosis." European Neurology. 29:150-155, 1989.


13. Joh J. Halpersin, MD "Lyme Neuroborreliosis." Laborabory Medicine. 21:5; May 1990.


14. Louis Reik, Jr., MD et al. "Demyelinating Encephalopathy in Lyme Disease. Neurology. 46:790-795, July, 1989.


16. Presentation to Rocky Mountain Lab by Kenneth Liegner, MD from Armonk, New York, re: growing evidence for link between Lyme and MS. Missoulian Newspaper. Wed August 15, 1990. Gred Lakes. Hamilton, Montana, Rocky Mountain Lab; NIH facility where Dr. Willy Burgdorfer discovered the spirochetal etiology of Lyme disease.


17. R. Ackerman, E. Gollmer and B. Rehse-Kupper. "Progressive Borrelial Encephalomyelitis": The Chronic Neurologic Manifestations of Erythema Chronicum Migrans {ECM} Disease." Lyme Times Newsletter. April, 1993, p. 48 Phyllis Mervine, Editor. Reprint of German publication called Deutsche Medizinische Wochenschrift 110. 1995. Translated by Ron Ferris, Calgary, Alberta, Canada.


Reprinted with persmission. English title, "Untreated neuroborreliosis progresses over years to cause serious MS-like encephalomyelitis."


18. J.H.J. Wokke, MD:,.van Gign, MD; A. Elderson, MD; and G. Stanek, MD. "Chronic Forms of Borrelia burgdorferi infection of the nervous system," Neurology 37:1031-1034: 1987.


19. Michael B. chancellor, MD; David E. McGinnis. Patrick J. Shenot, MS et al. Dept. Urology, Jefferson Medical College. Thomas Jefferson University, PA 19107. "lette" The Lancet. Vol 339: May 16, 1992 p.1237-1238.


20. Keffreu A. Nelson, MD; Mitchel, D. Wolf, MD; William T.c. Yuh, MD et al. "Cranial nerve involvement with Lyme borreliosis demonstrated by magnetic resonance imaging". Neurology. 42:671-673. March 1992.


21. P.K. Coyle,MD;Z.Deng, MS; S.E. Schutzer, MD; A.L. Gelman,MD et al. "Detection of Borrelia buergdoferi antigens in cerebrospinal fluid." Neurology. 43:1093-1097, 1993.


22. Saul Rosen, PhD, MD, Section Editor. "Current Perspectives on Lyme Borreliosis". Journal American medical Association. 276;10, March 11, 1992. "Gran Rounds at the Clinical Center of the National Institute of Health.".


23 Ackerman, R,MD; Rehse-Kupper, B. MD, "Chronic Neurologic manifestations of erythema chronicum migrans borreliosis". Annals NY Academy of Science. 539-16-23.


24. Matuschka, Fr. and Spielman, A. The emergence of Lyme disease in a changing encironment in North American and Central Europe". Experimental and Applied Acarology. 2: 1986; 1337-1353.


25. JJ Halpersin, MD; Raymond Dattwyler, MD et al. "Lyme Disease: Cause of a Treatable Peripheral Neuropathy." Neurology. 37; No 11; 1700-06; 1987.


26. Belman, A.L.; Coyle, Patricia K.; Nachman, S. and Roche, C. "Brain MRI abnormalities in children infected by Borrelia burgdorferi." Neurology. 41 {Suppl 1} Item 73 P: March 1991.


27. Vincent Marshal, DVM, "Multiple Sclerosis is a chronic central nervous system infection by a spirochetal agent." Medical Hypothesis. 25:89-92, 1988.


28 A. Kirk E. winward, MD; J. Lawton Smith, MD et al. "Ocular Lyme Borreliosis." { Ed. note: eye diseases found in MS patients called "pars planitis" and uveitis, scotomas, disk edema, optic neuritis and neuropathy, blurred vision etc. are implicated in this article as Lyme disease eye phenomenon as well}.


"A similar association with pars planitis has been reported in multiple sclerosis {18} Because a demyelinating syndrome nearly indistinguishable from multiple sclerosis may also occur in Lyme disease, it is possible that Lyme borreliosis, pars planitis, and demyelinating disease may, in some cases, share a common pathogenic mechanism." p. 656. American Journal of Ophthalmology 108:651-657, 1989.


30. A. Berger, B.C., and Leopold, I.H. "The incidence of uveitis in mutiple sclerosis." American Journal of Ophthalmology. 62-540., 1966.


31.DuPuis, MJ , Multiple neurologic manifestations of Borrelia burgdorferi infection , Reviews in Neurology {Paris}, 1988;144{12}:765-775.

{Article in French, English abstract available on Medline}
Exerpt: The central nervous system involvement is characterised by slowly progressive or fluctuating course during month or years,


ataxic or spastic gait disorder,
bladder disturbances,
cranial nerve sydrunction including
optic atrophy and
hypoacusia,
dysarthria,
focal and diffuse encephalopathy.
This chronic central nervous system disease can mimic multiple sclerosis psychic disorders or subacute presentile dementia. It is often associated with
pelocytosis,
abnormal EEG and
evoked potentials,
sometimes multifocal and mainly periventricular white matter lesions visualized by CT or MRI......


Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parencymetous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator...and can cause


acute transverse myelitis,
severe encephalitis,
myositis,
chronic neuropathy...
recurrent strokes...
meningoradiculitis...
lyphocytic meningitis with an acute or even relapsing course,
apparently idiopathic facial palsy,
neuritis of other cranial nerves,
polyneuritis cranialis,
Argyll-Robertson sign and so on.



32. Baig S., Osson T, Hojeberg G, Link H., Dept. of Neurology, Karolinska Institute, Hugginge Unversity Hospital, Stockholm, Sweden, Cells secreting antibodies to myelin basic protein in cerebrospinal fluid of patients with Lyme neuroborreliosis. Neurology 1991; April, 41{4}:581-587.


33. Lyme borreliosis neuropathy. A Case report Am J. Phys. Medicine and Rehabilitation, 1996 Jul;75{4}:314-316.


34. Coyle, PK, Dept. of Neurology, School of Medicine, State University of New York, Stony Brook, Neurologic complications of Lyme disease. Rheumatologic Discussion Clinical North American, 1993, Nov;19{4}993-1009.

______________________

" In 84% of multiple sclerosis patients we were able to demonstrate intrathecal antibody production against measles, rubella or mumps virus............"



{This quote is from the first of the following abstracts.


I find it interesting because these three viruses are also included in one shot for vaccinations. What are these antibodies doing in the spinal fluid and being used as a marker for MS?


Does anyone know?


Georgia}

Heller J, Holzer G, Schimrigk K. Immunological differentiation between neuroborreliosis and multiple sclerosis. J Neurol. 1990 Dec;237{8}:465-70.


Heller J, Holzer G, Schimrigk K. {ELISA for specifying oligoclonal bands of isoelectric focusing of cerebrospinal fluid in patients with neuroborreliosis and multiple sclerosis}, Nervenarzt. 1990 Apr;61(4):248-9. German.


--------------------------------------------------------------------------------

Further Reading on neuroborreliosis/MS
Lawrence C, Lipton RB, Lowy FD, Coyle PK, Seronegative chronic relapsing neuroborreliosis. Eur Neurol 995;35{2}:113-7.


Garcia-Monco JC, Seidman RJ, Benach JL, Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides.Infect Immun 1995 Oct;63{10}:4130-7 {Full text}
Mattman L, Spirochaeta Myelophthora in Multiple Sclerosis, in: Cell Wall Deficient Forms: Stealth Pathogens, 2nd Edition, CRC Press, Boca Raton, Boston, London, New York, Washington D.C., 1993
Martin Roland, Cellular Immunology Section, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, Research Interests:


"In treatment trials as well as in longitudinal studies of disease activity in MS patients immunologic disease markers
-measured by


ELISA,
quantitative PCR,
cDNA microarrays,
T cell frequencies and specificity-
are correlated with
the clinical course and
disease activity as assessed by MRI."
Dr. Martin's laboratory investigates the cellular immune system in multiple sclerosis and chronic Lyme disease and, together with Henry McFarland, develops novel treatment modalities for MS."


Example:.


In the case of a
a history of Lyme disease and
a neurological picture compatible with atypical multiple sclerosis, that seems to improve with intravenous antibiotics and relapse when antibiotics.have been discontinued
it seems a probably safe option to use of both,
i.v. antibiotics directed against Lyme and simultaneously
copaxone to reduce autoimmune damage.


Background of this is the lack of diagnostic tests that actually verify an active infection, i.e. the persistence and reproduction of a B. burgdorferi population {personal communication from Roland Martin}.


Martin R, Gran B, Zhao Y, Markovic-Plese S, Bielekova B, Marques A, Sung MH, Hemmer B, Simon R, McFarland HF, Pinilla C., Molecular mimicry and antigen-specific T cell responses in multiple sclerosis and chronic CNS Lyme disease, J Autoimmun 2001 May;16{3}:187-92
Immunology Division, Department of Pathology, University of Cambridge:


"The implications of this are
that the continuous stimulation of T cells is required to maintain the inflammatory process and
that TNFalpha plays a key role in that process.
The currently accepted view is that whatever initiates the disease, once joint damage is established it is a self-perpetuating process in which
auto-antigens released as a result of the damage
stimulate T cells
which recruit and activate macrophages
which lead in turn to further damage, the maintenance of inflammation - via vascular endothelial activation - and the perpetuation of the proliferation and cytokine secretion of local TH1 cells.
Presumptively the key cytokines are
TNFalpha and IL-12 released by macrophages and
IFNgamma from T cells."

http://www.path.cam.ac.uk/immuno/part1/lec13/lec13_97.html

Activity of Copaxone:
Li QQ, Burt DR, Bever CT., Glatiramer acetate inhibition of tumor necrosis factor-alpha-induced RANTES expression and release from U-25 MG human astrocytic cells. J Neurochem. 2001 Jun;77{5}:1208-17.

--------------------------------------------------------------------------------


Antimyelin antibodies in Lyme

Epidemiol Mikrobiol Imunol 2002 Apr;51{2}:60-5


{Article in Czech}


Ryskova O, Vyslouzil L, Honegr K, Lesna J, Horacek J, Skrabkova Z.
Ustav klinicke mikrobiologie, UK Praha, LF Hradec Kralove. [email protected]


The method of enzyme immunoassay {ELISA} was used for detection of antibodies against the basic protein myelin {antimyelin antibodies} for a group of serum samples {n 36} with positive anti-borrelia immunoglobulins IgG and IgM {ELISA-Borrelia afzelii} and their immune complexes {ELISA-PEG}.


Antimyelin antibodies {ELISA-Doxa Kit-Myelin Basic Protein Antibodies} were assessed in 31% {n 11} of examined serum samples of patients with the working diagnosis of Lyme borreliosis.
Statistical analysis {p 0.07} confirmed a more frequent incidence of antimyelin antibodies in younger female subjects {age 31 years} as compared with a group of sera {n 25} where the authors did not record the formation of immunoglobulins against the basic myelin protein {age 51 years}.

Neither the value of titres nor the frequency of detected anti-borrelia IgG and IgM and immune complexes differed significantly in the two groups.


From the assembled results ensues that in the course of Lyme borreliosis, in chronic affection of organs an autoimmune reaction may develop where the basic myelin protein is damaged {demyelinizatio} and subsequently antimyelin antibodies are formed.
PMID: 11987581 {PubMed - in process}

--------------------
Do unto others as you would have them do unto you.
Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.

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