Sveitsiläisessä artikkelissa pohditaan MS-taudin ja Borrelioosin välistä yhteyttä.
1. "MS-tautiin ei ole edelleenkään kyetty löytämään parantavaa hoitoa. Maailmanlaajuisesti MS-tautia ja borrelioosia esiintyy maantieteellisesti samoilla alueilla. Samoin vuodenajalla jolloin ihminen on syntynyt (punkkien aktiivisuus) on havaittu olevan yhtenevyyttä MS-tautiin myöhemmin sairastuviin.
Millään muulla taudinaiheuttajalla ei ole havaittu tällaista alueellista ja vuodenaikayhteyttä.
Lisäksi MS-tautia sairastavien aivoista on löydetty borrelia-bakteerin spirokeetta ja kystamuotoja. Koska minosykliini, tinidatsoli ja hydroksiklorokiini kykenevät raporttien mukaan tuhoamaan borrelia-bakteereita, tarjoaa se uutta toivoa sairastuneille. Minosykliinistä on hyötyä myös sellaisissa tapauksissa joissa taudilla ei ole yhteyttä borrelia-bakteeriin. Sellaiset potilaat, jotka ovat saaneet yhdistelmähoitoja ovat parantuneet tai päässeet pidempään remissioon kuin ne potilaat, jotka eivät ole saaneet hoitoa. Tarvitaan lisätutkimuksia nimenomaan sellaisilla alueilla joilla punkkeja esiintyy runsaasti. Tutkimuksissa tulee selvittää ennenkaikkea borrelia-bakteerin L-muotojen esiintymistä MS-tautia sairastavien selkäydinnesteessä."
Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?
Fritzsche M.
Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland. markus.fritzsche@gmx.ch
Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks.
In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation.
Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls.
Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study.
PMID: 15617845 [PubMed - indexed for MEDLINE]
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2. Epstein Barr-viruksen epäillään olevan yhteydesssä riskiin sairastua MS-tautiin. (suom.huom. Useilla Borrelioosia sairastavilla on lisäinfektiona mm. tämä herpes viruksiin kuuluva virus)
http://archneur.ama-assn.org/cgi/conten ... ct/64/1/72
Archives of Neurology
Vol. 64 No. 1, January 2007
? Online Features
Original Contribution
Multiple Sclerosis After Infectious Mononucleosis
Trine Rasmussen Nielsen, MD; Klaus Rostgaard, MSc; Nete Munk Nielsen, MSc, MD, PhD; Nils Koch-Henriksen, MD, DMSc; Sven Haahr, MD, DMSc; Per Soelberg Sørensen, MD, DMSc; Henrik Hjalgrim, MD, PhD
Arch Neurol. 2007;64:72-75.
Background
Infectious mononucleosis caused by the Epstein-Barr virus has been associated with increased risk of multiple sclerosis. However, little is known about the characteristics of this association.
Objective
To assess the significance of sex, age at and time since infectious mononucleosis, and attained age to the risk of developing multiple sclerosis after infectious mononucleosis.
Design
Cohort study using persons tested serologically for infectious mononucleosis at Statens Serum Institut, the Danish Civil Registration System, the Danish National Hospital Discharge Register, and the Danish Multiple Sclerosis Registry.
Setting
Statens Serum Institut.
Patients
A cohort of 25 234 Danish patients with mononucleosis was followed up for the occurrence of multiple sclerosis beginning on April 1, 1968, or January 1 of the year after the diagnosis of mononucleosis or after a negative Paul-Bunnell test result, respectively, whichever came later and ending on the date of multiple sclerosis diagnosis, death, emigration, or December 31, 1996, whichever came first.
Main Outcome Measure
The ratio of observed to expected multiple sclerosis cases in the cohort (standardized incidence ratio).
Results
A total of 104 cases of multiple sclerosis were observed during 556 703 person-years of follow-up, corresponding to a standardized incidence ratio of 2.27 (95% confidence interval, 1.87-2.75). The risk of multiple sclerosis was persistently increased for more than 30 years after infectious mononucleosis and uniformly distributed across all investigated strata of sex and age. The relative risk of multiple sclerosis did not vary by presumed severity of infectious mononucleosis.
Conclusions
The risk of multiple sclerosis is increased in persons with prior infectious mononucleosis, regardless of sex, age, and time since infectious mononucleosis or severity of infection. The risk of multiple sclerosis may be increased soon after infectious mononucleosis and persists for at least 30 years after the infection.
Author Affiliations: Department of Epidemiology Research, Statens Serum Institut, Copenhagen (Drs T. R. Nielsen, N. M. Nielsen, and Hjalgrim and Mr Rostgaard), National Institute of Public Health and Department of Neurology, Aalborg Hospital, Aalborg, (Dr Koch-Henriksen), Department of Medical Microbiology and Immunology, University of Aarhus, Aarhus (Dr Haahr), and Danish Multiple Sclerosis Research Centre, Department of Neurology, Copenhagen University Hospital, Copenhagen (Dr Sørensen), Denmark.
3. "MS-oireiden hoidossa on saatu lupaavia tuloksia matala-annoksisella naltreksonilla. Wilkinson sairastui MS-tautiin 30-vuotiaana. Hän on vuoteen 2004 saakka käyttänyt MS-taudin hoidossa käytettäviä tavanomaisia lääkkeitä. Niistä ei ollut apua. Tauti eteni ja hän joutui ottamaan kävelykepit avukseen. Vuoden 2003 lopulla hänelle oltiin tilaamassa sähkökäyttöistä pyörätuolia. "Aloitin naltreksoni-hoidon helmikuussa 2004. Sen jälkeen olen tullut koko ajan parempaan kuntoon ilman pahenemiskausia." Koska naltreksoni on edullinen, geneerinen lääke, lääketeollisuudella ei ole suuria intressejä lääkkeen tunnetuksi tekemiseen. Siksi sairastuneet ovat ottaneet asiakseen tuoda asian julkisuuteen omatoimisesti.."
Article URL: http://www.medicalnewstoday.com/medical ... <o:p></o:p>
Patient Advocates With Multiple Sclerosis Fund Clinical Trial Of Promising Drug That Has Already Helped Thousands<o:p></o:p>
13 Feb 2007
Over the last decade, anecdotal reports suggested that a very low dose of an FDA-approved drug called naltrexone provides effective symptom relief for many patients who suffer from Multiple Sclerosis. Frustrated by the lack of scientific research, volunteers began raising money to fund a human clinical trial of Low Dose Naltrexone (LDN) for MS. This effort culminated in awarding a $25,000 gift to the University of California, San Francisco Multiple Sclerosis Research Center.
Naltrexone was approved by the FDA 20 years ago for treating addiction, but researchers at Penn State University discovered its ability to normalize a dysfunctional immune system when used in very low doses. Dr Bernard Bihari, a Harvard trained neurologist in New York City, observed positive results in his patients using LDN for MS and other immune system disorders. His observations were published at http://www.ldninfo.org, which is where an MS patient named SammyJo Wilkinson learned of it.
Wilkinson was diagnosed with MS in 1995 at age 30. For years she used the injectable drugs approved by the FDA for MS but to no avail; the disease progressed to walking with a cane, and she had to give up her technology career. By the end of 2003, she was falling so often that a motorized wheelchair was on order.
"In February of 2004 I took my first 4.5 mg capsule" recalls Wilkinson, "and I have recovered without setbacks ever since." In 2005 she attended the 1st LDN Conference, and in conjunction with other patient advocates including the nonprofit Accelerated Cure Project for MS, formed a committee to raise funds to stimulate research for LDN treatment of MS. Because naltrexone is an inexpensive generic drug, the concern was that there would be little commercial interest in research, so they felt it was up to patients themselves to lead the way. In addition to Wilkinson, this committee also consisted of Robert Lester and Art Mellor.
They set up a website, http://www.LDNers.org, and received enthusiastic support from other patients who had benefited from LDN. The culmination of the fundraising effort was a gala benefit in California attended by over 250. The organizer, Vicky Finlayson, had experienced an amazing recovery from 10 years of painful MS attacks after taking LDN, and felt passionately about funding the research, so that others with MS could gain the relief she had.
Following the benefit, $25,000 had been raised, and word arrived that the UCSF Multiple Sclerosis Center was interested in conducting the first human trial in the US, to measure the impact of LDN on MS. The funds were donated to UCSF, and a 3 month double-blind crossover trial involving 80 patients is expected to start this Spring.
About UCSF MS Center
The Multiple Sclerosis Center at the University of California serves the MS community of Northern California through a commitment to providing the highest standard of integrated patient care, innovative basic science and clinical research, and education. The UCSF MS center cares for approximately 3,500 patients who suffer from MS and provides consultation for many more patients who geographically are unable to receive continuity of care in San Francisco. The MS Center is committed to developing improved therapies for MS through clinical trials as well as basic science research oriented at understanding why patients develop MS and uncovering novel therapeutic strategies. For more information about the UCSF MS Center please visit the website: http://www.ucsf.edu/msc/index.html
About Accelerated Cure Project for MS
Accelerated Cure Project for Multiple Sclerosis, www.acceleratedcure.org, is a national nonprofit organization dedicated to curing Multiple Sclerosis (MS) by determining its causes. Accelerated Cure Project believes this effort can be accelerated by organizing the research process and encouraging collaboration between research organizations and clinicians. A "Cure Map" is currently being developed by Accelerated Cure Project to establish what is known and what is not known about the causes of MS. From the Cure Map, Accelerated Cure Project will facilitate research most likely to reveal the causes of MS in the shortest time through a large-scale, multidisciplinary, MS Repository. For more information about Accelerated Cure Project or to make a corporate or individual donation, call 781/487-0008, visit http://acceleratedcure.org, or send an email to info-pr@acceleratedcure.org.
About Multiple Sclerosis
Multiple Sclerosis is a chronic demyelinating disorder of the central nervous system that often results in severe disability including the inability to walk, blindness, cognitive dysfunction, extreme fatigue and other serious symptoms. MS affects over 400,000 people in the US and 2 million individuals worldwide. The disorder occurs twice as often in women as in men. The cause is not known and there is no known cure.
4. Prolaktiini-hormoni saattaa auttaa MS-oireisiin, selkäydinvammoihin ja aivohalvauksiin. Raskaana olevilla hiirillä esiintyi kaksi kertaa enemmän myeliiniä tuottavia soluja ja synnytyksen jälkeen niillä oli 50% enemmän myeliiniä hermosolujen suojana kuin sellaisilla hiirillä jotka eivät olleet raskaana. Prolaktiini jäljittelee raskautta ja lisää myeliinin tuotantoa ja korjaantumista.
Pregnancy Hormone may Treat MS
Ivanhoe Newswire
(Ivanhoe Newswire) -- A hormone women produce during pregnancy may help treat multiple sclerosis.
University of Calgary researchers report prolactin increases myelin, which improves signaling within the nervous system and helps repair damage in the brain and spinal cord. Prolactin could be used to help treat MS patients.
MS causes the body's immune system to attack myelin, which insulates nerve cells and is critical to maintaining the speed of messages being transmitted from cell to cell. A decrease in myelin leads to a progressive loss of sensation and movement.
Researchers compared pregnant and virgin female mice of the same age. When researchers compared cells in the animals' brains and spinal cords, they found pregnant mice had twice as many myelin-producing cells and kept generating new ones during pregnancy. The mice also had 50-percent more myelin coating their nerve cells after giving birth.
During pregnancy, the body appears to be able to repair nerve cells with destroyed myelin faster. Prolactin mimics the effects of pregnancy, increasing both myelin production and repair. The researchers suggest the hormone, which increases during pregnancy, may help trigger the production of new myelin.
MS is more common in women than men. Previous studies have shown women often experience remission of their symptoms during pregnancy. Researchers report more research on prolactin will be done in animals before the hormone can be tested in humans. The findings also have implications for the other neurological disorders, like spinal cord injuries and stroke.
This article was reported by Ivanhoe.com, which offers Medical Alerts by e-mail every day of the week. To subscribe, click on:
http://www.ivanhoe.com/newsalert/.
SOURCE: The Journal of Neuroscience, 2007;27:1812-1823
Source:
University of California - Los Angeles
Date: March 25, 2007
More on: Multiple Sclerosis, Multiple Sclerosis Research, Pregnancy and Childbirth, Diseases and Conditions, Disorders and Syndromes, Immune System
5. Raskaana olevilla, MS-tautia sairastavilla, naisilla esiintyy normaalia vähemmän oireita raskauden aikana. Syynä siihen näyttäisi olevan naissukuhormoni Estrioli jolla on tulehdusta hillitsevä että hermostoa suojeleva vaikutus. Aiheesta on alkamassa tutkimus.
Could Estriol Be The Elixir For Multiple Sclerosis?
Science Daily â?? It has long been common knowledge that pregnant women with multiple sclerosis (MS) experience a sharp drop in the disease's symptoms during the course of their pregnancy.
Some years back, Dr. Rhonda Voskuhl, director of UCLA's Multiple Sclerosis Program, and her colleagues discovered the cause. They found that a female sex hormone called estriol, which is produced during pregnancy, was responsible for the suppression. Four years ago, Voskuhl followed that discovery with a pilot study in which 10 non-pregnant women with MS were given estriol, yielding what she described as "pretty remarkable" results â?? an 80 percent drop in inflammatory lesions in the brain, a hallmark of the disease.
This month, Voskuhl begins a much larger trial of estriol, one that will involve 150 patients at multiple locations over the next two years. The prospects, she said, are exciting.
Multiple sclerosis is an autoimmune disease of the central nervous system that attacks the tissue surrounding the brain's nerve fibers. This tissue, called myelin, can be thought of as the insulation wrapped around an electrical wire. When the myelin is damaged, the nerve's ability to send signals to and from the brain is interfered with, resulting in symptoms common to MS, including problems with balance, memory, vision loss and more.
Currently, anti-inflammatory drugs used to treat MS lessen the symptoms and slow the progression of the disease. But they must be given by injection daily, weekly or monthly â?? depending on the drug â?? and are expensive, costing between $12,000 to $24,000 a year.
Estriol is a hormone produced by the placenta that is virtually undetectable until pregnancy, when it progressively increases. It is thought that its role is to suppress a woman's immune system when she is pregnant, so that the fetus will not be seen by the body as a foreign "invader."
"The beauty of estriol is that it can be given as a pill, not a shot, and also that it's not a new drug; it has decades of safety behind it," said Voskuhl, who holds the Jack H. Skirball Chair for Multiple Sclerosis in the UCLA Department of Neurology. For years estriol has been in widespread use in Europe and Asia as hormone replacement therapy for women with menopausal symptoms. The fact that the pill already exists, she said, should dramatically reduce the cost of treatment.
Most important of all, though, is that the drug potentially provides a one-two punch against MS, both reducing the ability of immune cells to attack the brain, as well as making the brain more resistant to damage if any immune cells do make it through.
"It's a two-pronged approach an anti-inflammatory prong to reduce the attacks, but also a neuroprotective prong to make the brain suffer less damage in case of an attack," said Voskuhl. In all, seven institutions from around the nation will be involved in the two-year study. The investigators plan to recruit 150 women who have not previously been treated for MS. They will be given either estriol along with Copaxone, an MS drug currently in use, or a placebo along with Copaxone. "That way, no one will receive less than the standard of care," Voskuhl said. The team will measure relapse rates over the course of the trial.
Initial funding of $667,000 for the trial is being provided by the Southern California Chapter of the National Multiple Sclerosis Society. The total cost of the trial is expected to be $4.7 million.
Note: This story has been adapted from a news release issued by University of California - Los Angeles.
BORRELIOOSI/MS-TAUTI
Valvojat:Jatta1001, Borrelioosiyhdistys, Waltari, Bb
Viimeksi muokannut soijuv, Pe Loka 14, 2011 21:25. Yhteensä muokattu 2 kertaa.
Neuroboorelioosin/MS-taudin yhteys lymfoomiin.
MS & NEUROBORRELIOSIS Department of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia.
Batinac T, Petranovic D, Zamolo G, Petranovic D, Ruzic A.
Department of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia.
Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by chronic inflammation and demyelination. Studies suggested that the viral, especially Epstein-Barr virus infection, and bacterial infections, especially Borrelia burgodorferi infection, play a role in etiology of MS. MS prevalence parallels the distribution of the Lyme disease pathogen B. burgdorferi. Criteria used for diagnosis of MS can also be fulfilled in other conditions such as Lyme disease, a multisystem disorder resulting from infection by the tick-borne spirochete, B. burgdorferi. In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed. A Lyme borreliosis can mimick central nervous system lymphoma. Also, B. burgdorferi has been implicated not only in etiology of MS, but also in etiology of lymphoma. Studies suggested that there is an increased risk of non-Hodgkin lymphoma in patients, who had a history of autoimmune diseases such as MS and that both non-Hodgkin's lymphomas and Hodgkin's disease were associated with Epstein-Barr virus infection. A small group of lymphomas called primary effusion lymphomas (PEL) is a recently individualized form of non-Hodgkin's lymphoma (WHO classification) that exhibit exclusive or dominant involvement of serous cavities, without a detectable solid tumor mass. These lymphomas have also been linked to Epstein-Barr virus and human herpes virus type 8 infections but virus negative cases have been described. Therefore, we propose that MS and neuroborreliosis are linked to central nervous system primary effusion lymphomas. As a first step in confirming or refuting our hypotheses, we suggest a thorough study of CSF in the patients suspected for the diagnosis of MS and Lyme borreliosis.
PMID: 17197115 [PubMed - in process]
MS & NEUROBORRELIOSIS Department of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia.
Batinac T, Petranovic D, Zamolo G, Petranovic D, Ruzic A.
Department of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia.
Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by chronic inflammation and demyelination. Studies suggested that the viral, especially Epstein-Barr virus infection, and bacterial infections, especially Borrelia burgodorferi infection, play a role in etiology of MS. MS prevalence parallels the distribution of the Lyme disease pathogen B. burgdorferi. Criteria used for diagnosis of MS can also be fulfilled in other conditions such as Lyme disease, a multisystem disorder resulting from infection by the tick-borne spirochete, B. burgdorferi. In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed. A Lyme borreliosis can mimick central nervous system lymphoma. Also, B. burgdorferi has been implicated not only in etiology of MS, but also in etiology of lymphoma. Studies suggested that there is an increased risk of non-Hodgkin lymphoma in patients, who had a history of autoimmune diseases such as MS and that both non-Hodgkin's lymphomas and Hodgkin's disease were associated with Epstein-Barr virus infection. A small group of lymphomas called primary effusion lymphomas (PEL) is a recently individualized form of non-Hodgkin's lymphoma (WHO classification) that exhibit exclusive or dominant involvement of serous cavities, without a detectable solid tumor mass. These lymphomas have also been linked to Epstein-Barr virus and human herpes virus type 8 infections but virus negative cases have been described. Therefore, we propose that MS and neuroborreliosis are linked to central nervous system primary effusion lymphomas. As a first step in confirming or refuting our hypotheses, we suggest a thorough study of CSF in the patients suspected for the diagnosis of MS and Lyme borreliosis.
PMID: 17197115 [PubMed - in process]
Italialaisella Elena Ravallilla alkoivat oudot huimaus, puutumus, fatiikki ja silmäoireet 37-vuotiaana v. 1995. Hänen miehensä, lääketieteen professori Paolo Zamboni, alkoi taistella vaimonsa terveyden puolesta ja etsiä apua vaimolleen. Vaimon oireet oli diagnosoitu MS-oireiksi. MS-oireisiin ei ole löydetty selkeää syytä eikä hoitoa.
Zamboni havaitsi että MS ei ole autoimmuunitauti vaan verisuonisairaus. Etsiessään ratkaisua hän suoritti kokeellisen aivoleikkauksen vaimolleen.
Kirjallisuudessa on vuosikymmenten ajan esitetty olettamuksia että liiallinen raudan kertyminen verisuoniin aiheuttaa MS-oireet. Raskasmetalli aiheuttaa verisuonitulehduksia ja solukuolemaa. Zamboni havaitsi että yli 90 %:lla MS-oireista kärsivistä esiintyi aivoverisuonissa epämuodostumia ja tukoksia. Zamboni epäili että rauta saattaisi olla syynä siihen.
Zamboni suoritti yksinkertaisen leikkauksen jossa tukkeutuneet suonet avattiin. Sen seurauksena veri pääsi jälleen normaalisti aivoihin ja suurin osa MS-oireista hävisi. Hän suoritti leikkauksen vaimolleen 3 vuotta sitten ja tämä on ollut siitä lähtien oireeton. Italiassa 65 MS-potilaalle suoritettiin aivoverisuonten avausleikkaus. Kahden vuoden seuranta-ajan jälkeen 73 % potilaista oli edelleen oireettomia.
40-vuotias Augusto Zeppi sairastui MS-oireisiin 9 vuotta sitten. Oireet tulivat päälle 4 kk:n välein ja kestivät n. viikon kerrallaan. Hänellä oli vaikeuksia liikuttaa käsiä ja jalkoja sekä paha fatiikki. Aivokuvauksessa huomattiin kaksi tukkeutunutta suonta. Hänelle tehtiin leikkaus v. 2007. Leikkaus toistettiin vuotta myöhemmin sillä toinen suonista oli tukkeutunut uudelleen. Sen jälkeen hän sai elämänsä takaisin.
USA:ssa ja Kanadassa on juuri alkanut tukimus jossa selvitetään MS:n/verisuonitukkeumien välistä yhteyttä (2009).
Professori Zambonin mukaan lääketieteessä hyväksytään hitaasti uusia teorioita ja vielä hitaammin otetaan käyttöön uusia hoitomenetelmiä.
Suom.huom. Borreliabakteeri aiheuttaa verisuonitulehduksia ja tukoksia. Sivuillamme on kerrottu esim. suomalaisen naisen tapaus. Hän kuoli Bb:n aiheuttamaan verisuonitulehdukseen/tukokseen.
http://www.theglobeandmail.com/news/nat ... le1372414/
Researcher's labour of love leads to MS breakthrough
André Picard and Avis Favaro
From Saturday's Globe and Mail Published on Friday, Nov. 20, 2009 9:07PM EST Last updated on Monday, Nov. 23, 2009 3:07AM EST
Elena Ravalli was a seemingly healthy 37-year-old when she began to experience strange attacks of vertigo, numbness, temporary vision loss and crushing fatigue. They were classic signs of multiple sclerosis, a potentially debilitating neurological disease.
It was 1995 and her husband, Paolo Zamboni, a professor of medicine at the University of Ferrara in Italy, set out to help. He was determined to solve the mystery of MS ? an illness that strikes people in the prime of their lives but whose causes are unknown and whose effective treatments are few.
What he learned in his medical detective work, scouring dusty old books and using ultra-modern imaging techniques, could well turn what we know about MS on its head: Dr. Zamboni's research suggests that MS is not, as widely believed, an autoimmune condition, but a vascular disease.
More radical still, the experimental surgery he performed on his wife offers hope that MS, which afflicts 2.5 million people worldwide, can be cured and even largely prevented.
?I am confident that this could be a revolution for the research and diagnosis of multiple sclerosis,? Dr. Zamboni said in an interview.
Not everyone is so bullish: Skeptics warn the evidence is too scant and speculative to start rewriting medical textbooks. Even those intrigued by the theory caution that MS sufferers should not rush off to get the surgery ? nicknamed the ?liberation procedure? ? until more research is done.
U.S. and Canadian researchers are trying to test Dr. Zamboni's premise.
For the Italian professor, however, the quest was both personal and professional and the results were stunning.
Fighting for his wife's health, Dr. Zamboni looked for answers in the medical literature. He found repeated references, dating back a century, to excess iron as a possible cause of MS. The heavy metal can cause inflammation and cell death, hallmarks of the disease. The vascular surgeon was intrigued ? coincidentally, he had been researching how iron buildup damages blood vessels in the legs, and wondered if there could be a similar problem in the blood vessels of the brain.
Using ultrasound to examine the vessels leading in and out of the brain, Dr. Zamboni made a startling find: In more than 90 per cent of people with multiple sclerosis, including his spouse, the veins draining blood from the brain were malformed or blocked. In people without MS, they were not.
He hypothesized that iron was damaging the blood vessels and allowing the heavy metal, along with other unwelcome cells, to cross the crucial brain-blood barrier. (The barrier keeps blood and cerebrospinal fluid separate. In MS, immune cells cross the blood-brain barrier, where they destroy myelin, a crucial sheathing on nerves.)
More striking still was that, when Dr. Zamboni performed a simple operation to unclog veins and get blood flowing normally again, many of the symptoms of MS disappeared. The procedure is similar to angioplasty, in which a catheter is threaded into the groin and up into the arteries, where a balloon is inflated to clear the blockages. His wife, who had the surgery three years ago, has not had an attack since.
The researcher's theory is simple: that the underlying cause of MS is a condition he has dubbed ?chronic cerebrospinal venous insufficiency.? If you tackle CCSVI by repairing the drainage problems from the brain, you can successfully treat, or better still prevent, the disease.
?If this is proven correct, it will be a very, very big discovery because we'll completely change the way we think about MS, and how we'll treat it,? said Bianca Weinstock-Guttman, an associate professor of neurology at the State University of New York at Buffalo.
The initial studies done in Italy were small but the outcomes were dramatic. In a group of 65 patients with relapsing-remitting MS (the most common form) who underwent surgery, the number of active lesions in the brain fell sharply, to 12 per cent from 50 per cent; in the two years after surgery, 73 per cent of patients had no symptoms.
Augusto Zeppi, a 40-year-old resident of the northern Italian city of Ferrara, was one of those patients. Diagnosed with MS nine years ago, he suffered severe attacks every four months that lasted weeks at a time ? leaving him unable to use his arms and legs and with debilitating fatigue. ?Everything I was dreaming for my future adult life, it was game over,? he said.
Scans showed that his two jugular veins were blocked, 60 and 80 per cent respectively. In 2007, he was one of the first to undergo the experimental surgery to unblock the veins. He had a second operation a year later, when one of his jugular veins was blocked anew.
After the procedures, Mr. Zeppi said he was reborn. ?I don't remember what it's like to have MS,? he said. ?It gave me a second life.?
Buffalo researchers are now recruiting 1,700 adults and children from the United States and Canada. They plan to test MS sufferers and non-sufferers alike and, using ultrasound and magnetic resonance imaging, do detailed analyses of blood flow in and out of the brain and examine iron deposits.
Another researcher, Mark Haacke, an adjunct professor at McMaster University in Hamilton, is urging patients to send him MRI scans of their heads and necks so he can probe the Zamboni theory further. Dr. Haacke is a world-renowned expert in imaging who has developed a method of measuring iron buildup in the brain.
?Patients need to speak up and say they want something like this investigated ? to see if there's credence to the theory,? he said.
MS societies in Canada and the United States, however, have reacted far more cautiously to Dr. Zamboni's conclusion. ?Many questions remain about how and when this phenomenon might play a role in nervous system damage seen in MS, and at the present time there is insufficient evidence to suggest that this phenomenon is the cause of MS,? said the Multiple Sclerosis Society of Canada.
The U.S. society goes further, discouraging patients from getting tested or seeking surgical treatment. Rather, it continues to promote drug treatments used to alleviate symptoms, which include corticosteroids, chemotherapy agents and pain medication.
Many people with multiple sclerosis, though, are impatient for results. Chatter about CCSVI is frequent in online MS support groups, and patients are scrambling to be part of the research, particularly when they hear the testimonials.
Kevin Lipp, a 49-year-old resident of Buffalo, was diagnosed with MS a decade ago and has suffered increasingly severe attacks, especially in the heat. (Heat sensitivity is a common symptom of MS.) His symptoms were so bad that he was unable to work and closed his ice-cream shop.
Mr. Lipp was tested and doctors discovered blockages in both his jugular and azygos veins. In January of this year, he travelled to Italy for surgery, which cleared five blockages, and he began to feel better almost immediately.
?I felt good. I felt totally normal. I felt like I did years ago,? he said. He has not had an attack since.
As part of the research project, Mr. Lipp's siblings have also been tested. His two sisters, both of whom have MS, have significant blockages and iron deposits, while his brother, who does not have MS, has neither iron buildup nor blocked arteries.
While it has long been known that there is a genetic component to multiple sclerosis, the new theory is that it is CCSVI that is hereditary ? that people are born with malformed valves and strictures in the large veins of the neck and brain. These problems lead to poor blood drainage and even reversal of blood flow direction that can cause inflammation, iron buildup and the brain lesions characteristic of multiple sclerosis.
It is well-established that the symptoms of MS are caused by a breakdown of myelin, a fatty substance that coats nerve cells and plays a crucial role in transmitting messages to the central nervous system. When those messages are blurred, nerves malfunction, causing all manner of woes, including blurred eyesight, loss of sensation in the limbs and even paralysis.
However, it is unclear what triggers the breakdown of myelin. There are various theories, including exposure to a virus in childhood, vitamin D deficiency, hormones ? and now, buildup of iron in the brain because of poor blood flow.
While he is convinced of the significance of his discovery, Dr. Zamboni recognizes that medicine is slow to accept new theories and even slower to act on them. Regardless, he can take satisfaction in knowing that the woman who inspired the quest, and perhaps a dramatic breakthrough, has benefited tremendously.
Dr. Zamboni's wife, Elena, has undergone a battery of scans and neurological tests and her multiple sclerosis is, for all intents and purposes, gone.
?This is probably the best prize of the research,? he said.
André Picard is the public health reporter at The Globe and Mail. Avis Favaro is the medical correspondent at CTV News.
With reports from Elizabeth St. Philip, CTV News
W5 DOCUMENTARY
Watch W5's documentary on the groundbreaking new treatment for multiple sclerosis, which includes the first time the ?liberation? surgery was filmed.
It is available on the Web at www.W5.ctv.ca, and will be replayed Sunday on CTV Newschannel.
MS IN CANADA
An estimated 55,000-75,000 Canadians have multiple sclerosis, and every day three more people in Canada are diagnosed with the disease. Canada has one of the highest rates of MS in the world. MS is the most common neurological disease affecting young adults in Canada.
* Women are more than three times as likely as men to develop MS.
* MS can cause loss of balance, heat sensitivity, impaired speech, extreme fatigue, double vision and paralysis. The disease is characterized by lesions on the brain, a result of the breakdown of myelin, the protective covering wrapped around the nerves of the central nervous system.
* The most common treatment for MS is corticosteroids. Steroids reduce inflammation at the site of new demyelination, lessening symptoms.
* MS was first identified and described by French neurologist Jean-Martin Charcot in 1868.
* MS is widely believed to be an autoimmune disorder, but the cause or causes are unknown. There are a number of theories about what might trigger the disease, including exposure to a virus in childhood; exposure to tobacco smoke; lack of the female sex hormone prolactin, which plays a role in the development of myelin; and vitamin D deficiency. Vitamin D may play a role in MS because it helps to construct the interior layer of blood vessels.
* Despite the long-held assumption that MS is an autoimmune disorder, new research suggests it is actually a vascular disease triggered by a buildup of iron in the brain due to problems in blood flow.
Source: MS Society of Canada
Zamboni havaitsi että MS ei ole autoimmuunitauti vaan verisuonisairaus. Etsiessään ratkaisua hän suoritti kokeellisen aivoleikkauksen vaimolleen.
Kirjallisuudessa on vuosikymmenten ajan esitetty olettamuksia että liiallinen raudan kertyminen verisuoniin aiheuttaa MS-oireet. Raskasmetalli aiheuttaa verisuonitulehduksia ja solukuolemaa. Zamboni havaitsi että yli 90 %:lla MS-oireista kärsivistä esiintyi aivoverisuonissa epämuodostumia ja tukoksia. Zamboni epäili että rauta saattaisi olla syynä siihen.
Zamboni suoritti yksinkertaisen leikkauksen jossa tukkeutuneet suonet avattiin. Sen seurauksena veri pääsi jälleen normaalisti aivoihin ja suurin osa MS-oireista hävisi. Hän suoritti leikkauksen vaimolleen 3 vuotta sitten ja tämä on ollut siitä lähtien oireeton. Italiassa 65 MS-potilaalle suoritettiin aivoverisuonten avausleikkaus. Kahden vuoden seuranta-ajan jälkeen 73 % potilaista oli edelleen oireettomia.
40-vuotias Augusto Zeppi sairastui MS-oireisiin 9 vuotta sitten. Oireet tulivat päälle 4 kk:n välein ja kestivät n. viikon kerrallaan. Hänellä oli vaikeuksia liikuttaa käsiä ja jalkoja sekä paha fatiikki. Aivokuvauksessa huomattiin kaksi tukkeutunutta suonta. Hänelle tehtiin leikkaus v. 2007. Leikkaus toistettiin vuotta myöhemmin sillä toinen suonista oli tukkeutunut uudelleen. Sen jälkeen hän sai elämänsä takaisin.
USA:ssa ja Kanadassa on juuri alkanut tukimus jossa selvitetään MS:n/verisuonitukkeumien välistä yhteyttä (2009).
Professori Zambonin mukaan lääketieteessä hyväksytään hitaasti uusia teorioita ja vielä hitaammin otetaan käyttöön uusia hoitomenetelmiä.
Suom.huom. Borreliabakteeri aiheuttaa verisuonitulehduksia ja tukoksia. Sivuillamme on kerrottu esim. suomalaisen naisen tapaus. Hän kuoli Bb:n aiheuttamaan verisuonitulehdukseen/tukokseen.
http://www.theglobeandmail.com/news/nat ... le1372414/
Researcher's labour of love leads to MS breakthrough
André Picard and Avis Favaro
From Saturday's Globe and Mail Published on Friday, Nov. 20, 2009 9:07PM EST Last updated on Monday, Nov. 23, 2009 3:07AM EST
Elena Ravalli was a seemingly healthy 37-year-old when she began to experience strange attacks of vertigo, numbness, temporary vision loss and crushing fatigue. They were classic signs of multiple sclerosis, a potentially debilitating neurological disease.
It was 1995 and her husband, Paolo Zamboni, a professor of medicine at the University of Ferrara in Italy, set out to help. He was determined to solve the mystery of MS ? an illness that strikes people in the prime of their lives but whose causes are unknown and whose effective treatments are few.
What he learned in his medical detective work, scouring dusty old books and using ultra-modern imaging techniques, could well turn what we know about MS on its head: Dr. Zamboni's research suggests that MS is not, as widely believed, an autoimmune condition, but a vascular disease.
More radical still, the experimental surgery he performed on his wife offers hope that MS, which afflicts 2.5 million people worldwide, can be cured and even largely prevented.
?I am confident that this could be a revolution for the research and diagnosis of multiple sclerosis,? Dr. Zamboni said in an interview.
Not everyone is so bullish: Skeptics warn the evidence is too scant and speculative to start rewriting medical textbooks. Even those intrigued by the theory caution that MS sufferers should not rush off to get the surgery ? nicknamed the ?liberation procedure? ? until more research is done.
U.S. and Canadian researchers are trying to test Dr. Zamboni's premise.
For the Italian professor, however, the quest was both personal and professional and the results were stunning.
Fighting for his wife's health, Dr. Zamboni looked for answers in the medical literature. He found repeated references, dating back a century, to excess iron as a possible cause of MS. The heavy metal can cause inflammation and cell death, hallmarks of the disease. The vascular surgeon was intrigued ? coincidentally, he had been researching how iron buildup damages blood vessels in the legs, and wondered if there could be a similar problem in the blood vessels of the brain.
Using ultrasound to examine the vessels leading in and out of the brain, Dr. Zamboni made a startling find: In more than 90 per cent of people with multiple sclerosis, including his spouse, the veins draining blood from the brain were malformed or blocked. In people without MS, they were not.
He hypothesized that iron was damaging the blood vessels and allowing the heavy metal, along with other unwelcome cells, to cross the crucial brain-blood barrier. (The barrier keeps blood and cerebrospinal fluid separate. In MS, immune cells cross the blood-brain barrier, where they destroy myelin, a crucial sheathing on nerves.)
More striking still was that, when Dr. Zamboni performed a simple operation to unclog veins and get blood flowing normally again, many of the symptoms of MS disappeared. The procedure is similar to angioplasty, in which a catheter is threaded into the groin and up into the arteries, where a balloon is inflated to clear the blockages. His wife, who had the surgery three years ago, has not had an attack since.
The researcher's theory is simple: that the underlying cause of MS is a condition he has dubbed ?chronic cerebrospinal venous insufficiency.? If you tackle CCSVI by repairing the drainage problems from the brain, you can successfully treat, or better still prevent, the disease.
?If this is proven correct, it will be a very, very big discovery because we'll completely change the way we think about MS, and how we'll treat it,? said Bianca Weinstock-Guttman, an associate professor of neurology at the State University of New York at Buffalo.
The initial studies done in Italy were small but the outcomes were dramatic. In a group of 65 patients with relapsing-remitting MS (the most common form) who underwent surgery, the number of active lesions in the brain fell sharply, to 12 per cent from 50 per cent; in the two years after surgery, 73 per cent of patients had no symptoms.
Augusto Zeppi, a 40-year-old resident of the northern Italian city of Ferrara, was one of those patients. Diagnosed with MS nine years ago, he suffered severe attacks every four months that lasted weeks at a time ? leaving him unable to use his arms and legs and with debilitating fatigue. ?Everything I was dreaming for my future adult life, it was game over,? he said.
Scans showed that his two jugular veins were blocked, 60 and 80 per cent respectively. In 2007, he was one of the first to undergo the experimental surgery to unblock the veins. He had a second operation a year later, when one of his jugular veins was blocked anew.
After the procedures, Mr. Zeppi said he was reborn. ?I don't remember what it's like to have MS,? he said. ?It gave me a second life.?
Buffalo researchers are now recruiting 1,700 adults and children from the United States and Canada. They plan to test MS sufferers and non-sufferers alike and, using ultrasound and magnetic resonance imaging, do detailed analyses of blood flow in and out of the brain and examine iron deposits.
Another researcher, Mark Haacke, an adjunct professor at McMaster University in Hamilton, is urging patients to send him MRI scans of their heads and necks so he can probe the Zamboni theory further. Dr. Haacke is a world-renowned expert in imaging who has developed a method of measuring iron buildup in the brain.
?Patients need to speak up and say they want something like this investigated ? to see if there's credence to the theory,? he said.
MS societies in Canada and the United States, however, have reacted far more cautiously to Dr. Zamboni's conclusion. ?Many questions remain about how and when this phenomenon might play a role in nervous system damage seen in MS, and at the present time there is insufficient evidence to suggest that this phenomenon is the cause of MS,? said the Multiple Sclerosis Society of Canada.
The U.S. society goes further, discouraging patients from getting tested or seeking surgical treatment. Rather, it continues to promote drug treatments used to alleviate symptoms, which include corticosteroids, chemotherapy agents and pain medication.
Many people with multiple sclerosis, though, are impatient for results. Chatter about CCSVI is frequent in online MS support groups, and patients are scrambling to be part of the research, particularly when they hear the testimonials.
Kevin Lipp, a 49-year-old resident of Buffalo, was diagnosed with MS a decade ago and has suffered increasingly severe attacks, especially in the heat. (Heat sensitivity is a common symptom of MS.) His symptoms were so bad that he was unable to work and closed his ice-cream shop.
Mr. Lipp was tested and doctors discovered blockages in both his jugular and azygos veins. In January of this year, he travelled to Italy for surgery, which cleared five blockages, and he began to feel better almost immediately.
?I felt good. I felt totally normal. I felt like I did years ago,? he said. He has not had an attack since.
As part of the research project, Mr. Lipp's siblings have also been tested. His two sisters, both of whom have MS, have significant blockages and iron deposits, while his brother, who does not have MS, has neither iron buildup nor blocked arteries.
While it has long been known that there is a genetic component to multiple sclerosis, the new theory is that it is CCSVI that is hereditary ? that people are born with malformed valves and strictures in the large veins of the neck and brain. These problems lead to poor blood drainage and even reversal of blood flow direction that can cause inflammation, iron buildup and the brain lesions characteristic of multiple sclerosis.
It is well-established that the symptoms of MS are caused by a breakdown of myelin, a fatty substance that coats nerve cells and plays a crucial role in transmitting messages to the central nervous system. When those messages are blurred, nerves malfunction, causing all manner of woes, including blurred eyesight, loss of sensation in the limbs and even paralysis.
However, it is unclear what triggers the breakdown of myelin. There are various theories, including exposure to a virus in childhood, vitamin D deficiency, hormones ? and now, buildup of iron in the brain because of poor blood flow.
While he is convinced of the significance of his discovery, Dr. Zamboni recognizes that medicine is slow to accept new theories and even slower to act on them. Regardless, he can take satisfaction in knowing that the woman who inspired the quest, and perhaps a dramatic breakthrough, has benefited tremendously.
Dr. Zamboni's wife, Elena, has undergone a battery of scans and neurological tests and her multiple sclerosis is, for all intents and purposes, gone.
?This is probably the best prize of the research,? he said.
André Picard is the public health reporter at The Globe and Mail. Avis Favaro is the medical correspondent at CTV News.
With reports from Elizabeth St. Philip, CTV News
W5 DOCUMENTARY
Watch W5's documentary on the groundbreaking new treatment for multiple sclerosis, which includes the first time the ?liberation? surgery was filmed.
It is available on the Web at www.W5.ctv.ca, and will be replayed Sunday on CTV Newschannel.
MS IN CANADA
An estimated 55,000-75,000 Canadians have multiple sclerosis, and every day three more people in Canada are diagnosed with the disease. Canada has one of the highest rates of MS in the world. MS is the most common neurological disease affecting young adults in Canada.
* Women are more than three times as likely as men to develop MS.
* MS can cause loss of balance, heat sensitivity, impaired speech, extreme fatigue, double vision and paralysis. The disease is characterized by lesions on the brain, a result of the breakdown of myelin, the protective covering wrapped around the nerves of the central nervous system.
* The most common treatment for MS is corticosteroids. Steroids reduce inflammation at the site of new demyelination, lessening symptoms.
* MS was first identified and described by French neurologist Jean-Martin Charcot in 1868.
* MS is widely believed to be an autoimmune disorder, but the cause or causes are unknown. There are a number of theories about what might trigger the disease, including exposure to a virus in childhood; exposure to tobacco smoke; lack of the female sex hormone prolactin, which plays a role in the development of myelin; and vitamin D deficiency. Vitamin D may play a role in MS because it helps to construct the interior layer of blood vessels.
* Despite the long-held assumption that MS is an autoimmune disorder, new research suggests it is actually a vascular disease triggered by a buildup of iron in the brain due to problems in blood flow.
Source: MS Society of Canada
Tutkimuksen mukaan MS-tauti on usein borreliabakteerin aiheuttama.
Chmielewska-Badora J, Cisak E, Dutkiewicz J.Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study.
Department of Occupational Biohazards, Institute of Agricultural Medicine, Jaczewskiego 2, 20-090 Lublin, Poland.
A total of 769 adult neurological patients hospitalised in clinics and hospitals situated in the Lublin region (eastern Poland) were examined during the years 1997-2000 with ELISA test for the presence of anti-Borrelia burgdorferi sensu lato antibodies. A statististically significant (p=0.0422) relationship was found between the clinically confirmed diagnosis of multiple sclerosis and the positive serologic reaction with Borrelia antigen. Ten out 26 patients with multiple sclerosis (38.5%) showed positive serologic reaction to Borrelia, whereas among the total number of examined neurological patients the frequency of positive findings was twice as low (19.4%). The result suggests that multiple sclerosis may be often associated with Borrelia infection
Chmielewska-Badora J, Cisak E, Dutkiewicz J.Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study.
Department of Occupational Biohazards, Institute of Agricultural Medicine, Jaczewskiego 2, 20-090 Lublin, Poland.
A total of 769 adult neurological patients hospitalised in clinics and hospitals situated in the Lublin region (eastern Poland) were examined during the years 1997-2000 with ELISA test for the presence of anti-Borrelia burgdorferi sensu lato antibodies. A statististically significant (p=0.0422) relationship was found between the clinically confirmed diagnosis of multiple sclerosis and the positive serologic reaction with Borrelia antigen. Ten out 26 patients with multiple sclerosis (38.5%) showed positive serologic reaction to Borrelia, whereas among the total number of examined neurological patients the frequency of positive findings was twice as low (19.4%). The result suggests that multiple sclerosis may be often associated with Borrelia infection
2010 Kroatia: Useat eri taudinaiheuttajat esim. borreliabakteeri voivat aiheuttaa MS-oireiston:
Clin Neurol Neurosurg. 2010 May 1; [Epub ahead of print]
Rare infections mimicking MS.
Brinar VV, Habek M.
University of Zagreb, School of Medicine and University Hospital Centre Zagreb,
Department of Neurology and Refferal Center for Demyelinating Diseases of the
Central Nervous System, Zagreb, Croatia.
The diagnosis of multiple sclerosis (MS), despite well defined clinical criteria
is not always simple. On many occasions it is difficult to differentiate MS from
various non-MS idiopathic demyelinating disorders, specific and infectious
inflammatory diseases or non-inflammatory demyelinating diseases. Clinicians
should be aware of various clinical and MRI "red flags" that may point to the
other diagnosis and demand further diagnostic evaluation. It is generally
accepted that atypical clinical symptoms or atypical neuroimaging signs
determine necessity for broad differential diagnostic work up. Of the infectious
diseases that are most commonly mistaken for MS the clinician should take into
account Whipple's disease, Lyme disease, Syphilis, HIV/AIDS, Brucellosis, HHV-6
infection, Hepatitis C, Mycoplasma and Creutzfeld-Jacob disease, among others.
Cat scratch disease caused by Bartonella hensellae, Mediterranean spotted fever
caused by Riketssia connore and Leptospirosis caused by different Leptospira
serovars rarely cause focal neurological deficit and demyelinating MRI changes
similar to MS. When atypical clinical and neuroimaging presentations are
present, serology on rare infectious diseases that may mimic MS may be
warranted. This review will focus on the infectious diseases mimicking MS with
presentation of rare illustrative cases. Copyright (c) 2010. Published by
Elsevier B.V.
http://eutils.ncbi.nlm.nih.gov/entrez/e ... md=prlinks
PMID: 20439131 [PubMed - as supplied by publisher]
Clin Neurol Neurosurg. 2010 May 1; [Epub ahead of print]
Rare infections mimicking MS.
Brinar VV, Habek M.
University of Zagreb, School of Medicine and University Hospital Centre Zagreb,
Department of Neurology and Refferal Center for Demyelinating Diseases of the
Central Nervous System, Zagreb, Croatia.
The diagnosis of multiple sclerosis (MS), despite well defined clinical criteria
is not always simple. On many occasions it is difficult to differentiate MS from
various non-MS idiopathic demyelinating disorders, specific and infectious
inflammatory diseases or non-inflammatory demyelinating diseases. Clinicians
should be aware of various clinical and MRI "red flags" that may point to the
other diagnosis and demand further diagnostic evaluation. It is generally
accepted that atypical clinical symptoms or atypical neuroimaging signs
determine necessity for broad differential diagnostic work up. Of the infectious
diseases that are most commonly mistaken for MS the clinician should take into
account Whipple's disease, Lyme disease, Syphilis, HIV/AIDS, Brucellosis, HHV-6
infection, Hepatitis C, Mycoplasma and Creutzfeld-Jacob disease, among others.
Cat scratch disease caused by Bartonella hensellae, Mediterranean spotted fever
caused by Riketssia connore and Leptospirosis caused by different Leptospira
serovars rarely cause focal neurological deficit and demyelinating MRI changes
similar to MS. When atypical clinical and neuroimaging presentations are
present, serology on rare infectious diseases that may mimic MS may be
warranted. This review will focus on the infectious diseases mimicking MS with
presentation of rare illustrative cases. Copyright (c) 2010. Published by
Elsevier B.V.
http://eutils.ncbi.nlm.nih.gov/entrez/e ... md=prlinks
PMID: 20439131 [PubMed - as supplied by publisher]
Borrelia-bakteeri voi aiheuttaa MS-oireiston. Alla useita sivustoja aiheesta. Linkit aktivoituvat sivulta
http://www.lymeinfo.net/multiplesclerosis.html
Lyme Disease Misdiagnosed as Multiple Sclerosis
The following articles compiled by LymeInfo provide information about Lyme disease being misdiagnosed as Multiple Sclerosis. The differential diagnosis can be tricky, as Lyme tests can be falsely negative. Disseminated Lyme disease is also very complicated to treat. Therefore, it is important for those diagnosed with Multiple Sclerosis to be thoroughly evaluated by a physician skilled at diagnosing Lyme disease. After reviewing the below articles, please browse around the Lyme Info website to learn more about Lyme disease and other tick-borne illnesses. Be sure to visit our Lyme Disease Diagnosis & Treatment page. The list below is merely an introduction and does not cover all articles on this topic.
Medical Abstracts:
Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma. (2007)
"In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed."
Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable? (2005)
"As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted."
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis. (2004)
"Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described. In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI."
Bacterial infection as a cause of multiple sclerosis. (2002)
"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."
Association between multiple sclerosis and cystic structures in cerebrospinal fluid. (2001)
"Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS."
Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. (2001)
"Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum."
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. (2000)
"The result suggests that multiple sclerosis may be often associated with Borrelia infection."
Multiple sclerosis vs Lyme disease: a case presentation to a discussant and a review of the literature.(1999)
Read the first page here.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. (1996)
"We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection."
The presence of anti-Borrelia burgdorferi antibodies in a group of multiple sclerosis patients in eastern Sicily. Preliminary data. (1993)
"The authors evaluate the presence of anti-Borrelia burgdorferi antibodies in a group of polysclerotic patients of Eastern Sicily, in order to verify or dismiss a correlation between Borrelia infection and demyelinizing syndrome."
Diseases that mimic multiple sclerosis. (1991)
"Dr Scott compares typical findings of multiple sclerosis with those of the four diseases that are sometimes mistaken for this syndrome."
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion. (1990)
"In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed."
Neurologic manifestations of Lyme disease, the new "great imitator". (1989)
"Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements."
Clinical manifestations of Lyme disease in the United States. (1989)
Conn Med. 1989 Jun;53(6):327-30.
Clinical pathologic correlations of Lyme disease. (1989)
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Chronic central nervous system involvement in Lyme borreliosis. (1988)
"We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis."
Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. (1988)
"Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement."
Demyelinating encephalopathy in Lyme disease. (1985)
"A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later."
Conferences:
Lyme Borreliosis and Related Disorders
by Liegner
11th International Scientific Conference on Lyme Disease and Other Spirochetal & Tick-Borne Disorders, 1998
Subtle Injury to Transformed Neural Cell Lines by Bb
by Benach
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, 1997
Spectrum of Antibiotic-Responsive Meningoencephalomyelitides
by Liegner
8th Annual LDF International Scientific Conference on Lyme Borreliosis and other Spirochetal and Tick-borne Diseases, 1995
Patient Stories:
Multiple Sclerosis & Lyme Blog
"I was content with the Multiple Sclerosis, and the routine that I had gotten into; both with the treatments and understanding the disease. Now I am thrown into something that I do not understand all that well. Furthermore, I am having a difficult time finding a doctor that is skilled in treating Lyme, especially now that I have long entered chronic/3rd stage Lyme (and all those doses of Solu-medrol only made things worse)."
Doctors can misdiagnose Lyme disease for MS, April 2010
"In a recent thesis, Winnipeg researcher Kathleen Crang found that some Manitobans diagnosed with MS and other chronic conditions may actually be suffering from the borrelia bacteria, a tick-borne 'biological evil genius' that causes Lyme disease."
Lyme disease sufferer spent years being misdiagnosed
"One neurologist told her she had multiple sclerosis. It's common, she says, for people with Lyme disease to be misdiagnosed as having multiple sclerosis, lupus, arthritis, or other illnesses with similar symptoms."
Patients, doctors debate Lyme
"Plagued witt unexplained fatigue, muscle aches, eye pain and other problems for years, Tierney was diagnosed with multiple sclerosis last year." (Free registration to LymeInfo required.)
Not Giving Up, The Corning Leader, December 2004 (expired link)
"Until January, Heininger lived for 20 years believing that multiple sclerosis was the cause of her growing disability. She is one of an increasing number of people who are learning that Lyme is a "disease in disguise," according to an Aug. 23 Newsweek article."
Lyme disease can get very severe without antibiotics, The Daily Review, September 2002
"Probably 10 percent of multiple sclerosis cases are actually Lyme's," Stricker said. "There's really not a lot of expertise in this area, sadly. It's really amazing how many patients will come in and say their doctor says Lyme disease doesn't happen here." (Free registration to LymeInfo required.)
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005 (expired link)
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
Misc:
Research by Gabriel Steiner on spirochetes and MS.
"In this respect the discovered spirochetes were totally different from the treponema-type and resembled the borrelia-type of spirochetes."
Systemic Intracellular Bacterial Infections
Article addresses Mycoplasma, Chlamydia, Borrelia species in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseases. Excerpt: "When these infections are released from cells, they contain host cell antigens in their exterior membranes, and these normal cell membrane antigens could stimulate autoimmune responses. Alternatively, the microorganisms may express antigens that mimic normal surface antigens." (Published April 2008)
Multiple Sclerosis Patients Should Be Tested for Lyme Disease
"Because both Multiple Sclerosis and Lyme Disease are diseases of the central nervous system, they both manifest themselves in ways that are different person to person."
Book: Multiple Sclerosis Through History and Human Life
Covers history of spirochete research as a cause of MS.
Editorial on MS & Lyme
"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."
Video: Chronic Lyme Disease: Connection to MS- Facts behind the controversy
This lecture was recorded at the Lyme Symposium held at the University of New Haven on May 12, 2006.
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lyme/MS Journal References
"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."
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
Multiple Sclerosis Sites:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
http://www.lymeinfo.net/multiplesclerosis.html
Lyme Disease Misdiagnosed as Multiple Sclerosis
The following articles compiled by LymeInfo provide information about Lyme disease being misdiagnosed as Multiple Sclerosis. The differential diagnosis can be tricky, as Lyme tests can be falsely negative. Disseminated Lyme disease is also very complicated to treat. Therefore, it is important for those diagnosed with Multiple Sclerosis to be thoroughly evaluated by a physician skilled at diagnosing Lyme disease. After reviewing the below articles, please browse around the Lyme Info website to learn more about Lyme disease and other tick-borne illnesses. Be sure to visit our Lyme Disease Diagnosis & Treatment page. The list below is merely an introduction and does not cover all articles on this topic.
Medical Abstracts:
Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma. (2007)
"In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed."
Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable? (2005)
"As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted."
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis. (2004)
"Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described. In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI."
Bacterial infection as a cause of multiple sclerosis. (2002)
"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."
Association between multiple sclerosis and cystic structures in cerebrospinal fluid. (2001)
"Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS."
Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. (2001)
"Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum."
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. (2000)
"The result suggests that multiple sclerosis may be often associated with Borrelia infection."
Multiple sclerosis vs Lyme disease: a case presentation to a discussant and a review of the literature.(1999)
Read the first page here.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. (1996)
"We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection."
The presence of anti-Borrelia burgdorferi antibodies in a group of multiple sclerosis patients in eastern Sicily. Preliminary data. (1993)
"The authors evaluate the presence of anti-Borrelia burgdorferi antibodies in a group of polysclerotic patients of Eastern Sicily, in order to verify or dismiss a correlation between Borrelia infection and demyelinizing syndrome."
Diseases that mimic multiple sclerosis. (1991)
"Dr Scott compares typical findings of multiple sclerosis with those of the four diseases that are sometimes mistaken for this syndrome."
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion. (1990)
"In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed."
Neurologic manifestations of Lyme disease, the new "great imitator". (1989)
"Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements."
Clinical manifestations of Lyme disease in the United States. (1989)
Conn Med. 1989 Jun;53(6):327-30.
Clinical pathologic correlations of Lyme disease. (1989)
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Chronic central nervous system involvement in Lyme borreliosis. (1988)
"We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis."
Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. (1988)
"Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement."
Demyelinating encephalopathy in Lyme disease. (1985)
"A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later."
Conferences:
Lyme Borreliosis and Related Disorders
by Liegner
11th International Scientific Conference on Lyme Disease and Other Spirochetal & Tick-Borne Disorders, 1998
Subtle Injury to Transformed Neural Cell Lines by Bb
by Benach
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, 1997
Spectrum of Antibiotic-Responsive Meningoencephalomyelitides
by Liegner
8th Annual LDF International Scientific Conference on Lyme Borreliosis and other Spirochetal and Tick-borne Diseases, 1995
Patient Stories:
Multiple Sclerosis & Lyme Blog
"I was content with the Multiple Sclerosis, and the routine that I had gotten into; both with the treatments and understanding the disease. Now I am thrown into something that I do not understand all that well. Furthermore, I am having a difficult time finding a doctor that is skilled in treating Lyme, especially now that I have long entered chronic/3rd stage Lyme (and all those doses of Solu-medrol only made things worse)."
Doctors can misdiagnose Lyme disease for MS, April 2010
"In a recent thesis, Winnipeg researcher Kathleen Crang found that some Manitobans diagnosed with MS and other chronic conditions may actually be suffering from the borrelia bacteria, a tick-borne 'biological evil genius' that causes Lyme disease."
Lyme disease sufferer spent years being misdiagnosed
"One neurologist told her she had multiple sclerosis. It's common, she says, for people with Lyme disease to be misdiagnosed as having multiple sclerosis, lupus, arthritis, or other illnesses with similar symptoms."
Patients, doctors debate Lyme
"Plagued witt unexplained fatigue, muscle aches, eye pain and other problems for years, Tierney was diagnosed with multiple sclerosis last year." (Free registration to LymeInfo required.)
Not Giving Up, The Corning Leader, December 2004 (expired link)
"Until January, Heininger lived for 20 years believing that multiple sclerosis was the cause of her growing disability. She is one of an increasing number of people who are learning that Lyme is a "disease in disguise," according to an Aug. 23 Newsweek article."
Lyme disease can get very severe without antibiotics, The Daily Review, September 2002
"Probably 10 percent of multiple sclerosis cases are actually Lyme's," Stricker said. "There's really not a lot of expertise in this area, sadly. It's really amazing how many patients will come in and say their doctor says Lyme disease doesn't happen here." (Free registration to LymeInfo required.)
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005 (expired link)
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
Misc:
Research by Gabriel Steiner on spirochetes and MS.
"In this respect the discovered spirochetes were totally different from the treponema-type and resembled the borrelia-type of spirochetes."
Systemic Intracellular Bacterial Infections
Article addresses Mycoplasma, Chlamydia, Borrelia species in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseases. Excerpt: "When these infections are released from cells, they contain host cell antigens in their exterior membranes, and these normal cell membrane antigens could stimulate autoimmune responses. Alternatively, the microorganisms may express antigens that mimic normal surface antigens." (Published April 2008)
Multiple Sclerosis Patients Should Be Tested for Lyme Disease
"Because both Multiple Sclerosis and Lyme Disease are diseases of the central nervous system, they both manifest themselves in ways that are different person to person."
Book: Multiple Sclerosis Through History and Human Life
Covers history of spirochete research as a cause of MS.
Editorial on MS & Lyme
"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."
Video: Chronic Lyme Disease: Connection to MS- Facts behind the controversy
This lecture was recorded at the Lyme Symposium held at the University of New Haven on May 12, 2006.
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lyme/MS Journal References
"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."
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
Multiple Sclerosis Sites:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
2011: Borrelia-bakteerin aiheuttaman infektion seurauksena voi esiintyä keskushermoston valkean aineen vaurioita (demyelinisaatioprosessi kuten esim. MS taudissa).
Infection with B. burgdorferi s.l., and the CNS Demyelinating Disease. A Case Report.
Durovska J
Neuro Endocrinol Lett 2011 08 30; 32 (4)
The work describes three cases of patients at various ages, diagnosed for CNS demyelinating disease. The presence of specific antibodies to B. burgdorferi sensu lato, and findings of B. burgdorferi s.l. DNA, identified in one case as the genospecies B. garinii in the liquor, indicated previous experience with the infection. Presumably, persistence of borrelia in the organism could act as one of the autoimmune process triggers, resulting in the demyelinating disease.
Infection with B. burgdorferi s.l., and the CNS Demyelinating Disease. A Case Report.
Durovska J
Neuro Endocrinol Lett 2011 08 30; 32 (4)
The work describes three cases of patients at various ages, diagnosed for CNS demyelinating disease. The presence of specific antibodies to B. burgdorferi sensu lato, and findings of B. burgdorferi s.l. DNA, identified in one case as the genospecies B. garinii in the liquor, indicated previous experience with the infection. Presumably, persistence of borrelia in the organism could act as one of the autoimmune process triggers, resulting in the demyelinating disease.
Borrelia-bakteeri kykenee läpäisemään aivo-veriesteen jo taudin varhaisvaiheessa. Allaolevassa tapausselostuksessa potilaalla ei ollut ihomuutosta (rengasmaista ihomuutosta) eikä niveloireita. Magneettikuvassa havaittiin verisuonitulehduksia ja MS taudillekin tyypillisiä valkean aineen vaurioita aivoissa. Selkäydinnesteestä löytyi borrelia vasta-aineita.
Neurol Sci. 2010 Apr;31(2):193-6. Epub 2009 Nov 6.
Borrelia burgdorferi, a great chameleon: know it to recognize it!
Santino I, Comite P, Gandolfo GM.
Source
Department of Public Health Sciences, Sapienza University of Rome, Rome, Italy. iolanda.santino@uniroma1.it
Abstract
Borrelia burgdorferi is a spirochaete that can penetrate the blood-brain barrier in early infection and can cause endothelial damage other than central nervous system lesions. We describe a clinical case of neuroborreliosis that occurred in the absence of classical erythema migrans or arthralgia. Magnetic resonance imaging findings compatible with simil-vasculitis and demyelinating lesions associated with the presence of anti-B. burgdorferi antibodies in the plasma or cerebrospinal liquid is an indication for antimicrobial treatment against B. burgdorferi. An early diagnosis and a prompt establishment of an adequate antibiotic treatment is needed for a successful recovery.
PMID:
19894021
[PubMed - indexed for MEDLINE]
Neurol Sci. 2010 Apr;31(2):193-6. Epub 2009 Nov 6.
Borrelia burgdorferi, a great chameleon: know it to recognize it!
Santino I, Comite P, Gandolfo GM.
Source
Department of Public Health Sciences, Sapienza University of Rome, Rome, Italy. iolanda.santino@uniroma1.it
Abstract
Borrelia burgdorferi is a spirochaete that can penetrate the blood-brain barrier in early infection and can cause endothelial damage other than central nervous system lesions. We describe a clinical case of neuroborreliosis that occurred in the absence of classical erythema migrans or arthralgia. Magnetic resonance imaging findings compatible with simil-vasculitis and demyelinating lesions associated with the presence of anti-B. burgdorferi antibodies in the plasma or cerebrospinal liquid is an indication for antimicrobial treatment against B. burgdorferi. An early diagnosis and a prompt establishment of an adequate antibiotic treatment is needed for a successful recovery.
PMID:
19894021
[PubMed - indexed for MEDLINE]
Venäjä 2011. Jaroslavin alueella on runsaasti Borrelioosia. Kroonista neuroborrelioosia on erittäin vaikea erottaa MS-taudista. Diagnostiikkaa helpottaa mikäli potilaalla on/on ollut vaeltava ihomuutos, punkinpurema, muutoksia keskushermostossa jne.
Differential aspects of multiple sclerosis and chronic borrelial encephalomyelitis.]
Spirin NN, Baranova NS, Fadeeva OA, Shipova EG, Stepanov IO
Zh Nevrol Psikhiatr Im S S Korsakova 2011 9; 111 (7): 8-12
The Yaroslavl region is an endemic area for Lyme disease (LD) with one of the highest levels of morbidity in Russia. Chronic neuroborreliosis can mimic multiple sclerosis and cause considerable difficulties in differential diagnosis. A comparative clinical-instrumental analysis of patients with definite multiple sclerosis (n=65) and chronic borrelial encephalomyelitis (n=11) was carried out.
The key differential-diagnostic features of multiple sclerosis and borrelial encephalomyelitis were specified. Migrating erythema and tick's bite in the anamnesis, combined with lesions of the central and peripheral nervous systems, the absence of retrobulbar neuritis in the anamnesis, artralgia and myalgia, the high blood sedimentation rate were not characteristic of multiple sclerosis. A patient with above mentioned findings should be tested for the presence of antibodies to Borrelia burgdorferi in the blood serum and, if necessary, in the cerebrospinal fluid to exclude the diagnosis o f Lyme disease.
Differential aspects of multiple sclerosis and chronic borrelial encephalomyelitis.]
Spirin NN, Baranova NS, Fadeeva OA, Shipova EG, Stepanov IO
Zh Nevrol Psikhiatr Im S S Korsakova 2011 9; 111 (7): 8-12
The Yaroslavl region is an endemic area for Lyme disease (LD) with one of the highest levels of morbidity in Russia. Chronic neuroborreliosis can mimic multiple sclerosis and cause considerable difficulties in differential diagnosis. A comparative clinical-instrumental analysis of patients with definite multiple sclerosis (n=65) and chronic borrelial encephalomyelitis (n=11) was carried out.
The key differential-diagnostic features of multiple sclerosis and borrelial encephalomyelitis were specified. Migrating erythema and tick's bite in the anamnesis, combined with lesions of the central and peripheral nervous systems, the absence of retrobulbar neuritis in the anamnesis, artralgia and myalgia, the high blood sedimentation rate were not characteristic of multiple sclerosis. A patient with above mentioned findings should be tested for the presence of antibodies to Borrelia burgdorferi in the blood serum and, if necessary, in the cerebrospinal fluid to exclude the diagnosis o f Lyme disease.
Otteita artikkelista:
http://www.newswithviews.com/Howenstine/james26.htm
"Borrelioosissa esiintyy yleisesti neurologisia ongelmia sillä bakteerin erittämät neurotoksiinit sitoutuvat rasvakudoksiin. Rasvakudosta on runsaasti mm aivoissa ja äärihermostossa. Neurotoksiinit voivat aiheuttaa äkillisen kuuroutumisen, kasvohermohalvauksen, Parkinsonin oireet, MS oireet, hermotulehduksia, kroonista kipua ym neurologisia ongelmia. Kissankynsi näyttäisi korjaavan immuunipuolustuksen toimintaa, tuhoavan mikrobeja ja estävän hermomyrkkyjen vaikutuksen soluihin, entsyymeihin ja hormoneihin.
Tri Joanne Whitakerin potilailla lähes jokaisen Parkinson oireita sairastavan borrelia-testi on ollut positiivinen. Tri Louis Romero kertoo kolmen Parkinson potilaansa olevan lähes oireettomia (99%) TOA vapaan kissankynsihoidon jälkeen.
Tapausselostuksia:
Larry Powers sairastui Parkinson taudin oireisiin v.1990. Hän käytti taudin hoidossa yleisesti käytettyä Sinemet hoitoa kahdeksan vuoden ajan. Hoidosta huolimatta hänen tilansa heikkeni heikkenemistään. Lopulta hän joutui pyörätuoliin eikä kyennyt syömään ilman apua. Kun hän sai tietää että Parkinson voi johtua borrelia-bakteerista, hän alkoi käyttää TOA vapaata kissankynttä. Kolmessa viikossa hänen tilansa parani niin paljon että hän pääsi pois pyörätuolista ja kävi kalastamassa.
Tom Coffey sai ALS diagnoosin 34-vuotiaana. Kesäkuussa 2001 hän ei kyennyt nielemään sylkeä eikä syömään. Hänelle laitettiin ruokintaletku. Hänen painonsa putosi nopeasti. Tom konsultoi Borrelioosiin erikoistunutta lääkäriä. Tämä aloitti suonensisäisen Tomille antibioottihoidon (Rocephalin) ja Tom tuli kuntoon."
Dr. Joanne Whitaker relates that nearly every patient with Parkinson?s Disease (PD). has tested positive for Bb. Dr. Louis Romero reports that 3 patients with PD are 99 % better after TOA-free cat?s claw (Uncaria tomentosa) therapy.
....
Case Reports Illustrating The Critical Importance Of Establishing The Diagnosis Of Lyme Disease
Case 1 Larry Powers, a former Mr. America in 1962, became ill with the symptoms of Parkinson?s Disease in 1990. Sinemet therapy was taken for eight years but he gradually became worse. He became confined to a wheel chair and required help with eating. After learning that Lyme Disease might be causing his symptoms of PD he started taking TOA free cat?s claw (Uncaria tormentosa). Within three weeks he was out of his wheelchair and fishing for 100 pound tarpon.
Case 2 Tom Coffey at age 34 developed diplopia, severe hypertension uncontrolled by drugs, and impaired balance. A diagnosis of amyotrophic lateral sclerosis was made. Surgery was performed to correct the diplopia. By June 2001 he was unable to swallow saliva and feeding tube nutrition was begun. His weight had fallen by 100 pounds. Nutritional support from the tube feedings produced slow resolution of the swallowing problem. Consultation with a Lyme expert uncovered the history of a bulls-eye rash after a tick bite. Therapy with Rocephin led to complete recovery.
Case 3 A young male college student developed such severe cognitive difficulties he was forced to drop out of school. A RIBb test was positive for LD and he resumed a normal life after receiving 4 months of antibiotic therapy...
.....Lyme Disease frequently exhibits neurologic abnormalities because the Bb neurotoxins are drawn to the fatty tissue found in the brain and peripheral nerves. As a consequence sudden deafness, Bells palsy, Parkinson?s Disease, Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis, chronic pain, and a multitude of other neurologic disorders may appear.
....The Influence of Toxins from Bb On The Symptoms and Course of Lyme Disease
Nuorilla Parkinsonin oireisiin kuolleilla tehdyissä ruumiinavauksissa on toistuvasti huomattu että aivovauriot eivät ole samanlaisia kuin tyypillisissä Parkinson tapauksissa vanhemmilla henkilöillä. Osa potilaista on saanut vuosikausiksi virheellisen Parkinson, ALS, MS diagnoosin. Osa on saanut nopean avun kissankynsivalmisteesta. Nopea apu ei selity immuunipuolustuksen vahvistumisella eikä valmisteen bakteereja tuhoavasta ominaisuudesta. Borrelia-bakteeri erittää erilaisia hermomyrkkyjä. Kissankynsi (Uncaria tomentosa) näyttäisi estävän hermomyrkkyjen vaikutuksen rasvakudoksiin.
Autopsy examinations of young persons (30s) dying from what appeared to be Parkinson?s disease PD have frequently failed to confirm the basal ganglion damage that would be expected in the classic PD seen in the elderly. Some patients with illnesses of many years duration misdiagnosed as Amyotrphic Lateral Sclerosis, Multiple Sclerosis, and Parkinson?s Disease have made incredible recoveries within periods as short as 24 to 72 hours when placed on TOA-free uncaria tormentosa (cat?s claw) for LD.. This rapid response could not rationally be attributed to improved immune function or bacteriocidal effects on spirochetes. Bb is known to produce a group of neurotoxins. The most sensible explanation for this recovery lies in turning off or blocking the neurotoxic effects of Bb on the lipid containing structures that the Bb neurotoxins are attracted to (central nervous system, peripheral nerves, muscles, joints etc.). This sudden improvement appears to be the result of blockage and inhibition of the neurotoxins[5]. The most important example of a ?Biotoxin Illness? appears to be Lyme Disease[6]. Patients with symptoms of Parkinson?s Disease at a young age caused by neurotoxins would not be expected to show permanent structural destruction in the basal ganglia. These neurotoxins probably act at specific sites such as neurotransmitters-pre- and- post synaptic membranes, altering dopamine, serotonin, GABA, and acetylcholine molecules, thereby blocking surface membrane receptors of various kinds which would interfere with the proper action of enzymes, coenzymes and hormones. This is only one of the damaging mechanisms of action of the neurotoxins.
The TOA free form of cat?s claw (Samento) may have three direct beneficial effects in humans with LD:
Immune modulation (correcting immune dysfunction)
Direct broad spectrum anti-microbial effect on spirochetes. Quinovic acid glycosides found in TAO-free cat?s claw are similar to the quinilones widely used as antibiotics.
Blocking the adverse neurotoxic effects on cells, enzymes, and hormones
Whether the serious lack of energy and fatigue seen in LD are similar to the cyanate[7] induced damage to the mitochondria?s ability to produce energy in the motor neurone found in amyotrophic lateral sclerosis or is due to failure of proper calcium channel function is not clear.
http://www.newswithviews.com/Howenstine/james26.htm
"Borrelioosissa esiintyy yleisesti neurologisia ongelmia sillä bakteerin erittämät neurotoksiinit sitoutuvat rasvakudoksiin. Rasvakudosta on runsaasti mm aivoissa ja äärihermostossa. Neurotoksiinit voivat aiheuttaa äkillisen kuuroutumisen, kasvohermohalvauksen, Parkinsonin oireet, MS oireet, hermotulehduksia, kroonista kipua ym neurologisia ongelmia. Kissankynsi näyttäisi korjaavan immuunipuolustuksen toimintaa, tuhoavan mikrobeja ja estävän hermomyrkkyjen vaikutuksen soluihin, entsyymeihin ja hormoneihin.
Tri Joanne Whitakerin potilailla lähes jokaisen Parkinson oireita sairastavan borrelia-testi on ollut positiivinen. Tri Louis Romero kertoo kolmen Parkinson potilaansa olevan lähes oireettomia (99%) TOA vapaan kissankynsihoidon jälkeen.
Tapausselostuksia:
Larry Powers sairastui Parkinson taudin oireisiin v.1990. Hän käytti taudin hoidossa yleisesti käytettyä Sinemet hoitoa kahdeksan vuoden ajan. Hoidosta huolimatta hänen tilansa heikkeni heikkenemistään. Lopulta hän joutui pyörätuoliin eikä kyennyt syömään ilman apua. Kun hän sai tietää että Parkinson voi johtua borrelia-bakteerista, hän alkoi käyttää TOA vapaata kissankynttä. Kolmessa viikossa hänen tilansa parani niin paljon että hän pääsi pois pyörätuolista ja kävi kalastamassa.
Tom Coffey sai ALS diagnoosin 34-vuotiaana. Kesäkuussa 2001 hän ei kyennyt nielemään sylkeä eikä syömään. Hänelle laitettiin ruokintaletku. Hänen painonsa putosi nopeasti. Tom konsultoi Borrelioosiin erikoistunutta lääkäriä. Tämä aloitti suonensisäisen Tomille antibioottihoidon (Rocephalin) ja Tom tuli kuntoon."
Dr. Joanne Whitaker relates that nearly every patient with Parkinson?s Disease (PD). has tested positive for Bb. Dr. Louis Romero reports that 3 patients with PD are 99 % better after TOA-free cat?s claw (Uncaria tomentosa) therapy.
....
Case Reports Illustrating The Critical Importance Of Establishing The Diagnosis Of Lyme Disease
Case 1 Larry Powers, a former Mr. America in 1962, became ill with the symptoms of Parkinson?s Disease in 1990. Sinemet therapy was taken for eight years but he gradually became worse. He became confined to a wheel chair and required help with eating. After learning that Lyme Disease might be causing his symptoms of PD he started taking TOA free cat?s claw (Uncaria tormentosa). Within three weeks he was out of his wheelchair and fishing for 100 pound tarpon.
Case 2 Tom Coffey at age 34 developed diplopia, severe hypertension uncontrolled by drugs, and impaired balance. A diagnosis of amyotrophic lateral sclerosis was made. Surgery was performed to correct the diplopia. By June 2001 he was unable to swallow saliva and feeding tube nutrition was begun. His weight had fallen by 100 pounds. Nutritional support from the tube feedings produced slow resolution of the swallowing problem. Consultation with a Lyme expert uncovered the history of a bulls-eye rash after a tick bite. Therapy with Rocephin led to complete recovery.
Case 3 A young male college student developed such severe cognitive difficulties he was forced to drop out of school. A RIBb test was positive for LD and he resumed a normal life after receiving 4 months of antibiotic therapy...
.....Lyme Disease frequently exhibits neurologic abnormalities because the Bb neurotoxins are drawn to the fatty tissue found in the brain and peripheral nerves. As a consequence sudden deafness, Bells palsy, Parkinson?s Disease, Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis, chronic pain, and a multitude of other neurologic disorders may appear.
....The Influence of Toxins from Bb On The Symptoms and Course of Lyme Disease
Nuorilla Parkinsonin oireisiin kuolleilla tehdyissä ruumiinavauksissa on toistuvasti huomattu että aivovauriot eivät ole samanlaisia kuin tyypillisissä Parkinson tapauksissa vanhemmilla henkilöillä. Osa potilaista on saanut vuosikausiksi virheellisen Parkinson, ALS, MS diagnoosin. Osa on saanut nopean avun kissankynsivalmisteesta. Nopea apu ei selity immuunipuolustuksen vahvistumisella eikä valmisteen bakteereja tuhoavasta ominaisuudesta. Borrelia-bakteeri erittää erilaisia hermomyrkkyjä. Kissankynsi (Uncaria tomentosa) näyttäisi estävän hermomyrkkyjen vaikutuksen rasvakudoksiin.
Autopsy examinations of young persons (30s) dying from what appeared to be Parkinson?s disease PD have frequently failed to confirm the basal ganglion damage that would be expected in the classic PD seen in the elderly. Some patients with illnesses of many years duration misdiagnosed as Amyotrphic Lateral Sclerosis, Multiple Sclerosis, and Parkinson?s Disease have made incredible recoveries within periods as short as 24 to 72 hours when placed on TOA-free uncaria tormentosa (cat?s claw) for LD.. This rapid response could not rationally be attributed to improved immune function or bacteriocidal effects on spirochetes. Bb is known to produce a group of neurotoxins. The most sensible explanation for this recovery lies in turning off or blocking the neurotoxic effects of Bb on the lipid containing structures that the Bb neurotoxins are attracted to (central nervous system, peripheral nerves, muscles, joints etc.). This sudden improvement appears to be the result of blockage and inhibition of the neurotoxins[5]. The most important example of a ?Biotoxin Illness? appears to be Lyme Disease[6]. Patients with symptoms of Parkinson?s Disease at a young age caused by neurotoxins would not be expected to show permanent structural destruction in the basal ganglia. These neurotoxins probably act at specific sites such as neurotransmitters-pre- and- post synaptic membranes, altering dopamine, serotonin, GABA, and acetylcholine molecules, thereby blocking surface membrane receptors of various kinds which would interfere with the proper action of enzymes, coenzymes and hormones. This is only one of the damaging mechanisms of action of the neurotoxins.
The TOA free form of cat?s claw (Samento) may have three direct beneficial effects in humans with LD:
Immune modulation (correcting immune dysfunction)
Direct broad spectrum anti-microbial effect on spirochetes. Quinovic acid glycosides found in TAO-free cat?s claw are similar to the quinilones widely used as antibiotics.
Blocking the adverse neurotoxic effects on cells, enzymes, and hormones
Whether the serious lack of energy and fatigue seen in LD are similar to the cyanate[7] induced damage to the mitochondria?s ability to produce energy in the motor neurone found in amyotrophic lateral sclerosis or is due to failure of proper calcium channel function is not clear.
BORRELIOOSI VAI MS-TAUTI?
Lukuisille Borrelioosiin sairastuneille on kerrottu heidän sairastavan MS-tautia. MS-taudin syytä ei tunneta, mutta näyttää siltä, että borrelia-bakteeri on yksi MS-taudille tyypillisten neurologisten oireiden aiheuttajista. Oireiden todellisen aiheuttajan selvittäminen saattaa toisinaan olla vaikeaa, sillä nykyisin yleisimmin käytössä olevat borreliatestit ovat epäluotettavia ja tulokset voivat olla virheellisesti negatiiviset. Siksi Borrelioosidiagnoosi on vielä tänä päivänä kliininen eikä sitä voida tehdä yksinomaan laboratoriotutkimusten perusteella.
?MS on krooninen tulehduksellinen, demyelinisoiva keskushermostosairaus. Vaikka sen syytä ei vielä varmuudella tiedetä, tiedetään, että tauti aiheuttaa vaurioita aksoneihin ja keskushermoston valkeaan aineeseen. Vauriot saattavat johtua joko infektiosta tai autoimmuunireaktiosta. ?
(http://www.acceleratedcure.org/download ... hogens.pdf )
?MS-taudin oirekuvan aiheuttavat todennäköisesti useat eri tekijät eikä mikään yksittäinen tekijä. Mikäli tutkimme 100 MS-tautia sairastavaa, löydämme todennäköisesti ainakin viisi erilaista syytä oireiden aiheuttajiksi. Se mikä aiheuttaa oireet yhdelle, ei välttämättä ole sama asia, joka on aiheuttanut oireet toiselle. MS-tautia ei aiheuta yksittäinen geeni, mikrobi, ravitsemusvirhe jne. Sen ajatellaan johtuvan useista geeneistä ja eri ympäristötekijöistä.?
(http://www.acceleratedcure.org/download ... sitory.pdf)
Vaikka MS-taudin aiheuttajaksi ei ole löydetty 140 vuoden aikana yhtään yksittäistä syytä, on epidemiologisten ja perinnöllisyystieteellisten tutkimusten pohjalta tultu siihen tulokseen, että ympäristötekijöillä (esim. ravinto, sukupuoli, elinympäristö jne.) on merkittävä osuus oireiden syntymisessä ja kehittymisessä. Ravitsemuksellisia seikkoja ei yleensä huomioida, vaikka niiden merkitys on tärkeä elämän kaikilla osa-alueilla. Elimistöllä on tietyt tarkat ravitsemukselliset vaatimukset. Mikäli niitä ei täytetä, on seurauksena sairastuminen.
(http://www.acceleratedcure.org/download ... rition.pdf)
Ympäristötekijöiden lisäksi erilaisten bakteerien ja virusten epäillään laukaisevan MS-taudin. Tutkijat ovat löytäneet useita mahdollisia taudinaiheuttajia, mutta eivät yhtään yksittäistä mikrobia, joka selittäisi jokaisen MS-tapauksen. Yksi listassa mainituista bakteereista on Borrelia burgdorferi. Sekään ei todennäköisesti selitä kaikkia MS-tapauksia.
(http://www.acceleratedcure.org/download ... tables.pdf )
Seuraavalta sivulta löytyy runsaasti tietoa Borrelioosin diagnosoinnista MS-taudiksi/ borreliabakteerin aiheuttama MS- oireisto:
http://www.lymeinfo.net/multiplesclerosis.html
Lyme Disease Misdiagnosed as Multiple Sclerosis
The following articles compiled by LymeInfo provide information about Lyme disease being misdiagnosed as Multiple Sclerosis. The differential diagnosis can be tricky, as Lyme tests can be falsely negative. Disseminated Lyme disease is also very complicated to treat. Therefore, it is important for those diagnosed with Multiple Sclerosis to be thoroughly evaluated by a physician skilled at diagnosing Lyme disease. After reviewing the below articles, please browse around the Lyme Info website to learn more about Lyme disease and other tick-borne illnesses. Be sure to visit our Lyme Disease Diagnosis & Treatment page. The list below is merely an introduction and does not cover all articles on this topic.
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Lääketieteellisiä tutkimuksia:
Antibiooteista minosykliini, tinidatsoli ja hydroksiklorokiini tappavat borreliabakteerin spirokeetta ja kystamuotoja, joita on löydetty MS-tautia sairastavien aivoista.
Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable? (2005)
"As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted."
MRI:ssä myöhäisvaiheen Borrelioosia sairastavan henkilön aivoista löydettiin aivojen valkean aineen muutoksia.
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis. (2004)
"Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described. In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI."
Borrelioosin aiheuttaa borreliabakteeri. Tauti saattaa aiheuttaa keskushermosto-oireita, jotka ovat samantyyppisiä kuin MS-taudissa.
Bacterial infection as a cause of multiple sclerosis. (2002)
"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."
Mikrobiologisissa ja kliinisissä tutkimuksissa on löydetty tukea olettamukselle, että MS-tauti saattaa johtua spirokeetoista. MS-potilaiden selkäydinnesteestä on löydetty kystamuotoisia bakteereita, jotka saattavat olla lähtöisin spirokeetoista.
Association between multiple sclerosis and cystic structures in cerebrospinal fluid. (2001)
"Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS."
Useat sairaudet kuten Borrelioosi (Lymen tauti), neurosarkoidoosi, lupus jne aiheuttavat samanlaisia tulehduksellisiia aivomuutoksia aivorunkoon ja pikkuaivoihin kuin MS-tauti.
Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. (2001)
"Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum."
Lopputuloksena voidaan todeta, että MS-tautia esiintyy usein Borreliainfektion yhteydessä.
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. (2000)
"The result suggests that multiple sclerosis may be often associated with Borrelia infection."
Tulehdukselliset muutokset aivoissa Borrelioosin yhteydessä. Kolmen potilaan tapausselostus + kirjallisuuskatsaus.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. (1996)
"We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection."
Borreliavasta-aineiden esiintyminen demyelinisoivissa aivosairauksissa.
The presence of anti-Borrelia burgdorferi antibodies in a group of multiple sclerosis patients in eastern Sicily. Preliminary data. (1993)
"The authors evaluate the presence of anti-Borrelia burgdorferi antibodies in a group of polysclerotic patients of Eastern Sicily, in order to verify or dismiss a correlation between Borrelia infection and demyelinizing syndrome."
Sairaudet, jotka muistuttavat MS-tautia.
Diseases that mimic multiple sclerosis. (1991)
"Dr Scott compares typical findings of multiple sclerosis with those of the four diseases that are sometimes mistaken for this syndrome."
Myöhäisvaiheen Borrelioosi diagnosoidaan MS-taudiksi.
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion. (1990)
"In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed."
Borrelioosin aiheuttamat neurologiset oireet.
Neurologic manifestations of Lyme disease, the new "great imitator". (1989)
"Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements."
Clinical manifestations of Lyme disease in the United States. (1989)
Conn Med. 1989 Jun;53(6):327-30.
Clinical pathologic correlations of Lyme disease. (1989)
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Neljä potilastapausta, joissa Borrelioosia sairastavilla esiintyi krooninen aivokalvo-aivoselkäydintulehdus.
Chronic central nervous system involvement in Lyme borreliosis. (1988)
"We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis."
MS-tauti on keskushermoston krooninen infektio, joka muistuttaa Borrelioosia ja neurosyfilistä.
Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. (1988)
"Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement."
38-vuotiaalla miehellä oli tajunnanmenetyksiä, myöhemmin niveltulehduksia, tietokonetomografiassa aivojen valkean aineen muutoksia jne. Borrelioosi diagnosoitiin 4 v myöhemmin.
Demyelinating encephalopathy in Lyme disease. (1985)
"A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later."
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Conferences:
Lyme Borreliosis and Related Disorders
by Liegner
11th International Scientific Conference on Lyme Disease and Other Spirochetal & Tick-Borne Disorders, 1998
Subtle Injury to Transformed Neural Cell Lines by Bb
by Benach
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, 1997
Spectrum of Antibiotic-Responsive Meningoencephalomyelitides
by Liegner
8th Annual LDF International Scientific Conference on Lyme Borreliosis and other Spirochetal and Tick-borne Diseases, 1995
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Potilastarinoita:
Heininger luuli 20 vuoden ajan sairastavansa MS-tautia.
I'm Not Giving Up, The Corning Leader, December 2004
"Until January, Heininger lived for 20 years believing that multiple sclerosis was the cause of her growing disability. She is one of an increasing number of people who are learning that Lyme is a "disease in disguise," according to an Aug. 23 Newsweek article."
Tri Strickerin mukaan todennäköisesti noin 10% MS-tautia sairastavista sairastaa Borrelioosia.
Lyme disease can get very severe without antibiotics, The Daily Review, September 2002
"Probably 10 percent of multiple sclerosis cases are actually Lyme's," Stricker said. "There's really not a lot of expertise in this area, sadly. It's really amazing how many patients will come in and say their doctor says Lyme disease doesn't happen here." (Free registration
Lääkäreiden mukaan naisella on MS-tauti (aivomuutokset MRI:ssä), vaikka hänen borreliavasta-ainetestinsä olivat positiiviset. Kukaan lääkäreistä ei halunnut hoitaa Borrelioosia.
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
Viimeaikaisten tutkimusten mukaan Borrelioosin aiheuttamat neurologiset ongelmat ovat hyvin smankaltaisia kuin MS-taudissa.
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
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Aiheeseen liittyviä sivustoja:
Lukuisia tutkimuksia Borrelioosista ja MS-taudista
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
Borrelioosi on viimeisin suuri matkija. Sen mahdollisuus tulee ottaa huomioon useissa neurologisissa taudeissa kuten Ms-tauti, Als, ADHD yms.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lista tutkimuksista joissa todetaan Borrelioosin ja MS-taudin samanlaisuus.
Lyme/MS Journal References
"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."
Milloin tulee epäillä Borrelioosia? Useille sairastuneille kerrotaan, että magneettikuvauksen ja selkäydinnestenäytteen tulosten perusteella heillä on MS-tauti. Lääketieteellinen kirjallisuus on kuitenkin yhtä mieltä siitä, että niiden perusteella diagnoosia ei voida tehdä. Kummassakin esiintyy samanlaisia muutoksia eivätkä selkäydinnestetutkimukset kykene kertomaan demyelinaation syytä.
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
22-vuotiaalla opiskelijalla esiintyi 3 1/2 vuoden ajan alaraajojejn puutumista ja viimeksi oikean käden heikkoutta. Borrelioositestit olivat positiiviset.
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirokeettojen kystamuodot MS-taudissa.
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Borrelioosi vai MS-tauti? Ennenkuin testit on suoritettu laboratoriossa, joka on erikoistunut ainoastaan punkkien levittämien sairauksien tutkimiseen, olisin erittäin varovainen tekemään lopullista diagnoosia.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Yleinen infektiotautien hoidossa käytetty antibiootti saattaa olla potentiaalinen MS-taudin hoidossa.
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
Tri Mattman on löytänyt borrelia spirokeettoja 8 Parkinsonin- 41 MS-, 21 ALS- tautia sairastavilta sekä kaikilta tutkimiltaan Alzheimerin tautia sairastavilta,
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Borreliabakteeri saattaa aiheuttaa keskushermostossa demyelinisoivan sairauden, joka muistuttaa suuresti MS-tautia.
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
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MS-taudista kertovia sivuja:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
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Aiheeseen liittyviä sivustoja:
Lukuisia tutkimuksia Borrelioosista ja MS-taudista
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
Borrelioosi on viimeisin suuri matkija. Sen mahdollisuus tulee ottaa huomioon useissa neurologisissa taudeissa kuten Ms-tauti, Als, ADHD yms.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lista tutkimuksista joissa todetaan Borrelioosin ja MS-taudin samanlaisuus.
Lyme/MS Journal References
"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."
Milloin tulee epäillä Borrelioosia? Useille sairastuneille kerrotaan, että magneettikuvauksen ja selkäydinnestenäytteen tulosten perusteella heillä on MS-tauti. Lääketieteellinen kirjallisuus on kuitenkin yhtä mieltä siitä, että niiden perusteella diagnoosia ei voida tehdä. Kummassakin esiintyy samanlaisia muutoksia eivätkä selkäydinnestetutkimukset kykene kertomaan demyelinaation syytä.
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
22-vuotiaalla opiskelijalla esiintyi 3 1/2 vuoden ajan alaraajojejn puutumista ja viimeksi oikean käden heikkoutta. Borrelioositestit olivat positiiviset.
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirokeettojen kystamuodot MS-taudissa.
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Borrelioosi vai MS-tauti? Ennenkuin testit on suoritettu laboratoriossa, joka on erikoistunut ainoastaan punkkien levittämien sairauksien tutkimiseen, olisin erittäin varovainen tekemään lopullista diagnoosia.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Yleinen infektiotautien hoidossa käytetty antibiootti saattaa olla potentiaalinen MS-taudin hoidossa.
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
Tri Mattman on löytänyt borrelia spirokeettoja 8 Parkinsonin- 41 MS-, 21 ALS- tautia sairastavilta sekä kaikilta tutkimiltaan Alzheimerin tautia sairastavilta,
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Borreliabakteeri saattaa aiheuttaa keskushermostossa demyelinisoivan sairauden, joka muistuttaa suuresti MS-tautia.
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
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MS-taudista kertovia sivuja:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
Lukuisille Borrelioosiin sairastuneille on kerrottu heidän sairastavan MS-tautia. MS-taudin syytä ei tunneta, mutta näyttää siltä, että borrelia-bakteeri on yksi MS-taudille tyypillisten neurologisten oireiden aiheuttajista. Oireiden todellisen aiheuttajan selvittäminen saattaa toisinaan olla vaikeaa, sillä nykyisin yleisimmin käytössä olevat borreliatestit ovat epäluotettavia ja tulokset voivat olla virheellisesti negatiiviset. Siksi Borrelioosidiagnoosi on vielä tänä päivänä kliininen eikä sitä voida tehdä yksinomaan laboratoriotutkimusten perusteella.
?MS on krooninen tulehduksellinen, demyelinisoiva keskushermostosairaus. Vaikka sen syytä ei vielä varmuudella tiedetä, tiedetään, että tauti aiheuttaa vaurioita aksoneihin ja keskushermoston valkeaan aineeseen. Vauriot saattavat johtua joko infektiosta tai autoimmuunireaktiosta. ?
(http://www.acceleratedcure.org/download ... hogens.pdf )
?MS-taudin oirekuvan aiheuttavat todennäköisesti useat eri tekijät eikä mikään yksittäinen tekijä. Mikäli tutkimme 100 MS-tautia sairastavaa, löydämme todennäköisesti ainakin viisi erilaista syytä oireiden aiheuttajiksi. Se mikä aiheuttaa oireet yhdelle, ei välttämättä ole sama asia, joka on aiheuttanut oireet toiselle. MS-tautia ei aiheuta yksittäinen geeni, mikrobi, ravitsemusvirhe jne. Sen ajatellaan johtuvan useista geeneistä ja eri ympäristötekijöistä.?
(http://www.acceleratedcure.org/download ... sitory.pdf)
Vaikka MS-taudin aiheuttajaksi ei ole löydetty 140 vuoden aikana yhtään yksittäistä syytä, on epidemiologisten ja perinnöllisyystieteellisten tutkimusten pohjalta tultu siihen tulokseen, että ympäristötekijöillä (esim. ravinto, sukupuoli, elinympäristö jne.) on merkittävä osuus oireiden syntymisessä ja kehittymisessä. Ravitsemuksellisia seikkoja ei yleensä huomioida, vaikka niiden merkitys on tärkeä elämän kaikilla osa-alueilla. Elimistöllä on tietyt tarkat ravitsemukselliset vaatimukset. Mikäli niitä ei täytetä, on seurauksena sairastuminen.
(http://www.acceleratedcure.org/download ... rition.pdf)
Ympäristötekijöiden lisäksi erilaisten bakteerien ja virusten epäillään laukaisevan MS-taudin. Tutkijat ovat löytäneet useita mahdollisia taudinaiheuttajia, mutta eivät yhtään yksittäistä mikrobia, joka selittäisi jokaisen MS-tapauksen. Yksi listassa mainituista bakteereista on Borrelia burgdorferi. Sekään ei todennäköisesti selitä kaikkia MS-tapauksia.
(http://www.acceleratedcure.org/download ... tables.pdf )
Seuraavalta sivulta löytyy runsaasti tietoa Borrelioosin diagnosoinnista MS-taudiksi/ borreliabakteerin aiheuttama MS- oireisto:
http://www.lymeinfo.net/multiplesclerosis.html
Lyme Disease Misdiagnosed as Multiple Sclerosis
The following articles compiled by LymeInfo provide information about Lyme disease being misdiagnosed as Multiple Sclerosis. The differential diagnosis can be tricky, as Lyme tests can be falsely negative. Disseminated Lyme disease is also very complicated to treat. Therefore, it is important for those diagnosed with Multiple Sclerosis to be thoroughly evaluated by a physician skilled at diagnosing Lyme disease. After reviewing the below articles, please browse around the Lyme Info website to learn more about Lyme disease and other tick-borne illnesses. Be sure to visit our Lyme Disease Diagnosis & Treatment page. The list below is merely an introduction and does not cover all articles on this topic.
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Lääketieteellisiä tutkimuksia:
Antibiooteista minosykliini, tinidatsoli ja hydroksiklorokiini tappavat borreliabakteerin spirokeetta ja kystamuotoja, joita on löydetty MS-tautia sairastavien aivoista.
Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable? (2005)
"As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted."
MRI:ssä myöhäisvaiheen Borrelioosia sairastavan henkilön aivoista löydettiin aivojen valkean aineen muutoksia.
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis. (2004)
"Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described. In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI."
Borrelioosin aiheuttaa borreliabakteeri. Tauti saattaa aiheuttaa keskushermosto-oireita, jotka ovat samantyyppisiä kuin MS-taudissa.
Bacterial infection as a cause of multiple sclerosis. (2002)
"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."
Mikrobiologisissa ja kliinisissä tutkimuksissa on löydetty tukea olettamukselle, että MS-tauti saattaa johtua spirokeetoista. MS-potilaiden selkäydinnesteestä on löydetty kystamuotoisia bakteereita, jotka saattavat olla lähtöisin spirokeetoista.
Association between multiple sclerosis and cystic structures in cerebrospinal fluid. (2001)
"Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS."
Useat sairaudet kuten Borrelioosi (Lymen tauti), neurosarkoidoosi, lupus jne aiheuttavat samanlaisia tulehduksellisiia aivomuutoksia aivorunkoon ja pikkuaivoihin kuin MS-tauti.
Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. (2001)
"Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum."
Lopputuloksena voidaan todeta, että MS-tautia esiintyy usein Borreliainfektion yhteydessä.
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. (2000)
"The result suggests that multiple sclerosis may be often associated with Borrelia infection."
Tulehdukselliset muutokset aivoissa Borrelioosin yhteydessä. Kolmen potilaan tapausselostus + kirjallisuuskatsaus.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. (1996)
"We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection."
Borreliavasta-aineiden esiintyminen demyelinisoivissa aivosairauksissa.
The presence of anti-Borrelia burgdorferi antibodies in a group of multiple sclerosis patients in eastern Sicily. Preliminary data. (1993)
"The authors evaluate the presence of anti-Borrelia burgdorferi antibodies in a group of polysclerotic patients of Eastern Sicily, in order to verify or dismiss a correlation between Borrelia infection and demyelinizing syndrome."
Sairaudet, jotka muistuttavat MS-tautia.
Diseases that mimic multiple sclerosis. (1991)
"Dr Scott compares typical findings of multiple sclerosis with those of the four diseases that are sometimes mistaken for this syndrome."
Myöhäisvaiheen Borrelioosi diagnosoidaan MS-taudiksi.
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion. (1990)
"In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed."
Borrelioosin aiheuttamat neurologiset oireet.
Neurologic manifestations of Lyme disease, the new "great imitator". (1989)
"Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements."
Clinical manifestations of Lyme disease in the United States. (1989)
Conn Med. 1989 Jun;53(6):327-30.
Clinical pathologic correlations of Lyme disease. (1989)
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Neljä potilastapausta, joissa Borrelioosia sairastavilla esiintyi krooninen aivokalvo-aivoselkäydintulehdus.
Chronic central nervous system involvement in Lyme borreliosis. (1988)
"We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis."
MS-tauti on keskushermoston krooninen infektio, joka muistuttaa Borrelioosia ja neurosyfilistä.
Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. (1988)
"Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement."
38-vuotiaalla miehellä oli tajunnanmenetyksiä, myöhemmin niveltulehduksia, tietokonetomografiassa aivojen valkean aineen muutoksia jne. Borrelioosi diagnosoitiin 4 v myöhemmin.
Demyelinating encephalopathy in Lyme disease. (1985)
"A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later."
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Conferences:
Lyme Borreliosis and Related Disorders
by Liegner
11th International Scientific Conference on Lyme Disease and Other Spirochetal & Tick-Borne Disorders, 1998
Subtle Injury to Transformed Neural Cell Lines by Bb
by Benach
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, 1997
Spectrum of Antibiotic-Responsive Meningoencephalomyelitides
by Liegner
8th Annual LDF International Scientific Conference on Lyme Borreliosis and other Spirochetal and Tick-borne Diseases, 1995
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Potilastarinoita:
Heininger luuli 20 vuoden ajan sairastavansa MS-tautia.
I'm Not Giving Up, The Corning Leader, December 2004
"Until January, Heininger lived for 20 years believing that multiple sclerosis was the cause of her growing disability. She is one of an increasing number of people who are learning that Lyme is a "disease in disguise," according to an Aug. 23 Newsweek article."
Tri Strickerin mukaan todennäköisesti noin 10% MS-tautia sairastavista sairastaa Borrelioosia.
Lyme disease can get very severe without antibiotics, The Daily Review, September 2002
"Probably 10 percent of multiple sclerosis cases are actually Lyme's," Stricker said. "There's really not a lot of expertise in this area, sadly. It's really amazing how many patients will come in and say their doctor says Lyme disease doesn't happen here." (Free registration
Lääkäreiden mukaan naisella on MS-tauti (aivomuutokset MRI:ssä), vaikka hänen borreliavasta-ainetestinsä olivat positiiviset. Kukaan lääkäreistä ei halunnut hoitaa Borrelioosia.
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
Viimeaikaisten tutkimusten mukaan Borrelioosin aiheuttamat neurologiset ongelmat ovat hyvin smankaltaisia kuin MS-taudissa.
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
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Aiheeseen liittyviä sivustoja:
Lukuisia tutkimuksia Borrelioosista ja MS-taudista
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
Borrelioosi on viimeisin suuri matkija. Sen mahdollisuus tulee ottaa huomioon useissa neurologisissa taudeissa kuten Ms-tauti, Als, ADHD yms.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lista tutkimuksista joissa todetaan Borrelioosin ja MS-taudin samanlaisuus.
Lyme/MS Journal References
"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."
Milloin tulee epäillä Borrelioosia? Useille sairastuneille kerrotaan, että magneettikuvauksen ja selkäydinnestenäytteen tulosten perusteella heillä on MS-tauti. Lääketieteellinen kirjallisuus on kuitenkin yhtä mieltä siitä, että niiden perusteella diagnoosia ei voida tehdä. Kummassakin esiintyy samanlaisia muutoksia eivätkä selkäydinnestetutkimukset kykene kertomaan demyelinaation syytä.
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
22-vuotiaalla opiskelijalla esiintyi 3 1/2 vuoden ajan alaraajojejn puutumista ja viimeksi oikean käden heikkoutta. Borrelioositestit olivat positiiviset.
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirokeettojen kystamuodot MS-taudissa.
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Borrelioosi vai MS-tauti? Ennenkuin testit on suoritettu laboratoriossa, joka on erikoistunut ainoastaan punkkien levittämien sairauksien tutkimiseen, olisin erittäin varovainen tekemään lopullista diagnoosia.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Yleinen infektiotautien hoidossa käytetty antibiootti saattaa olla potentiaalinen MS-taudin hoidossa.
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
Tri Mattman on löytänyt borrelia spirokeettoja 8 Parkinsonin- 41 MS-, 21 ALS- tautia sairastavilta sekä kaikilta tutkimiltaan Alzheimerin tautia sairastavilta,
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Borreliabakteeri saattaa aiheuttaa keskushermostossa demyelinisoivan sairauden, joka muistuttaa suuresti MS-tautia.
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
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MS-taudista kertovia sivuja:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
--------------------------------------------------------------------------------
Aiheeseen liittyviä sivustoja:
Lukuisia tutkimuksia Borrelioosista ja MS-taudista
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
Borrelioosi on viimeisin suuri matkija. Sen mahdollisuus tulee ottaa huomioon useissa neurologisissa taudeissa kuten Ms-tauti, Als, ADHD yms.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lista tutkimuksista joissa todetaan Borrelioosin ja MS-taudin samanlaisuus.
Lyme/MS Journal References
"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."
Milloin tulee epäillä Borrelioosia? Useille sairastuneille kerrotaan, että magneettikuvauksen ja selkäydinnestenäytteen tulosten perusteella heillä on MS-tauti. Lääketieteellinen kirjallisuus on kuitenkin yhtä mieltä siitä, että niiden perusteella diagnoosia ei voida tehdä. Kummassakin esiintyy samanlaisia muutoksia eivätkä selkäydinnestetutkimukset kykene kertomaan demyelinaation syytä.
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
22-vuotiaalla opiskelijalla esiintyi 3 1/2 vuoden ajan alaraajojejn puutumista ja viimeksi oikean käden heikkoutta. Borrelioositestit olivat positiiviset.
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirokeettojen kystamuodot MS-taudissa.
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Borrelioosi vai MS-tauti? Ennenkuin testit on suoritettu laboratoriossa, joka on erikoistunut ainoastaan punkkien levittämien sairauksien tutkimiseen, olisin erittäin varovainen tekemään lopullista diagnoosia.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Yleinen infektiotautien hoidossa käytetty antibiootti saattaa olla potentiaalinen MS-taudin hoidossa.
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
Tri Mattman on löytänyt borrelia spirokeettoja 8 Parkinsonin- 41 MS-, 21 ALS- tautia sairastavilta sekä kaikilta tutkimiltaan Alzheimerin tautia sairastavilta,
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Borreliabakteeri saattaa aiheuttaa keskushermostossa demyelinisoivan sairauden, joka muistuttaa suuresti MS-tautia.
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
--------------------------------------------------------------------------------
MS-taudista kertovia sivuja:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
Re: BORRELIOOSI/MS-TAUTI
Med Hypotheses. 2005;64(3):438-48.
Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?
Fritzsche M.
Source
Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland. markus.fritzsche@gmx.ch
Abstract
Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks. In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation. Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls. Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study.
PMID:
15617845
[PubMed - indexed for MEDLINE]
Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?
Fritzsche M.
Source
Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland. markus.fritzsche@gmx.ch
Abstract
Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks. In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation. Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls. Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study.
PMID:
15617845
[PubMed - indexed for MEDLINE]
Re: BORRELIOOSI/MS-TAUTI
Ei tutkimus, mutta mielenkiintoinen kirjoitus MS/Borrelioosista. Artikkelin kirjoittajalla on mys omakohtainen kokemus aiheesta:
http://www.betterhealthguy.com/topics/m ... -sclerosis
Multiple Sclerosis
Last Updated: April 27 2013
It pains me to see how many different maladies people struggle with on a daily basis only to later find that they were improperly diagnosed and that something could have been done to help their condition sooner. This was what happened to me for a long, eight years. Once I finally was diagnosed and properly treated, the improvement has been remarkable.
MS, ALS, Parkinson's, Alzheimer's and a host of other diseases are, in my opinion, "labels" that are attached to someone that may actually be suffering with chronic Lyme disease. That was certainly my experience.
Healthcare professionals suggested that I had MS, Fibromyalgia, Chronic Fatigue Syndrome and a host of other "labels" that in my opinion often mean that the practitioner has not looked deeply enough to find the actual cause of illness.
MS is very real. Fibromyalgia is very real. CFS is very real. All of these conditions are very real and the struggles that they pose to those that suffer with them are many. Where I differ though in my thought process from many others is that I do not think that one should stop with these "labels". With appropriate medical guidance and lots of detective work, I do believe that any of these conditions can be treated. I believe that they all have a cause, or more likely, multiple causes. I believe that Lyme disease is in many cases one of the causes of these neurological diseases. I have heard MDs suggest that MS may actually be caused by or triggered by Lyme disease in over 50% of cases.
Looking more specifically at MS, it is my opinion that MS can be triggered by an infection with Borrelia burgdoferi, the causative agent in Lyme Disease. It may also be caused by a host of viruses such as HHV-6, HHV-8, CMV and others. Mycoplasmal infections are implicated in some cases of MS. Bottom line in my experience is that stopping at the label "MS" may be missing an opportunity to improve one's current state of health.
MS is in fact an autoimmune disorder and is a very serious condition. My belief (and maybe I will be proven wrong) is that almost all, if not all, cases of MS are triggered by an infection. It is also my opinion that there is a genetic component involved and that someone else that has the same combination of microbes may be entirely unaffected and live a perfectly healthy life. For others, this genetic predisposition combined with a combination of infectious organisms may trigger an autoimmune response that results in MS (or an MS-like presentation).
A compelling research study entitled "A Geostatistical Analysis of Possible Spirochetal Involvement in Multiple Sclerosis and Other Related Diseases" was conducted by Megan Blewett and was published in 2006. It compares the prevalence of MS and of Lyme Disease by geographic region. When you take the resulting distributions and compare the two, the result is a near-identical map. The study suggests a common spirochetal cause for both Lyme and MS. The details can be found here.
Other good sources of information suggesting a link between MS and Lyme can be found here.
I'll briefly relay a personal story about a friend that was diagnosed with MS. I worked with her for several years and knew that she had been diagnosed with MS. She was on heavy MS drugs to keep her symptoms under control. After I was myself diagnosed with Lyme disease and began attending conferences and researching these illnesses, I suggested to her that I questioned her MS diagnosis as the end of the journey and felt that she should look further into causes for her condition. I suspected infections that had not previously been diagnosed.
Having been aware of the potential link between MS and Lyme, I finally convinced her to dig deeper. Through energetic testing, it appeared that she did in fact have indications of Borrelia, Bartonella (a common Lyme co-infection) and a host of viral and parasitic stressors. This was enough for me to convince her to look further. She sought out further testing to confirm or deny what I had suspected. The results were consistent with Lyme Disease. Sadly, shortly after she started working with an LLMD and began antibiotic treatment, she felt worse and decided to go back to her MS drugs and stopped all Lyme treatment.
Another concern that I have with those diagnosed with MS is that it is often the case that steroids are used to help control the symptoms. If one has an infectious origin to their MS condition, steroids only further suppress the immune system and allow these infections to become more aggressive and problematic. I am of the opinion that taking steroids in absence of proof of a lack of an infectious component is unwise and potentially further risks one's health.
All of this has been such a journey for me and for so many that I have met along the way. I have met several people that once had an "MS" diagnosis only later to find that there was a more clearly identifiable potential cause. With that new understanding, a whole new world of treatment options were now available and improvement once again a reality.
If you are reading this and you have an "MS" diagnosis or any other diagnosis where the true cause is unknown, consider looking further into potential causes of your illness. If you have accepted the diagnosis which you currently have, I truly hope you are finding options that work well for you. If you, on the other hand, believe your diagnosis to be a "label" and not the true cause, I urge you to continue your search for answers with great vigor. I did and I am a different and better person for having done so.
-----------------------------------------------------------------------------------------------
MS tautia sairastavan blogi ja kokemuksia Puolan MS-klinikan hoidoista:
http://ms-patienten.blogspot.se/p/pa-va ... ameds.html
------------------------------------------------------------------------------------------------
Kirja MS-taudin hoidosta:
Ann Boroch: Healing Multiple Sclerosis: Diet, Detox & Nutritional Makeover for Total Recovery
http://www.amazon.com/gp/product/097734 ... 0977344606
Kirjan sisältö:
http://www.amazon.com/gp/product/097734 ... 0977344606
http://www.betterhealthguy.com/topics/m ... -sclerosis
Multiple Sclerosis
Last Updated: April 27 2013
It pains me to see how many different maladies people struggle with on a daily basis only to later find that they were improperly diagnosed and that something could have been done to help their condition sooner. This was what happened to me for a long, eight years. Once I finally was diagnosed and properly treated, the improvement has been remarkable.
MS, ALS, Parkinson's, Alzheimer's and a host of other diseases are, in my opinion, "labels" that are attached to someone that may actually be suffering with chronic Lyme disease. That was certainly my experience.
Healthcare professionals suggested that I had MS, Fibromyalgia, Chronic Fatigue Syndrome and a host of other "labels" that in my opinion often mean that the practitioner has not looked deeply enough to find the actual cause of illness.
MS is very real. Fibromyalgia is very real. CFS is very real. All of these conditions are very real and the struggles that they pose to those that suffer with them are many. Where I differ though in my thought process from many others is that I do not think that one should stop with these "labels". With appropriate medical guidance and lots of detective work, I do believe that any of these conditions can be treated. I believe that they all have a cause, or more likely, multiple causes. I believe that Lyme disease is in many cases one of the causes of these neurological diseases. I have heard MDs suggest that MS may actually be caused by or triggered by Lyme disease in over 50% of cases.
Looking more specifically at MS, it is my opinion that MS can be triggered by an infection with Borrelia burgdoferi, the causative agent in Lyme Disease. It may also be caused by a host of viruses such as HHV-6, HHV-8, CMV and others. Mycoplasmal infections are implicated in some cases of MS. Bottom line in my experience is that stopping at the label "MS" may be missing an opportunity to improve one's current state of health.
MS is in fact an autoimmune disorder and is a very serious condition. My belief (and maybe I will be proven wrong) is that almost all, if not all, cases of MS are triggered by an infection. It is also my opinion that there is a genetic component involved and that someone else that has the same combination of microbes may be entirely unaffected and live a perfectly healthy life. For others, this genetic predisposition combined with a combination of infectious organisms may trigger an autoimmune response that results in MS (or an MS-like presentation).
A compelling research study entitled "A Geostatistical Analysis of Possible Spirochetal Involvement in Multiple Sclerosis and Other Related Diseases" was conducted by Megan Blewett and was published in 2006. It compares the prevalence of MS and of Lyme Disease by geographic region. When you take the resulting distributions and compare the two, the result is a near-identical map. The study suggests a common spirochetal cause for both Lyme and MS. The details can be found here.
Other good sources of information suggesting a link between MS and Lyme can be found here.
I'll briefly relay a personal story about a friend that was diagnosed with MS. I worked with her for several years and knew that she had been diagnosed with MS. She was on heavy MS drugs to keep her symptoms under control. After I was myself diagnosed with Lyme disease and began attending conferences and researching these illnesses, I suggested to her that I questioned her MS diagnosis as the end of the journey and felt that she should look further into causes for her condition. I suspected infections that had not previously been diagnosed.
Having been aware of the potential link between MS and Lyme, I finally convinced her to dig deeper. Through energetic testing, it appeared that she did in fact have indications of Borrelia, Bartonella (a common Lyme co-infection) and a host of viral and parasitic stressors. This was enough for me to convince her to look further. She sought out further testing to confirm or deny what I had suspected. The results were consistent with Lyme Disease. Sadly, shortly after she started working with an LLMD and began antibiotic treatment, she felt worse and decided to go back to her MS drugs and stopped all Lyme treatment.
Another concern that I have with those diagnosed with MS is that it is often the case that steroids are used to help control the symptoms. If one has an infectious origin to their MS condition, steroids only further suppress the immune system and allow these infections to become more aggressive and problematic. I am of the opinion that taking steroids in absence of proof of a lack of an infectious component is unwise and potentially further risks one's health.
All of this has been such a journey for me and for so many that I have met along the way. I have met several people that once had an "MS" diagnosis only later to find that there was a more clearly identifiable potential cause. With that new understanding, a whole new world of treatment options were now available and improvement once again a reality.
If you are reading this and you have an "MS" diagnosis or any other diagnosis where the true cause is unknown, consider looking further into potential causes of your illness. If you have accepted the diagnosis which you currently have, I truly hope you are finding options that work well for you. If you, on the other hand, believe your diagnosis to be a "label" and not the true cause, I urge you to continue your search for answers with great vigor. I did and I am a different and better person for having done so.
-----------------------------------------------------------------------------------------------
MS tautia sairastavan blogi ja kokemuksia Puolan MS-klinikan hoidoista:
http://ms-patienten.blogspot.se/p/pa-va ... ameds.html
------------------------------------------------------------------------------------------------
Kirja MS-taudin hoidosta:
Ann Boroch: Healing Multiple Sclerosis: Diet, Detox & Nutritional Makeover for Total Recovery
http://www.amazon.com/gp/product/097734 ... 0977344606
Kirjan sisältö:
http://www.amazon.com/gp/product/097734 ... 0977344606
Re: BORRELIOOSI/MS-TAUTI
MS-taudin yhteys muihin tauteihin:"MS saattaa puhjeta borreliatartunnan seurauksena:"
http://www.esri.com/news/arcuser/1207/ticks.html
Spatial Statistics Provide New Insights Researcher sees possible links between MS and other diseases
By Susan Harp, Esri Writer
Summary
Spatial statistics have opened up a new way of looking at a debilitating disease that reportedly affects 400,000 people worldwide.
Normalized count of multiple sclerosis deaths by county for 1998 over 1990 census data
George de Mestral envisioned the design of the Velcro fastener in 1948 while picking burr-covered seedpods from his dog's fur after a mountain hike. As the story goes, the Swiss citizen stopped to observe the sticking qualities of Mother Nature's design and made the leap to a new, creative application. With the avalanche of information available to researchers today, the catalyst that helps produce this kind of "ah hah!" moment is extremely valuable.
For Megan M. Blewett, a young 21st-century researcher, spatial geography played a role in both her ah-hah! experience and her research. Blewett turned 18 in 2007, but five years ago, she was already reading a neuroscience textbook and asking questions about a mysterious disease—multiple sclerosis (MS)—that she found described in its pages. Blewett said, "I started researching MS when I was 12 and have since fallen in love with discovering the insights spatial statistics can give."
MS affects the central nervous system. Although its cause is unknown, many researchers think environmental triggers might be a factor. This unsolved puzzle caught Blewett's attention. She started collecting data about MS cases in her home state of New Jersey, learned to map their distribution with GIS, and has been using spatial statistics tools to analyze that distribution. She has continued reading about the neurological and biochemical aspects of the disease. However, her ah hah! moment occurred at a science fair while she was talking with one of the judges about her map of MS distribution in New Jersey.
"I just got lucky there," commented Blewett. "I was looking at a state map of MS distribution and saw that my county, Morris County, has a high incidence of MS. You could see individual towns, and I knew the town next to me had a high incidence of Lyme disease." A bacterial infection, Lyme disease is spread by tick-borne spirochetes. She was already using ArcGIS Desktop to map MS distribution, so when she started thinking about a possible Lyme disease correlation, she added Lyme data to her map layers.
click to enlarge
Normalized count of Lyme disease deaths by county for 1998 over 1990 census data
"I saw all these correlations and results that I hadn't been able to see before and still don't think I would have been able to see if I had been using more conventional chemical research to look at individual proteins at work," Blewett added. "Spatial statistics allowed me to see the bigger picture. Then I zoomed in to look at proteins at work in MS and related demyelinating diseases. I like to say my research path is analogous to reading the summary before reading the book."
The data collection process was one of the harder parts her research. Data came from TheDataWeb, an online set of libraries, and DataFerrett, a data mining tool, both provided free to the public by the United States Bureau of the Census and the Centers for Disease Control and Prevention (CDC). When Lyme disease data was not available online, Blewett had to contact the state epidemiologist and request data. Eventually she received data from every state. "To my knowledge, it is the largest standardized dataset of Lyme information in existence," saidBlewett about the dataset. She also said she is willing to make the data available to other researchers.
Blewett ran a correlation analysis. She calculated a Pearson's correlation coefficient (r) (for the normally distributed variables) or Kendall's tau-b or Spearman's rho for data that was not normally distributed. All correlation analyses assumed a linear relationship between the variables so the appropriate coefficient was calculated for pairs of variables in three datasets. All variable values were converted to z-scores for use in a regression analysis. Finally, cartographic analyses compared MS, Lyme (from other specified arthropod-borne diseases data), and control data from external cause of death data.
"The two disease distributions were pretty similar—they correlate and the control doesn't," explained Blewett.
"Biochemically they are also very similar, so it has just taken off from there." She hypothesizes that both diseases may share a common spirochetal basis, and MS might develop from a secondary tick bite.
Control data: normalized count of external causes of death by county for 1998 over 1990 census data
Blewett consulted with Esri spatial statistics expert Lauren Scott on using GIS in her research. "While biologists and medical researchers investigate this hypothesis at the cellular level, Megan's work examines the spatial fingerprint of these two diseases at broad spatial scales and then tests hypotheses regarding their spatial correlation," said Scott.
"I wish to expand my research from a national to a global scale, while also testing my models in smaller geographic areas," Blewett said. "A recent study suggests that MS is, in fact, 50 percent more common than previously predicted."
Blewett presented her work at the 2006 Esri International User Conference and participated in the Academic Fair during the 2006 Esri Health GIS Conference. In 2007, she was accepted into several top universities and awarded seventh place in the prestigious 66th Annual Intel Science Talent Search. For more information, contact Megan Blewett at megan.blewett@att.net or mblewett@mit.edu or visit www.msgeographics.com.
http://www.esri.com/news/arcuser/1207/ticks.html
Spatial Statistics Provide New Insights Researcher sees possible links between MS and other diseases
By Susan Harp, Esri Writer
Summary
Spatial statistics have opened up a new way of looking at a debilitating disease that reportedly affects 400,000 people worldwide.
Normalized count of multiple sclerosis deaths by county for 1998 over 1990 census data
George de Mestral envisioned the design of the Velcro fastener in 1948 while picking burr-covered seedpods from his dog's fur after a mountain hike. As the story goes, the Swiss citizen stopped to observe the sticking qualities of Mother Nature's design and made the leap to a new, creative application. With the avalanche of information available to researchers today, the catalyst that helps produce this kind of "ah hah!" moment is extremely valuable.
For Megan M. Blewett, a young 21st-century researcher, spatial geography played a role in both her ah-hah! experience and her research. Blewett turned 18 in 2007, but five years ago, she was already reading a neuroscience textbook and asking questions about a mysterious disease—multiple sclerosis (MS)—that she found described in its pages. Blewett said, "I started researching MS when I was 12 and have since fallen in love with discovering the insights spatial statistics can give."
MS affects the central nervous system. Although its cause is unknown, many researchers think environmental triggers might be a factor. This unsolved puzzle caught Blewett's attention. She started collecting data about MS cases in her home state of New Jersey, learned to map their distribution with GIS, and has been using spatial statistics tools to analyze that distribution. She has continued reading about the neurological and biochemical aspects of the disease. However, her ah hah! moment occurred at a science fair while she was talking with one of the judges about her map of MS distribution in New Jersey.
"I just got lucky there," commented Blewett. "I was looking at a state map of MS distribution and saw that my county, Morris County, has a high incidence of MS. You could see individual towns, and I knew the town next to me had a high incidence of Lyme disease." A bacterial infection, Lyme disease is spread by tick-borne spirochetes. She was already using ArcGIS Desktop to map MS distribution, so when she started thinking about a possible Lyme disease correlation, she added Lyme data to her map layers.
click to enlarge
Normalized count of Lyme disease deaths by county for 1998 over 1990 census data
"I saw all these correlations and results that I hadn't been able to see before and still don't think I would have been able to see if I had been using more conventional chemical research to look at individual proteins at work," Blewett added. "Spatial statistics allowed me to see the bigger picture. Then I zoomed in to look at proteins at work in MS and related demyelinating diseases. I like to say my research path is analogous to reading the summary before reading the book."
The data collection process was one of the harder parts her research. Data came from TheDataWeb, an online set of libraries, and DataFerrett, a data mining tool, both provided free to the public by the United States Bureau of the Census and the Centers for Disease Control and Prevention (CDC). When Lyme disease data was not available online, Blewett had to contact the state epidemiologist and request data. Eventually she received data from every state. "To my knowledge, it is the largest standardized dataset of Lyme information in existence," saidBlewett about the dataset. She also said she is willing to make the data available to other researchers.
Blewett ran a correlation analysis. She calculated a Pearson's correlation coefficient (r) (for the normally distributed variables) or Kendall's tau-b or Spearman's rho for data that was not normally distributed. All correlation analyses assumed a linear relationship between the variables so the appropriate coefficient was calculated for pairs of variables in three datasets. All variable values were converted to z-scores for use in a regression analysis. Finally, cartographic analyses compared MS, Lyme (from other specified arthropod-borne diseases data), and control data from external cause of death data.
"The two disease distributions were pretty similar—they correlate and the control doesn't," explained Blewett.
"Biochemically they are also very similar, so it has just taken off from there." She hypothesizes that both diseases may share a common spirochetal basis, and MS might develop from a secondary tick bite.
Control data: normalized count of external causes of death by county for 1998 over 1990 census data
Blewett consulted with Esri spatial statistics expert Lauren Scott on using GIS in her research. "While biologists and medical researchers investigate this hypothesis at the cellular level, Megan's work examines the spatial fingerprint of these two diseases at broad spatial scales and then tests hypotheses regarding their spatial correlation," said Scott.
"I wish to expand my research from a national to a global scale, while also testing my models in smaller geographic areas," Blewett said. "A recent study suggests that MS is, in fact, 50 percent more common than previously predicted."
Blewett presented her work at the 2006 Esri International User Conference and participated in the Academic Fair during the 2006 Esri Health GIS Conference. In 2007, she was accepted into several top universities and awarded seventh place in the prestigious 66th Annual Intel Science Talent Search. For more information, contact Megan Blewett at megan.blewett@att.net or mblewett@mit.edu or visit www.msgeographics.com.
Re: BORRELIOOSI/MS-TAUTI
Tutkimuksia joissa Borrelioosi diagnosoitiin MS-taudiksi:
Allaolevien tutkimusten linkit avautuvat sivuulta:
http://www.lymeinfo.net/multiplesclerosis.html
Lyme Disease Misdiagnosed as Multiple Sclerosis
The following articles compiled by LymeInfo provide information about Lyme disease being misdiagnosed as Multiple Sclerosis. The differential diagnosis can be tricky, as Lyme tests can be falsely negative. Disseminated Lyme disease is also very complicated to treat. Therefore, it is important for those diagnosed with Multiple Sclerosis to be thoroughly evaluated by a physician skilled at diagnosing Lyme disease. After reviewing the below articles, please browse around the Lyme Info website to learn more about Lyme disease and other tick-borne illnesses. Be sure to visit our Lyme Disease Diagnosis & Treatment page. The list below is merely an introduction and does not cover all articles on this topic.
Medical Abstracts:
Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma. (2007)
"In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed."
Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable? (2005)
"As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted."
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis. (2004)
"Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described. In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI."
Bacterial infection as a cause of multiple sclerosis. (2002)
"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."
Association between multiple sclerosis and cystic structures in cerebrospinal fluid. (2001)
"Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS."
Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. (2001)
"Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum."
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. (2000)
"The result suggests that multiple sclerosis may be often associated with Borrelia infection."
Multiple sclerosis vs Lyme disease: a case presentation to a discussant and a review of the literature.(1999)
Read the first page here.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. (1996)
"We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection."
The presence of anti-Borrelia burgdorferi antibodies in a group of multiple sclerosis patients in eastern Sicily. Preliminary data. (1993)
"The authors evaluate the presence of anti-Borrelia burgdorferi antibodies in a group of polysclerotic patients of Eastern Sicily, in order to verify or dismiss a correlation between Borrelia infection and demyelinizing syndrome."
Diseases that mimic multiple sclerosis. (1991)
"Dr Scott compares typical findings of multiple sclerosis with those of the four diseases that are sometimes mistaken for this syndrome."
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion. (1990)
"In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed."
Neurologic manifestations of Lyme disease, the new "great imitator". (1989)
"Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements."
Clinical manifestations of Lyme disease in the United States. (1989)
Conn Med. 1989 Jun;53(6):327-30.
Clinical pathologic correlations of Lyme disease. (1989)
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Chronic central nervous system involvement in Lyme borreliosis. (1988)
"We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis."
Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. (1988)
"Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement."
Demyelinating encephalopathy in Lyme disease. (1985)
"A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later."
Conferences:
Lyme Borreliosis and Related Disorders
by Liegner
11th International Scientific Conference on Lyme Disease and Other Spirochetal & Tick-Borne Disorders, 1998
Subtle Injury to Transformed Neural Cell Lines by Bb
by Benach
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, 1997
Spectrum of Antibiotic-Responsive Meningoencephalomyelitides
by Liegner
8th Annual LDF International Scientific Conference on Lyme Borreliosis and other Spirochetal and Tick-borne Diseases, 1995
Patient Stories:
Multiple Sclerosis & Lyme Blog
"I was content with the Multiple Sclerosis, and the routine that I had gotten into; both with the treatments and understanding the disease. Now I am thrown into something that I do not understand all that well. Furthermore, I am having a difficult time finding a doctor that is skilled in treating Lyme, especially now that I have long entered chronic/3rd stage Lyme (and all those doses of Solu-medrol only made things worse)."
Doctors can misdiagnose Lyme disease for MS, April 2010
"In a recent thesis, Winnipeg researcher Kathleen Crang found that some Manitobans diagnosed with MS and other chronic conditions may actually be suffering from the borrelia bacteria, a tick-borne 'biological evil genius' that causes Lyme disease."
Lyme disease sufferer spent years being misdiagnosed
"One neurologist told her she had multiple sclerosis. It's common, she says, for people with Lyme disease to be misdiagnosed as having multiple sclerosis, lupus, arthritis, or other illnesses with similar symptoms."
Patients, doctors debate Lyme
"Plagued witt unexplained fatigue, muscle aches, eye pain and other problems for years, Tierney was diagnosed with multiple sclerosis last year." (Free registration to LymeInfo required.)
Not Giving Up, The Corning Leader, December 2004 (expired link)
"Until January, Heininger lived for 20 years believing that multiple sclerosis was the cause of her growing disability. She is one of an increasing number of people who are learning that Lyme is a "disease in disguise," according to an Aug. 23 Newsweek article."
Lyme disease can get very severe without antibiotics, The Daily Review, September 2002
"Probably 10 percent of multiple sclerosis cases are actually Lyme's," Stricker said. "There's really not a lot of expertise in this area, sadly. It's really amazing how many patients will come in and say their doctor says Lyme disease doesn't happen here." (Free registration to LymeInfo required.)
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005 (expired link)
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
Misc:
Research by Gabriel Steiner on spirochetes and MS.
"In this respect the discovered spirochetes were totally different from the treponema-type and resembled the borrelia-type of spirochetes."
Systemic Intracellular Bacterial Infections
Article addresses Mycoplasma, Chlamydia, Borrelia species in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseases. Excerpt: "When these infections are released from cells, they contain host cell antigens in their exterior membranes, and these normal cell membrane antigens could stimulate autoimmune responses. Alternatively, the microorganisms may express antigens that mimic normal surface antigens." (Published April 2008)
Multiple Sclerosis Patients Should Be Tested for Lyme Disease
"Because both Multiple Sclerosis and Lyme Disease are diseases of the central nervous system, they both manifest themselves in ways that are different person to person."
Book: Multiple Sclerosis Through History and Human Life
Covers history of spirochete research as a cause of MS.
Editorial on MS & Lyme
"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."
Video: Chronic Lyme Disease: Connection to MS- Facts behind the controversy
This lecture was recorded at the Lyme Symposium held at the University of New Haven on May 12, 2006.
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lyme/MS Journal References
"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."
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
Multiple Sclerosis Sites:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
Allaolevien tutkimusten linkit avautuvat sivuulta:
http://www.lymeinfo.net/multiplesclerosis.html
Lyme Disease Misdiagnosed as Multiple Sclerosis
The following articles compiled by LymeInfo provide information about Lyme disease being misdiagnosed as Multiple Sclerosis. The differential diagnosis can be tricky, as Lyme tests can be falsely negative. Disseminated Lyme disease is also very complicated to treat. Therefore, it is important for those diagnosed with Multiple Sclerosis to be thoroughly evaluated by a physician skilled at diagnosing Lyme disease. After reviewing the below articles, please browse around the Lyme Info website to learn more about Lyme disease and other tick-borne illnesses. Be sure to visit our Lyme Disease Diagnosis & Treatment page. The list below is merely an introduction and does not cover all articles on this topic.
Medical Abstracts:
Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma. (2007)
"In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed."
Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable? (2005)
"As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted."
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis. (2004)
"Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described. In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI."
Bacterial infection as a cause of multiple sclerosis. (2002)
"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."
Association between multiple sclerosis and cystic structures in cerebrospinal fluid. (2001)
"Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS."
Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. (2001)
"Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum."
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. (2000)
"The result suggests that multiple sclerosis may be often associated with Borrelia infection."
Multiple sclerosis vs Lyme disease: a case presentation to a discussant and a review of the literature.(1999)
Read the first page here.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. (1996)
"We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection."
The presence of anti-Borrelia burgdorferi antibodies in a group of multiple sclerosis patients in eastern Sicily. Preliminary data. (1993)
"The authors evaluate the presence of anti-Borrelia burgdorferi antibodies in a group of polysclerotic patients of Eastern Sicily, in order to verify or dismiss a correlation between Borrelia infection and demyelinizing syndrome."
Diseases that mimic multiple sclerosis. (1991)
"Dr Scott compares typical findings of multiple sclerosis with those of the four diseases that are sometimes mistaken for this syndrome."
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion. (1990)
"In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed."
Neurologic manifestations of Lyme disease, the new "great imitator". (1989)
"Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements."
Clinical manifestations of Lyme disease in the United States. (1989)
Conn Med. 1989 Jun;53(6):327-30.
Clinical pathologic correlations of Lyme disease. (1989)
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Chronic central nervous system involvement in Lyme borreliosis. (1988)
"We describe four patients with marked chronic meningoencephalomyelitis caused by tick-transmitted Borrelia burgdorferi infection. Imaging techniques showed either MS-like lesions or evidence of vascular involvement, as in other spirochetal infections, especially in meningovascular syphilis."
Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. (1988)
"Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement."
Demyelinating encephalopathy in Lyme disease. (1985)
"A 38-year-old man from southeastern Connecticut developed a diffuse encephalopathy with partial complex seizures, followed weeks later by arthritis, cryoglobulinemia, and increased serum IgM. CT showed confluent low-density lesions in the deep cerebral white matter consistent with demyelination. Neither the encephalopathy nor the CT abnormalities improved. Lyme disease was diagnosed serologically 4 years later."
Conferences:
Lyme Borreliosis and Related Disorders
by Liegner
11th International Scientific Conference on Lyme Disease and Other Spirochetal & Tick-Borne Disorders, 1998
Subtle Injury to Transformed Neural Cell Lines by Bb
by Benach
10th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders, 1997
Spectrum of Antibiotic-Responsive Meningoencephalomyelitides
by Liegner
8th Annual LDF International Scientific Conference on Lyme Borreliosis and other Spirochetal and Tick-borne Diseases, 1995
Patient Stories:
Multiple Sclerosis & Lyme Blog
"I was content with the Multiple Sclerosis, and the routine that I had gotten into; both with the treatments and understanding the disease. Now I am thrown into something that I do not understand all that well. Furthermore, I am having a difficult time finding a doctor that is skilled in treating Lyme, especially now that I have long entered chronic/3rd stage Lyme (and all those doses of Solu-medrol only made things worse)."
Doctors can misdiagnose Lyme disease for MS, April 2010
"In a recent thesis, Winnipeg researcher Kathleen Crang found that some Manitobans diagnosed with MS and other chronic conditions may actually be suffering from the borrelia bacteria, a tick-borne 'biological evil genius' that causes Lyme disease."
Lyme disease sufferer spent years being misdiagnosed
"One neurologist told her she had multiple sclerosis. It's common, she says, for people with Lyme disease to be misdiagnosed as having multiple sclerosis, lupus, arthritis, or other illnesses with similar symptoms."
Patients, doctors debate Lyme
"Plagued witt unexplained fatigue, muscle aches, eye pain and other problems for years, Tierney was diagnosed with multiple sclerosis last year." (Free registration to LymeInfo required.)
Not Giving Up, The Corning Leader, December 2004 (expired link)
"Until January, Heininger lived for 20 years believing that multiple sclerosis was the cause of her growing disability. She is one of an increasing number of people who are learning that Lyme is a "disease in disguise," according to an Aug. 23 Newsweek article."
Lyme disease can get very severe without antibiotics, The Daily Review, September 2002
"Probably 10 percent of multiple sclerosis cases are actually Lyme's," Stricker said. "There's really not a lot of expertise in this area, sadly. It's really amazing how many patients will come in and say their doctor says Lyme disease doesn't happen here." (Free registration to LymeInfo required.)
Beyond Lyme disease's symptoms lies the truth, The Star-Ledger, May 2002
"She tested positive for Lyme but no one, she said, would treat her. Brain abnormalities showed up on an MRI and doctors told her she had multiple sclerosis." (Free registration to LymeInfo required.)
A Guide to Multiple Sclerosis, Wichita Eagle, March 2005 (expired link)
"Recent reports suggest that the neurological problems associated with Lyme disease may present a clinical picture much like MS."
Misc:
Research by Gabriel Steiner on spirochetes and MS.
"In this respect the discovered spirochetes were totally different from the treponema-type and resembled the borrelia-type of spirochetes."
Systemic Intracellular Bacterial Infections
Article addresses Mycoplasma, Chlamydia, Borrelia species in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseases. Excerpt: "When these infections are released from cells, they contain host cell antigens in their exterior membranes, and these normal cell membrane antigens could stimulate autoimmune responses. Alternatively, the microorganisms may express antigens that mimic normal surface antigens." (Published April 2008)
Multiple Sclerosis Patients Should Be Tested for Lyme Disease
"Because both Multiple Sclerosis and Lyme Disease are diseases of the central nervous system, they both manifest themselves in ways that are different person to person."
Book: Multiple Sclerosis Through History and Human Life
Covers history of spirochete research as a cause of MS.
Editorial on MS & Lyme
"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."
Video: Chronic Lyme Disease: Connection to MS- Facts behind the controversy
This lecture was recorded at the Lyme Symposium held at the University of New Haven on May 12, 2006.
Art's Lyme Misdiagnosed As...
Provides a comprehensive listing of abstracts about Lyme disease and Multiple Sclerosis.
ILADS Basic Information
"Lyme disease is the latest great imitator and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, as well as arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes."
Lyme/MS Journal References
"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."
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
Case 59 - White Matter Lesions
"This 22 year old male college student from western Pennsylvania was seen by a neurologist in late 1994 with a 3 1/2 year history of vague complaints of lower extremity numbness and new onset right arm/hand weakness. A Lyme titer was strongly positive and confirmed by Western blot in the spring of 1995."
Spirochaeta Myelophthora in Multiple Sclerosis
Cell Wall Deficient Forms: Stealth Pathogens Research Summary.
Lyme Disease and Multiple Sclerosis
"Until I have testing done at labs that specialize only in tick disease, I would be careful about rushing to a final diagnosis."
Antibiotic may be a potential therapy for MS
"A common antibiotic, long used to treat infections in humans, may have potential as a treatment for multiple sclerosis."
New Ideas About the Cause, Spread and Therapy of Lyme Disease
"Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson's Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer's Disease."
Neurologic Lyme Disease
"Patients with new onset Bb infection may develop an acute CNS demyelinated disease that looks much like multiple sclerosis."
Multiple Sclerosis Sites:
Accelerated Cure Project for Multiple Sclerosis
"We believe to develop a cure, the causes of the disease first need to be identified. We are driving this process through a logical and systematic plan called the Cure Map. The Cure Map looks at the five possible causes of any known disease: genetics, toxic agents, pathogens, trauma, and nutrition. It identifies and outlines what existing research has already uncovered in each of those areas, and identifies what remains to be researched."
Friends with MS
"Friends with MS is an online interactive support group for people with MS, those not yet diagnosed and those who love them. Our mission is to end the isolation that people feel when faced with a chronic illness, Multiple Sclerosis."
National Multiple Sclerosis Society
"The mission of the National Multiple Sclerosis Society is to end the devastating effects of MS."
All About Multiple Sclerosis
"All About Multiple Sclerosis aims to provide accurate and comprehensive medical information about multiple sclerosis (MS) written in plain English by people living with the disease and its symptoms."
Re: BORRELIOOSI/MS-TAUTI
Tutkijat selvittivät neuroborrelioosia sairastavien amyloidiaineenvaihduntaa. Borreliabakteerin todettiiin vaikuttavan amyloidien aineenvaihduntaan.
Amyloidiaineenvaihdunnassa on todettu poikkeavuuksia Alzheimerin, MS-taudin, SLE:n ja HIV:in kohdallla.
http://www.biomedcentral.com/content/pd ... -10-51.pdf
Neuroinflammation in Lyme neuroborreliosis affects amyloid metabolism
Niklas Mattsson*, Daniel Bremell, Rolf Anckarsäter, Kaj Blennow, Henrik Anckarsäter, Henrik Zetterberg,and Lars Hagberg
Abstract
Background:
The metabolism of amyloid precursor protein (APP) an
d β-amyloid (Aβ) is widely studied in Alzheimer's
disease, where Aβ deposition and plaque development are
essential components of the pathogenesis. However, the
physiological role of amyloid in the adult nervous system remains largely unknown. We have previously found altered
cerebral amyloid metabolism in other neuroinflammatory conditions. To further elucidate this, we investigated amyloid
metabolism in patients with Lyme neuroborreliosis (LNB).
Methods:
The first part of the study was a cro
ss-sectional cohort study in
61 patients with acute facial palsy (19 with
LNB and 42 with idiopathic facial pare
sis, Bell's palsy) and 22 healthy controls. CSF was analysed for the β-amyloid
peptides Aβ38, Aβ40 and Aβ42, and the amyloid precursor pr
otein (APP) isoforms α-sAPP and β-sAPP. CSF total-tau (T-
tau), phosphorylated tau (P-tau) and neurofilament protein
(NFL) were measured to moni
tor neural cell damage. The
second part of the study was a prospective cohort-study in
26 LNB patients undergoing consecutive lumbar punctures
before and after antibiotic treatment to study time-dependent dynamics of the biomarkers.
Results:
In the cross-sectional st
udy, LNB patients had lower levels of CSF α-sAPP, β-sAPP and P-tau, and higher levels of
CSF NFL than healthy controls and patients with Bell's palsy.
In the prospective study, LNB patients had low levels of
CSF α-sAPP, β-sAPP and P-tau at baseline, whic
h all increased towards normal at follow-up.
Conclusions:
Amyloid metabolism is altered in LNB. CSF levels
of α-sAPP, β-sAPP and P-tau are decreased in acute
infection and increase after treatment. In combination with ea
rlier findings in multiple sc
lerosis, cerebral SLE and HIV
with cerebral engagement, this points to an infl
uence of neuroinflammation on amyloid metabolism.
Background
The trans-membranous protein amyloid precursor pro-
tein (APP) has been intensely studied in Alzheimer's dis-
ease (AD), since it is the source of β-amyloid (Aβ)
peptides, recognized as key-components in AD
pathophysiology [1]. Although ubiquitously expressed,
the physiological role of APP in the adult organism
remains largely unknown. APP may undergo non-amy-
loidogenic cleavage at the α-site, which inhibits formation
of Aβ and releases an extracellular soluble α-sAPP frag-
ment. Alternatively, APP is processed by combined cleav-
ages by β-secretase and γ-secretase, releasing Aβ and β-
sAPP. Aβ peptides vary in length due to variability in the
γ-secretase cleavage site. Although CSF levels of α-sAPP
and β-sAPP generally correlate tightly [2], it is not known
how these pathways are orchestrated
in vivo
. CSF levels of
α-sAPP and β-sAPP are reduced in MS and cerebral sys-
temic lupus erythematosus SLE [3], and even lower levels
are seen in HIV patients with cerebral engagement [4].
Lyme neuroborreliosis (LNB) is caused by a central ner-
vous system (CNS) infection by the tick-borne spirochete
Borrelia burgdorferi
. LNB is often manifested by cranial
nerve engagement, and common clinical findings are
facial nerve palsy and radiculitic pain [5,6]. Common lab-
oratory findings are increased albumin ratio, indicating
impaired blood-brain barrier function, and CSF monocy-
tosis. In this study, we investigated CSF markers of amy-
loid metabolism and neural cell damage in LNB, to
elucidate the influence of neuroinflammation on amyloid
metabolism.
* Correspondence: niklas.mattsson@neuro.gu.se
1
Clinical Neuroc
hemistry Laboratory, Institute of
Neuroscience and Physiology,
Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy,
University of Gothenburg, Mölndal, Sweden
Full list of author information is
available at the end of the article
Mattsson
et al.
BMC Neurology
2010,
10
:51
http://www.biomedcentra
l.com/1471-2377/10/51
Page 2 of 7
The project contained two clinical studies. The first
was a cross-sectional study in patients with acute facial
palsy caused by either LNB or idiopathic Bell's palsy. The
second was a longitudinal prospective cohort-study,
where LNB patients were followed with successive lum-
bar punctures to investigate time-dependent biomarker
dynamics.
Methods
Study participants
We enrolled different study participants for the cross-
sectional study and the longitudinal study. Participants
included LNB patients, Bell's palsy patients and controls.
Diagnostic criteria for LNB were: I. Clinical symptoms
consistent with neuroborreliosis and alternative explana-
tions excluded; II Inflammatory CSF with mononuclear
cell count >5 × 10
6
/l and erythrocytes <100 × 10
6
/L; III.
One or more of the following: a) Intrathecal antibody
production against
B burgdorferi sp
. b) Antibodies against
B burgdorferi sp
. in serum. c) Erythema migrans within
three months; and IV. One or more of the following: a)
CSF albumin >400 mg/L. b) Oligoclonal IgG and/or IgM-
synthesis on CSF protein electrophoresis. c) IgG index
(CSF/serum IgG ratio)/(CSF/serum albumin ratio) > .70.
Bell's palsy (idiopathic facial palsy) was defined as acute,
monosymptomatic, unilateral peripheral facial paresis of
unknown etiology. Bell's palsy patients were included as
non-infectious palsy controls.
In the cross-sectional part of the study we investigated
61 patients of whom 19 fulfilled criteria for LNB and 42
were classified as Bell's palsy. Twenty-two individuals for
whom CSF analysis was done because of headache or ver-
tigo, but infection and other diseases were excluded (CSF
albumin and cell count were normal), served as controls.
The longitudinal study included 26 LNB patients with
radiculitic pain and sensory disturbances. In addition, 3
patients had facial palsy, 3 had paraparesis, 1 had paresis
of the accessorius nerve, and 1 had a trigeminus paresis.
There was no overlap with the patients in the cross-sec-
tional study. Ten patients without any neurological disor-
ders, undergoing knee replacements, where CSF was
drawn before surgery (Table 1) served as controls in the
longitudinal study. These subjects are described in detail
elsewhere [7]. All LNB patients were given oral treatment
with doxycycline 200-400 mg daily for 10-14 days, which
is the standard treatment in Sweden [8]. CSF was drawn
before start of treatment and at follow-up. The median
duration between the samplings was 45 days (range 33-
61). All subjects gave informed consent to participate.
The study was approved by the ethics committee of Uni-
versity of Gothenburg.
Sampling
CSF samples were collected by lumbar puncture in the
L3/L4 or L4/L5 interspace. Four mL of CSF was collected
in a polypropylene tube and immediately transported to
the local laboratory for centrifugation at 2.000 g at +4°C
for 10 minutes. The supernatant was pipetted off, gently
mixed to avoid possible gradient effects, and aliquoted in
polypropylene tubes that were stored at -70°C pending
biochemical analyses, without being thawed and re-fro-
zen.
Biochemical procedures
All biochemical analyses were performed at the Clinical
Neurochemistry Laboratory in Mölndal, Sweden, by
experienced laboratory technicians who were blinded to
the clinical diagnoses and other clinical information.
Markers of amyloid metabolism
CSF levels of Aβ38, Aβ40 and Aβ42 were measured using
the MSD
®
Human/Rodent (4G8) Abeta Triplex Assay as
described by the manufacturer (Meso Scale Discovery,
MSD
®
, Gaithersburg, MD, USA). This assay employs the
4G8 antibody to capture Aβ and C-terminal specific anti-
bodies to specifically capture Aβ38, Aβ40 and Aβ42. All
isoforms are detected by SULFO-TAG™-labeled anti-4G8
detection antibody. CSF concentrations of α-sAPP and β-
sAPP were determined using the MSD
®
sAPPα/sAPPβ
Multiplex Assay as described by the manufacturer. This
assay employs the 6E10 antibody to capture α-sAPP and a
neoepitope-specific antibody to capture β-sAPP. Both
isoforms are detected by SULFO-TAG™-labeled anti-APP
antibody p2-1.
Markers of neural cell damage
The axonal damage marker CSF T-tau was measured
using a sandwich ELISA (INNOTEST
®
hTAU-Ag, Innoge-
netics, Ghent, Belgium) specifically constructed to mea-
sure all tau isoforms irrespectively of phosphorylation
status (T-tau), as previously described [9]. CSF concen-
trations of tau phosphorylated at threonine 181 (P-tau)
was measured using a sandwich ELISA (INNOTEST
®
PHOSPHO-TAU(181P), Innogenetics), as previously
described [10]. CSF NFL, which is increased following
damage to large myelinated axon, was analyzed using an
ELISA, as previously described [11]. The detection limit
for the NFL ELISA was 125 ng/L.
Albumin
Quantitative determination of albumin in serum and CSF
was performed using the Behring Nephelometer Analyser
(Behringwerke AG, Marburg, Germany). The CSF/serum
albumin ratio was calculated as: CSF albumin (mg/l)/
serum-albumin (g/l).
Statistical analyses
All statistical calculations were performed using SPSS
15.0 (SPSS Inc, Chicago, USA). As the distribution of
quantitative measures was significantly skewed, statistical
tests involving these variables were conducted using the
Mattsson
et al.
BMC Neurology
2010,
10
:51
http://www.biomedcentra
l.com/1471-2377/10/51
Page 3 of 7
non-parametric Kuskal-Wallis test for comparisons of
multiple groups and the Mann-Whitney U test for pair-
wise comparisons between groups. Quantitative variables
are presented as median (range). The Spearman correla-
tion coefficient was used for analyses of correlation
between variable levels in different study groups. Statisti-
cal significance was determined at P < .05.
Role of the funding source
The sponsors of the study had no role in study design,
data collection, data analysis, data interpretation, or writ-
ing of the report. The corresponding author had full
access to all the data in the study and had final responsi-
bility for the decision to submit for publication.
Results
In the cross-sectional study all groups were comparable
in age. The only exception was that Bell's palsy patients
were slightly younger than th
e controls (P = .023, Table
1). LNB patients had longer history of neurological symp-
toms before the time of lumbar puncture than Bell's palsy
patients (Table 1).
In the longitudinal study, LNB patients were younger
than the controls (P = .031, Table 1). The median dura-
tion of neurologic symptoms was 7 days longer than in
the cross-sectional study (21 days compared with 28
days). At follow-up, all LNB patients had improved in
their clinical symptoms and their inflammatory reactions
had diminished, with decreased CSF monocytic cell
counts (Table 1).
Amyloid metabolism
In the cross-sectional study, LNB patients had lower α-
sAPP and β-sAPP than the other groups (Figure 1), but
there were no differences in Aβ38, Aβ40 or Aβ42 (Table
2). α-sAPP and β-sAPP correlated to most Aβ peptides in
Bell's palsy patients (R = .47-.60, P ≤ .002) and controls (R
= .42-.55, P < .05; the only exception was α-sAPP and
Aβ38 in controls, where there was a trend towards signif-
icance, R = .40, P = .065), but not in LNB patients (P >
.05).
In the longitudinal study, LNB patients had lower base-
line levels of α-sAPP and β-sAPP (Figure 2) and Aβ pep-
tides than controls (Table 3). α-sAPP and β-sAPP
increased after treatment (Figure 2), while Aβ levels were
unaffected (Table 3). Conversely to what was seen in the
cross-sectional study, α-sAPP and β-sAPP correlated to
all Aβ peptides in LNB in the longitudinal study (R = .71-
.98, P < .001), but not in controls (P > .05).
Table 1: Study participants and routine CSF analysis
a
Group N M/F Age
years
Disease
duration
b
CSF monocytes
×10
6
/L
CSF albumin ratio CSF albumin (mg/l)
mean (range)
Cross-sectional study
Controls 22 9/13 44
(25-67)
-1
(1 - 34)
4.65
(2.7-10.5)
222
(83 - 411)
LNB with
facial palsy
19 11/8 42
(8 - 72)
21 136
(14 - 534)
16.3
c
(3.8-49.9)
861
c
(166 - 2850)
Bell's palsy 42 18/24 36
(16-70)
52
(1 - 39)
4.7
d
(2.3-11.5)
206
d
(114 - 569)
Follow-up study
Controls 10 6/4 63
(51-70)
-Missing data 6.4
(4.7-10.1)
302
(192 - 579)
Baseline Follow-up Baseline Follow-up Baseline Follow-up
LNB 26 17/9 49
(12-74)
28 105
(14-590)
12
(2-21)
15
c
(5.7-49.3)
6.1
e
(4.7-13.6)
816
c
(267-2180)
322
e
(146-707)
CSF, cerebrospinal fluid; LN
B, Lyme neuroborreliosis;
a
data presented as median (range
), if not stated otherwise;
b
any neurologic symptom
including radiculitic pain before study
inclusion, presented
as days (median);
c
P < .001 vs controls;
d
P < .001 vs LNB;
e
P < .001 vs LNB baseline.
Amyloidiaineenvaihdunnassa on todettu poikkeavuuksia Alzheimerin, MS-taudin, SLE:n ja HIV:in kohdallla.
http://www.biomedcentral.com/content/pd ... -10-51.pdf
Neuroinflammation in Lyme neuroborreliosis affects amyloid metabolism
Niklas Mattsson*, Daniel Bremell, Rolf Anckarsäter, Kaj Blennow, Henrik Anckarsäter, Henrik Zetterberg,and Lars Hagberg
Abstract
Background:
The metabolism of amyloid precursor protein (APP) an
d β-amyloid (Aβ) is widely studied in Alzheimer's
disease, where Aβ deposition and plaque development are
essential components of the pathogenesis. However, the
physiological role of amyloid in the adult nervous system remains largely unknown. We have previously found altered
cerebral amyloid metabolism in other neuroinflammatory conditions. To further elucidate this, we investigated amyloid
metabolism in patients with Lyme neuroborreliosis (LNB).
Methods:
The first part of the study was a cro
ss-sectional cohort study in
61 patients with acute facial palsy (19 with
LNB and 42 with idiopathic facial pare
sis, Bell's palsy) and 22 healthy controls. CSF was analysed for the β-amyloid
peptides Aβ38, Aβ40 and Aβ42, and the amyloid precursor pr
otein (APP) isoforms α-sAPP and β-sAPP. CSF total-tau (T-
tau), phosphorylated tau (P-tau) and neurofilament protein
(NFL) were measured to moni
tor neural cell damage. The
second part of the study was a prospective cohort-study in
26 LNB patients undergoing consecutive lumbar punctures
before and after antibiotic treatment to study time-dependent dynamics of the biomarkers.
Results:
In the cross-sectional st
udy, LNB patients had lower levels of CSF α-sAPP, β-sAPP and P-tau, and higher levels of
CSF NFL than healthy controls and patients with Bell's palsy.
In the prospective study, LNB patients had low levels of
CSF α-sAPP, β-sAPP and P-tau at baseline, whic
h all increased towards normal at follow-up.
Conclusions:
Amyloid metabolism is altered in LNB. CSF levels
of α-sAPP, β-sAPP and P-tau are decreased in acute
infection and increase after treatment. In combination with ea
rlier findings in multiple sc
lerosis, cerebral SLE and HIV
with cerebral engagement, this points to an infl
uence of neuroinflammation on amyloid metabolism.
Background
The trans-membranous protein amyloid precursor pro-
tein (APP) has been intensely studied in Alzheimer's dis-
ease (AD), since it is the source of β-amyloid (Aβ)
peptides, recognized as key-components in AD
pathophysiology [1]. Although ubiquitously expressed,
the physiological role of APP in the adult organism
remains largely unknown. APP may undergo non-amy-
loidogenic cleavage at the α-site, which inhibits formation
of Aβ and releases an extracellular soluble α-sAPP frag-
ment. Alternatively, APP is processed by combined cleav-
ages by β-secretase and γ-secretase, releasing Aβ and β-
sAPP. Aβ peptides vary in length due to variability in the
γ-secretase cleavage site. Although CSF levels of α-sAPP
and β-sAPP generally correlate tightly [2], it is not known
how these pathways are orchestrated
in vivo
. CSF levels of
α-sAPP and β-sAPP are reduced in MS and cerebral sys-
temic lupus erythematosus SLE [3], and even lower levels
are seen in HIV patients with cerebral engagement [4].
Lyme neuroborreliosis (LNB) is caused by a central ner-
vous system (CNS) infection by the tick-borne spirochete
Borrelia burgdorferi
. LNB is often manifested by cranial
nerve engagement, and common clinical findings are
facial nerve palsy and radiculitic pain [5,6]. Common lab-
oratory findings are increased albumin ratio, indicating
impaired blood-brain barrier function, and CSF monocy-
tosis. In this study, we investigated CSF markers of amy-
loid metabolism and neural cell damage in LNB, to
elucidate the influence of neuroinflammation on amyloid
metabolism.
* Correspondence: niklas.mattsson@neuro.gu.se
1
Clinical Neuroc
hemistry Laboratory, Institute of
Neuroscience and Physiology,
Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy,
University of Gothenburg, Mölndal, Sweden
Full list of author information is
available at the end of the article
Mattsson
et al.
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The project contained two clinical studies. The first
was a cross-sectional study in patients with acute facial
palsy caused by either LNB or idiopathic Bell's palsy. The
second was a longitudinal prospective cohort-study,
where LNB patients were followed with successive lum-
bar punctures to investigate time-dependent biomarker
dynamics.
Methods
Study participants
We enrolled different study participants for the cross-
sectional study and the longitudinal study. Participants
included LNB patients, Bell's palsy patients and controls.
Diagnostic criteria for LNB were: I. Clinical symptoms
consistent with neuroborreliosis and alternative explana-
tions excluded; II Inflammatory CSF with mononuclear
cell count >5 × 10
6
/l and erythrocytes <100 × 10
6
/L; III.
One or more of the following: a) Intrathecal antibody
production against
B burgdorferi sp
. b) Antibodies against
B burgdorferi sp
. in serum. c) Erythema migrans within
three months; and IV. One or more of the following: a)
CSF albumin >400 mg/L. b) Oligoclonal IgG and/or IgM-
synthesis on CSF protein electrophoresis. c) IgG index
(CSF/serum IgG ratio)/(CSF/serum albumin ratio) > .70.
Bell's palsy (idiopathic facial palsy) was defined as acute,
monosymptomatic, unilateral peripheral facial paresis of
unknown etiology. Bell's palsy patients were included as
non-infectious palsy controls.
In the cross-sectional part of the study we investigated
61 patients of whom 19 fulfilled criteria for LNB and 42
were classified as Bell's palsy. Twenty-two individuals for
whom CSF analysis was done because of headache or ver-
tigo, but infection and other diseases were excluded (CSF
albumin and cell count were normal), served as controls.
The longitudinal study included 26 LNB patients with
radiculitic pain and sensory disturbances. In addition, 3
patients had facial palsy, 3 had paraparesis, 1 had paresis
of the accessorius nerve, and 1 had a trigeminus paresis.
There was no overlap with the patients in the cross-sec-
tional study. Ten patients without any neurological disor-
ders, undergoing knee replacements, where CSF was
drawn before surgery (Table 1) served as controls in the
longitudinal study. These subjects are described in detail
elsewhere [7]. All LNB patients were given oral treatment
with doxycycline 200-400 mg daily for 10-14 days, which
is the standard treatment in Sweden [8]. CSF was drawn
before start of treatment and at follow-up. The median
duration between the samplings was 45 days (range 33-
61). All subjects gave informed consent to participate.
The study was approved by the ethics committee of Uni-
versity of Gothenburg.
Sampling
CSF samples were collected by lumbar puncture in the
L3/L4 or L4/L5 interspace. Four mL of CSF was collected
in a polypropylene tube and immediately transported to
the local laboratory for centrifugation at 2.000 g at +4°C
for 10 minutes. The supernatant was pipetted off, gently
mixed to avoid possible gradient effects, and aliquoted in
polypropylene tubes that were stored at -70°C pending
biochemical analyses, without being thawed and re-fro-
zen.
Biochemical procedures
All biochemical analyses were performed at the Clinical
Neurochemistry Laboratory in Mölndal, Sweden, by
experienced laboratory technicians who were blinded to
the clinical diagnoses and other clinical information.
Markers of amyloid metabolism
CSF levels of Aβ38, Aβ40 and Aβ42 were measured using
the MSD
®
Human/Rodent (4G8) Abeta Triplex Assay as
described by the manufacturer (Meso Scale Discovery,
MSD
®
, Gaithersburg, MD, USA). This assay employs the
4G8 antibody to capture Aβ and C-terminal specific anti-
bodies to specifically capture Aβ38, Aβ40 and Aβ42. All
isoforms are detected by SULFO-TAG™-labeled anti-4G8
detection antibody. CSF concentrations of α-sAPP and β-
sAPP were determined using the MSD
®
sAPPα/sAPPβ
Multiplex Assay as described by the manufacturer. This
assay employs the 6E10 antibody to capture α-sAPP and a
neoepitope-specific antibody to capture β-sAPP. Both
isoforms are detected by SULFO-TAG™-labeled anti-APP
antibody p2-1.
Markers of neural cell damage
The axonal damage marker CSF T-tau was measured
using a sandwich ELISA (INNOTEST
®
hTAU-Ag, Innoge-
netics, Ghent, Belgium) specifically constructed to mea-
sure all tau isoforms irrespectively of phosphorylation
status (T-tau), as previously described [9]. CSF concen-
trations of tau phosphorylated at threonine 181 (P-tau)
was measured using a sandwich ELISA (INNOTEST
®
PHOSPHO-TAU(181P), Innogenetics), as previously
described [10]. CSF NFL, which is increased following
damage to large myelinated axon, was analyzed using an
ELISA, as previously described [11]. The detection limit
for the NFL ELISA was 125 ng/L.
Albumin
Quantitative determination of albumin in serum and CSF
was performed using the Behring Nephelometer Analyser
(Behringwerke AG, Marburg, Germany). The CSF/serum
albumin ratio was calculated as: CSF albumin (mg/l)/
serum-albumin (g/l).
Statistical analyses
All statistical calculations were performed using SPSS
15.0 (SPSS Inc, Chicago, USA). As the distribution of
quantitative measures was significantly skewed, statistical
tests involving these variables were conducted using the
Mattsson
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non-parametric Kuskal-Wallis test for comparisons of
multiple groups and the Mann-Whitney U test for pair-
wise comparisons between groups. Quantitative variables
are presented as median (range). The Spearman correla-
tion coefficient was used for analyses of correlation
between variable levels in different study groups. Statisti-
cal significance was determined at P < .05.
Role of the funding source
The sponsors of the study had no role in study design,
data collection, data analysis, data interpretation, or writ-
ing of the report. The corresponding author had full
access to all the data in the study and had final responsi-
bility for the decision to submit for publication.
Results
In the cross-sectional study all groups were comparable
in age. The only exception was that Bell's palsy patients
were slightly younger than th
e controls (P = .023, Table
1). LNB patients had longer history of neurological symp-
toms before the time of lumbar puncture than Bell's palsy
patients (Table 1).
In the longitudinal study, LNB patients were younger
than the controls (P = .031, Table 1). The median dura-
tion of neurologic symptoms was 7 days longer than in
the cross-sectional study (21 days compared with 28
days). At follow-up, all LNB patients had improved in
their clinical symptoms and their inflammatory reactions
had diminished, with decreased CSF monocytic cell
counts (Table 1).
Amyloid metabolism
In the cross-sectional study, LNB patients had lower α-
sAPP and β-sAPP than the other groups (Figure 1), but
there were no differences in Aβ38, Aβ40 or Aβ42 (Table
2). α-sAPP and β-sAPP correlated to most Aβ peptides in
Bell's palsy patients (R = .47-.60, P ≤ .002) and controls (R
= .42-.55, P < .05; the only exception was α-sAPP and
Aβ38 in controls, where there was a trend towards signif-
icance, R = .40, P = .065), but not in LNB patients (P >
.05).
In the longitudinal study, LNB patients had lower base-
line levels of α-sAPP and β-sAPP (Figure 2) and Aβ pep-
tides than controls (Table 3). α-sAPP and β-sAPP
increased after treatment (Figure 2), while Aβ levels were
unaffected (Table 3). Conversely to what was seen in the
cross-sectional study, α-sAPP and β-sAPP correlated to
all Aβ peptides in LNB in the longitudinal study (R = .71-
.98, P < .001), but not in controls (P > .05).
Table 1: Study participants and routine CSF analysis
a
Group N M/F Age
years
Disease
duration
b
CSF monocytes
×10
6
/L
CSF albumin ratio CSF albumin (mg/l)
mean (range)
Cross-sectional study
Controls 22 9/13 44
(25-67)
-1
(1 - 34)
4.65
(2.7-10.5)
222
(83 - 411)
LNB with
facial palsy
19 11/8 42
(8 - 72)
21 136
(14 - 534)
16.3
c
(3.8-49.9)
861
c
(166 - 2850)
Bell's palsy 42 18/24 36
(16-70)
52
(1 - 39)
4.7
d
(2.3-11.5)
206
d
(114 - 569)
Follow-up study
Controls 10 6/4 63
(51-70)
-Missing data 6.4
(4.7-10.1)
302
(192 - 579)
Baseline Follow-up Baseline Follow-up Baseline Follow-up
LNB 26 17/9 49
(12-74)
28 105
(14-590)
12
(2-21)
15
c
(5.7-49.3)
6.1
e
(4.7-13.6)
816
c
(267-2180)
322
e
(146-707)
CSF, cerebrospinal fluid; LN
B, Lyme neuroborreliosis;
a
data presented as median (range
), if not stated otherwise;
b
any neurologic symptom
including radiculitic pain before study
inclusion, presented
as days (median);
c
P < .001 vs controls;
d
P < .001 vs LNB;
e
P < .001 vs LNB baseline.
Re: BORRELIOOSI/MS-TAUTI
Bakteeri- ja virusinfektioiden merkitys neurologisissa sairauksissa kuten Alzheimer, Parkinson, MS jne.
http://www.bjmp.org/content/role-chroni ... hiatric-au
Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1
Garth L. Nicolson and Jörg Haier
Cite this article as: BJMP 2009:2(4) 20-28
Download PDF
Abstract
Chronically ill patients with neurodegenerative, neurobehavioral and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections. In addition, other chronic illnesses where neurological manifestations are routinely found, such as fatiguing and autoimmune diseases, Lyme disease and Gulf War illnesses, also show systemic bacterial and viral infections that could be important in disease inception and progression or in increasing the number and severity of signs and symptoms. Evidence of Mycoplasma species, Chlamydia pneumoniae, Borrelia burgdorferi, human herpesvirus-1, -6 and -7 and other bacterial and viral infections revealed high infection rates in the above illnesses that were not found in controls. Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.
Abbreviations: Ab beta amyloid; AD Alzheimer’s disease; ADHD attention-deficit/hyperactivity disorder; ALS amyotrophic lateral sclerosis; ASD autism spectrum disorders; EBV Epstein-Barr virus; CFS chronic fatigue syndrome; CFS/ME chronic fatigue syndrome/myalgic encephalomyopathy; CI confidence interval; CMV cytomegalovirus; CSF cerebrospinal fluid; CNS central nervous system; ELISA enzyme linked immunoabsorbant assay; GWI Gulf War illnesses; HHV human herpes virus; HSV herpes simplex virus; PCR polymerase chain reaction; PD Parkinson’s disease
Introduction
Chronic infections appear to be common features of various diseases, including neurodegenerative, psychiatric and neurobehavioral diseases, autoimmune diseases, fatiguing illnesses and other conditions.1-4 Neurodegenerative diseases, chronic degenerative diseases of the central nervous system (CNS) that cause dementia, are mainly diseases of the elderly. In contrast, neurobehavioral diseases are found mainly in younger patients and include autism spectrum disorders (ASD), such as autism, attention deficit disorder, Asperger’s syndrome and other disorders.5 For the most part, the causes of these neurological diseases remain largely unknown.2 Neurodegenerative diseases are characterized by molecular and genetic changes in nerve cells that result in nerve cell degeneration and ultimately nerve cell dysfunction and death, resulting in neurological signs and symptoms and dementia.2,3 On the other hand, neurobehavioral diseases are related to fetal brain development but are less well characterized at the cellular level and involve both genetic and environmental factors.6, 7 Even less well characterized at the cellular and genetic level are the psychiatric disorders, such as schizophrenia, paranoia, bipolar disorders, depression and obsessive-compulsive disorders.
Genetic linkages have been found in neurodegenerative and neurobehavioral diseases, but the genetic changes that occur and the changes in gene expression that have been found are complex and usually not directly related to simple genetic alterations.2, 6-8 In addition, it is thought that nutritional deficiencies, environmental toxins, heavy metals, chronic bacterial and viral infections, autoimmune immunological responses, vascular diseases, head trauma and accumulation of fluid in the brain, changes in neurotransmitter concentrations, among others, are involved in the pathogenesis of various neurodegenerative and neurobehavioral diseases.2, 3, 5-16 One of the biochemical changes found in essentially all neurological, neurodegenerative and neurobehavioral diseases is the over-expression of oxidative free radical compounds (oxidative stress) that cause lipid, protein and genetic structural changes.9-11 Such oxidative stress can be caused by a variety of environmental toxic insults, and when combined with genetic factors could result in pathogenic changes.14
Neurodegenerative diseases
Infectious agents are important factors in neurodegenerative and neurobehavioral diseases and may enter the brain within infected migratory macrophages. They may also gain access by transcytosis across the blood-brain-barrier or enter by intraneuronal transfer from peripheral nerves.15 Cell wall-deficient bacteria, such as species of Mycoplasma, Chlamydia (Chlamydophila), Borrelia and Brucella, among others, and various viruses are candidate brain infectious agents that may play important roles in neurodegenerative and neurobehavioral diseases.16-19 Such infections are systemic and can affect the immune system and essentially any organ system, resulting in a variety of systemic signs and symptoms.4, 15, 16, 19, 20
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) is an adult-onset, idiopathic, progressive neurodegenerative disease that affects both central and peripheral motor neurons.21 Patients show gradual progressive weakness and paralysis of muscles due to destruction of upper motor neurons in the motor cortex and lower motor neurons in the brain stem and spinal cord. This ultimately results in death, usually by respiratory failure.21, 22 The overall clinical picture of ALS can vary, depending on the location and progression of pathological changes.23
The role of chronic infections has attracted attention with the finding of enterovirus sequences in a majority of ALS spinal cord samples by polymerase chain reaction (PCR).24 However, others have failed to detect enterovirus sequences in spinal cord samples from patients with or without ALS.25-26 In spite of the mixed findings on enterovirus, infectious agents that penetrate the CNS could play a role in the aetiology of ALS. Evidence for transmission of an infectious agent or transfer of an ALS-like disease from man-to-man or man-to-animals has not been found.27
Using PCR methods systemic mycoplasmal infections have been found in a high percentage of ALS patients.28, 29 We found that 100% of Gulf War veterans from three nations diagnosed with ALS had systemic mycoplasmal infections.28 All but one patient had M. fermentans, and one veteran from Australia had a systemic M. genitalium infection. In nonmilitary ALS patients systemic mycoplasmal infections of various species were found in approximately 80% of cases.28 Of the mycoplasma-positive civilian patients who were further tested for various species of Mycoplasma, most were positive for M. fermentans (59%), but other Mycoplasma species, such as M. hominis (31%) and M. pneumoniae infections (9%) were also present. Some of the ALS patients had multiple infections; however, multiple mycoplasmal infections were not found in the military patients with ALS.28 In another study 50% of ALS patients showed evidence of systemic Mycoplasma species by PCR analysis.29
ALS patients who live in certain areas often have infections of Borrelia burgdorferi, the principal aetiological agent in Lyme disease. For example, ALS patients who live in a Lyme-prevalent area were examined for B. burgdorferi infections, and over one-half were found to be seropositive for Borrelia compared to 10% of matched controls.30 In addition, some patients diagnosed with ALS were subsequently diagnosed with neuroborreliosis.31 Spirochetal forms have been observed in the brain tissue of ALS patients and in patients with other neurodegenerative diseases.32 In general, however, the incidence of Lyme infections in ALS patients is probably much lower. In one recent study on 414 ALS patients only about 6% showed serological evidence of Borrelia infections.33 Some Lyme Disease patients may progress to ALS, but this is probably only possible in patients who have the genetic susceptibility genes for ALS as well as other environmental toxic exposures.34, 35
Additional chronic infections have been found in ALS patients, including human herpes virus-6 (HHV-6), Chlamydia pneumoniae andother infections.36, 37 There is also a suggestion that retroviruses might be involved in ALS and other motorneuron diseases.38 McCormick et al.39 looked for reverse transcriptase activity in serum and cerebrospinal fluid of ALS and non-ALS patients and found reverse transcriptase activity in one-half of ALS serum samples tested but in only 7% of controls. Interestingly, only 4% of ALS cerebrospinal fluid samples contained reverse transcriptase activity.39
Although the exact cause of ALS remains to be determined, there are several hypotheses on its pathogenesis: (1) accumulation of glutamate causing excitotoxicity; (2) autoimmune reactions against motor neurons; (3) deficiency of nerve growth factor; (4) dysfunction of superoxide dismutase due to mutations; and (5) chronic infection(s).24, 27-40 None of these hypotheses have been ruled out or are exclusive, and ALS may have a complex pathogenesis involving multiple factors. 28, 36
It is tempting to propose that infections play an important role in the pathogenesis or progression of ALS.28, 40 Infections could be cofactors in ALS pathogenesis, or they could simply be opportunistic, causing morbidity in ALS patients. For example, infections could cause the respiratory and rheumatic symptoms and other problems that are often found in ALS patients. Since the patients with multiple infections were usually those with more rapidly progressive disease,28 infections likely promote disease progression. Indeed, when Corcia et al.41 examined the cause of death in 100 ALS patients, the main causes were broncho-pneumonia and pneumonia. Finally, there are a number of patients who have ALS-like signs and symptoms but fall short of diagnostic criteria. Although a careful study has not been attempted on these patients, there is an indication that they have the same infections as those found in patients with a full diagnosis of ALS (personal communication). Thus ALS-like diseases may represent a less progressive state, in that they may lack additional changes or exposures necessary for full ALS.
Multiple sclerosis
Multiple sclerosis (MS) is the most common demyelinating neurological disease. It can occur in young or older people and is a cyclic (relapsing-remitting) or progressive disease that continues progressing without remitting.42 Inflammation and the presence of autoimmune antibodies against myelin and other nerve cell antigens are thought to cause the myelin sheath to break down, resulting in decrease or loss of electrical impulses along the nerve fibers.42, 43 In the progressive subset of MS neurological damage occurs additionally by the deposition of plaques on the nerve cells to the point where nerve cell death occurs. In addition, breakdown of the blood-brain barrier in MS is associated with local inflammation caused by glial cells.42, 43 The clinical manifestations of demyelinization, plaque damage and blood-brain barrier disruptions cause variable symptoms, but they usually include impaired vision, alterations in motor, sensory and coordination systems and cognitive dysfunction.43
There is strong evidence for a genetic component in MS.44, 45 Although it has been established that there is a genetic susceptibility component to MS, epidemiological and twin studies suggest that MS is an acquired, rather than an inherited, disease.46
MS has been linked to chronic infection(s).46, 47 For example, patients show immunological and cytokine elevations consistent with chronic infections.48-50 An infectious cause for MS has been under examination for some time, and patients have been tested for various viral and bacterial infections. 44, 45,47, 48, 51 One of the most common findings in MS patients is the presence of C. pneumoniae antibodies and DNAin their cerebrospinal fluid.51-53 By examining relapsing-remitting and progressive MS patients for the presence of C. pneumoniae in cerebrospinal fluid by culture, PCR and immunoglobulin reactivity Sriram et al.52 were able to identify C. pneumoniae in 64% of MS cerebrospinal fluid versus 11% of patients with other neurological diseases. They also found high rates (97% positive) of PCR-positive MOMP gene in MS- patients versus 18% in other neurological diseases, and this correlated with 86% of MS patients being serology-positive patients by ELISA and Western blot analysis.52 Examination of MS patients for oligoclonal antibodies against C. pneumoniae revealed that 82% of MS patients were positive, whereas none of the control non-MS neurological patients had antibodies that were absorbed by C. pneumoniae elemental body antigens.53 Similarly, Contini et al.54 found that the DNA and RNA transcript levels in mononuclear cells and cerebrospinal fluid of 64.2% of MS patients but in only 3 controls.
Using immunohistochemistry Sriram et al.55 later examined formalin-fixed brain tissue from MS and non-MS neurological disease controls and found that in a subset of MS patients (35%) chlamydial antigens were localized to ependymal surfaces and periventricular regions. Staining was not found in brain tissue samples from other neurological diseases. Frozen tissues were available in some of these MS cases, and PCR amplification of C. pneumoniae genes was accomplished in 63% of brain tissue samples from MS patients but none in frozen brain tissues from other neurological diseases. In addition, using immuno-gold-labeled staining and electron microscopy they examined cerebrospinal fluid sediment for chlamydial antigens and found that the electron dense bodies resembling bacterial structures correlated with PCR-positive results in 91% of MS cases.55 They also used different nested PCR methods to examine additional C. pneumoniae gene sequences in the cerebrospinal fluid of 72 MS patients and linked these results to MS-associated lesions seen by MRI.56
MRI was used by Grimaldi et al.57 to link the presence of C. pneumoniae infection with abnormal MRI results and found linkage in 21% of MS patients. These turned out to be MS patients with more progressive disease.58 In addition, higher rates of C. pneumoniae transcription were found by Dong-Si et al.58 in the cerebrospinal fluid of 84 MS patients. The data above and other studies strongly support the presence of C. pneumoniae in the brains of MS patients,59-61 at least in the more progressed subset of MS patients.
Other research groups have also found evidence for C. pneumoniae in MS patients but at lower incidence. Fainardi et al.62 used ELISA techniques and found that high-affinity antibodies against C. pneumoniae were present in the cerebrospinal fluid of 17% of MS cases compared to 2% of patients with non-inflammatory neurological disorders. They found that the majority of the progressive forms of MS were positive compared to patients with remitting-relapsing MS. The presence of C. pneumoniae antibodies was also found in other inflammatory neurological disorders; thus it was not found to be specific for MS.62
In contrast to the studies above, other researchers have not found the presence of C. pneumoniaeor other bacteriain the brains of MS patients.63-65 For example, Hammerschlag et al.66 used nested PCR and culture to examine frozen brain samples from MS patients but could not find any evidence for C. pneumoniae. However, in one study C. pneumoniae was found at similar incidence in MS and other neurological diseases, but only MS patients had C. pneumoniae in their cerebrospinal fluid.64 Swanborg et al.67 reviewed the evidence linking C. pneumoniae infection with MS and concluded that it is equivocal, and they also speculated that specific genetic changes may be necessary to fulfill the role of such infections in the aetiology of MS.
Another possible reason for the equivocal evidence linking MS with infections, such as C. pneumoniae, is that multiple co-infections could be involved rather than one specific infection. In addition to C. pneumoniae found in most studies, MS patients could also have Mycoplasma species, B. burgdorferi and other bacterial infections as well as viral infections.68 When multiple infections are considered, it is likely that >90% of MS patients have obligate intracellular bacterial infections caused by Chlamydia (Chlamydophila), Mycoplasma, Borrelia or other intracellular bacterial infections. These infections were found only singly and at very low incidence in age-matched subjects.68 In spite of these findings, others did not find evidence of Mycoplasma species in MS brain tissue, cerebrospinal fluid or peripheral blood.69
Viruses have also been found in MS. For example, HHV-6 has been found at higher frequencies in MS patients, but this virus has also been found at lower incidence in control samples.70 Using PCR Sanders et al.70 examined postmortem brain tissue and controls for the presence of various neurotrophic viruses. They found that 57% of MS cases and 43% of non-MS neurological disease controls were positive for HHV-6, whereas 37% and 28%, respectively, were positive for herpes simplex virus (HSV-1 and -2) and 43% and 32%, respectively, were positive for varicella zoster virus. However, these differences did not achieve statistical significance, and the authors concluded “an etiologic association to the MS disease process [is] uncertain.” They also found that 32% of the MS active plaques and 17% of the inactive plaque areas were positive for HHV-6.70 Using sequence difference analysis and PCR Challoner et al.71 searched for pathogens in MS brain specimens. They found that >70% of the MS specimens were positive for infection-associated sequences. They also used immunocytochemistry and found staining around MS plaques more frequently than around white matter. Nuclear staining of oligodendrocytes was also seen in MS samples but not in controls.71 Using immunofluorescent and PCR methods HHV-6 DNA has also been found in peripheral leukocytes in the systemic circulation of MS patients.72, 73 However, using PCR methods, others did not found herpes viruses in the peripheral blood or CSF of MS patients.74, 75 Evidence that prior infection with EBV could be related to the development of MS was proposed; however, EBV infects more than 90% of humans without evidence of health problems and 99% of MS patients.76 The difference in MS patients could be the presence of multiple infections, including EBV. Recently Willis et al.77 used multiple molecular techniques to examine MS tissue but failed to find EBV in any MS tissues but could find EBV in CNS lymphomas.
Current reviews and the information above points to an infectious process in MS.47, 48, 75, 76, 78-80 Although a few studies did not come to this conclusion,74, 75 most studies have found infections in MS patients. It is interesting that it is the progressive rather than relapsing-remitting forms of MS which have been associated with chronic infections; therefore, infections might be more important in MS progression than in its inception. Various infections may also nonspecifically stimulate the immune system.47, 48 Infections may also invade immune cells and alter immune cell function in a way that promotes inflammation and autoimmune activity.78 If infections like C. pneumoniae and Mycoplasma species are important in MS, then antibiotics effective against these infections should improve clinical status. Although preliminary, that is in fact what has been seen, but not in all patients.81 As in other neurodegenerative diseases, multiple factors appear to be involved in the pathogenesis of MS.
Alzheimer’s disease
Alzheimer’s Disease (AD) is a family of brain disorders usually found in elderly patients and is the most common cause of dementia. AD is characterized by slow, progressive loss of brain function, notable lapses in memory, disorientation, confusion, mood swings, changes in personality, language problems, such as difficulty in finding the right words for everyday objects, loss of behavioral inhibitions and motivation and paranoia. The course of AD varies widely, and the duration of illness can range from a few years to over 20 years. During this period the parts of the brain that control memory and thinking are among the first affected, followed by other brain changes that ultimately result in brain cell death.82
AD is characterized by distinct neuropathological changes in brain tissues and cells. Among the most notable are the appearance of plaques and tangles of neurofibrils within brain nerve cells that affect synapses and nerve-nerve cell communication. These structural alterations involve the deposition of altered amyloid proteins.83, 84 Although the cause of AD is not known, the formation of the amyloid plaques and neurofibrillary tangles may be due to genetic defects and resulting changes in the structure of beta amyloid proteins. This in turn may be caused by chemicals or other toxic events, inflammatory responses, excess oxidative stress and increases in reactive oxygen species, loss of nerve trophic factors and reductions in nerve cell transmission.83-87
Recently AD brain infections have become important.88-90 For example, one pathogen that has attracted considerable attention is C. pneumoniae.91, 92 As mentioned above, this intracellular bacterium has a tropism for neural tissue, and it has been found at high incidence in the brains of AD patients by PCR and immunohistochemistry.92 C. pneumoniae has also been found in nerve cells in close proximity to neurofibrillary tangles.92, 93 Similarly to Mycoplasma species, C. pneumoniae can invade endothelial cells and promote the transmigration of monocytes through human brain endothelial cells into the brain parenchyma.94 C. pneumoniae has been found in the brains of most AD patients,91 and it has been cultured from AD brain tissue.95 Injection of C. pneumoniae into mice stimulates beta amyloid plaque formation.96 Although the data are compelling, some investigators have not found C. pneumoniae infections in AD.97, 98
AD patients also have other bacterial infections, such as B. burgdorferi.99 Using serology, culture, Western blot and immunofluorenscence methods this Lyme Disease infection has been examined in AD.100, 101 Not all researchers, however, have found evidence of B. burgdorferi in AD patients.102, 103 The presence of intracellular infections like B. burgdorferi in AD patients has been proposed to be a primary event in the formation of AD beta amyloid plaques. This is thought to occur by the formation of “congophilic cores” that attract beta amyloid materials.104 Multiple reports indicate that AD nerve cells are often positive for B. burgdorferi, indicating that this intracellular bacteria could be important in the pathogenesis of AD.99, 100, 104, 105
The hypothesis in AD that intracellular microorganisms could provide “cores” for the attraction of beta amyloid materials is appealing, but other factors, including the induction of reactive oxygen species, lipid peroxidation and the breakdown of the lysosomal membranes releasing lysosomal hydrolases, are also thought to be important in beta amyloid deposition.105 That infections may be important in AD pathogenesis is attractive; however, some negative reports have not confirmed the presence of infections like B. burgdorferi in AD patients.99-101 This suggests that the infection theory, although compelling, remains controversial.102, 105
Herpes virus infections have also been found in AD,especially HSV-1.106, 107 Previously it was determined that HSV-1 but not a related neurotrophic virus (varicella zoster virus) is present more often in AD brains, and this could be linked to AD patients who have the risk factor ApoE e4 allele.108, 109 HSV-1 is thought to be involved in the abnormal aggregation of beta amyloid fragments within the AD brain by reducing the amount of full-length beta amyloid precursor protein and increasing the amounts of their fragments.110 HSV-1 infection of glial and neuronal cells results in a dramatic increase in the intracellular levels of beta amyloid forms, whereas the levels of native beta amyloid precursor protein are decreased.111 This is similar to what has been found in mice infected with HSV-1, indicating that HSV-1 is probably involved directly in the development of senile-associated plaques. Another herpes virus, HHV-6, has also been found in AD patients, but it is thought that this virus is not directly involved in AD pathogenesis. HHV-6 may exacerbate the effects of HSV-1 in AD ApoE e4 carriers.112
Other infections have been found in AD patients, for example, C. pneumoniae, Helicobacter pylori amongst others.113 It has been proposed that such infections may act as a trigger or co-factor in AD.114 Although experimental evidence that pathogens can elicit the neuropathological changes and cognitive deficits that characterize AD is lacking, this approach may yield interesting and important results. These authors also stressed that systemic infections must be considered as potential contributors to the pathogenesis of AD.114
Parkinson’s disease
Parkinson’s disease (PD) is characterized by akinesia, muscular rigidity and resting tremor.103 In addition, autonomic dysfunction, olfactory disturbances, depression, sensory and sleep disturbances and frequently dementia characterize this disease.115 The pathology of PD indicates a progressive loss of the dopamine neurons of the substantia nigra together with the presence of Lewy bodies and alpha-synuclein. More extensive brain degeneration also occurs, from the medulla oblongata to the cerebral cortex.116, 117
Age-related inclusion bodies and protein aggregations or defects in their degradation characteristically occur in PD, but their role in PD pathogenesis remains unclear.117, 118 Some evidence suggests a relationship between PD and specific genetic changes, such as changes in the genes affecting mitochondria, protein degradation, organelle trafficking and vesicular fusion, and in proteins involved in oxidative stress or antioxidant function.102 Inflammation has also been associated with PD pathology.119
The pathogenesis of PD has been proposed to be due to multiple genetic and neurotoxic events that produce oxidative damage and cell death. In the case of PD the relevant targets of toxic events are neuromelanin-containing dopaminergic neurons of the substantia nigra.118, 120 A case-control study indicated that multiple environmental factors and genetic background were statistically related risk factors for PD.121 Prominent among these were long-term toxic exposures and trauma early in life.122 For example,early life exposure to brain injury, chemicals and/or infections may initiate a cyclic inflammatory process involving oxidative damage, excitotoxicity, mitochondrial dysfunction and altered proteolysis that later in life results in substantia nigra neuron death.123, 124
A role for chronic infections in PD pathogenesis has been proposed.123, 124 One infection found in PD that has aroused considerable interest is the presence of chronic gastrointestinal Helicobacter pylori.125 Indeed, treatment of this infection offers relief to late stage cachexia in PD patients receiving L-dopa.126 Helicobacter pylori-infected PD patients showed reduced L-dopa absorption and increased clinical disability,127 whereas treatment of this infection increased L-dopa absorption and decreased clinical disability.128 H. pylori may not be directly involved in the pathogenesis of PD, but its systemic presence could affect the progression and treatment of PD, probably by stimulating inflammation and autoimmunity.128
Chronic infections in PD have been linked to inflammation and autoimmune responses.129-131 Experimental models of PD have been developed using neurological viral or bacterial infections to initiate the pathogenic process.132, 133 Spirochetes have also been found in Lewy bodies of PD patients.30 Other infections, such as viral encephalitis,134 AIDS-associated opportunistic infections of the basal ganglia,135 coronavirus,136 among other infections,68, 137, 138 have been found in PD and could be important in stimulating inflammation and autoimmune responses. It has been stressed that additional research will be necessary to establish whether a causal link exists between PD and chronic infections.139
Neurobehavioral diseases
Autism spectrum disorders
ASD, such as autism, Asperger’s syndrome, etc., are neurobehavioral diseases of primarily the young where patients generally suffer from an inability to communicate properly, form relationships with others and respond appropriately to their environment. Such patients do not all share the same signs and symptoms but tend to share certain social, communication, motor and sensory problems that affect their behavior in predictable ways. These patients often display repetitive actions and develop troublesome fixations with specific objects, and they are often painfully sensitive to certain sounds, tastes and smells.140, 141
ASD cases are likely to be caused by multiple factors, including genetic defects, heavy metal, chemical and biological exposures, among other important events, which are probably different in each patient. ASD patients appear to have similarities in genetic defects and environmental exposures that are important in patient morbidity or in illness progression.5-8, 140-142
Chronic infections appear to be an important element in the development of ASD.6, 16, 143, 144 In ASD patients more than 50 different bacterial, viral and fungal infections have been found,6 some apparently more important than others in causing symptoms. It has been known for some time that ASD patients have a number of nonspecific chronic signs and symptoms, such as fatigue, headaches, gastrointestinal, vision problems, occasional intermittent low-grade fevers and other signs and symptoms that are generally excluded in the diagnosis of ASD but are consistent with the presence of infections.143 Indeed, increased titres to various viruses as well as bacterial and fungal infections have been commonly seen in ASD patients.6, 16, 19, 143-145 Not withstanding these reports, epidemiological evidence for an association of childhood infections in the first two years of life and ASD has been mixed.146
Environmental exposures to chemicals and heavy metals also appear to be important in the development of ASD.140, 141, 147, 148 The relationship between ASD and heavy metals may involve the role of multiple vaccines in ASD pathogenesis.130, 141 ASD patients often show their first signs and symptoms after multiple childhood immunizations, and the sharp increase in Autism rates occurred only after the multiple MMR vaccine came into widespread use.141 In some states in the U.S. children receive as many as 33 vaccines before they can enroll in school.140 Such vaccines can contain mercury and other toxic preservatives, and some may also contain contaminating bacteria, as found in veterinary vaccines.149
There are very few studies that have followed the transmission of infections and subsequent autism. Previously we found that veterans of the Gulf War with chronic fatiguing illnesses (Gulf War illnesses, GWI) exhibited multiple nonspecific signs and symptoms similar to chronic fatigue syndrome/myalgic encephalomyopathy (CFS/ME).150, 151 After returning to the home with GWI, their children subsequently became symptomatic, and these children were often diagnosed with ASD.152, 153 Symptomatic children (mostly diagnosed with ASD) were infected with the same Mycoplasma species, M. fermentans, that was found in the veterans and their symptomatic family members, and this was not seen in aged-matched control subjects or in military families without GWI. In the GWI families some non-symptomatic family members did have mycoplasmal infections (~10%), but this was not significantly different from the incidence of mycoplasmal infections in healthy control subjects.152, 153
Subsequently ASD patients who were not in military families were examined for systemic mycoplasmal infections.153 The majority (~54%) were positive for mycoplasmal infections. However, in contrast to the children of GWI patients who for the most part had only M. fermentans, the civilian children tested positive for a variety of Mycoplasma species. We also tested a few siblings without apparent signs and symptoms, and for the most part few had these infections.153 In another study we examined the blood of ASD patients from Central and Southern California and found that a large subset (>58%) of patients showed evidence of Mycoplasma infections compared to age-matched control subjects (Odds Ratio=13.8, p<0.001).19 ASD patients were also examined for C. pneumoniae (8.3% positive, Odds Ratio=5.6, p<0.01) and HHV-6 (29.2% positive, Odds Ratio=4.5, p<0.01). The results indicated that a large subset of ASD patients display evidence of bacterial and/or viral infections (Odds Ratio=16.5, p<0.001).19
ASD patients have been examined for B. burgdorferi infections.154 Various studies revealed that 22-30% of ASD patients (N=76) have Borrelia infections.6, 154 The incidence of Borrelia infections in ASD patients may be related to Lyme disease distribution, with some Lyme-intense areas having high prevalence, and other areas having a low prevalence. Other infections, such as Lyme-associated Bartonella, Babesia, Ehrlichia and non-Lyme-associated CMV, Plasmodium species, Toxoplasma species and Treponema species may also be associated with ASD.6
Final comments to part 1
When neurological symptoms are present, infections of the CNS must be considered. Brain infections can stimulate glial responses, and the presence of viral and bacterial infections in nerve cells, can stimulate autoimmune responses against nerve cell antigens as well as the infections within them.155 For example, in MS some 20 different bacterial and viral infections have been found, but the link between these infections and the pathogenesis of MS is still being debated.16, 47, 75 One or even a few types of infections cannot be causally linked to MS, and the reason for this is that there may be too many possibilities. No one infection or a group of infections needs to be the trigger in MS to be important in the pathogenesis of MS. In time combinations of certain infections may eventually be identified at least in a subset of MS patients, and this will allow the development of new therapeutic approaches for many MS patients that are not recognized today.
One problem that is rarely discussed is the apparent disparity between the laboratory results from different laboratories. Often different laboratories cannot agree on types of infections found in various chronic diseases.47 There are a number of reasons for this, including differences in the source of materials, qualities of reagents and techniques used.16 Some procedures, such as PCR, have specific challenges that must be overcome in the handling of specimens, their stability, presence of interfering substances, contamination, sensitivity and specificity of the tests and interpretation of the results. Variability in results from different laboratories will remain a problem unless research groups work closely together to solve these problems. One example of how this has been overcome is a multi-centre research study on the presence of C. pneumoniae in the cerebrospinal fluid of clinically defined, mono-symptomatic MS patients.156 Sriram et al.156 conducted this diagnostic trial with good concordance of results between different laboratories. Cooperative studies such as this should eventually alleviate discrepancies in the types of infections found by different research groups.
This review continues in Part 2 with psychiatric diseases, autoimmune diseases, fatiguing illnesses, and other infectious diseases with neurological aspects and an overall discussion of the topic. 157
Competing Interests
None Declared
Author Details
GARTH L. NICOLSON, Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA JORG HAIER, Department of General and Visceral Surgery, University Hospital, Münster 48149, Germany
CORRESSPONDENCE: Prof. Garth L. Nicolson, Office of the President, The Institute for Molecular Medicine, P.O. Box 9355, S. Laguna Beach, California, 92652 USA
Email: gnicolson@immed.org
References
1.Nicolson GL, Nasralla M, Haier J, et al. Mycoplasmal infections in chronic illnesses: Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis. Med Sentinel1999; 4: 172-176.
jne
http://www.bjmp.org/content/role-chroni ... hiatric-au
Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1
Garth L. Nicolson and Jörg Haier
Cite this article as: BJMP 2009:2(4) 20-28
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Abstract
Chronically ill patients with neurodegenerative, neurobehavioral and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections. In addition, other chronic illnesses where neurological manifestations are routinely found, such as fatiguing and autoimmune diseases, Lyme disease and Gulf War illnesses, also show systemic bacterial and viral infections that could be important in disease inception and progression or in increasing the number and severity of signs and symptoms. Evidence of Mycoplasma species, Chlamydia pneumoniae, Borrelia burgdorferi, human herpesvirus-1, -6 and -7 and other bacterial and viral infections revealed high infection rates in the above illnesses that were not found in controls. Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.
Abbreviations: Ab beta amyloid; AD Alzheimer’s disease; ADHD attention-deficit/hyperactivity disorder; ALS amyotrophic lateral sclerosis; ASD autism spectrum disorders; EBV Epstein-Barr virus; CFS chronic fatigue syndrome; CFS/ME chronic fatigue syndrome/myalgic encephalomyopathy; CI confidence interval; CMV cytomegalovirus; CSF cerebrospinal fluid; CNS central nervous system; ELISA enzyme linked immunoabsorbant assay; GWI Gulf War illnesses; HHV human herpes virus; HSV herpes simplex virus; PCR polymerase chain reaction; PD Parkinson’s disease
Introduction
Chronic infections appear to be common features of various diseases, including neurodegenerative, psychiatric and neurobehavioral diseases, autoimmune diseases, fatiguing illnesses and other conditions.1-4 Neurodegenerative diseases, chronic degenerative diseases of the central nervous system (CNS) that cause dementia, are mainly diseases of the elderly. In contrast, neurobehavioral diseases are found mainly in younger patients and include autism spectrum disorders (ASD), such as autism, attention deficit disorder, Asperger’s syndrome and other disorders.5 For the most part, the causes of these neurological diseases remain largely unknown.2 Neurodegenerative diseases are characterized by molecular and genetic changes in nerve cells that result in nerve cell degeneration and ultimately nerve cell dysfunction and death, resulting in neurological signs and symptoms and dementia.2,3 On the other hand, neurobehavioral diseases are related to fetal brain development but are less well characterized at the cellular level and involve both genetic and environmental factors.6, 7 Even less well characterized at the cellular and genetic level are the psychiatric disorders, such as schizophrenia, paranoia, bipolar disorders, depression and obsessive-compulsive disorders.
Genetic linkages have been found in neurodegenerative and neurobehavioral diseases, but the genetic changes that occur and the changes in gene expression that have been found are complex and usually not directly related to simple genetic alterations.2, 6-8 In addition, it is thought that nutritional deficiencies, environmental toxins, heavy metals, chronic bacterial and viral infections, autoimmune immunological responses, vascular diseases, head trauma and accumulation of fluid in the brain, changes in neurotransmitter concentrations, among others, are involved in the pathogenesis of various neurodegenerative and neurobehavioral diseases.2, 3, 5-16 One of the biochemical changes found in essentially all neurological, neurodegenerative and neurobehavioral diseases is the over-expression of oxidative free radical compounds (oxidative stress) that cause lipid, protein and genetic structural changes.9-11 Such oxidative stress can be caused by a variety of environmental toxic insults, and when combined with genetic factors could result in pathogenic changes.14
Neurodegenerative diseases
Infectious agents are important factors in neurodegenerative and neurobehavioral diseases and may enter the brain within infected migratory macrophages. They may also gain access by transcytosis across the blood-brain-barrier or enter by intraneuronal transfer from peripheral nerves.15 Cell wall-deficient bacteria, such as species of Mycoplasma, Chlamydia (Chlamydophila), Borrelia and Brucella, among others, and various viruses are candidate brain infectious agents that may play important roles in neurodegenerative and neurobehavioral diseases.16-19 Such infections are systemic and can affect the immune system and essentially any organ system, resulting in a variety of systemic signs and symptoms.4, 15, 16, 19, 20
Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) is an adult-onset, idiopathic, progressive neurodegenerative disease that affects both central and peripheral motor neurons.21 Patients show gradual progressive weakness and paralysis of muscles due to destruction of upper motor neurons in the motor cortex and lower motor neurons in the brain stem and spinal cord. This ultimately results in death, usually by respiratory failure.21, 22 The overall clinical picture of ALS can vary, depending on the location and progression of pathological changes.23
The role of chronic infections has attracted attention with the finding of enterovirus sequences in a majority of ALS spinal cord samples by polymerase chain reaction (PCR).24 However, others have failed to detect enterovirus sequences in spinal cord samples from patients with or without ALS.25-26 In spite of the mixed findings on enterovirus, infectious agents that penetrate the CNS could play a role in the aetiology of ALS. Evidence for transmission of an infectious agent or transfer of an ALS-like disease from man-to-man or man-to-animals has not been found.27
Using PCR methods systemic mycoplasmal infections have been found in a high percentage of ALS patients.28, 29 We found that 100% of Gulf War veterans from three nations diagnosed with ALS had systemic mycoplasmal infections.28 All but one patient had M. fermentans, and one veteran from Australia had a systemic M. genitalium infection. In nonmilitary ALS patients systemic mycoplasmal infections of various species were found in approximately 80% of cases.28 Of the mycoplasma-positive civilian patients who were further tested for various species of Mycoplasma, most were positive for M. fermentans (59%), but other Mycoplasma species, such as M. hominis (31%) and M. pneumoniae infections (9%) were also present. Some of the ALS patients had multiple infections; however, multiple mycoplasmal infections were not found in the military patients with ALS.28 In another study 50% of ALS patients showed evidence of systemic Mycoplasma species by PCR analysis.29
ALS patients who live in certain areas often have infections of Borrelia burgdorferi, the principal aetiological agent in Lyme disease. For example, ALS patients who live in a Lyme-prevalent area were examined for B. burgdorferi infections, and over one-half were found to be seropositive for Borrelia compared to 10% of matched controls.30 In addition, some patients diagnosed with ALS were subsequently diagnosed with neuroborreliosis.31 Spirochetal forms have been observed in the brain tissue of ALS patients and in patients with other neurodegenerative diseases.32 In general, however, the incidence of Lyme infections in ALS patients is probably much lower. In one recent study on 414 ALS patients only about 6% showed serological evidence of Borrelia infections.33 Some Lyme Disease patients may progress to ALS, but this is probably only possible in patients who have the genetic susceptibility genes for ALS as well as other environmental toxic exposures.34, 35
Additional chronic infections have been found in ALS patients, including human herpes virus-6 (HHV-6), Chlamydia pneumoniae andother infections.36, 37 There is also a suggestion that retroviruses might be involved in ALS and other motorneuron diseases.38 McCormick et al.39 looked for reverse transcriptase activity in serum and cerebrospinal fluid of ALS and non-ALS patients and found reverse transcriptase activity in one-half of ALS serum samples tested but in only 7% of controls. Interestingly, only 4% of ALS cerebrospinal fluid samples contained reverse transcriptase activity.39
Although the exact cause of ALS remains to be determined, there are several hypotheses on its pathogenesis: (1) accumulation of glutamate causing excitotoxicity; (2) autoimmune reactions against motor neurons; (3) deficiency of nerve growth factor; (4) dysfunction of superoxide dismutase due to mutations; and (5) chronic infection(s).24, 27-40 None of these hypotheses have been ruled out or are exclusive, and ALS may have a complex pathogenesis involving multiple factors. 28, 36
It is tempting to propose that infections play an important role in the pathogenesis or progression of ALS.28, 40 Infections could be cofactors in ALS pathogenesis, or they could simply be opportunistic, causing morbidity in ALS patients. For example, infections could cause the respiratory and rheumatic symptoms and other problems that are often found in ALS patients. Since the patients with multiple infections were usually those with more rapidly progressive disease,28 infections likely promote disease progression. Indeed, when Corcia et al.41 examined the cause of death in 100 ALS patients, the main causes were broncho-pneumonia and pneumonia. Finally, there are a number of patients who have ALS-like signs and symptoms but fall short of diagnostic criteria. Although a careful study has not been attempted on these patients, there is an indication that they have the same infections as those found in patients with a full diagnosis of ALS (personal communication). Thus ALS-like diseases may represent a less progressive state, in that they may lack additional changes or exposures necessary for full ALS.
Multiple sclerosis
Multiple sclerosis (MS) is the most common demyelinating neurological disease. It can occur in young or older people and is a cyclic (relapsing-remitting) or progressive disease that continues progressing without remitting.42 Inflammation and the presence of autoimmune antibodies against myelin and other nerve cell antigens are thought to cause the myelin sheath to break down, resulting in decrease or loss of electrical impulses along the nerve fibers.42, 43 In the progressive subset of MS neurological damage occurs additionally by the deposition of plaques on the nerve cells to the point where nerve cell death occurs. In addition, breakdown of the blood-brain barrier in MS is associated with local inflammation caused by glial cells.42, 43 The clinical manifestations of demyelinization, plaque damage and blood-brain barrier disruptions cause variable symptoms, but they usually include impaired vision, alterations in motor, sensory and coordination systems and cognitive dysfunction.43
There is strong evidence for a genetic component in MS.44, 45 Although it has been established that there is a genetic susceptibility component to MS, epidemiological and twin studies suggest that MS is an acquired, rather than an inherited, disease.46
MS has been linked to chronic infection(s).46, 47 For example, patients show immunological and cytokine elevations consistent with chronic infections.48-50 An infectious cause for MS has been under examination for some time, and patients have been tested for various viral and bacterial infections. 44, 45,47, 48, 51 One of the most common findings in MS patients is the presence of C. pneumoniae antibodies and DNAin their cerebrospinal fluid.51-53 By examining relapsing-remitting and progressive MS patients for the presence of C. pneumoniae in cerebrospinal fluid by culture, PCR and immunoglobulin reactivity Sriram et al.52 were able to identify C. pneumoniae in 64% of MS cerebrospinal fluid versus 11% of patients with other neurological diseases. They also found high rates (97% positive) of PCR-positive MOMP gene in MS- patients versus 18% in other neurological diseases, and this correlated with 86% of MS patients being serology-positive patients by ELISA and Western blot analysis.52 Examination of MS patients for oligoclonal antibodies against C. pneumoniae revealed that 82% of MS patients were positive, whereas none of the control non-MS neurological patients had antibodies that were absorbed by C. pneumoniae elemental body antigens.53 Similarly, Contini et al.54 found that the DNA and RNA transcript levels in mononuclear cells and cerebrospinal fluid of 64.2% of MS patients but in only 3 controls.
Using immunohistochemistry Sriram et al.55 later examined formalin-fixed brain tissue from MS and non-MS neurological disease controls and found that in a subset of MS patients (35%) chlamydial antigens were localized to ependymal surfaces and periventricular regions. Staining was not found in brain tissue samples from other neurological diseases. Frozen tissues were available in some of these MS cases, and PCR amplification of C. pneumoniae genes was accomplished in 63% of brain tissue samples from MS patients but none in frozen brain tissues from other neurological diseases. In addition, using immuno-gold-labeled staining and electron microscopy they examined cerebrospinal fluid sediment for chlamydial antigens and found that the electron dense bodies resembling bacterial structures correlated with PCR-positive results in 91% of MS cases.55 They also used different nested PCR methods to examine additional C. pneumoniae gene sequences in the cerebrospinal fluid of 72 MS patients and linked these results to MS-associated lesions seen by MRI.56
MRI was used by Grimaldi et al.57 to link the presence of C. pneumoniae infection with abnormal MRI results and found linkage in 21% of MS patients. These turned out to be MS patients with more progressive disease.58 In addition, higher rates of C. pneumoniae transcription were found by Dong-Si et al.58 in the cerebrospinal fluid of 84 MS patients. The data above and other studies strongly support the presence of C. pneumoniae in the brains of MS patients,59-61 at least in the more progressed subset of MS patients.
Other research groups have also found evidence for C. pneumoniae in MS patients but at lower incidence. Fainardi et al.62 used ELISA techniques and found that high-affinity antibodies against C. pneumoniae were present in the cerebrospinal fluid of 17% of MS cases compared to 2% of patients with non-inflammatory neurological disorders. They found that the majority of the progressive forms of MS were positive compared to patients with remitting-relapsing MS. The presence of C. pneumoniae antibodies was also found in other inflammatory neurological disorders; thus it was not found to be specific for MS.62
In contrast to the studies above, other researchers have not found the presence of C. pneumoniaeor other bacteriain the brains of MS patients.63-65 For example, Hammerschlag et al.66 used nested PCR and culture to examine frozen brain samples from MS patients but could not find any evidence for C. pneumoniae. However, in one study C. pneumoniae was found at similar incidence in MS and other neurological diseases, but only MS patients had C. pneumoniae in their cerebrospinal fluid.64 Swanborg et al.67 reviewed the evidence linking C. pneumoniae infection with MS and concluded that it is equivocal, and they also speculated that specific genetic changes may be necessary to fulfill the role of such infections in the aetiology of MS.
Another possible reason for the equivocal evidence linking MS with infections, such as C. pneumoniae, is that multiple co-infections could be involved rather than one specific infection. In addition to C. pneumoniae found in most studies, MS patients could also have Mycoplasma species, B. burgdorferi and other bacterial infections as well as viral infections.68 When multiple infections are considered, it is likely that >90% of MS patients have obligate intracellular bacterial infections caused by Chlamydia (Chlamydophila), Mycoplasma, Borrelia or other intracellular bacterial infections. These infections were found only singly and at very low incidence in age-matched subjects.68 In spite of these findings, others did not find evidence of Mycoplasma species in MS brain tissue, cerebrospinal fluid or peripheral blood.69
Viruses have also been found in MS. For example, HHV-6 has been found at higher frequencies in MS patients, but this virus has also been found at lower incidence in control samples.70 Using PCR Sanders et al.70 examined postmortem brain tissue and controls for the presence of various neurotrophic viruses. They found that 57% of MS cases and 43% of non-MS neurological disease controls were positive for HHV-6, whereas 37% and 28%, respectively, were positive for herpes simplex virus (HSV-1 and -2) and 43% and 32%, respectively, were positive for varicella zoster virus. However, these differences did not achieve statistical significance, and the authors concluded “an etiologic association to the MS disease process [is] uncertain.” They also found that 32% of the MS active plaques and 17% of the inactive plaque areas were positive for HHV-6.70 Using sequence difference analysis and PCR Challoner et al.71 searched for pathogens in MS brain specimens. They found that >70% of the MS specimens were positive for infection-associated sequences. They also used immunocytochemistry and found staining around MS plaques more frequently than around white matter. Nuclear staining of oligodendrocytes was also seen in MS samples but not in controls.71 Using immunofluorescent and PCR methods HHV-6 DNA has also been found in peripheral leukocytes in the systemic circulation of MS patients.72, 73 However, using PCR methods, others did not found herpes viruses in the peripheral blood or CSF of MS patients.74, 75 Evidence that prior infection with EBV could be related to the development of MS was proposed; however, EBV infects more than 90% of humans without evidence of health problems and 99% of MS patients.76 The difference in MS patients could be the presence of multiple infections, including EBV. Recently Willis et al.77 used multiple molecular techniques to examine MS tissue but failed to find EBV in any MS tissues but could find EBV in CNS lymphomas.
Current reviews and the information above points to an infectious process in MS.47, 48, 75, 76, 78-80 Although a few studies did not come to this conclusion,74, 75 most studies have found infections in MS patients. It is interesting that it is the progressive rather than relapsing-remitting forms of MS which have been associated with chronic infections; therefore, infections might be more important in MS progression than in its inception. Various infections may also nonspecifically stimulate the immune system.47, 48 Infections may also invade immune cells and alter immune cell function in a way that promotes inflammation and autoimmune activity.78 If infections like C. pneumoniae and Mycoplasma species are important in MS, then antibiotics effective against these infections should improve clinical status. Although preliminary, that is in fact what has been seen, but not in all patients.81 As in other neurodegenerative diseases, multiple factors appear to be involved in the pathogenesis of MS.
Alzheimer’s disease
Alzheimer’s Disease (AD) is a family of brain disorders usually found in elderly patients and is the most common cause of dementia. AD is characterized by slow, progressive loss of brain function, notable lapses in memory, disorientation, confusion, mood swings, changes in personality, language problems, such as difficulty in finding the right words for everyday objects, loss of behavioral inhibitions and motivation and paranoia. The course of AD varies widely, and the duration of illness can range from a few years to over 20 years. During this period the parts of the brain that control memory and thinking are among the first affected, followed by other brain changes that ultimately result in brain cell death.82
AD is characterized by distinct neuropathological changes in brain tissues and cells. Among the most notable are the appearance of plaques and tangles of neurofibrils within brain nerve cells that affect synapses and nerve-nerve cell communication. These structural alterations involve the deposition of altered amyloid proteins.83, 84 Although the cause of AD is not known, the formation of the amyloid plaques and neurofibrillary tangles may be due to genetic defects and resulting changes in the structure of beta amyloid proteins. This in turn may be caused by chemicals or other toxic events, inflammatory responses, excess oxidative stress and increases in reactive oxygen species, loss of nerve trophic factors and reductions in nerve cell transmission.83-87
Recently AD brain infections have become important.88-90 For example, one pathogen that has attracted considerable attention is C. pneumoniae.91, 92 As mentioned above, this intracellular bacterium has a tropism for neural tissue, and it has been found at high incidence in the brains of AD patients by PCR and immunohistochemistry.92 C. pneumoniae has also been found in nerve cells in close proximity to neurofibrillary tangles.92, 93 Similarly to Mycoplasma species, C. pneumoniae can invade endothelial cells and promote the transmigration of monocytes through human brain endothelial cells into the brain parenchyma.94 C. pneumoniae has been found in the brains of most AD patients,91 and it has been cultured from AD brain tissue.95 Injection of C. pneumoniae into mice stimulates beta amyloid plaque formation.96 Although the data are compelling, some investigators have not found C. pneumoniae infections in AD.97, 98
AD patients also have other bacterial infections, such as B. burgdorferi.99 Using serology, culture, Western blot and immunofluorenscence methods this Lyme Disease infection has been examined in AD.100, 101 Not all researchers, however, have found evidence of B. burgdorferi in AD patients.102, 103 The presence of intracellular infections like B. burgdorferi in AD patients has been proposed to be a primary event in the formation of AD beta amyloid plaques. This is thought to occur by the formation of “congophilic cores” that attract beta amyloid materials.104 Multiple reports indicate that AD nerve cells are often positive for B. burgdorferi, indicating that this intracellular bacteria could be important in the pathogenesis of AD.99, 100, 104, 105
The hypothesis in AD that intracellular microorganisms could provide “cores” for the attraction of beta amyloid materials is appealing, but other factors, including the induction of reactive oxygen species, lipid peroxidation and the breakdown of the lysosomal membranes releasing lysosomal hydrolases, are also thought to be important in beta amyloid deposition.105 That infections may be important in AD pathogenesis is attractive; however, some negative reports have not confirmed the presence of infections like B. burgdorferi in AD patients.99-101 This suggests that the infection theory, although compelling, remains controversial.102, 105
Herpes virus infections have also been found in AD,especially HSV-1.106, 107 Previously it was determined that HSV-1 but not a related neurotrophic virus (varicella zoster virus) is present more often in AD brains, and this could be linked to AD patients who have the risk factor ApoE e4 allele.108, 109 HSV-1 is thought to be involved in the abnormal aggregation of beta amyloid fragments within the AD brain by reducing the amount of full-length beta amyloid precursor protein and increasing the amounts of their fragments.110 HSV-1 infection of glial and neuronal cells results in a dramatic increase in the intracellular levels of beta amyloid forms, whereas the levels of native beta amyloid precursor protein are decreased.111 This is similar to what has been found in mice infected with HSV-1, indicating that HSV-1 is probably involved directly in the development of senile-associated plaques. Another herpes virus, HHV-6, has also been found in AD patients, but it is thought that this virus is not directly involved in AD pathogenesis. HHV-6 may exacerbate the effects of HSV-1 in AD ApoE e4 carriers.112
Other infections have been found in AD patients, for example, C. pneumoniae, Helicobacter pylori amongst others.113 It has been proposed that such infections may act as a trigger or co-factor in AD.114 Although experimental evidence that pathogens can elicit the neuropathological changes and cognitive deficits that characterize AD is lacking, this approach may yield interesting and important results. These authors also stressed that systemic infections must be considered as potential contributors to the pathogenesis of AD.114
Parkinson’s disease
Parkinson’s disease (PD) is characterized by akinesia, muscular rigidity and resting tremor.103 In addition, autonomic dysfunction, olfactory disturbances, depression, sensory and sleep disturbances and frequently dementia characterize this disease.115 The pathology of PD indicates a progressive loss of the dopamine neurons of the substantia nigra together with the presence of Lewy bodies and alpha-synuclein. More extensive brain degeneration also occurs, from the medulla oblongata to the cerebral cortex.116, 117
Age-related inclusion bodies and protein aggregations or defects in their degradation characteristically occur in PD, but their role in PD pathogenesis remains unclear.117, 118 Some evidence suggests a relationship between PD and specific genetic changes, such as changes in the genes affecting mitochondria, protein degradation, organelle trafficking and vesicular fusion, and in proteins involved in oxidative stress or antioxidant function.102 Inflammation has also been associated with PD pathology.119
The pathogenesis of PD has been proposed to be due to multiple genetic and neurotoxic events that produce oxidative damage and cell death. In the case of PD the relevant targets of toxic events are neuromelanin-containing dopaminergic neurons of the substantia nigra.118, 120 A case-control study indicated that multiple environmental factors and genetic background were statistically related risk factors for PD.121 Prominent among these were long-term toxic exposures and trauma early in life.122 For example,early life exposure to brain injury, chemicals and/or infections may initiate a cyclic inflammatory process involving oxidative damage, excitotoxicity, mitochondrial dysfunction and altered proteolysis that later in life results in substantia nigra neuron death.123, 124
A role for chronic infections in PD pathogenesis has been proposed.123, 124 One infection found in PD that has aroused considerable interest is the presence of chronic gastrointestinal Helicobacter pylori.125 Indeed, treatment of this infection offers relief to late stage cachexia in PD patients receiving L-dopa.126 Helicobacter pylori-infected PD patients showed reduced L-dopa absorption and increased clinical disability,127 whereas treatment of this infection increased L-dopa absorption and decreased clinical disability.128 H. pylori may not be directly involved in the pathogenesis of PD, but its systemic presence could affect the progression and treatment of PD, probably by stimulating inflammation and autoimmunity.128
Chronic infections in PD have been linked to inflammation and autoimmune responses.129-131 Experimental models of PD have been developed using neurological viral or bacterial infections to initiate the pathogenic process.132, 133 Spirochetes have also been found in Lewy bodies of PD patients.30 Other infections, such as viral encephalitis,134 AIDS-associated opportunistic infections of the basal ganglia,135 coronavirus,136 among other infections,68, 137, 138 have been found in PD and could be important in stimulating inflammation and autoimmune responses. It has been stressed that additional research will be necessary to establish whether a causal link exists between PD and chronic infections.139
Neurobehavioral diseases
Autism spectrum disorders
ASD, such as autism, Asperger’s syndrome, etc., are neurobehavioral diseases of primarily the young where patients generally suffer from an inability to communicate properly, form relationships with others and respond appropriately to their environment. Such patients do not all share the same signs and symptoms but tend to share certain social, communication, motor and sensory problems that affect their behavior in predictable ways. These patients often display repetitive actions and develop troublesome fixations with specific objects, and they are often painfully sensitive to certain sounds, tastes and smells.140, 141
ASD cases are likely to be caused by multiple factors, including genetic defects, heavy metal, chemical and biological exposures, among other important events, which are probably different in each patient. ASD patients appear to have similarities in genetic defects and environmental exposures that are important in patient morbidity or in illness progression.5-8, 140-142
Chronic infections appear to be an important element in the development of ASD.6, 16, 143, 144 In ASD patients more than 50 different bacterial, viral and fungal infections have been found,6 some apparently more important than others in causing symptoms. It has been known for some time that ASD patients have a number of nonspecific chronic signs and symptoms, such as fatigue, headaches, gastrointestinal, vision problems, occasional intermittent low-grade fevers and other signs and symptoms that are generally excluded in the diagnosis of ASD but are consistent with the presence of infections.143 Indeed, increased titres to various viruses as well as bacterial and fungal infections have been commonly seen in ASD patients.6, 16, 19, 143-145 Not withstanding these reports, epidemiological evidence for an association of childhood infections in the first two years of life and ASD has been mixed.146
Environmental exposures to chemicals and heavy metals also appear to be important in the development of ASD.140, 141, 147, 148 The relationship between ASD and heavy metals may involve the role of multiple vaccines in ASD pathogenesis.130, 141 ASD patients often show their first signs and symptoms after multiple childhood immunizations, and the sharp increase in Autism rates occurred only after the multiple MMR vaccine came into widespread use.141 In some states in the U.S. children receive as many as 33 vaccines before they can enroll in school.140 Such vaccines can contain mercury and other toxic preservatives, and some may also contain contaminating bacteria, as found in veterinary vaccines.149
There are very few studies that have followed the transmission of infections and subsequent autism. Previously we found that veterans of the Gulf War with chronic fatiguing illnesses (Gulf War illnesses, GWI) exhibited multiple nonspecific signs and symptoms similar to chronic fatigue syndrome/myalgic encephalomyopathy (CFS/ME).150, 151 After returning to the home with GWI, their children subsequently became symptomatic, and these children were often diagnosed with ASD.152, 153 Symptomatic children (mostly diagnosed with ASD) were infected with the same Mycoplasma species, M. fermentans, that was found in the veterans and their symptomatic family members, and this was not seen in aged-matched control subjects or in military families without GWI. In the GWI families some non-symptomatic family members did have mycoplasmal infections (~10%), but this was not significantly different from the incidence of mycoplasmal infections in healthy control subjects.152, 153
Subsequently ASD patients who were not in military families were examined for systemic mycoplasmal infections.153 The majority (~54%) were positive for mycoplasmal infections. However, in contrast to the children of GWI patients who for the most part had only M. fermentans, the civilian children tested positive for a variety of Mycoplasma species. We also tested a few siblings without apparent signs and symptoms, and for the most part few had these infections.153 In another study we examined the blood of ASD patients from Central and Southern California and found that a large subset (>58%) of patients showed evidence of Mycoplasma infections compared to age-matched control subjects (Odds Ratio=13.8, p<0.001).19 ASD patients were also examined for C. pneumoniae (8.3% positive, Odds Ratio=5.6, p<0.01) and HHV-6 (29.2% positive, Odds Ratio=4.5, p<0.01). The results indicated that a large subset of ASD patients display evidence of bacterial and/or viral infections (Odds Ratio=16.5, p<0.001).19
ASD patients have been examined for B. burgdorferi infections.154 Various studies revealed that 22-30% of ASD patients (N=76) have Borrelia infections.6, 154 The incidence of Borrelia infections in ASD patients may be related to Lyme disease distribution, with some Lyme-intense areas having high prevalence, and other areas having a low prevalence. Other infections, such as Lyme-associated Bartonella, Babesia, Ehrlichia and non-Lyme-associated CMV, Plasmodium species, Toxoplasma species and Treponema species may also be associated with ASD.6
Final comments to part 1
When neurological symptoms are present, infections of the CNS must be considered. Brain infections can stimulate glial responses, and the presence of viral and bacterial infections in nerve cells, can stimulate autoimmune responses against nerve cell antigens as well as the infections within them.155 For example, in MS some 20 different bacterial and viral infections have been found, but the link between these infections and the pathogenesis of MS is still being debated.16, 47, 75 One or even a few types of infections cannot be causally linked to MS, and the reason for this is that there may be too many possibilities. No one infection or a group of infections needs to be the trigger in MS to be important in the pathogenesis of MS. In time combinations of certain infections may eventually be identified at least in a subset of MS patients, and this will allow the development of new therapeutic approaches for many MS patients that are not recognized today.
One problem that is rarely discussed is the apparent disparity between the laboratory results from different laboratories. Often different laboratories cannot agree on types of infections found in various chronic diseases.47 There are a number of reasons for this, including differences in the source of materials, qualities of reagents and techniques used.16 Some procedures, such as PCR, have specific challenges that must be overcome in the handling of specimens, their stability, presence of interfering substances, contamination, sensitivity and specificity of the tests and interpretation of the results. Variability in results from different laboratories will remain a problem unless research groups work closely together to solve these problems. One example of how this has been overcome is a multi-centre research study on the presence of C. pneumoniae in the cerebrospinal fluid of clinically defined, mono-symptomatic MS patients.156 Sriram et al.156 conducted this diagnostic trial with good concordance of results between different laboratories. Cooperative studies such as this should eventually alleviate discrepancies in the types of infections found by different research groups.
This review continues in Part 2 with psychiatric diseases, autoimmune diseases, fatiguing illnesses, and other infectious diseases with neurological aspects and an overall discussion of the topic. 157
Competing Interests
None Declared
Author Details
GARTH L. NICOLSON, Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA JORG HAIER, Department of General and Visceral Surgery, University Hospital, Münster 48149, Germany
CORRESSPONDENCE: Prof. Garth L. Nicolson, Office of the President, The Institute for Molecular Medicine, P.O. Box 9355, S. Laguna Beach, California, 92652 USA
Email: gnicolson@immed.org
References
1.Nicolson GL, Nasralla M, Haier J, et al. Mycoplasmal infections in chronic illnesses: Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis. Med Sentinel1999; 4: 172-176.
jne
Re: BORRELIOOSI/MS-TAUTI
http://yle.fi/uutiset/ranskalaisyhtio_i ... sa/7954085
Tiede 25.4.2015 klo 1:35 | päivitetty 25.4.2015 klo 1:38
Ranskalaisyhtiö ilmoitti läpimurrosta ms-taudin lääketesteissä
Yhtiön mukaan testattu lääke vähensi taudin etenemistä ja johti joissakin tapauksissa "merkittävään kohentumiseen" taudista kärsiville.
Ranskalainen bioteknologian yhtiö MedDay kertoi perjantaina rohkaisevista tuloksista kokeissa, joissa kehitetään uutta lääkettä keskushermostoon vaikuttavaan ms-tautiin.
– Tämä on ensimmäinen kerta, kun lääke on kyennyt vähentämään taudin etenemisen astetta sekä kohentamaan merkittävää osaa potilaista, joilla on jatkuvasti etenevä ms-tauti, MedDayn toimitusjohtaja Frederic Sedel sanoo tiedotteessa.
Myös tutkimuksen päätarkastaja, professori Ayman Tourbah, piti testien tuloksia rohkaisevina. Hänen mukaansa uudesta lääkkeestä voi tulla merkittävä hoitomuoto ms-taudista kärsiville potilaille.
Uuden lääkkeen lupaprosessin odotetaan alkavan vuoden lopulla, kun kaikki koetulokset ovat valmistuneet.
Lähteet: Yle Uutiset, AFP
Iiro-Matti Nieminen
Yle Uutiset
Tiede 25.4.2015 klo 1:35 | päivitetty 25.4.2015 klo 1:38
Ranskalaisyhtiö ilmoitti läpimurrosta ms-taudin lääketesteissä
Yhtiön mukaan testattu lääke vähensi taudin etenemistä ja johti joissakin tapauksissa "merkittävään kohentumiseen" taudista kärsiville.
Ranskalainen bioteknologian yhtiö MedDay kertoi perjantaina rohkaisevista tuloksista kokeissa, joissa kehitetään uutta lääkettä keskushermostoon vaikuttavaan ms-tautiin.
– Tämä on ensimmäinen kerta, kun lääke on kyennyt vähentämään taudin etenemisen astetta sekä kohentamaan merkittävää osaa potilaista, joilla on jatkuvasti etenevä ms-tauti, MedDayn toimitusjohtaja Frederic Sedel sanoo tiedotteessa.
Myös tutkimuksen päätarkastaja, professori Ayman Tourbah, piti testien tuloksia rohkaisevina. Hänen mukaansa uudesta lääkkeestä voi tulla merkittävä hoitomuoto ms-taudista kärsiville potilaille.
Uuden lääkkeen lupaprosessin odotetaan alkavan vuoden lopulla, kun kaikki koetulokset ovat valmistuneet.
Lähteet: Yle Uutiset, AFP
Iiro-Matti Nieminen
Yle Uutiset
BORRELIOOSI/MS-TAUTI
MULTIPPELISKLEROOSIN HISTORIAA JA SEN LINKIT BORRELIA INFEKTIOIHIN
Joanne Drayson • ProHealth.com • 14. joulukuuta 2018
Painettu LookingAtLyme.blogspot.comista Joanne Draysonin luvan perusteella. Voit lukea alkuperäisen artikkelin napsauttamalla tätä
Toimittajan huomautus: Tässä artikkelissa tarkastellaan multippeliskleroosin varhaisia tutkimuksia ja sen myöhempiä linkkejä Lymen tautiin.
"DR. Gabriel Steiner oli selvästi osoittanut, että noin yhdellä kymmenestä aivojen autopsiosta hän löysi spirokeet käyttämällä omaa hopeanvärjäystä. Käytämme edelleen Steinerin tahraa tänään havaitsemaan spirokeetit, mutta jostain syystä emme tunnusta hänen löytöjään spirokeetoista, jotka ovat yhteydessä multippeliskleroosiin. "
https://durayresearch.wordpress.com/…/s ... ocative-fi…/
Joanne Drayson • ProHealth.com • 14. joulukuuta 2018
Painettu LookingAtLyme.blogspot.comista Joanne Draysonin luvan perusteella. Voit lukea alkuperäisen artikkelin napsauttamalla tätä
Toimittajan huomautus: Tässä artikkelissa tarkastellaan multippeliskleroosin varhaisia tutkimuksia ja sen myöhempiä linkkejä Lymen tautiin.
"DR. Gabriel Steiner oli selvästi osoittanut, että noin yhdellä kymmenestä aivojen autopsiosta hän löysi spirokeet käyttämällä omaa hopeanvärjäystä. Käytämme edelleen Steinerin tahraa tänään havaitsemaan spirokeetit, mutta jostain syystä emme tunnusta hänen löytöjään spirokeetoista, jotka ovat yhteydessä multippeliskleroosiin. "
https://durayresearch.wordpress.com/…/s ... ocative-fi…/