posted
Can any of you explain ALS and the connection to or with Lyme Disease?
Does ALS go along with Lyme or is it 2 seperate diseases?
How are you tested for ALS?
The reason I ask is I just found out thru a neigbhor about our "dare officier" for the schools that he has Lyme and or ALS, our town is running a fund raiser tonight to benfit his medical treatments that are not covered by insurance. (stem cell treatments)
I was told this man had cancer, the newspaper said he had Lyme disease and or ALS.
I'd like to meet him and go and talk to him and see what his treatment has been for Lyme thus far etc. as there have been many new different treatments for Lyme since the earlier yrs.
Posts: 374 | From NJ | Registered: Aug 2006
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posted
According to Dr Lida Mattman, ALS is caused by a nasty, fast growing, Borrelia Strain, which has specific features like segmented fimbriae, unusual cysts. Simply, it is thought to be a 'specific' type of Borreliosis bacterium.
Posts: 638 | From Wroclaw, Poland | Registered: Mar 2004
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CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
The Tick Borne Encephalitis Virus is shortened to TBE Virus. There are many TBE Viruses around the world. The Russians did a great deal of work on the connection between ALS and TBE. However, spirochetes can also cause ALS by themselves as seen in the next abstract after the TBE one.
: Zh Nevropatol Psikhiatr Im S S Korsakova. 1983;83(8):1173-9. Links [Structure of progressive forms of tick-borne encephalitis] [Article in Russian] Umanekii KG, Dekonenko EP. 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.
PMID: 6414202 [PubMed - indexed for MEDLINE] Amyotrophic Lateral Sclerosis Syndrome of Syphilitic Origin. 5 Cases el Alaoui-Faris M, Medejel A, al Zemmouri K, Yahyaoui M, Chkili T Service de Neurologie, Hopital des specialites Rabat, Maroc. 1: Rev Neurol (Paris) 1990;146(1):41-4
Amyotrophic lateral sclerosis syndrome of syphilitic origin. 5 cases.
[Article in French]
We studied 5 cases of syphilitic lateral amyotrophic sclerosis. The diagnosis was based on the presence of a lymphocytic reaction in the CSF and positive VDRL and TPHA reactions in both blood and CSF. Clinically, the disease affected the arms in 3 cases and produced paraplegia in 2 cases. The gradual extension of amyotrophy over several months, the diffusion of electromyographic abnormalities and the finding of spinal cord atrophy at myelography and CT suggested a subacute ischemic mechanism with meningo-myelic arteritis involving the anterior horns. After treatment with penicillin G in high doses, the outcome was constantly favourable, with improvement of motor deficit in 4 cases and stabilisation in 1 case in a 5 to 13 years' follow-up. Publication Types: Review Review of reported cases MeSH Terms: Adult Amyotrophic Lateral Sclerosis/physiopathology Amyotrophic Lateral Sclerosis/etiology* Amyotrophic Lateral Sclerosis/drug therapy Cerebrospinal Fluid/analysis Cerebrospinal Fluid Proteins/analysis English Abstract Female Follow-Up Studies Human Lymphocytosis/cerebrospinal fluid Male Middle Age Neurosyphilis/complications* Penicillin G/therapeutic use Syndrome Syphilis Serodiagnosis
Substances: Penicillin G Cerebrospinal Fluid Proteins
PMID: 2408129, UI: 90176246
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
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I'm wondering what his course of treatment has been up to this point, as I will find out that out when I meet him.
Also I would like to invite him to come to this site as it is so informative.
It's just so unreal what many of us have to go thru with the many other possible dignoses MS - Lupus - etc leaving one unsure about alot of things - and possbily leading to no getting proper treatment that could make a differance in our lives and or save our lives.
Posts: 374 | From NJ | Registered: Aug 2006
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ILADS WELCOMES PHYSICIAN RECOVERING FROM ALS
DOCTOR'S CASE SUPPORTS THEORY LYME DISEASE MAY BE THE CAUSE OF ALS
Bethesda MD September 2, 2004 - The International Lyme and Associated Diseases Society (ILADS) strengthened its impressive membership today with the addition of Dr. Dave Martz of Colorado Springs, who joined ILADS 15 months after being diagnosed with Amyotrophic Lateral Sclerosis (ALS). In April of 2003, Dr. Martz began suffering weakness and pain in his muscles. Dr. Martz soon lost much of his mobility. His condition worsened forcing him to retire from the medical practice he loves.
After six frustrating months with hope fading, Dr. Martz discovered the work of Dr. Gregory Bach of Colmar, Pennsylvania. Dr. Bach, who is a member of ILADS, suggested a link between ALS and Lyme disease. IGeneX Reference Laboratory of Palo Alto then confirmed Lyme bacteria in Dr. Martz. Dr. Martz then sought out a local ILADS physician who started Lyme disease treatment based on the recommendations of Dr. Bach. The results were dramatic.
"Before I found Lyme "literate" professionals, I could only function at a level of about 20 percent," says Dr. Martz. "But now that I'm in expert hands, I am up to 75 percent of full function and I hope to return to work soon as a physician, helping others with Chronic Lyme Disease." An internist, and Past President of the Colorado Medical Society, he is committed to giving others opportunities that have been given to him.
The Centers for Disease Controls says that Lyme disease may be under-reported by as much as ten-fold. This means as many as a quarter of a million Americans may contract Lyme disease each year, yet most of them are unaware of it. ILADS will hold its annual meeting in October of this year in Rye, New York.
ILADS president, Dr. Steven Phillips, says, "Dr. Martz is an example of the many physicians and medical experts we encourage to join ILADS so we can continue to raise awareness and make vital advances in the world-wide fight against Lyme disease."
For more information about Lyme disease go to www.ilads.org
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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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.
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.
posted
*Note that this poor fella was treated by the IDSA guidelines initially, and that initial treatment failed. I am curious what the outcome of this case was several years later.
Neurol Neurosurg Psychiatry 1997;63:257-258 August
Letters to the editor
Generalised motor neuron disease as an unusual manifestation of Borrelia burgdorferi infection
Lyme borreliosis is a well known multisystem disease caused by the spirochete Borrelia burgdorferi and can produce a wide array of neurological abnormalities in humans. The most frequent are meningitis, cranial neuritis, and painful radiculoneuritis.1 Other clinical manifestations include chronic encephalomyelitis, spastic paraplegia, and axonal polyneuropathy.
Our report concerns what we think to be the first case of a patient with upper and lower motor neuron disease and Borrelia burgdorferi infection of the CNS. A causal relation is strongly supported by an evaluation of the Borrelia burgdorferi specific antibody index and the patient's favourable response to medical treatment.
Fifteen months before admission a 33 year old patient noticed weakness in his right hand followed by weakness of the left hand and a progressive gait disturbance. Although he had no pain or sensory disturbance and no history of a tick bite, an erythema migrans, or arthralgias, his physician tested him for Borrelia burgdorferi specific antibodies in the serum because he lived in an endemic region. The test disclosed high concentrations of specific IgG antibodies [1:1200, cut off <1:200]. The patient was treated with doxycyclin for two weeks.
A control examination performed in a different laboratory still disclosed high concentrations of specific IgG antibodies [1:160, cut off 1:40]. Treatment was started again with cefotaxim [2g intravenously for five days].
Six months later he was admitted to our hospital because of persisting paresis and muscle atrophy. On admission, clinical examination disclosed hyperactive deep tendon reflexes with a clonus in both ankles. The muscles of both hands and forearms showed atrophy and severe paresis [figure]. His gait was clumsy and stiff, and there was mild spastic paraparesis. There was no sensory loss, and cerebellar function was normal.
Image Severe atrophy of hand muscles.
Needle EMG disclosed severe active denervation in the small hand muscles bilaterally. Mild to moderate signs of axonal damage were seen in the right anterior tibial muscle and in the left masseter muscle. Motor and sensory nerve conduction velocities were normal. No conduction block could be detected. F waves were abolished. Visual and sensory evoked potentials were normal. Motor evoked potentials disclosed prolonged central conduction times to both anterior tibial muscles and to the left abductor digiti minimi muscle.
Routine blood chemistry was normal. Serum Treponema pallidum and GM1-specific antibodies were not detected. Borrelia serology tests showed slightly raised concentrations of Borrelia burgdorferi specific IgG antibodies in serum and clearly raised concentrations in the CSF. At the time of the first lumbar puncture [after antibiotic treatment], CSF contained five white blood cells/�l and a total protein concentration of 410 mg/l. Reiber-formula analysis2 indicated an intrathecal synthesis of IgG and IgA.
Employing a sensitive affinity blotting technique most of the oligoclonal IgG bands in the CSF were shown to be specific for Borrelia burgdorferi This finding was confirmed by western blotting using identical concentrations of IgG in the CSF and serum. A higher number of Borrelia burgdorferi specific antibody bands were found in the CSF than in serum. Calculation of the Borrelia burgdorferi specific antibody index from enzyme linked immunosorbent assay [ELISA] studies disclosed raised values for IgG and IgA. Specificity of intrathecally produced IgG antibodies for Borrelia burgdorferi was confirmed by employing a highly specific 14 kDa fragment of the flagellin as antigen in enzyme linked immunosorbent assay [ELISA].3 The table shows the detailed data of the antibody tests on admission and on follow up examination five months later. MRI of the cervical spinal cord and the brain disclosed no abnormalities.
View this table: [in this window] [in a new window] Summary of antibody tests
The patient was treated with ceftriaxone intravenously for two weeks, followed by oral prednisone for 10 weeks. After this treatment the patient's condition improved slowly but continuously. At the time of the last clinical control examination 18 months after hospital discharge the patient was able to work without physical impairment.
Clinical and electrophysiological findings met all the criteria for the diagnosis of motor neuron disease. Clinical signs of lower motor neuron involvement were present in both arms. Electromyographic studies disclosed axonal loss at three different levels namely, lumbar [anterior tibial muscle], cervical [hand muscles], and supraspinal [masseter muscle].
Clear signs of damage to the upper motor neuron were also present. Although the symptoms of the patient could be explained by cervical myelitis the EMG findings with evidence of axonal damage in the anterior tibial and masseter muscle as well as the lack of any sensory abnormalities argue strongly against this possibility. In addition, signs of inflammation in the CSF were not consistent with a diagnosis of amyotrophic lateral sclerosis.
We identified a Borrelia burgdorferi infection of the CNS as the cause of the inflammation. Evidence included a raised specific IgG and IgA antibody index, the demonstration of Borrelia burgdorferi specific oligoclonal IgG bands in the CSF and the predominance of individual Borrelia burgdorferi specific antibody bands in CSF [as indicated by western blotting]. The absence of a high white cell count and protein in the CSF could be attributed to prior antibiotic treatment. Optimising dose and duration, antibiotic treatment was renewed and combined with a long term steroid therapy. Four months later a CSF examination showed a considerable decrease in specific antibody concentrations, and the patient's condition continued to improve.
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 L�CKING Department of Neurology and Clinical Neurophysiology, University of Freiburg , Germany G DEUSCHL Department of Neurology and Clinical Neurophysiology, University of Kiel, Germany Correspondence to: Dr Franz X Glocker, Neurologische Universit�tsklinik Breisacher Strasse 64, D-79106 Freiburg, Germany. References
1. Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme disease: meningitis, cranial neuritis, and radiculoneuritis. Neurology 1985;35:47-53[Abstract].
2. Reiber H, Felgenhauer K. Protein transfer at the blood cerebrospinal fluid barrier and the quantitation of the humoral immune response within the central nervous system. Clin Chim Acta 1987;163:319-328[Medline].
3. Kaiser R, Rasiah C, Gassmann G, Vogt A, L�cking C. Intrathecal antibody synthesis in Lyme neuroborreliosis: use of recombinant p41 and a 14-kDa flagellin fragment in ELISA. J Med Microbiol 1993;39:290-297[Abstract].
4. ElAlaouli F, Medejel A, AlZemmouri K, Yahyaoui M, Chkili T. Syphilitic lateral amyotrophic sclerosis. A study of 5 cases. Rev Neurol 1990;146:41-44[Medline].
5. Fredrikson S, Link H. CNS-borreliosis selectively affecting central motor neurons. Acta Neurol Scand 1988;78:181-184[Medline].
6. Halperin JJ, Kaplan GP, Brazinsky S, et al. Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease. Arch Neurol 1990;47:586-594[Abstract].
� 1997 by Journal of Neurology, Neurosurgery, and Psychiatry
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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He had both Lyme and AlS. I don't know what kind of medical treatment he received.
Posts: 449 | From Pasadena, CA, usa | Registered: Aug 2005
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