Dear Chris,
    Please let me know how much value you find in the medical info and possibly
the book referred to in the enclosed attachment.
Yours, David Dunlop and Jason Becker

[ Lyme1.htm 5K ]
 

(2)
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ALS & Lyme
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Subject   : ALS med. journal articles

Date      : Mon, 04 May 1998 22:34:31 -0500
Newsgroups: sci.med.diseases.lyme

Since 1990, as many of you know, I have been accummulating data to implicate
Lyme as the possible underlying etiology of many autoimmune diseases: ALS
being one of them. (see Laura Mermin's book, Lyme Disease, Patient/Physician
Perspectives, 1991).

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 {*filter*} 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?

Kathy Cavert