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Myasthenia gravis after
general anesthesia and hepatitis B vaccine.
Biron P, Montpetit P, Infante-Rivard C, Lery L.
Department of Pharmacology, Faculty of Medicine, University
of Montreal, Quebec, Canada.
Arch Intern Med. 1988 Dec;148(12):2685.
A 48-year-old man presented with the first symptoms of
myasthenia gravis one month after a general anesthesia and
a second dose of hepatitis B plasma vaccine. Whether either
event may have acted as a nonspecific challenge to the
patient's immune system is speculative, but the case is
described to discover similar observations, if any.
Neurological conditions
resulting from prolonged and severe dietary
restriction.
Denny-Brown, D.
Medicine 1947; 26: 41.
No abstract available.
Myasthenia gravis,
manganese and the thymus.
Josephson, E.M.
Presented to Section N, American Association for
Advancement of Science, December 30, 1946. Boston, MA:
Harvard School of Public Health.
Thymus, Manganese, and
Myasthenia Gravis 1961.
Josephson, E.M.
Ferndale, MI: A-albionic Research (www.msen.com or
www.addall.com).
Response of peripheral
and central nerve pathology to mega-doses of the vitamin
B-complex and other metabolites.
Klenner, F.R
J. Appl. Nutr. 1973; 25: 16.
No abstract available.
Effects of thiamine,
ascorbic acid and alpha tocopherol on neuronal and muscular
function
McGraw C.P.; Metcalf D.L. Bowman Gray Sch. Med., Wake
Forest Coll., Winston Salem, N.C. United States
Journal of Applied Nutrition ( J. APPL. NUTR. ) 1975,
27/1 (51-63)
Stimulated by a patient's report that all symptoms of
myasthenia gravis disappeared when she took vitamins in
large doses, the authors review the literature reporting
the relationship between vitamins and neuromuscular
function. Of particular interest was Denny Brown's report
on outbreaks of myasthenia gravis like symptoms in
prisoners of war maintained on low nutritional diets. They
found that three vitamins, thiamine (vitamin B1), ascorbic
acid (vitamin C) and alpha tocopherol (vitamin E), have
been reported to play specific roles in neuronal and
muscular function. Those roles and the possible use of
those vitamins in the treatment of neuromuscular disorders
are the subject of this report. The papers reviewed are
those that they believe to be the most relevant to this
report.
Study of megavitamin
therapy on experimental myasthenia gravis in Guinea pigs by
electromyographic monitoring
McGraw C.P.; Paschold E.H.; Currin J.M. Bowman Gray Sch.
Med., Wake Forest Univ., Winston-Salem, N.C. United
States
Journal of Applied Nutrition ( J. APPL. NUTR. ) (United
States) 1980, 32/1 (37-43)
The underlying defect is myasthenia gravis is not known,
but it is manifested as a premature fatigue of the
neuromuscular junction upon repeated stimulation. It is
generally accepted that the activity at that junctin can be
compromised by an autoimmune reaction, and it is postulated
that the autoantigen of muscle tisse may be released by
some pathological occcurrence such as loss of cell membrane
or chronic autolysis. The resulting autoantibodies may then
attack the neuromuscular junction and cause further damage,
producing a maysthenia-like syndrome. If this is true, then
the goals of therapy should be: restoration of the
integrity of the muscle cell membranes with subsequent
cessation of the release of autoantigen; facilitation of
the neurotransmitter-producing activity of the neuron; and
enhancement of the effectivenss of the neurotransmitter
after its release from the neuron. Classical therapy
acieves only the third goal. Theoretically, on the basis of
their physiological activity, thiamine , ascorbic acid and
alpha-tocopherol given in megadoses should accomplish the
first and second goals as well. In this study, an
immunologically induced myasthenia gravis model was used in
an attempt to prove that point. The immunological method of
Goldstein and Kalden was used in 40 guinea pigs to produce
a partial neuromuscular block. Ten healthy nonimmunized
guinea pigs served as controls. Half of the animals
received megavitamin therapy in whole milk; half received
whole milk only. Megavitamin therapy consisted of massive
doses of thiamine , ascorbic acid, and alpha-tocopherol.
The presence of a neural deficit and the effects of therapy
were determined electromyographically. Although the model
was produced in 73% of animals, we could show no difference
in response of the animals, regardless of therapy. Despite
the fact that we were unable to show a favorable effect of
megavitamin therapy in this myasthenia gravis model, we
believe that the theories that support such an effect are
valid and that further study in this area should be
pursured with a more satisfactory model.
The effect of thiamine,
ascorbic acid and alphatocopherol on experimental
autoimmune myasthenia gravis (EMG) in rats and
rabbits.
Peeler, R.H., McGraw, C.P., Wagoner, R.O.
J. Appl. Nutr. 1979; 31: 34-44.
No abstract available.
Effects of resistance
exercise and creatine supplementation on myasthenia gravis:
a case study.
Stout JR, Eckerson JM, May E, Coulter C,
Bradley-Popovich GE. Exercise Science Department, Creighton
University, Omaha, NE 68178, USA.
jstout@nutriciausa.com
Med Sci Sports Exerc 2001 Jun;33(6):869-72
PURPOSE: The purpose of this case study was to determine
the effects of 15 wk of resistance exercise and creatine
(Cr) supplementation on body composition, training volume,
peak strength, and complete blood chemistry in a patient
with myasthenia gravis (MG).
METHODS: The patient was a 26-yr-old man who was taking
prednisone and azathioprine for his condition. The patient
self-administered 5 g of Cr per day in addition to
resistance exercise 3 times per week. Fasting blood samples
were obtained and body weight (BW) and fat free mass (FFM;
via hydrostatic weighing) were measured before and after
training and Cr supplementation. In addition, isokinetic
(Cybex II) peak strength for leg extension (LE), leg
flexion (LF), and volume load (repetition x mass lifted)
for the first and last resistance training session were
determined.
RESULTS: After Cr supplementation and training, the
results demonstrated increases in BW (6.8%), FFM (4.3%),
upper body volume load (37.0%), lower body volume load
(15.0%), and peak strength for LE (37.0%) and LF (12.5%).
Moreover, blood chemistry values remained within normal
limits for the duration of the 15-wk study.
CONCLUSION: These data suggest that resistance exercise
plus Cr supplementation may promote gains in strength and
FFM in patients with MG.
The preskeletal phase
of chronic fluoride intoxication.
Waldbott, G.L.
Fluoride 1998; 31(1): 13-20.
No abstract available.
Suggested
Reading
Recent studies on
traditional Chinese medicinal plants.
Da-Yuan, Z., Dong-Lu, B., Xi-Can, T.
Drug Dev. Res. 1996; 39(2): 147-57.
No abstract available.
Dietary precursors and
brain neurotransmitter formation.
Fernstrom JD.
Annu Rev Med. 1981;32:413-25.
The rates of synthesis of serotonin, acetylcholine, and,
under certain circumstances, dopamine and norepinephrine by
brain neurons depend considerably on the availability to
brain of the respective dietary precursors. This precursor
dependence seems to be related to the fact that the enzyme
catalyzing the rate-limiting step in the synthetic pathway
for each transmitter is unsaturated with substrate at
normal brain concentrations. Moreover, brain levels of the
individual precursors rise following oral or parenteral
administration of the pure compound or the ingestion of
certain foods. Precursor-induced increases in brain
transmitter formation seem to influence a variety of brain
functions and behaviors, which suggests that transmitter
release has been enhanced. It now appears that these
precursors may become useful as therapeutic agents for the
treatment of selected disease states, wherein the disease
is related to reduced release of transmitter. Examples of
Parkinson's disease (tyrosine), myasthenia gravis (choline
or phosphatidylcholine), depression (tyrosine), and
possibly abnormal appetite (tryptophan). Perhaps the future
will bring the identification of still other
neurotransmitters, whose rates of synthesis depend on
precursor availability. Two potential candidates for which
some information is already available are glycine (a spinal
cord transmitter) and the prostaglandins (some of which may
function as neuromodulators or transmitters) (48, 49). Each
time a new precursor-product relationship is described, an
opportunity becomes available for determining whether the
precursor might be useful in treating disease states
related to reduced transmitter release by neurons. The
opportunities are worth exploring, since the use of a
natural dietary constituent, even in purified form, is
likely to produce fewer unwanted side-effects than are seen
following administration of synthetic drugs.
[Myasthenia and
pernicious anemia or Biermer's (author's transl)]
[Article in French]
Goulon M, Zittoun J, Tulliez M, Estournet B.
Rev Neurol (Paris). 1979 Oct;135(8-9):605-14.
The association of myasthenia and Biermer's anemia is
very rarely reported. In a series of 138 cases of
myasthenia, this association was found in only one patient,
in whom the anemia developed 19 years after the discovery
of a calcified thymoma and 13 years after the appearance of
the first signs of myasthenia. This led the authors to
conduct a prospective study for the presence of intrinsic
antifactor antibodies. A total of 81 patients (20 men and
61 women) with myasthenia were studied. The myasthenia had
appeared after 35 years of age in 40 patients and 19 had a
thymoma. The results of the study for the antibodies was
positive in 3 women, as was the test of inhibition of
leucocyte migration, but none of them had anemia, vitamin
B12 malabsorption, achlorhydria, or gastric atrophy. The
discovery of these immunological disorders raises the
problem of their significance ; two hypotheses can be
discussed : pre-Biermer state or immunological disturbance
without pathogenetic significance. The problem can probably
only be resolved by studying these antibody levels in a
very much larger number of patients with myasthenia.
Neurological
complications of pregnancy and anaesthesia.
Graham, J.G.
Clin. Obstet. Gynaecol. 1982; 9(2): 333-50.
No abstract available.
[Diagnosis and
treatment of eye muscle palsies (author's transl)]
[Article in German]
Huber A.
Klin Monatsbl Augenheilkd. 1978 Feb;172(2):138-40.
After the discussion of the clinical symptomatology of
paralytic squint (diplopia, variable angle of squint,
compensatory head posture etc.) the importance of modern
electromyography for differentiation between myopathy
(affection of the eye muscles), myastherias (affection of
the neuromuscular transmission) and peripheral neurogenic
palsies (affection of the peripheral neuron up to the
nuclear region) is discussed. The clinical symptomatology
of these affections of different levels is discussed as
well as the differential diagnosis. The treatment of eye
muscle palsies in principle consists in: 1. medical
treatment (local and general), 2. optical treatment
(glasses, occlusions, prisms etc.), 3. orthoptic treatment,
4. surgical treatment.
[The role of nutrition
in the synthesis of neurotransmitters and in cerebral
functions: clinical implications] [Article in
French]
Martin-Du Pan RC, Wurtman RJ.
Schweiz Med Wochenschr. 1981 Sep 26;111(39):1422-34.
Much experimental evidence shows that intracerebral
synthesis of various neurotransmitters (serotonin,
acetylcholine, and catecholamines) may be affected by the
amount of their respective precursors (tryptophan, choline
and tyrosine) in food. Changes in cerebral functions
secondary to the administration of each of these three
precursors have been reviewed in physiological and
pathological conditions, and in particular in different
neuro-psychiatric diseases due to a lack of synthesis or
release of neurotransmitters. Possible interactions between
digestive and cerebral diseases are considered in relation
to lack or excess of precursors.
Humoral and cellular
immunity to intrinsic factor in myasthenia
gravis.
Zittoun J, Tulliez M, Estournet B, Goulon M.
Scand J Haematol. 1979 Nov;23(5):442-8.
Myasthenia gravis (MG) is an autoimmune disease often
associated with other autoimmune disorders. A case history
of MG with a coexisting atypical megaloblastic anaemia with
vitamin B12 deficiency and anti Intrinsic Factor (IF)
antibodies, led to a study of humoral and cellular immunity
to IF in 81 MG patients. Within this series, 3 other
patients had a disturbed humoral and cellular immunity to
IF. These 3 patients presented no other features of
pernicious anaemia. The possible origins and significance
of the anti IF antibodies in MG patients are discussed.
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