In article <[log in to unmask]>, dated Wed, 21 Apr
1999 at 10:06:56, Harries <[log in to unmask]> writes
>Allan,
>i don't know about your case, but try and contact dr. karen e. pape at the
>magee clinic, suite 505,5160 young st. north york, ontario, m2n 6l9 canada.
>she is using the t.e.s (therapeutic electrical stimulation) method for c.p,
>polio, spina bifida etc. last paper i found in the jornal of developmental
>medicine and child neurology 1997, 39:515-520.
>hope it helps,
>netta harries
First, regarding the Magee clinic, I received the following (unconfirmed and
unsolicited) information on 9th July 1998 from P. Bonish of Mayatek Inc.:
"I would like to inform you that The Magee Clinics has been closed since March
of 1996. TES is now available through a network of trained Practitioners and
would like to encourage you to visit our website www.mayatek.com for updated
information."
Secondly, I would advise caution regarding use of TES in patients with a history
of polio. Dr. Richard Louis Bruno PhD of the Post-Polio Institute at New
Jersey's Englewood Hospital and Medical Center reported the following in an
article entitled "Post-Polio Research: The State of the Art, 1998" published in
New Mobility Magazine, April 1998.
"The most important and sobering finding of 1997 was a study by A.J. McComas of
Canada's McMaster University. McComas and his group tested the most widely
accepted hypothesis for late-onset muscle weakness in polio survivors: that
motor neurons are breaking down and sometimes dying as a result of the initial
poliovirus damage and decades of overuse abuse.
McComas actually performed two studies. First, using a technique he developed
and has used for 25 years, he counted the number of motor neurons in polio
survivors. Muscles known to have been affected by the original polio were found
to have lost 59 percent of their motor neurons. Sixty-five percent of muscles
thought not to have been affected had lost 40 percent of their motor neurons.
These percentages mirror precisely the findings of pathologist David Bodian, who
50 years ago showed that at least 60 percent of motor neurons had to be killed
by the poliovirus for a muscle to show any weakness, and argued that there was
no such thing as an "unaffected muscle" in someone who had had paralytic polio.
McComas' second study was equally revealing but more disturbing. He counted
motor neurons in 18 subjects, then followed them for two years. At follow-up, 78
percent of the subjects reported a decrease in muscle strength and had lost an
average of 13.5 percent of their motor neurons, approximately twice the rate of
loss expected in healthy subjects. Most alarming was the finding that the two
survivors who reported the greatest decrease in strength had each lost 50
percent of their motor neurons during the two years. While these findings are
frightening, they are also a guide to a rational treatment for PPS. "Our
findings make clear that polio survivors should not be treated using electrical
stimulation that causes muscle contraction, warns McComas, "nor should they
engage in fatiguing exercise or activities that further stress metabolically
damaged neurons that are already overworking.""
End Quote
The article Dr. Bruno referred to is
Brain 1997 Aug;120 ( Pt 8):1415-21
Early and late losses of motor units after poliomyelitis.
McComas AJ, Quartly C, Griggs RC
Department of Medicine, McMaster University, Hamilton, Canada.
Abstract:Motor unit number estimation was employed to assess muscle innervation
in 76 patients with prior poliomyelitis. Of the 68 patients who were < 70 years
of age, new musculoskeletal symptoms had appeared in all but four; the mean
latent interval was 38.0 +/- 10.1 years. As expected, there was a high incidence
of muscles exhibiting denervation in previously affected limbs (87%). However,
the incidence in supposedly unaffected limbs was also high (65%). Significant
differences in the degree of denervation were found between muscles of the same
hands and feet. Judged on the basis of their potential amplitudes, the surviving
motor units in partially denervated muscles tended to be enlarged. The
enlargement was proportional to the extent of the denervation and was comparable
to that found in amyotrophic lateral sclerosis. In some muscles, possibly those
innervated by failing motor neurons, motor-unit enlargement was not present.
Needle examination confirmed the high incidences of denervation in affected and
allegedly unaffected limbs. Of the 188 muscles with EMG features of chronic
denervation, only nine exhibited fibrillations or positive sharp waves (4.8%).
Ninety-five muscles of 18 patients were studied a second time after an interval
of 2 years. Overall, there was a 13.4% reduction in motor-unit number and a
18.4% diminution in M-wave amplitude (P < 0.001). The rate of motor-unit loss
was twice that occurring in healthy subjects aged > 60 years. Analysis of
individual patients indicated that some were deteriorating more rapidly than
others. These studies confirm that denervation progresses in patients with prior
poliomyelitis in both clinically affected and unaffected muscles, and indicate
that this progression is more rapid than that occurring in normal ageing.
PMID: 9278631, UI: 97424518
Finally, it is important to emphasise that the denervation considerations also
apply to so-called "non-paralytic" polio.
>From "NON-PARALYTIC POLIO AND PPS"
Marcia Falconer, Ph.D. cell biology and Eddie Bollenbach, M.A. biology
A Lincolnshire Post-Polio Library Publication - January 1999
http://www.zynet.co.uk/ott/polio/lincolnshire/library/falconer/nonparalytic.html
"In acute polio, the degree of nerve involvement varies within the entire
nervous system. Some areas appear clinically unaffected while, in paralytic
polio cases, other regions show flaccid paralysis. In abortive polio the nervous
system appears undamaged at the symptomatic level. However the symptoms listed
for non-paralytic polio are suggestive of neurological involvement. For nerve
damage to be visible as weakness or paralysis a threshold of damage to the
neuron population must be involved (Sharrard, 1955). When few neurons are
damaged or destroyed, the patient presents with no specific muscle weakness or
paralysis but can have undetected neuronal damage (Dalakas (a), 1995). We do not
know how this will manifest in later life. There were undoubtedly mistakes in
diagnosis and misdiagnosis for many patients. Many people with non-paralytic
polio probably were paralytic cases with diffuse weakness that recovered quickly
(Dalakas (b), 1995)."
--
Chris Salter (Vice Chairman) Lincolnshire Post-Polio Network
Registered Charity No. 1064177
<URL:http://www.zynet.co.uk/ott/polio/lincolnshire/>
Web Site & Vice Chairman Email: [log in to unmask]
Honorary Secretary Email: [log in to unmask]
Member of the British Healthcare Internet Association
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
|