Lyme & ALS/Motor Neurone
**Updated 4th March 2016
ALS and Lyme Pt 1
By Claire Culver
This is the first in a series. I’m discussing my husband’s story. He was first diagnosed with ALS before it was discovered he had Lyme Disease all along (the patient had bullseye rash following a tick bite, flu like symptoms then developed severe neurological symptoms). These videos are directed to those who are diagnosed with ALS (Lou Gherig’s Disease) and PLS (Primary Lateral Sclerosis).
Pt II is available at: https://www.youtube.com/watch?v=5CB-B0A38jc
Man Diagnosed With ALS Dies of Lyme Disease (Part 1 of 2)
On Dec. 22, three days before Christmas, (former high school principial) 55-year-old David A. Geraghty died from complications of a supposedly rarely fatal infection: Lyme disease. As reported in The Valley Breeze, a Lincoln, R.I. newspaper, Geraghty and his family found out conclusively that he has had Lyme disease just one year ago, last December. As was the case for me and is not uncommon in other cases of Lyme disease diagnoses, it was Geraghty and his wife — not his physicians — who pushed for investigation into the cause of his illness and ultimately were responsible for discovering that Lyme disease was at the root.
Also recommend this article by the same author:
**Updated 16th Jan 2014
Lyme Disease –Induced Polyradiculopathy
Mimicking Amyotrophic Lateral Sclerosis
Ahmet Z. Burakgazi, MD1
1Assistant Professor, Neuroscience Section, Department of Medicine, Virginia Tech Carilion School of Medicine, Roanoke, USA
Correspondence Author: Ahmet Z. Burakgazi, MD Carilion Clinic 3 Riverside Circle Roanoke, VA 24016
Importance: To describe a case of predominantly motor polyradiculopathy secondary to Lyme disease that can mimic motor neuron disease and has been rarely reported.
Observations: A 64 year-old man presented with a one-month history of rapidly progressive weakness involving bulbar, upper limb and lower limb muscles. The physical examination showed widespread weakness, atrophy, fasciculation and brisk reflexes. The initial electrodiagnostic test showed widespread active and chronic denervation findings. The initial physical and electrodiagnostic findings were suggestive of Amyotrophic Lateral Sclerosis (ALS). However blood serology indicated possible Lyme disease. Thus, the patient was treated with doxycycline. The clinical and electrodiagnostic findings were resolved with the treatment.
Conclusion and Relevance: The diagnosis of Lyme disease can be very challenging and it can mimic other neurological disorders such as ALS or Guillain-Barre syndrome (GBS). Careful and detailed examination and investigation are required to confirm the diagnosis and to prevent misleading inaccurate diagnoses.
For more on Lyme/ALS check out
**Updated 1st August 2013
Man finds ALS was undiagnosed Lyme Disease
The San Jose Mercury News writes a follow-up story on Bart Fenolio, who last December was told he had two months to live. Fenolio has been in a nursing home since then, receiving Lyme treatment. Now he’s well enough to go home.
Court finds Lyme led to ALS (motor neurone)
The court pointed out that the worker’s treating physician found that he suffered from significant muscle atrophy that rendered him totally disabled and was related to his Lyme disease. A neurologist also opined that the worker’s progressive muscle weakness and consequent total disability were causally related to his Lyme disease. His treating psychiatrist indicated that his Lyme disease prompted an autoimmune reaction that produced symptoms resembling amyotrophic lateral sclerosis. The psychiatrist also explained that the worker’s creatine phosphokinase levels improved when treated with antibiotics, establishing a connection between the infection and his muscle deterioration. The psychiatrist also opined that the worker suffered from anxiety and stress related to his diagnosis. The court noted that the carrier presented the opinions of several neurologists who could not state with certainty that the worker’s Lyme disease was the cause of his motor neuron disease. However, the court found that substantial evidence supported a determination of a causal relationship.
**Updated 24th April 2013
Details of Dr Martz & his fight against Lyme induced ALS…
Scott Brazil dies from Lyme Disease Complications
LOS ANGELES – Emmy-winning producer-director Scott Brazil, whose television shows included “The Shield” and “Hill Street Blues,” has died. He was 50.
Brazil died of respiratory failure due to Lou Gehrig’s disease and lyme disease complications..
Brazil was executive producer of “The Shield,” the first original drama series on FX Networks, and he directed 11 episodes. Brazil and “Shield” creator and executive producer Shawn Ryan won the 2002 Golden Globe for drama series.
Although his condition had worsened, Brazil used a motorized wheelchair to go about his duties as “The Shield” producer-director.
“He worked (last) Thursday, working to the very last day, talking to the writers, doing casting and prepping our next episode,” Ryan said Wednesday. “That’s what made all this so stunning for us. We’re kind of shocked.”
For more on the story go to: http://sci.tech-archive.net/Archive/sci.med.diseases.lyme/2006-04/msg00501.html
Patients grapple with Lyme disease
In 2001, doctors told Tony Coffey he had a form of amyotrophic lateral sclerosis – ALS, or Lou Gehrig’s disease – and gave him a few months to live. His steps were faltering, his speech slurred. He couldn’t swallow his own saliva, let alone food. He had Bell’s palsy, causing his facial muscles to droop.
“I couldn’t cough or laugh,” said Coffey of Fredericks County, Penn. who celebrated his 37th birthday Saturday at a symposium on Lyme disease at New Milford High School. “And I had what I can only describe as a constant pressure on my brain. I think my doctors thought I was faking it, or losing my mind.”
Coffey was lucky. His search for medical help took him to Dr. Gregory Bach, a Pennsylvania doctor who specializes in treating Lyme disease. Thanks to intensive, long-term regime of antibiotics, Coffey has recovered his health. He has a new son, named Gregory after Bach.
“I’m happy every day of my life,” he said. “I’m just so grateful to be
liberated from the hell of Lyme disease.”
More at: http://sci.tech-archive.net/Archive/sci.med.diseases.lyme/2006-04/msg00513.html
**Updated 2nd October 2012
Tit for tat, sides face off about the role of Lyme Disease in ALS cases…
From Dean Chioles Site – a sufferer of Lyme & ALS – he has sadly since passed away:
My name is Dean Chioles and I was diagnosed with Sporadic ALS (Amyotrophic Lateral Sclerosis) Lou Gehrig’s Disease in October of 1993. In January of 1998, I tested positive for Lyme disease!
It is becoming more and more apparent that ALS (Amyotrophic Lateral Sclerosis) and many other neurological degenerative diseases are actually quite often misdiagnosed Lyme disease. There is no definitive test for ALS, diagnoses is based upon symptoms and by ruling out other treatable afflictions. There is no known cause or cure for ALS. so the question I and others often ponder is how can I be absolutely positive that I have ALS and not some other treatable illness?
I was diagnosed as having ALS by some of the top neurologists in Chicago. After culturing my blood for four weeks by a research lab in Michigan, the results were positive in finding Borrelia Burgdorferi, the bacteria responsible for LYME DISEASE !!! I am not the only one, I know of thirty seven (37) other PALS who also have tested positive for Lyme.
Lyme disease is caused by the spirochete bacteria Borrelia burgdorferi and is transferred by a bite from a tick. Symptoms of Lyme disease can mimic those of ALS, the tests are unreliable and Lyme is very difficult to detect.
Below are three very compelling articles which unequivocably implicate Borrelia burgdorferi as the initiating infection which is capable of causing “classic ALS” symptoms:
1) “immunologic Reactivity Against Borrelia burgdorferi in Patient with Motor Neuron Disease”, John J. Halperin, MD, Gary P. Kaplan, MD, etal. Archives of Neurology-Vol47, May 1990.
This study first of all took a group of men with only classic ALS symptoms from a hyperendmic area of Suffolk county. In the study it was made clear that with a true ALS, there is nothing which can cause reversal of neurologic function once it is lost. IV rocephin however, did reverse neuro function in a statistically significant number of these men making this study exceptionally noteworthy.
It mentioned that the bulbar group progressively decline. Two reasons come to mind: For one, the bulbar group represents those patients with severe brainstem involvement. The brainstem being the control center for all bodily functioning; especially breathing, swallowing and movement etc. It is hypothesized that a very short course of IV was used in this group and the Jarisch-Herxheimer reaction caused a quickly progressive decline in this group as it hit the brainstem. We have had such a case close to home whereby a woman with severe brainstem demyelination began to improve on IV therapy and then within hours went into sudden respiratory adult distress and cardiac failure. Even though she was life-flighted to a nearby hospital, she could not be saved. Had a critical care physician, knowledgeable about Lyme been available, perhaps she could have been saved? Certainly in this study, the bulbar group may have had a chance had they been given longer term antibiotic and perhaps been weaned onto the IV with orals first? No one knows yet for sure.
2) “Borrelia burgdorferi Antibodies and Amyotrophic Lateral Sclerosis” Lancet, August 8, 1987; Russell Johnson, Ronald Schell, Burton Waisbren. Reference was made to Dr. Stanek, Pachner Reik, Steere and Dattwyler, the very men who downplay Lyme at this time. This article was published when these men were publishing Lyme for what it really is: a very serious neurologic disease implicating such symptoms as those that cause ALS.
In this study, case histories are taken of patients with “classic ALS”: taken from the State of Wisconsin and one from the Chicago area. Each patients had symptoms such as dysarthria, fasciculations (common to most Lyme patients), atrophy and latent infection of the central nervous system. Two patients ultimately died from respiratory failure but were never given treatment and one was allowed treatment and “seemed to stabilize”. The concluding remark was as follows: “Since there is no treatment for ALS and there for chronic Lyme disease, clinicians will ask if patients with ALS who have high titre-anti-Borrelia antibodies should be treated empirically with degtriaxone, one of the antibiotics of choice for chonric B. burgdorferi infection. At the least, it seems reasonable to find out if a patient with ALS does have B burgdoferi antibodies.”
3) “ALS-like sequelae in chronic neuroborreliosis”, Wien Med Wochenschr, 1995; 145(7-8):186-8. Hansel Y, Ackerl M, Stanek G.
One patient, a 61 YO female with clinical picture of motor neuron disease gave the physicians evidence of having possible Lyme disease. Improvement of her symptoms and her CSF findings occured after administration of antibiotic therapy. Her diagnosis was then switched from ALS to Lyme disease.
There are other studies about clusters of ALS in Wisconsin or in England and these same areas are also implicated as high rate areas for Lyme however the health depts do not make the parallel either intentionally or inadvertently. There are also studies of doctors such as one in California who gave ceftriaxone to a group of ALS patients and they did not respond to he declared it a waste of time. He, no doubt, gave a very short course and expected immediate reversal of symptoms and/or cure?
Arch Neurol. 1990 May;47(5):586-94.
Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease.
Halperin JJ, Kaplan GP, Brazinsky S, Tsai TF, Cheng T, Ironside A, Wu P, Delfiner J, Golightly M, Brown RH, et al.
Department of Neurology, State University of New York, Stony Brook 11794.
Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24 ALS patients–3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas.
PMID: 2334308 [PubMed – indexed for MEDLINE]
Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in chronic neuroborreliosis]
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Neurologischen Abteilung des Kaiser-Franz-Josef-Spitals, Wien.
CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
PMID: 7610670 [PubMed – indexed for MEDLINE]
Acta Neurol Scand. 2007 Feb;115(2):129-31.
Motor neuron disease recovery associated with IV ceftriaxone and anti-Babesia therapy.
Harvey WT, Martz D.
Rocky Mountain Chronic Disease Specialists, L.L.C., North Circle Drive, Colorado Springs, CO 80909, USA. firstname.lastname@example.org
* Acta Neurol Scand. 2008 Mar;117(3):217.
This report summarizes what we believe to be the first verifiable case of a significant and progressive motor neuron disease (MND) consistent with amyotrophic lateral sclerosis that resolved during treatment with i.v. ceftriaxone plus oral atovaquone and mefloquine. The rationale for use of these antibiotics was (i) positive testing for Borrelia burgdorferi and (ii) red blood cell ring forms consistent with Babesia species infection. The patient has continued to be free of MND signs and symptoms for 15 months, although some symptoms consistent with disseminated Borreliosis remain.
PMID: 17212618 [PubMed – indexed for MEDLINE]
P-glycoprotein and Multidrug Resistance
Donna C. King
Environmental Health Specialist
A subset of patients with encephalitis and subsequent paralysis, or a diagnosis of ALS has been correlated with the spirochete, Borrelia (BB) from ticks. Highly upregulated mRNA of MRP (lp38/5.48 fold upreg) has been observed in plasmids from BB after they enter a mammalian host. There appears to be a commonality in upregulated expression of MRP between the three disease states, ALS (non-BB ALS), TBE (Tick Born Encephalitis from Borreliosis) and ionizing radiation injury. ..
..ALS patients and mSOD1 mice may be resistant to therapeutic agents due to the upregulation of multi-drug resistant proteins which prevent therapeutic dose accumulation inside the cell.
Treatment of Amyotrophic Lateral Sclerosis and Multiple Sclerosis with Anti-Lyme Disease Antibiotics Being Used to Treat Lyme Disease
The concept of treating infections and other serious diseases based on possibility rather than probability is not new. Who among the readers of this essay have not added an antibiotic to the treatment of fever of unknown etiology because of the possibility that it may be associated with a bacterial infection?
Have not most oncologist given patients with serious cancer chemotherapy because of the possibility that it might help them? It is in this frame of reference that this essay suggests that ceftriaxone should be added to treatment programs for amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) because of their possible relationship to Lyme disease.
First we will discuss the lessons that can be learned from syphilis, which is the spirochetal disease most closely related to Lyme disease.1 Then, we will present anecdotes of cases of ALS and MS seen at the Waisbren Clinic. These anecdotes support the conclusion that there is a possibility that treatment for Lyme disease might help some patients who live in areas where Lyme disease is endemic and who present with syndromes compatible with MS and ALS. 2 Finally, articles in the literature will be alluded to that may help explain the anecdotes in this article.3-20
More at: http://www.waisbrenclinic.com/ALS-MS-lyme-disease.html
European Doctors Misdiagnosed Lyme Disease As ALS
Television-host Jodi Adamson was infected with Lyme disease for six years and the doctors of the region were not able to diagnose the disease. Earlier, Mr. Adamson was told by the doctors that he was infected with ALS also known as Lou Gehrig’s disease. Mr. Adamson had undergone a very terrible phase due to the disease.
The doctors of the Europe knew about the existence of such a disease from the past 100 years, but the health department wrongly diagnosed the disease as ALS. As per Jodi Adamson, the health departments need to work on various measures to detect the disease.
Finally, Mr. Adamson himself tallied the symptoms of Lyme disease with his own and realized that 75% of the symptoms matched. He appealed the neurologist, but they did not consider his suggestion. As per a research, the testing method for public health did not reveal exact result. The Eliza test needs to be replaced with the much more research-proven Western Blot. The Ontario Health Minister, Deb Matthews, should have refurbished the existing modes of Lyme detection.
Another case was from Pictou County, where a dog was diagnosed to have contracted with Lyme disease. A vaccine could treat Lyme disease in dogs, but unfortunately there was no such vaccine for humans or other animals.
Lyme as a Motor Neuron disease
J Neurol Neurosurg Psychiatry 1997;63:257-258 ( August )
Letters to the editor
A part of the dialogue…
In the light of the evidence, it seems safe to conclude that the patient’s symptoms were due to a CNS Borrelia burgdorferi infection which merely mimicked amyotrophic lateral sclerosis. Several reports have been published on spirochetal diseases leading to isolated damage to the motor system. Spinal meningovascular lues has been reported to cause a clinical syndrome mimicking motor neuron disease.4 Fredrikson and Link published a case report of a patient with isolated upper motor neuron symptoms due to CNS borreliosis who responded favourably to antibiotic treatment.5 Cases of painful motor neuropathy due to Borrelia burgdorferi specific infection have also been reported.1 Halperin et al6 found serological evidence of exposure to Borrelia burgdorferi in nine of 19 patients with motor neuron disease. However, none of them showed signs of Borrelia burgdorferi specific immunoreactivity in the CSF or favourable response to treatment.
It can be speculated that the spirochete Borrelia burgdorferi has the ability to induce an immune reaction that specifically affects motor neurons. This reaction may mimic different, non-curable diseases, such as spastic spinal paralysis, spinal muscle atrophy, and amyotrophic lateral sclerosis. Therefore, we suggest that patients diagnosed as having progressive motor neuron disease, who live in endemic areas, should be tested for Borrelia burgdorferi specific antibodies in serum and in CSF. The test could reliably detect a rare, but treatable disease mimicking motor neuron disease.
B HEMMER, F X GLOCKER, R KAISER, C H LÜCKING
Department of Neurology and Clinical Neurophysiology, University of Freiburg , Germany
Department of Neurology and Clinical Neurophysiology, University of Kiel, Germany
Correspondence to: Dr Franz X Glocker, Neurologische
Universitätsklinik Breisacher Strasse 64, D-79106 Freiburg, Germany.
Two Limestone women get reprieve from ALS diagnosis
Athens News-Courier, Athens , Alabama , USA
By Charlotte Fulton, email@example.com
“I never thought I’d be so happy to be diagnosed with Lyme Disease,” says 54-year-old Vickie Crawford, “but when you consider the alternative…”