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Lyme Disease Induced Neurodegeneration

(ALS) Amyotrophic Lateral Sclerosis or (MND) Motor Neurone Disease
are referred to as ALS/MND.

PALS is short for People (or a person) with ALS.

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Cowden Support Program W Lee Cowden, MD-MD(H)
Dr. Cowden can be emailed at , as Chairman of the Scientific Advisory Board of the Academy of Comprehensive Integrative Medicine (ACIM)
General Lyme Information
ALS and Borreliosis Information 

Igenex in California can test for Lyme, Babisiosis and Erlichiosis

Bowen Research and Training Institute FL, closed 22 Dec 2006. The Q-RIBb direct detection test is therefore no longer available.

The Central Florida Research Lab, a new laboratory at 245 N. Seminole Ave., Lake Alfred, FL  33850, phone 863-956-3538 is working on a new Lyme disease test. 

Basic Lyme Information

  1. Lyme disease is prevalent across the United States but one’s country of residence does not reflect one's Lyme disease risk, since people, pets and ticks travel. Also it has been shown that mosquito bites and human to human transmission of Lyme is possible.This dynamic situation provides many opportunities for exposure to the illness.

  2. Lyme disease is a spirochetal infection of multiple organ systems and causes a wide range of symptoms. Familiarity with its varied presentations is key to recognizing its protean manifestations.

  3. As few as 15% of patients with Lyme disease recall a tick bite.

  4. Fewer than 50% of patients with Lyme disease recall any rash.

  5. A bull's eye skin rash is considered classic but is not the most common manifestation of early-localized Lyme infection. Atypical forms of this rash are more common. The Erythema Migrans rash is sufficient proof of Lyme disease and the need to start 6 weeks of antibiotic therapy. Shorter treatment courses result in a relapse rate of over 40%.

  6. Most research indicates that active ongoing spirochetal infection is the cause of the persistent symptoms in chronic Lyme disease.

  7. No study has ever shown that 30 days of antibiotic treatment cures Lyme disease. Both US and European medical literature reports that, histologically and in culture, short courses of antibiotic treatment fail to eradicate the Lyme spirochete.

  8. Chronic Lyme disease requires an average of 6-12 months of high dose antibiotic therapy. Recurrent symptoms and the continued presence of Borrelia burgdorferi indicate the need for further treatment. Consequences of untreated chronic Lyme infection outweigh the potential consequences of long term antibiotic therapy.

  9. Many Lyme patients require treatment for 1- 4 years. Relapses occur and maintenance antibiotics may be required. There are few generally available tests to ensure the organism is eradicated or the patient cured.

  10. There are 5 subspecies of Borrelia burgdorferi, over 100 strains in the US, and 300 strains worldwide. This diversity is thought to contribute to Borrelia burgdorferi's antigenic variability and its various antibiotic resistances.

  11. Antibody titers for Babesia microti, HGE, HME and other tick transmitted diseases should be performed. The presence of co-infection implies probable Lyme infection and when left untreated increases morbidity and complicates successful treatment.

  12. Lyme disease is the latest “great imitator” and should be considered in the differential diagnosis of MS, ALS, seizure and other neurologic conditions, arthritis, CFS, Gulf war syndrome, ADHD, hypochondriasis, fibromyalgia, somatization disorder and patients with various difficult-to-diagnose multi-system syndromes.

  13. The ELISA test is unreliable and misses 35% of culture proven Lyme. A screening test should have 95% sensitivity.

  14. 20-30% of patients with acute culture proven Lyme disease remain seronegative on serial Western Blot sampling.

  15. Antibody titers decline over time so the IgG Western Blot is even less sensitive in detecting chronic Lyme infection, yet the IgM Western Blot may work. For epidemiological purposes the CDC eliminated from the Western Blot analysis the reading of bands 31 and 34. These bands are so specific to Borrelia burgdorferi that they have been chosen for vaccine development. For patients not vaccinated for Lyme, a positive 31 or 34 band is highly indicative of Borrelia burgdorferi exposure.

  16. Western Blot, if used at all, should be performed by a laboratory that reads and reports on all 16 bands as part of their routine comprehensive analysis. Laboratories that use FDA approved kits (for instance, Mardex's Marblot) must abide by the rules of the manufacturer and are restricted from reporting all of the bands. These rules are in accordance with the CDC’s surveillance criteria but increase the risk of false negative results. Such kits may be OK for surveillance purposes but are too inaccurate for adequate patient management.

This information was taken from the International Lyme and Associated Diseases Society (ILADS). Most Lyme Literate MDs belong to this organization.


The official position is that Lyme Disease/Borreliosis is not present in Australia but there is evidence to refute this. Lyme/Borreliosis was first noted in the Hunter Valley, at Branxton, between Singleton and Maitland, NSW in 1980 and 4 other continents.

Even if the disease were not normally found in Australia there are numerous people flying into the country every day who may have been exposed to the deer ticks that commonly carry the disease in the USA and Europe. It is possible that ticks found on Australian native animals may also carry and transmit borrelia spirochetes introduced in this way.

Lyme is a great imitator and can be incredibly deceptive. Symptoms for Lyme/Borreliosis can be similar to ALS/MND. Seek a Doctor experienced in the treatment of Lyme/Borreliosis as it should be considered in differential diagnosis for anyone who is suspected of having ALS/MND. Get tested before neurological symptoms become too severe. Educate yourself and arrange for accurate and appropriate testing for Borreliosis, even if you have to demand it.

There is a lot of information on the internet about International Tick Born Diseases.

Many people have tested positive for Lyme after being examined by several Doctors and Neurologists, none of whom suspected or tested for Lyme. Even if you test seronegative for Lyme, send blood samples to a Lab specializing in Tick Borne Diseases for a complete panel, as they may actually detect the infection where others have failed.

I was diagnosed with Borrelia and babesia infections in 2002 from blood samples sent the Bowen Laboratories in Florida, USA (which closed Dec 2006). My only typical Lyme symptom was initially the Erythema Migrans rash that is often considered sufficient proof of Lyme disease. I took doxycycline for months but other than that have not been able to receive treatment for Borrelia or Babesia under Australia's current health system because Lyme Disease is still inexplicably considered an "exotic illness" in Australia.SS


(Lyme Neurologic Infection)

as a Possible Cause of ALS

edited from an article contributed by Kathy Cavert

... I've been watching ALS research for over 10 years and the following is the best explanation I've seen that offers a cure in the short term, like now. The theory seems sound and those using anti-mycoplasmal meds are seeing positive results. This theory doesn't eliminate other causes/theories such as malformed EAAT2, glutamate excitotoxicity, or mitochondrial DNA mutation. Mycoplasmal infection may work together with other pieces of the ALS puzzle.


Some people think that ALS is just a variant of Lyme and that they are treating the Lyme spirochete. They are using doxycycline and doxycycline is one of the meds that Prof. Garth Nicolson has been using to successfully treat mycoplasma infections. I think that they are actually treating mycoplasmas. In an initial screening Prof. Nicolson found mycoplasmas in about 80% of ALS patients, so this only applies to a subgroup of ALS. Prof. Nicolson is now doing a formal study with ALS patients using doxycycline. He said that the preliminary results were positive and that fewer patients have died than would be expected in the normal course of ALS.

When mycoplasmas are in the blood they live in and on leukocytes, according to Prof. Nicolson. Mycoplasmas cannot cross the blood/brain barrier on their own, but can be carried across and deposited in the CNS when leukocytes respond to some CNS infection. This explains the coincidence of ALS with CNS infections such as Lyme disease. But many PALS don't test positive for Lyme. The CNS infection may be some other infection. Also, some PALS test positive for enterovirus but many don't. For more info on mycoplasmas

Tinidazole is an anti-parasitic, and mycoplasmas are parasites, so its use makes sense. Tinidazole has not been approved by the FDA because Pfizer has not tried for approval. Pfizer thinks that there would not be enough of a US market to justify the cost. A source for tinidazole is listed below.

Prof. Nicolson developed a new mycoplasma test that can be done by his lab, but it takes 10 to 15 working days to get results, if you care to wait. You can get info on their ALS test panel and the order form from the lab at 714-799-7177, ext. 202 (Client Services) or ext. 204 (Brant Blasingame, Lab Director). The protocol below is not Prof. Nicolson's, but it is possible that not enough research has been done to identify an optimal protocol.

"On the basis of long-term follow up (from 2 to 22 years) of 175 patients with various syndromes of progressive forms of tick-borne encephalitis (TBE), evaluation criteria of TBE progression are systematized. Two basic forms of disease progression are identified: amyotrophic and hyperkinetic, each of them breaking down into a series of leading syndromes.

Important for characterizing progressive forms of tick-borne encephalitis (PFTBE) are the time when the disease began to progress and the pattern of progression as well as its stage and severity. PFTBE are correlated with the acute period syndromes.

In long-term follow-up, 68% of patients with PFTBE display transformation of clinical forms of the disease, with the formation of the lateral amyotrophic sclerosis syndrome in the overwhelming majority of these patients".

1: Zh Nevropatol Psikhiatr Im SS Korsakova 1983;83(8):1173-9 Related Articles, Books [Structure of progressiveforms of tick-borne encephalitis]. [Article in Russian] Umanekii KG, DekonenkoEP.PMID: 6414202   [Pub MEd - indexed for MEDLINE]


"This discussion of neuroborreliosis (Lyme neurologic infection) includes a list of medical journal articles possibly indicating the Lyme spirochete is a cause of the neurologic syndrome of ALS.

  These studies reveal that parallels exists between the two diseases, one with and one without a known cause.  Both may be the same illness and ALS is an immune-mediated disease with an infectious underpinning. This information was gleaned from over 10 years of running a Lyme hotline and talking with thousands of patients, from researching medical journals re: ALS and Lyme and based on (more than) 14 years of personal experience with Lyme.

I was too weak to get up off the floor, had nocturnal dyspnea, fasciculations, profound fatigue and polio-like weakness, inability to pull a blanket over my body, inability to climb stairs, dysarthria during periods of extreme sleepiness and weakness, dysphagia, severe motor impairment of the right hand and moderate of the left, hospitalization with ataxia, foot dragging and using a walker. After antibiotic therapy, I experienced a complete turnaround.

At least 13 medical journal listings suggest ALS patients could have an infection with denervation caused by an infection vs. "auto-immune disease" out of "nowhere". Lyme is a bacterial infection and thus the neurologic bulbar and neuro weakness and atrophy should be treatable with antibiotic therapy. Below is an explanation of Lyme, the way it is treated and the reason for this article.

Lyme disease (Borrelia burgdorferi) and its cousin, syphilis, is known as "The Great Medical Imitator".  Both illnesses are multisystemic infections caused by chameleon-like, intracellular pathogens called spirochetes.  Syphilis was able to destroy the nervous system and other organs.  Lyme can do the same but the diagnosis of Lyme is often missed. 

Most physicians are either not familiar with the symptoms or the way Lyme can mimic other autoimmune diseases like MS (including demyelination, and exact parallel spinal fluid findings, etc.). 

Most physicians remain ill-informed and antibiotic therapy often required intravenously to get past the blood brain barrier is expensive. Lyme is primarily "neurotrophic" as it moves toward and attacks the nerves, both peripheral and central (spinal cord, etc.) 

Lyme can have an arthritic component perhaps depending on the individual's immune system or perhaps due to the strain variant. Lyme is a worldwide epidemic, found on all continents except Antarctica.

Few doctors understand how aggressive they must be with antibiotic therapy to successfully treat Lyme.  Borrelia is intracellular, like tuberculosis.  TB requires almost a year of antibiotics with a cocktail of 4 used concomitantly. Lyme physicians may also use combination therapy.

My disease was mixed before diagnosis. I had ALS symptoms, arthritic symptoms, fibromyalgia symptoms and eventually short term memory loss and occasional confused states. 

Common symptoms of Lyme are headache, stiff neck, backache, weakness, fasciculations, profound fatigue, migratory symptoms like diarrheoa, chest pain, shortness of breath, myalgias, hand or foot pain, stiffness in the morning or if sitting too long, connective tissue weakness, anxiety disorder, mood disorders, sleep disorders and more.

Unlike most other diseases this one is identifiable by clinical response to antibiotics.  The testing for Lyme is very unreliable.  One can get the Elisa and Western Blot done simultaneously and perhaps the Lyme urine antigen test done after taking antibiotics (looking for the dead protein from the bacteria in the first morning urine. Call 1-800-832-3200-IgeneX Lab, Palo Alto, CA, USA, run by Dr. Nick Harris).  In spite of DNA testing, there remains room for error. 

Some physicians talk of false positives but most do not buy this.  How can one have antibodies to an infection to which one has not been exposed?  It makes no sense but false negatives fill medical literature. 

The pathogen is able to hook up with antibodies that are supposed to be defending against it. It is then able to hide in spinal fluid and do its nasty work. Sometimes Lyme presents atypically as ALS, MS, polymyalgia rheumatica, Guillain Barre, transverse myelitis, polyneuropathies of unknown aetiology, brain swelling and or tumor, severe eye disease, cardiomyopathy, hepatitis and so on.

Sometimes it mimics lupus and its blood tests.  Entire families may have been infected but will each manifest the illness in different ways. Some will show CIFIDS, MS, fibromyalgia, ALS, etc. 

Lyme has been documented since the 1800s.  When you look back at your own illness, think f time when you first noticed signs of illness... perhaps a temperature, a headache or time of fatigue and weakness followed by feeling OK.

Perhaps you began with stumbling and typical ALS weakness and fasciculations.  It all varies person by person. People with Lyme may never show the same set of symptoms but there are always common threads unless one has classic ALS.

A study performed by President Bush Snr's neurologist, John J. Halperin, MD and others to following and preceding it, implicated classic ALS patients as having an infection triggering neurologic damage to the brainstem and nervous system in a gradual, predictable, degenerative way. 

The study showed that a statistically significant number of classic ALS patients had reversal of neurologic function after administration of intravenous Rocephin, an antibiotic used to treat Lyme. Most people with severe neurologic Lyme disease are first given intravenous rocephin because it has the ability to cross the blood brain barrier. It also has good tissue penetration and the ability to kill this particular bacteria.

The beauty of Lyme vs. ALS is that Lyme has a known cause.  ALS is just a description of a syndrome whereby the body becomes denervated and muscles atrophy.  Lyme can denervate, cause demyelination of the brainstem, cause respiratory distress syndrome, partial and total paralysis, seizures, weakness, fasciculations and more.

I was frequently misdiagnosed.  Many of my diagnoses were autoimmune, saying my body was turning on itself. I could not see my body turning on itself without something triggering it.  I felt that something was "causing" my body to go downhill. 

It took 27 specialists before I was diagnosed with this infection, not by tests (although some of them were positive at times and some negative) but by "clinical diagnosis".  Little is done to improve awareness of this disease but it has been stated in no uncertain terms that this is a "clinical diagnosis".

Surveillance for CDC epidemiological purposes requires a specific blood finding on Western Blot or other such test and to get a positive on the Western Blot takes an act of congress.  If you have had a lesion like a bull's eye or even another odd-looking rash that did not go away right away, (even one where the tissue fell off in the middle and it was not a recluse bite) or one which was irregularly shaped and red or purple or had bumps like chigger bites or looked like herpes, if a doctor saw your rash and documented it, you may have a case of Lyme with no tests needed. 

Having the erythema migrans or the rash that grows larger with time after a tick bite (whether you remember a tick bite or not), qualifies you to have Lyme and you need to be treated for Lyme with no questions asked.

Most of us do not remember a bite or rash and tick bites do not hurt. They feed and drop off.  You could have been infected years ago stayed healthy like syphilis patients and HIV patients do only to become sick after a surgical procedure or childbirth. 

Surgery and childbirth cause this infection and its cousin, syphilis, to come to the forefront.  People will have a surgery and suddenly become weak, fatigued and achy.  This is the way this infection works. 

I had carried the infection with all but a few leg pains and a few high fevers and otherwise felt great until after I had neck surgery. About 4 weeks later my entire body began to gradually break down.

For some the symptoms are migratory and come and go.  It may take years to get well.  It is considered treatable so those with ALS who take antibiotics and have this infection may get neurologic function back. They may not get it all back and they will have a chronic disease that can always go into complete remission as it finally did with me. 

After several rounds of IV antibiotic and several responses to it, feeling better, I would relapse and again have to have more antibiotics.  But this is OK.  I have never been as sick as I was initially.  I am 98% better now and have progressed from a walker and too weak to climb stairs or pull a blanket over me to playing racquetball!

The spirochete bacterias on earth are known to give off toxins when they are killed with antibiotic.  This was discovered after WWII when the men were treated with penicillin for syphilis. They had a drop in blood pressure, rapid heart rate, fever, chills, etc.Doctors in Europe called this the Jarisch-Herxheimer reaction. 

In extreme cases, this reaction can cause death and immense pain and suffering as one tries to eradicate the spirochete. The positive side is that if you feel you have allergies to antibiotics, it may be a JH reaction.  I had hives and a fat lip on iv claforan and it turned out my skin was having a herxheimer reaction.

This organism does not want to die and goes down fighting.  But we must stay strong. JH will cause exacerbation of pre-existing symptoms.  For seriously ill ALS patients this can be life threatening. 

Breathing may be compromised and heart failure due to bulbar involvement could occur. Ventilation assist may be needed, so critical care hospitalization may be necessary in some cases. 

The JH reaction usually causes periods of intense weakness. One must be fully aware of this possibility and not be afraid of it.  The weakness passes but can be very scary.  The weakness may be accompanied by new pains, aching or stabbing pains or more fasciculations.

As the treatment continues, many ALS patients begin to notice neurologic functions returning.  Fingers and arms will gain strength and move.  Toes move and internal feelings of energy and wellness begin to occur. 

It is a long and arduous process and only the most experienced Lyme doctors (or doctors willing to talk with the most experienced Lyme doctors) should take the helm. If you can find a Lyme doc in your area that is the way to go. 

Any caring doctor should give antibiotic treatment upon request from an ALS patient for possible Lyme, based on the literature included here. I say this because if it were them in your shoes and they had the information below, I would be willing to bet they would give the antibiotics a try.

I want to share all my years of research into Lyme and my own experience with it firsthand.  I have conducted formal clinical manifestations research into diseases that Lyme mimics, like ALS. I have collected powerful studies that imply ALS has an infectious underpinning.

If this is so, then anyone with ALS should be entitled to take antibiotics for a lengthy period. Lyme is slow to respond and is intracellular like tuberculosis which requires a good year of treatment. Many Lyme patients do very well on antibiotics but relapse when antibiotics are withdrawn. 

The reason for this article is simple.  Lyme borreliosis is often referred to as "neuroborreliosis" because it is mainly neurologic.  Lyme is an infection with a KNOWN cause.  Lyme is treatable with antibiotics and symptoms that are neurologic are able to be reversed in most patients with aggressive antibiotic therapy.

Find a Lyme doctor in your area.  This is run by knowledgeable Lyme persons who provide up to date medical information. On the web page "search", off to the left of the page, will lead to a medical search where you can type in a key word such as "denervation" and find research abstracts that lead directly to that topic.

When you consult the Lymenet web page look for support group listings by state and see if you can contact someone in your state listed in this grouping or if not in your state, call someone in a state close by. Begin to make appropriate calls.  If you can find a doctor who is very good with neurologic Lyme have your family doctor call that doctor and see if they would be willing to direct them in your treatment trial.

I cannot emphasize enough that with ALS all there is are yearly research solicitations for money to find a cause or cure.  There are medical pharmaceutical trials with drugs that may or may not help the illness. Nothing is really grounded in terms of offering definitive help.  Almost everyone is told that there is nothing that can be done and that they have "x" amount of time to live.

With Lyme, there are studies by extremely influential medical journals. Where studies have been done and where ALS patients have benefited dramatically from antibiotic therapy.  The bulbar group has had a more difficult time and for this reason, it is crucial that the bulbar involved group have critical care doctors who can work them through the treatment and herxheimer reaction without too much adverse reaction.

Lyme is not a "syndrome" or a "disease of unknown etiology".  Lyme disease is a cousin to syphilis and is a TREATABLE neurologic disease.

What could possibly be better than having something that is treatable?

There are a few books at Barnes and Noble or other book stores.  One is called "Coping with Lyme Disease" in which Denise Lang describes the disease and odd and varying ways in which it manifests.  Some of my research and quotes from my Lyme Aid newsletter were put in this book.  The other book is by Karen Forschner and it is called "Everything you wanted to know about Lyme disease".

This book also lists other tick-borne infections that can be in the body as well as Lyme. They are easy to read and offer a wealth of information about a disease that HAS A KNOWN CAUSE AND TREATMENT. Just think, if Lyme were caused by a virus, there would be no treatment.  It would be like HIV or herpes and nothing could be done to cure it.  But it is a bacteria; a spirochete. 

It is up to you.  It is your life and if you want to declare war on it why not?  What do you have to lose?  You will know if you were once infected with this bug because you will either remember a time in the past when you were exposed to ticks or when you first became ill and had odd symptoms and perhaps even fevers, etc. 

Or.. you will take antibiotics and eventually you will begin to notice improvement of some of your symptoms... very gradual but nonetheless improvement.

If your disease is something that came out of thin air and has no reason for being there or is caused by a virus then, after about 6 months of antibiotic or 3 months of IV, you have not seen a change in your neuro status you probably have something else.  But remember, the studies are out there to correlate the two diseases. So happy hunting and God bless you all with new hope.

For those of you who decide to take the antibiotic and "demand" it from your doctors should they become stubborn as we see so often, and you get better, be sure and keep a diary so that we can go on 20/20 and change the world of ALS someday.  Promise me that this long letter will not be in vain!"


1. "Borrelia burgdorferi antibodies and amyotrophic lateral sclerosis" The Lancet.  August 8, 1987 Russel Johnson, MD (famous Lyme researcher in the US) et al.

Case studies are discussed whereby persons who tested positive for Lyme on antibody tests showed classic ALS symptoms including denervation, atrophy, weakness, bulbar involvement, dysarthria, ataxia and so on. The end of the article states that any person with ALS should be given the opportunity for a Lyme diagnosis based on these compelling studies.

  1. 2."ALS-like sequelae in chronic neuroborreliosis" German newsletter entitled Wien Med Wochenschr, 1995;145(7-8);186-8 Hansel Y, Ackerl M, Stanek G (very well known Lyme European researchers)

    [Lyme was very common neurologic disease in Europe in even 1800s but no one knew the organism causing it!

    This study suggests that all persons diagnosed with ALS be suspect for having Lyme disease as this particular case study individual had her diagnosis changed from ALS to Lyme.  She had had Lyme for many years and the long-term sequelae of the infection caused an ALS misdiagnosis.

    3. "Neurologic Complications of Lyme Disease" Rheumatic Dis Clinical North America, 1993 Nov;19(4):993-1009 Coyle, Patricia K. (Neurologist at Stony Brook University, New York)

    Quote from the article:  "Lyme disease should be included in the differential diagnosis [editors note: by physicians] of most major neurologic syndromes."

    4. "Clinical and electrophyphsiologic findings in chronic neuropathy of Lyme Disease" Logigian El et al., Neurology 1992 Feb, 42(2):303-11.

    48% had distal neuropathy involvement with multifocal losses. Weakness, hyporeflexia were present in some and motor or sensory nerve conduction showed slowing in 64%.  48% had radicular (nerve root pains).

    75-80% of patients , with needle EMG studies showed DENERVATION IN PARASPINAL AND LIMB MUSCLES.   76% of patients showed improvement with intravenous rocephin therapy

    5. Immunologic Reactivity Against Borrelia burgdorferi in Patient with Motor Neuron Disease" Archives of Neurology-Vol 47, May1990, p. 586-594.  Author:  John J. Halperin, MD et al. (one of President Bush's doctors and many other [et al].

Lyme Disease/ALS Study

Abstract:  The findings of this study are the best of all studies done to date.  A group of Suffolk New York "Classic ALS" patients were taken for the study.  They were not classic Lyme patients. All were given antibiotic.  Some did not do anything, some did very well and the bulbar group deteriorated rapidly.

Remember, the reason for this Deterioration was hypothetically due to a very common research problem. Back then... the length and type of treatment given to the severe bulbar group was probably not only long enough. The rapid deterioration was a definite sign of the Lyme infection because of the Jarisch-Herxheimer Reaction.

This reaction only occurs with infections like lyme and the only way a group could either not respond or do a rapid decline on Treatment would be due to this endotoxin released by the spirochete Bacteria when antibiotics kill it. 

The endotoxin given off by the Spirochete causes an immunologic reaction which is very difficult for all Lyme patients but passes with time. No doubt the bulbar group received A short duration of therapy and no one was aware of this reaction and Their need for individualized therapy... even oral perhaps as opposed to IV or perhaps pulse therapy whereby the patient takes IVs only a few days a week as opposed to daily to try and minimize this reaction).

Similarly, those who did not respond, were probably like me.  It took me 16 weeks of intravenous antibiotic to get well my first treatment!  I am sure these research patients were given only 2-4 weeks of IV.

After 2-4 weeks of IV, I was so sick from the cyclical immunologic exacerbation of symptoms of the JH reaction that I could barely stand to be in my body from all the strange neurologic things going on.  I felt better in some ways but much worse in others and it took me 16 weeks straight on IVs to get well!

One case of a 35 yo male who was paralyzed from Lyme and on a ventilator, required a full year of IV claforan to bring him back to living alone and fully-functioning again, able to drive etc.  He had severe brain-stem demyelination and encephalitis and was very, very acutely ill.  He is fine now other than the damage from the dysarthria.  He sounds as if he has had a stroke.

The results of this study were profound:  There was a statistically significant reversal of neurologic function of classic ALS patients taking antibiotic for Lyme in this study!

If I were an ALS patient, this study alone would make me run for antibiotics treatment.  Now the Lyme specialists no longer use a short 4-6 week course of antibiotics but rather they individualize your length of therapy depending on the time it takes you to get better.

6. "Neuroborreliosis as a cause of respiratory failure", Journal of Neurology, 242:9, 1995 Sep.604-7.  Silva MT, et al. LaneFox Respiratory Unit, St. Thomas' Hospital, London, UK.

Three cases of Lyme causing acute respiratory impairment requiring ventilatory support.  TWO OF THE THREE HAD BRAINSTEM INVOLVEMENT. All of these patients ALSO had central apnoea requiring tracheostomy, etc.

7. "Chronic Neurologic Manifestations of Lyme Disease" Logigian et al.  New England Journal of Medicine, Nov. 1990.

Neurologic studies and neuropsychiatric studies were performed on a group of Lyme patients.  Findings showed that a group of Lyme patients had both proximal and distal paraspinal denervation on electromyographic testing (EMG) with clearly ALS signs. EMG studies revealed neuropathy both proximal and distal with noted denervation, atrophy and weakness.

8. "Pathogenesis of immune-mediated neuropathies" [Immune-meidated is a = way of avoiding the use of "autoimmune" meaning that something has "triggered" the immunologic damage of the nervous system such as the spirochete infection.]
Pediatr Res, 1993 Jan,33(1Suppl):S90-4 Dept. Neurology, University Pennsylvania School of Medicine

In this abstract, Guillain-Barre disease is the topic with Lyme mentioned as well.  NERVE CONDUCTION VELOCITY SLOWING AND SEGMENTAL DEMYELINATION IS MENTIONED. 

Many patients with Lyme disease have had a hard hit to their immune systems by this immune-suppressing infection and many of us have had to have gammaglobulin intravenously to help us fight the infection.  This study mentioned the use of gammaglobulin therapy IV for GB patients as well.

9. "Detection of Borrelia burgdorferi DNA and complement menbrane attack complex deposits in the sural nerve of a patient with chronic polyneuropathy and tertiary Lyme disease." Institute of Neurological Sciences, University of Siena, Italy. Muscle Nerve, 1997 Aug;20(8):969-75. Maimone D, Villanova M, et al.

This study delves into polyneuropathies, sural nerve biopsy showing spirochete infection, EMG findings etc.

10. Lyme Borreliosis neuropathy.  A case report." American Journal of Physician Medicine and Rehabilitation, 1996 Jul;75(4):314-316.

This study is significant for ALS in that "electro physiologic studies demonstrate a PROXIMAL AND DISTAL AXONAL INVOLVEMENT."  It even suggests that EMGs may show improvement in clinical changes as therapy begins to improve neurologic involvement.  This report suggests that some peripheral neuro involvements may resolve while other neuro symptoms may not. Responses vary.

11. "Myositis during Borrelia burgdorferi infection (Lyme Disease) Schoenen J., et al, Journal Neurology and Neurosurgical Psychiatry 1989, Aug;52(8):1002-5.

Patient developed myopathic syndrome with severe muscular pains, incapacitating weakness of the proximal limb and the neck, as well as the bulbar muscles.  Steroids stopped symptoms for a while but only antibiotics improved the paresis.

12. "Central nervous system manifestations of Lyme disease.  Pachner AR, Duray P, et al. Achives of Neurology, 1989 July;46(7):790-5

Weeks to years after this infection, behavioral changes, ataxia, and/or WEAKNESS IN BULBAR OR PERIPHERAL MUSCLES DEVELOPED."  All 6 patients in this study were treated with IV penicillin high dose but the length was not mentioned.  Four had response and 2 did not... again perhaps due to length of therapy not being long enough?

13. "Multiple Neurologic manifestations of Borrelia burgdorferi infection"  [article in French] Author-dupuis, MJ, Revue of Neurology (Paris) 1988;144(12):765-775. Clinique St.-Pierre, Ottignies, Belgique.

"The neurologic spectrum of Borrelia burgdorferi is still enlarging. The following neuro manifestations are mentioned:  meningitis, acute  or relapsing neuro symptoms such as palsies, cranial neuropathies, peripheral nerve involvement, acute transverse myelitis and paralysis, encephalitis, myositis, chronic neuropathy, sensory and  MOTOR IMPAIRMENT AND SIGNS, recurrent stroke, progressive neuro disease, optic atrophy, DYSARTHRIA, SLOWLY OR PROGRESSIVE  ATAXIA, SPASTIC GAIT DISORDER, ABNORMAL EMGs, etc.

Spirochetal cyst forms in neurodegenerative disorders...

Hiding in plain sight.

PubMedID:16828236 7/21/2006 Journal: Med Hypotheses Author(s):MacDonald Alan B

... Variously sized cystic spirochetal profiles within diseased nerve cells explain the following structures: Lewy body of Parkinson's disease, Pick body, ALS spherical body, Alzheimer plaque.

Borrelia infection is therefore a unifying concept to explain diverse neurodegenerative diseases, based not entirely on a corkscrew shaped profile in diseased tissue, but based on small, medium and large caliber rounded cystic profiles derived from pathogenic spirochetes which are "hiding in plain sight".

Lyme Neuroborreliosis (NB) is often thought to be mistaken for... (Neurological illnesses)

Neuroborreliosis (NB) is is also thought to be a form of (MS).  And NB is often thought to be the initiating cause of chronic neurological disease, without the infection being present.  There seems to be little difference clincally, and the statistic is 25% of MS cases are cases exposed to Borrelia burgdorferi (Coyle).  But if the testing was better, it might reveal a greater linkage. 

Approximately the same number is ~47% in endemic areas, that Borrelia burgdorferi exposure is associated with Amyotrophic Lateral Sclerosis (Dattyler, Halperin).  Even the markers are similar, in the the indices of these three diagnoses.  Two clinical trials are underway that suggest an association of ALS or MS to borreliosis


Artemisinin may be useful in treating Lyme/borrelia and related co-infections.

Some people claim that artemisinin, a compound found in Artemisia annua, is far more effective than simply taking the powdered leaves of the herb Artemisia annua.

Artemisinin is an antimalarial agent extracted from the Chinese herb artemisia annua (qinghaosu or sweet wormwood). This plant is grown from seed and only yields artemisinin under specific agricultural and climatological conditions. Wormwood cultivated in China, Vietnam (and pilot projects in Tanzania and India) produce artemisinin.

Artemisinin acts rapidly and potently against the malarial parasite, including some drug-resistant strains. Without significant side effects, it quickly reduces fever and lowers the blood levels of the parasite.

This helps to keep small outbreaks of malaria from becoming epidemics and to quell ongoing epidemics. In a malaria epidemic in the early 1990's in Vietnam, artemisinin reduced the death rate by 97%.

To decrease the risk of resistance, artemisinin is taken as part of a "cocktail." The cocktail of artemisinin and lumefantrine (Benflumetol) is marketed as Coartem and Riamet. Artemisinin was first isolated in 1965 by Chinese military researchers. Pronounced ar-te-mis'-in-in with the accent on the mis.

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