Page 1, 2, 3, 4,
5, 6, 7,
Next
Etiology of Multiple Sclerosis – Historical
As for the etiology of Multiple Sclerosis, a good history will tell the story.
I have one patient who was diagnosed with Polio in 1950. He experienced total
paralysis, but made a complete recovery. Five years ago, he began to demonstrate
the signs and symptoms of Multiple Sclerosis. He was given a "strong" course
of ACTH with relief of symptoms. Three months later, this had to be repeated,
but the results were not as good. Some three months later, a third series
of injections of ACTH was worthless. (This has been the pattern with the
use of ACTH, and represents nothing more than whipping a tired horse. In
my book, it borders on malpractice.) His myelin sheath has just about been
destroyed. He has so many areas of "no insulation" that his movements
are like that of a newborn baby. Had he received our treatment at the onset
of his illness, he would be in good health today without any physical handicap.
This individual never had Poliomyelitis. The virus that brought him down
was the coxsackie virus, and this explains his initial recovery. Another
case seen was a 31 year-old female. This young lady was diagnosed Poliomyelitis
when she was 19 years of age. Three years ago, she began developing signs
and symptoms of Multiple Sclerosis, and that is her present diagnosis. Her
neurologist, who made the diagnosis of Polio, now tells her that there is
no doubt in his mind that what she has now, actually started when she was
19. He is absolutely correct, because she had a coxsackie virus infection.
In 80% of the cases that have come under my supervision, an illness compatible
with a Summer virus has been entertained. Unless an illness is associated
with paralysis, it is understandable when a patient or the family have difficulty
in establishing a workable timetable.
Other Hypotheses on Etiology of Multiple Sclerosis
Dr. Henry Kempe, from the University of Colorado School of Medicine, as reported
by Medical World News, believes that
Multiple Sclerosis is caused by vaccinia virus. He found a correlation between
severity of the clinical disease and
antibody titer. He also observed that only in demyelinating disease were antibodies
to vaccinia virus in the cerebral spinal fluid. This brings to mind the work
of Horsefall and his co-workers at the Rockefeller Institute. They were able
to culture an organism, which they designated Streptococcus MG, from a large
percentage of their patients with primary atypical pneumonia. This proved later
to have no value, and the viral nature of the disease was recognized.
The sleeping virus theory of Dr. Milton Alter and others, as reported in Medical
Tribune, along with the environmental aspect
for Multiple Sclerosis is another "ripe apple" for public consumption and public
press exaggeration. Most of
this theory rests with the circumstantial evidence that filterable transmissible
agents having slow virus properties are present in other diseases.
Another theory, that of Dr. D.K. Schandl, a Nova University biochemist, in
Fort Lauderdale, Florida, and published in The Charlotte Observer,
relates it to an environmental agent, specifically carbon monoxide, and the
lack of
the vitamin pyridoxine (vitamin B6). Pyridoxine is concerned with the enzymatic
decarboxylation of amino acids and the incidence of Multiple Sclerosis is too
low in terms of the availability of carbon monoxide.
Still another theory has been advanced by Doris Dahl and Amico Bignami of Stanford
University, Palo Alto, California. They report the discovery of a substance
that "may" prevent the self-renewing of myelin. Scar tissue is
indeed the problem, but it is the end result of microscopic hemorrhages following
virus invasion.
Concepts Concerning Myasthenia Gravis
In Myasthenia Gravis, the accepted reasoning is initiated by Thymomas in 20%
of patients over forty, and hyperplasia of the thymus in others. Antibodies
to muscle have been reported in roughly 33%. Excessive pyruvates at the neuro-muscular
junction has been recognized but not appreciated.
Case Histories
Multiple Sclerosis: Male,
white, was in a wheelchair at a Veterans' Hospital for two years.
Patient seen while home
on 30-day vacation. Treatment given
every day with marked improvement. Upon returning to Veterans' Hospital,
the physician in charge recognized the improvement and advised the young
man to return home and continue the treatment. After three years,
he was given
a clean bill of health by three neurologists in three different places and
was given a responsible position. This was in 1950. The individual remains
in excellent health, but continues with modified therapy.
Myasthenia Gravis: Male, white, receiving treatment from nearby medical centre
for one year. He was receiving guanadine (amount unknown) and 90 mg. prostigmine
bromide each day. He was first seen in a Myasthenia Gravis crisis. The emergency
treatment consisted of two ampules of prostigmine methylsulfate of a strength
of 1:2000, and 5cc of coramine. Within a period of eight or ten minutes, the
patient experienced a generalized convulsive seizure which lasted some five
minutes and required 4 men to hold him on the bed. Prostigmine, by needle,
was continued for three weeks, and then 15mg. tablets every six hours. Thiamin
hydrochloride was given three times each day, intramuscularly, as well as other
fractions of the B complex. In one year's time, he had been "weaned
off" prostigmine. Although given only two weeks to live by the physicians
at the medical centre the day prior to our first visit, this individual lived
a normal life for 18 years. His death was due to a cerebral accident.
Female, white, with diagnosis (August 1967), Polyneuritis. Began with pain
and burning of legs associated with jerking. Ran high fever 10 days. Paralysis
started on left side along with weakness of hands, soon followed with complete
paralysis lower extremities. Seen first time 7/5/69. Paralysis and weakness
as described. Started on medication by mouth and intramuscular injections.
Several months later, began intravenous schedule. In approximately 16 months,
was able to move right leg. Upper extremities returned to normal. On 6/10/72,
began to move left foot. Patient now able to walk approximately 50 yards with
knee braces and walker. Does all the cooking for family of four, as well as
sewing clothes for herself and two daughters. (I can personally vouch for her
ability as a cook.) April 1973, she was able to go without a back brace that
was previously necessary for her to use to even get out of bed. One marvels
at her ability to pedal a stationary bicycle "contraption" made
for her by her husband so that she might exercise her legs. Our diagnosis in
this case is Transverse Myelitis. (200 grams ascorbic acid given IV, in divided
doses, would have saved this patient from paralysis.) She has also received
300mg ribonucleic acid four times each week.
Female, white, who developed weakness in extremities
around June 25, 1961. Sensory examination revealed hypalgesia over medial aspect of right foot and
calf. Motor examination revealed a partial foot drop on the right, with rather
marked weakness and inversion, eversion, and dorsiflexion of right foot. Reflexes
upper extremities 3-4 plus. Abdominal reflexes absent. Knee jerks were 3-4
plus with patellar clonus. Right ankle jerk was 4 plus and the left, 3 plus.
Bilateral, sustained, ankle clonus. Babinski's "brisk."
Later examined and hospitalized at a nearby medical centre where Medrol was
tried. She was sent home with a diagnosis of Multiple Sclerosis, superimposed
by a viral meningoencephalitis. Blurring of vision was established as due to
a left six-nerve paralysis. Seen in our office one month later, we concurred
with the impression of Multiple Sclerosis. Our treatment schedule became operative.
It has been a long journey since June 1961, but the results have been phenomenal.
This individual has been returned to full activities, and as a gesture of gratitude,
comes to my office to serve in the capacity of an office assistant several
days each week. She does, however, still maintain her treatment schedule. Whether
this is necessary or not, I follow the advice of another patient who has been
continuing modified treatment for 22 years: "Why stop when you feel so
good?"
Male, white, 28 years. Seen first time 2/26/72. History of numbness in lower
extremities with loss of muscle control from waist down. This started approximately
2 years before this visit. Difficulty with bladder control at times. Seen by
several neurologists at a nearby medical centre who failed to make a diagnosis
other than to say he had a Central Nervous System Pathology. Babinski's,
Gordon and Oppenheim signs were all positive, and ankle jerks were 4 plus.
Ankle clonus was bilateral and sustained on right. He demonstrated a right
foot drop. We entertained a diagnosis of Multiple Sclerosis. Treatment was
not started since he had an appointment to be examined at a nearby Veterans' Hospital
clinic. We advised him not to accept ACTH therapy. The following week we did
start treatment. After 5 weeks, we did not see the patient again for three
weeks, at which time he confessed that he thought that he was well and had
stopped treatment. The weakness and other symptoms were again returning. He
has been back to gainful employment for the past 12 months. Incidentally, he
has been a "crack" pistol shooter, and he still can hold a steady
hand on the gun.
|
