It took me a while before I noticed improvement on Mino, I herxed alot from it. At the time, the biggest difference I saw was an improvement with joint pains.

Mino has been a wonder drug for me..it took some getting use to, but well worth it in the long run.

I was on Mino for close to 2 years. i have been off all abx since April and am doing very well...

I wish you all wellness!!

Then I switched to omnicef, not realizing the mino had almost completed its job. For a month longer, I felt grumpy and sore, but not overwhelmed with symptoms, and then suddenly it was like I'd never been sick. Then my liver enzymes went up and my LLMD pulled me off all abx, leading to a total relapse, grr.

This time around, I've been on for six weeks along with ketek, and am starting to experience the exact same change in symptoms that I did last year. Except that ketek hits the neuro stuff like mino never did. I'm getting all these cravings for sugar and salt, I'm grouchy but also much more able to reason through my grouchiness and drop it, and even though I still feel yucky, with sore throat, fatigue, headache, etc., objectively I'm able to do more, at a higher quality level.

ALS has ( by matter of fact) been linked as having borrelia burgdorferi as ONE of the caustive agents.

You on meds for coinfections yet?

Sorry it took me so long to get back to you...now that I'm actually well enough to work, it's harder to find the time to log on the internet...

Thanks Joe for covering me..yes it took me about 3 months to notice a difference and by 9 months I was feeling pretty good.

I did have to stop taking the Mino a couple of times as the herxes got very severe.

The first time I took it (if memory serves me right) I was literally bed ridden for 11 days and I was so sick, my hubby was very nervous.

Turns out that too much of a herx, is NOT a good thing. SO I was pulled off the Mino for about a week and started back up on it and did much better.

I have been told by my LLMD and some pretty smart cookies here.... that if a herx gets bad, to take a break and give your body a chance to rest/detox and start back on the meds in a few days to a week.

Doing this really helped me be able to stay on this abx for the long haul, and I am so thankful today that I stuck to it.

But as always, make sure you talk to your LLMD before starting or stopping a abx.. ( a little disclaimer )

I sure hope you can stick with the Mino and hope it will do for you, what it has done for me...

Joe, so glad you are seeing a little improvement...some improvement is better than no improvement! and I will be keeping my fingers crossed that the mino will kick in soon and help you on your road to recovery!!!

Your choices are to take the treatment and kill all of the lyme or not take the treatment and have the same condition possibly occur due to more active lyme, just takes a little longer. The sooner you start the better. If you allow the lyme to spread throughout your body, it will take longer to get through the treatment.

quote:

---

Originally posted by TheCrimeOfLyme:
YOu stop it with treatment.

ALS has ( by matter of fact) been linked as having borrelia burgdorferi as ONE of the caustive agents.

You on meds for coinfections yet?

---

Here ya go tweety
http://www.geocities.com/lymeart3/als-abstracts.html

Medical and Scientific Abstracts
on
Lyme Disease and ALS or MND
A Bibliography with Highlighted Full Abstracts
Lyme disease is a serious bacterial infection caused by a tick bite and affects humans and animals.

Table of Contents
Medical and scientific citations or abstracts from the NIH, NLM MEDLINE database
Other medical or scientific information pertaining to Lyme disease and ALS or MND

Sources

Also see:
Lyme Disease Misdiagnosed as Amyotrophic Lateral Sclerosis (ALS)
For more information on Lyme disease

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

Medical and scientific citations or abstracts from the NIH, NLM MEDLINE database pertaining to Lyme disease and ALS or MND:

This section contains citations and complete abstracts for medical and scientific articles from the National Institutes of Health (NIH), National Library of Medicine (NLM) MEDLINE database about Lyme disease and amyotrophic lateral sclerosis (ALS) or motor neuron disease (MND). Citations are sorted by date within categories with particularly significant portions highlighted in bold red lettering.

Note: Most of the citations or abstracts in this section were gleaned from articles found by the following MEDLINE "search" link:

MEDLINE - ALS or MND or Gehrig or Charcot AND Lyme disease - 13 on 9 May 00

TITLE:
[Neuroborreliosis in a patient with progressive supranuclear paralysis. An association or the cause?]
AUTHORS:
Garcia-Moreno JM; Izquierdo G; Chacon J; Angulo S; Borobio MV
AUTHOR AFFILIATION:
Departamento de Inmunologia, Hospital Universitario Virgen de la Macarena, Sevilla, Espana. [email protected]
SOURCE:
Rev Neurol 1997 Dec;25(148):1919-21
ABSTRACT:
INTRODUCTION: Many different neurological conditions may be seen in the later stages of Lyme's Disease, such as blindness, epileptic crises, CVA, extrapyramidal disorders, amyotrophic lateral sclerosis, and dementia may be yet another form of presentation of chronic infection due to Borrelia burgdorferi (Bb). Progressive Supranuclear Paralysis (PSP), a disorder of unknown aetiology, considered to be the commonest cause of Parkinsonism-plus, one of the symptoms of which is dementia, has never been mentioned in this type of differential diagnosis. CLINICAL CASE: We present the case of a 78 year old man with sub-acute mental deterioration, Bb positive serology in both plasma and CSF, and with clinical and epidemiological features compatible with Lyme's Disease. Complementary tests were negative. The syndrome corresponded to Lyme's [sic] Disease and improved after treatment with ceftriaxona. CONCLUSIONS: We consider aspects of the aetiology of PSP which are still not clear. In our patient, the aetiology seemed to be Bb infection, according to the criteria of the original description of the disease and in view of the neuropathological findings which have shown Bb in the substancia nigra of the mid-brain and the existence of an animal model in which Bb shows a particular tendency to colonize infratentorial structures.

TITLE:
Generalised motor neuron disease as an unusual manifestation of Borrelia burgdorferi infection
[letter]
AUTHORS:
Hemmer B; Glocker FX; Kaiser R; Lucking CH; Deuschl G
SOURCE:
J Neurol Neurosurg Psychiatry 1997 Aug;63(2):257-8
No abstract available.

TITLE:
[Motor neuron syndrome and Lyme disease. Relation of causality or fortuitous association? (letter)]
AUTHORS:
Deibener J; Kaminsky P; Debouverie M; Aubrun P; Maurer P; Gerard A; Duc M
SOURCE:
Presse Med 1997 Jul 12;26(24):1144
No abstract available.

TITLE:
[ALS-like sequelae in chronic neuroborreliosis]
AUTHORS:
Hansel Y; Ackerl M; Stanek G
AUTHOR AFFILIATION:
Neurologischen Abteilung des Kaiser-Franz-Josef-Spitals, Wien.
SOURCE:
Wien Med Wochenschr 1995;145(7-8):186-8
ABSTRACT:
CSF investigation in a 61-year old female patient with clinical picture of motor neuron 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.

TITLE:
Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease.
AUTHORS:
Halperin JJ; Kaplan GP; Brazinsky S; Tsai TF; Cheng T; Ironside A; Wu P; Delfiner J; Golightly M; Brown RH; et al
AUTHOR AFFILIATION:
Department of Neurology, State University of New York, Stony Brook 11794.
SOURCE:
Arch Neurol 1990 May;47(5):586-94
ABSTRACT:
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.

TITLE:
Borrelia burgdorferi antibodies and amyotrophic lateral sclerosis [letter]
AUTHORS:
Waisbren BA; Cashman N; Schell RF; Johnson R
SOURCE:
Lancet 1987 Aug 8;2(8554):332-3
No abstract available.

Also see:
source: the Lancet, August 8, 1987
title: Borrelia Burgdorferi Antibodies And Amyotrophic Lateral Sclerosis
authors: Waisbren, Cashman, Schell, Johnson

"Sir,--Neurological involvement in Lyme disease usually takes the form of symptoms of meningoencephalitis, mononeuritis multiplex, radiculoneuritis, and/or cranial nerve neuritis developing within months of primary infection with Borrelia burgdorferi. Recently, however, long-term sequelae have been described; these include a remitting/relapsing neurological syndrome (simulating multiple sclerosis), focal encephalitis, psychiatric disease.(1-4) These tertiary symptoms are thought to be due to latent infection of the central nervous system.

"A patient's query as to whether her amyotrophic lateral sclerosis (ALS) could be caused by Lyme disease led us to test a series of ALS patients for B. burgdorferi antibodies in serum. 4 of 54 patients from Wisconsin and Illinois had antibodies at titres thought by the Wisconsin State Laboratory of Hygiene to be significant. (256 or greater).

"B. burgdorferi antibody was sought. (5) Briefly, antigen spotted slides were stored at -20 degrees C for no longer than four months before use. Spotting dilutions of sera on antigen slides were washed and overlaid with flourescein isothiocyanate-labelled sheep antihuman immunoglobulin (Wellcome Diagnostics) . Serum antibody titres were expressed as the highest dilution that exhibited barely visible staining of at least 50% of the spirochaetes per microscopic field. the results at the Wisconsin State Laboratory of Hygiene were confirmed by another of us (R.J.) in Minnieapolis.

"Case 1, -- A 65-year- old woman had slurred speech 3 months after she had a generalised rash while on holiday in Oxford, Wisconsin. 6 months later she saw a neurologist for progressive weakness, dysarthria, and dyspnoea " (air hunger resulting in labored or difficult breathing, sometimes accompanied by pain. It is normal when due to vigorous work or athletic activity.) .
"Atrophy, fasiculations "(Involuntary contraction or twitching of muscle fibers, visible under the skin. Spontaneous contractions of muscle fibers that do not cause movement at the joint.) "and brisk reflexes were observed on examination. An electromyogram (EMG) demonstated widespread denervation. Her B burgdorferi antibody titre in her serum was 512. She died of respiratory failure 3 years after onset. Her spinal fluid was never examined and cortical spinal tract degeneration were demonstrated at necropsy. Conventional stains for central nervous system (CNS) spirochaetes were negative.

"Case 2--A 42- year- old woman who had been on holiday in northern Wisconsin had arm weakness followed by dysarthria and weakness in all four limbs. There was no history of rash or arthritis. Atrophy and fasiculation were noted on examination. B. burgdorferi antibody titres ranged from 64 to 4096 in this patient. Her CSF was normal. In view of the rise in titre while she was getting progressively worse intravenous ceftriaxone (6) was administered.(6) Her disease seems to have stabilised.

"Case 3-- A 33 -year-old-man had left median prolonged motor and sensory distal latencies in September, 1985. He had previously been on holiday in northern Wisconsin. These findings progressed into hand weakness, generalised muscle fasiculation, and weakness characteristic of ALS. A first test for B burgdorferi was negative but a repeat test revealed a titire of 256.

"Case 4-- A 61-year-old-man from Chicago had developed bilateral arm weakness. There was no history of rash or arthritis. Wasting, fasiculations, and depressed reflexes were present in the arms. The serum anti-B burgdorferi titre was 512. He died of respiratory failure. No necropsy was done.

"The finding of cases of ALS with high titres of B burgdorferi antibodies should be viewed in the context of other CNS diseases as diverse as dementia and multiple sclerosis for which similar antibodies have been reported. This could mean that the cross-reactivity potential of B burgdorferi antigen is high--or that the spirochaete causes a wider diversity of common CNS syndromes than is generally recognised. Since there is no treatment for ALS and there is for chronic Lyme disease clinicians will ask if patients with ALS who have high titre anti- Borrelia antibodies should be treated empirically with ceftriaxone, one of the antibiotics of choice for chronic B. burgdorferi infection. (6, 7) At the least, it seems reasonable to find out if a patient with ALS does have B burgdorferi antibodies.

1. Reik, Steere, Bartenhagen, et al. Neurologic Abnormalities of Lyme disease. Ann Intern Med 1980; 93: 8-16.
2. Pachner, Steere. The triad of neurologic manifestations of Lyme disease. Neurology 1985;35:47-53.
3. Reik, Burgdorfer, Donaldson. Neurologic abnormalities in Lyme disease without erythema chronicum migrans. Am J Med 1986;81:73-77
4. Steere Spirochaetal disease of the CNS. Neurol Clin 1986; 4:207-22
5. Russell H, Sampson, Schmid, Wilkinson, Plikaytes. Enzyme linked immunosolvent assay and indirect immunofluorescent assay for Lyme disease. J Inf Dis 1984;149:465-470.
6. Dattwyler , Halperin, Pah, Luft. Ceftriaxone-effective therapy in refractory Lyme disease. J Inf Dis (in press)
7. Johnson, Codner, russell. In vitro and in vivo susceptibility of Lyme disease sprochetes, Borrelia burgdorferi to 4 antimicrobials. Antimicrob Ag Chemother (in press)

Source:

Subject: Re: Mis DX with MS or ALS????
Date: 15 Feb 1999 20:55:06 GMT
From: [email protected] (JWissmille)
Newsgroups: sci.med.diseases.lyme

sci.med.diseases.lyme: Subject: Re: Mis DX with MS or ALS???? [Lancet, August 8, 1987]

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Other medical or scientific information pertaining to Lyme disease and ALS or MND:

From
Journal of Spirochetal and Tick-borne Diseases

Letters to the Editor

[J Spiro Tick Diseases 2(3):64, 1995.]

Lyme-Related Relapsing Motor Neuron Disease

Gerald J. Ferencz, MD
Community Medical Center
Toms River, NJ 08755

To the Editor:

Motor neuron disease (MND), particularly amyotrophic lateral sclerosis, is generally considered to be a progressive nonremitting disease. Lyme neuroborreliosis is reported to cause various neurologic syndromes affecting both the central and peripheral nervous systems, including a rare association with amyotrophic lateral sclerosis [1]. Relapsing MND is distinctly uncommon.

A 71-year-old woman presented in 1989 with symptoms of Parkinson's disease. She was treated with levodopa and improved. In May 1990, she presented with fulminant weakness, dyspnea, and shaking chills. Testing revealed an erythrocyte sedimentation rate (ESR) of 93 mm/h, negative antinuclear antibody (ANA), normal creatine phosphokinase (CPK), polyclonal increase on immunoelectrophoresis, positive Lyme immunoblot for the 41 and 55 kda bands, and Lyme enzymelinked immunosorbent assay (ELISA) with IgM 1.63 normal (<0.8). Cerebrospinal fluid analysis was normal. Temporal artery biopsy was normal. Nerve conduction studies (NCV) were normal. Electromyography (EMG) revealed diffuse fasciculations, high-amplitude polyphasia, and giant motor unit action potentials with decreased recruitment pattern consistent with MND. Muscle biopsy revealed neurogenic atrophy. The patient was placed on ceftriaxone 2 g intravenously daily for 3 weeks. The patient's strength improved. Repeated EMG in October 190 revealed absent fasciculations, improved insertional activity with continued decreased recruitment pattern. The patient continued to improve, and EMG in August 1990 showed normal motor unit potentials.

In September 1992, the patient presented again with diffuse weakness, hyper-reflexia with extensor plantar responses. Cerebrospinal fluid was normal. Western blot for Lyme disease was negative, and B12, levels were normal. The ESR was elevated. She was placed on ceftriaxone 2 g daily with rapid improvement. On switching to oral antibiotics, she lapsed in November 1992, becoming unable to ambulate across a room. Reinstitution of intravenous ceftriaxone resulted in marked improvement within 1 week.

On examination in June 1993, patient exhibited hyperreflexia, left clonus with extensor plantar response, but well maintained strength. EMG did not reveal any evidence of active denervation, but polyphasia was still present.

This patient exhibited a fluctuating course of relapse and remission of MND over a 3-year period. Repeat neurophysiologic studies appeared consistent with MND rather than a syndrome mimicking it (i.e., polyneuropathy and radiculopathy). Evaluation suggested an initial acute presentation of Lyme neuroborreliosis. The mechanism of repeated improvements or exacerbations in unclear. Previous explanations include an intrinsic beneficial effect of third generation cephalosporins [2].

Further study of Lyme neuroborreliosis as a cause of potentially reversible MND would be beneficial.

References

1.Halperin JJ, Kaplan GP, et al. Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease. Arch. Neurol. 47: 586-594,1990.
2.Smith L. Improvement of patient with amyotrophic lateral sclerosis given ceftriaxone. Lancet 339:1417, 1992.

Letters to the Editor

-----
LATE-STAGE NEUROPSYCHIATRIC LYME BORRELIOSIS
DIFFERENTIAL DIAGNOSIS AND TREATMENT

Psychosomatics 1995;36:295-300.

Brian A. Fallon, Mori Schwartzberg, Robert Bransfield, Barry Zimmerman, Angelo Scotti, Charles, Webber, Michael Liebowitz
.
.
.
Lyme borreliosis is known to have protean manifestations, some of which do not include any of the typical features outlined by the CDC. Some of the presentations are listed in TABLE 1.

TABLE 1
DISORDERS ASSOCIATED WITH NEUROLOGIC LYME BORRELIOSIS

COMMON OR TYPICAL

Aseptic meningitis
Encephalopathy
Meningoencephalomyelitis
Cranial nerve palsies (e.g., Bell's palsy, optic neuritis)
Radiculoneuropathy
Chronic fatigue-like syndrome
Depression
Insomina
Mood lability and behavioral disorders in children

LESS COMMON

Spastic paresis or hemiparesis
Transverse myelitis
Cerebellar syndromes
Extrapyramidal syndromes
Seizure disorders
Dementia
Pseudo-tumor-like syndromes in children
Tulio phenomenon
Cerebrovascular disease
Demylinating-like disorders (e.g., multiple sclerosis-like)
Anterior horn cell-like disease (e.g., ALS-like, diffuse motor neuropathy)
Guillain-Barre-like syndrome
Psychotic or anxiety disorders

Because of lyme borreliosis's ability to mimic other known disease, it has been dubbed the "new great imitator" (11). As was true for syphilis - the former "great imitator" - late-stage Lyme borreliosis psychiatric disorders may appear as the predominant symptom. When Lyme borreliosis is suspected but not proven, either because the clinical profile is not typical or because the diagnostic tests are negative, some physicians opt to use a trial of antibiotics as both a diagnostic and therapeutic tool. If the patient improves, the diagnosis is supported.
.
.
.
See complete article at:
Late - Stage Neuropsychiatric Lyme Borreliosis
or
Late - Stage Neuropsychiatric Lyme Borreliosis

-----
THE NEUROPSYCHIATRIC MANIFESTATION OF LYME BORRELIOSIS

Brian A. Fallon, M.D. (1)
Jennifer A. Nields, M.D.
Joseph J. Burrascano, M.D.(2)
Kenneth Liegner, M.D. (3)
Donato DelBene, B.A. (1)
Michaell R. Liebowitz, M.D. (1)

PSYCHIATRIC QUARTERLY, Vol 63, No. 1 Spring 1992

"Case reports have linked a variety of neurologic syndromes to late Lyme disease, including blindness (21), progressive demyelinating-like syndromes (mimicking Multiple sclerosis) (2) or Amyotrophic lateral sclerosis (22), Guillain-barre (23), progressive dementias (24), seizure disorders (25), strokes (26), and extrapyramidal disorders (27)."

See complete document at:
The Neuropsychiatric Manifestation of Lyme Borreliosis

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Sources: