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Female,
white, 57 years. Seen first time 5/19/72. Chief complaint was fatigue. This started
approximately seven years before coming to our office. The onset
of illness was gradual. Generalized weakness as the day went on,
but was always feeling refreshed in the morning. Drooping of the
eyelids became a problem so that she automatically would tilt her
head backward so that the ptosed eyelids would be partially corrected.
Fatigue of the muscles of mastication on chewing became so embarrassing
that for the past several months, she avoided all social events,
even dinner with friends. Swallowing also became a serious problem
forcing her to a bland and sometimes liquid diet. Even a few minutes
talking, while taking the history, would so fatigue her that she
found it necessary to recline on the examining table so as to regain
her strength. She visited many clinics and medical centers in the
United States and Europe, but always was given the same diagnosis – her
review of conditions labeled her as psychosomatic. To us it was
obvious that she suffered from advanced Myasthenia Gravis. 1000mg.
Thiamin Hydrochloride and 300mg. pyridoxine given by needle had
her demonstrating jaw and face movements to her husband in less
than 10 minutes. She remarked that she had not been able to do
that in three years. She was given our schedule for treatment,
but had great difficulty getting her local physician or any physician
to give her the needed injections. In desperation, she returned
to one of the medical centres and confronted them with the diagnosis,
which they did not believe. She, however, demanded that they employ
their test for this disease, which they did. From the patient’s
description, given at a later visit, I surmised that Tensilon was
used. Her response was the greatest ever seen in that University.
She is also receiving RNA 300mg. tablets three times each week,
which we believe have stimulated or furthered her progress. She
no longer hesitates to eat in public, and her stamina is approaching
normal. During a visit to our office in April of 1973, she laughed
and joked about her experiences in getting the diagnosis confirmed
so that she could receive the vitamin injections under supervision.
She also favored us with a platter of delicious cakes that she
had baked.
Although we could write a book on cases treated and cured (or established a permanent
remission), time is a prohibiting factor.
Conclusion
The treatment of Multiple Sclerosis has been empiric since it was first described
by Sir Robert Carswell in 1838. Brickner, in 1936, gave a review on treatment
which included preparations of Antimony and Arsenic, fever induced by various
methods such as diathermy, malaria, typhoid vaccine, and fever brought on
with the use of drugs. Surgical procedures such as cervical sympathectomy
and root section were also employed. Serums, hypnotism and intraspinal injections
of lecithin had their day. Moore administered nicotinic acid and thiamin
following the dissertation by Zimmerman and Burack on diseases of the nervous
system resulting from a deficiency of the vitamin B-Complex, and the paper
by Spies and others on the use of nicotinic acid in the treatment of Pellagra
associated with mental pathology. Spies and Aring, in 1938, published a paper
on the effects of vitamin B1 on peripheral neuritis as associated with Pellagra.
Moore also had the benefit of the work of Stern, who published an article
on the intraspinal use of vitamin B1 for the relief of intractable pain,
and for inflammatory and degenerative diseases of the Central Nervous System.
We learned early in our approach to this disease that small and infrequent
doses of thiamin hydrochloride would not accomplish our purpose, and we also
realized that more than one unit of the B-Complex would be required, even
though the physiological chemistry relative to this phase of metabolism had
not been completely established. Although Moore used nicotinic acid for vasodilation
purposes, we rationalized that the degenerative process taking place in nerves,
and thus also in muscle, was of a greater magnitude. Inasmuch as the only
sickness remembered by the patient, family or relatives took place during
the summer months, we immediately suspected a virus to be the offending agent.
This idea gained momentum with the greater incidence of Multiple Sclerosis
following the epidemic of encephalitis lethargia of 1920 to 1926, and the epidemic
of encephalitis B in St. Louis and Toledo in 1934. However, the incidence of
Polio was also up. Mixed, abortive or unrecognized cases of Poliomyelitis became
a tantalizing factor. After the isolation of the Coxsackie virus with its mimicking
of Polio, and the knowledge that the paralysis with this type virus infection
was never permanent, the real devastating factor, in time and place, at least
to me, became apparent. Flexner and Lewis were able to demonstrate that in
Polio, vascular and lymphatic lesions constituted the primary causes of the
lesions of the nervous system. Multiple hemorrhagic accidents take place in
Multiple Sclerosis with ensuing scar tissue. As these microscopic scars contract,
they impinge on the vessels carrying nutrients to the Central Nervous System
cells. In muscle, the "devastation" is brought about through lack
of function, there being no "electrical charge" present to keep
muscle active. For this reason, the Sister Kenney treatment for Polio had merit,
since it helps to maintain muscle and muscle-nerve integrity. Our employment
of nicotinic acid is to effect adequate dilatation of existing vascular structures,
producing over time, chemically, what the Urologist accomplished with his catheters
in a mechanical fashion. Once these channels are sufficiently operative, the
metabolic factors that we supply will go about revamping the myelin sheaths.
Due to lack of full energy components, cells can temporarily lose the ability
of normal physiological activity. We can restore the normal function of cells
which depends upon their ability to extract and use the chemical potential
energy locked within the structure of organic molecules. We accomplish this
by placing massive amounts of the essential material at the disposal of cells.
We categorically make this statement: Any victim of Multiple Sclerosis who
will dramatically flush with the use of nicotinic acid, and who has not yet
progressed to the stage of myelin degeneration, as witnessed by sustained ankle
clonus elicited in the orthodox manner, can be cured with the adequate employment
of Thiamin Hydrochloride and other factors of the Vitamin B Complex in conjunction
with essential proteins, lipids, carbohydrates and injectable crude liver.
If sustained ankle clonus is not bilateral, then it is not a deterrent. We
have had patients who did demonstrate bilateral sustained ankle clonus, and
who were in wheelchairs, and who returned to normal activities after 5 to 8
years of treatment. These patients, fortunately, had not received ACTH. One
patient was given a single course of Medrol 4 mg. QID. This had little effect
on her pathology, and apparently no blocking action, on our treatment. The
general use of ACTH in Multiple Sclerosis will extend the recovery period by
a time directly proportional to the amount of the drug employed. It is hoped
that this paper will bring an end to this senseless practice of medicine, since
ACTH never works the third time.
The theories recognized as playing a part in Myasthenia Gravis still rest in
the main with Thymus enlargement or tumor, Endocrine dysfunction, Metabolic
fault, and the build-up of pyruvic acid in the vicinity of the motor end-plates.
In reality, it is a genetic fault involving a lethal intermediate gene or group
of genes. There is definitely an over-supply of pyruvates, and an under-supply
of acetylcholine. The cue in this drama is cocarboxylase. Coenzyme A is also
in limited supply. Two molecules of thiamin hydrochloride, and two molecules
of phosphoric acid yields cocarboxylase. One way of obtaining acetyl coenzyme
A, a by-product of coenzyme A and pyruvic acid, is in the reaction between
pyruvic acid, coenzyme A and diphosphopyridine nucleotide in the presence of
diphosphothiamine (cocarboxylase). Cocarboxylase is also involved in the synthesis
of acetylcholine and in the control of its hydrolysis. The activity of choline
esterase of serum is strongly inhibited by this same agent. Thiamin occupies
a key position in at least the terminal stages of carbohydrate metabolism.
Cocarboxylase plays an active role in the decarboxylation of pyruvic and other
keto acids. In the brain, cocarboxylase participates in the anaerobic dismutation
of pyruvates to lactate and acetate, and their subsequent oxidation to carbon
dioxide and water. In liver and other tissue cells, cocarboxylase is involved
in the conversion of pyruvates to oxalacetate which combines oxidatively and
irreversibly with another molecule of pyruvate to enter the tricarboxylic acid
cycle. In thiamin deficiency, a form of peripheral neuritis markedly demonstrated
in some cases of chronic alcoholism exists, affecting both sensory and motor
nerves.
The treatment of Myasthenia Gravis is that of any pathology dealing with the
interruption of the normal physiology of nerve cells. In years past, when we
were treating Poliomyelitis successfully with massive doses of ascorbic acid,
we would always follow with an indefinite timetable, giving the B vitamins
for nerve repair. We see the same results when treating damage to the spinal
cord, whether this is due to mechanical trauma, or to the inflammation caused
by a virus – any virus. As pointed out by Lipschitz et al., the replenishing
of vitamin B1 restores the ability of the nervous system to handle properly
pyruvic acid and dextrose. This action of thiamin makes its function in Myasthenia
Gravis seem elementary. A German scientist once speculated that cocarboxylase
was actually the "food" required for nerve life. In treating Myasthenia
Gravis with the schedule outlined, the intensity with which it is applied in
Multiple Sclerosis will never be necessary. We are not confronted with the
loss of myelin sheaths in extra vital areas. The chemistry, however, is more
complex than in Multiple Sclerosis, since it involves muscle cells to a greater
degree. Enzymes and their balance is a necessary approach. When we realize
that over 900 different enzymes have been identified, it makes more knowledgeable
the need for extensive vitamin therapy. This suggests that normal liver function
is necessary for good results. A simple liver function test can be used to
good advantage. One that I worked out many years ago to demonstrate "liver
stress" is performed as follows. Have patient bring 90cc from first voiding
upon arising. Fill ordinary test tube to within one cm. of top. Allow to set
for 24 hours and read. One will find, in most specimens, a gelatinous fluid
resting at the bottom of the test tube. The amount present, which can measure
2-1/2 cm., indicates the degree of liver stress present. Choline by needle
or by mouth will remove this finding from the urine. Some urine specimens will
show a heavy, white sediment obstructing proper reading of liver stress. Glacial
Acetic Acid alone, and/or heat will temporarily remove these phosphates. Should
the deposit of phosphate be exceedingly heavy, then it is advisable to secure
a bedtime specimen, or one 2 hours after breakfast. The night specimen should
be placed in a cool area until delivery. Occasionally, the urine specimen will
look like skim milk. This is due to earthy phosphates and can be cleared by
adding Glacial Acetic Acid to the tube. (After ascertaining liver stress, one
can then add 20 drops Glacial Acetic Acid to the specimen – if none was
previously added – and allow to remain an additional 48 hours to check
for Uric Acid Crystals. A red shower indicating an abnormal level for uric
acid.) This test must be run every week when administering ribonucleic acid
(RNA).
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