Download Word Count: 783 In 1890, German medical professor Wilhelm Erb

Word Count: 783
In 1890, German medical professor Wilhelm Erb and other physicians had been
observing several cases of a neuromuscular disease that they believed was affecting how
nerve impulses were transmitted to muscle at the neuromuscular junction. The patient’s
experienced a "grave muscular weakness" and Wilhelm named it
myasthenia gravis. Through further research, the physicians discovered whether it
affected the eye muscles first, or created difficulty in talking, chewing and swallowing, or
in using the arms and legs it was neither hereditary nor contagious. Their discoveries
lead to more detailed research.
In the early 1970s when Muscular Dystrophy Association, using snake venom,
observed that patients with the disease had decreased numbers of acetylcholine receptors.
Thus, discovering that the disease affected acetylcholine receptors of the skeletal
muscles. The Muscular Dystrophy Association also found that, in rabbits, an immune
attack against the acetylcholine receptors resulted in muscle membrane damage that is
similar to that seen in human myasthenia gravis. This rabbit experiment was responsible
for a large portion of what scientists now know about myasthenia gravis.
Myasthenia gravis causes a progressive and abnormally rapid fatigue of the voluntary
muscles. It is known as an autoimmune disease, in which the body generates an immune
system attack against its own skeletal muscles. This arises when lymphocytes in the
blood produce antibodies that destroy muscle-cell receptors for acetylcholine molecules,
preventing muscle contractions. The antibodies have been shown to decrease the
usefulness of acetylcholine receptors through accelerated endocytosis and blockade of the
receptor. Endocytosis is when extracellular substances are being incorporated into the
cell by vesicles forming inward through budding of the plasma membrane. Researchers
have been able to demonstrate the effect of antibodies on acetylcholine receptor by using
radioactively labeled alpha bungaroo toxin, a snake poison, to follow the rate of
degradation. Antibodies from patients with myasthenia gravis cause an increase in the
rate of degradation of acetylcholine receptors. Blockade of acetylcholine receptors is
another form of autoimmune attack from myasthenia gravis. Antibodies from these
patients have been shown to block the acetylcholine binding sites preventing
acetylcholine from binding to its receptor and opening the ion channel. The antibodies
may bind near the acetylcholine binding site rather than directly on it, because the
acetylcholine binding site is so small. In this case, the antibodies would prevent
acetylcholine from binding at the receptor by interfering with the acetylcholine molecule
as it moves towards its receptor.
Symptoms for some one with myasthenia gravis include a flattened smile and
droopy eyes, with slow pupillary light responses. The person with myasthenia gravis,
myasthenic patient, may have fixed column deformity or irregular posture after standing
for a short time period. Nasal speech, difficulty chewing and swallowing, dulled facial
expression, including difficulty smiling and an ineffective cough due to weak expiratory
muscles, are all also frequently associated with myasthenia gravis. The degree of muscle
weakness involved in myasthenia gravis varies greatly among patients. However, the
myasthenic patient has no loss of reflexes or alteration of sensation or coordination and
generally doesn’t complain about feelings of fatigue. Instead, they experience localized
fatigue in specific, repeatedly used muscle groups.
Who gets myasthenia gravis? Myasthenia gravis occurs in all ethnic groups and both
genders. It most commonly affects young adult women, under 40, and older men, over
60, but it can occur at any age. Studies showed that women were often affected more than
men were. Now, males are more often affected than females, and the onset of symptoms
is usually after age 50. In birth development stages, the fetus may acquire antibodies
from a mother affected with myasthenia gravis. Generally, cases of neonatal myasthenia
gravis are temporary and the child’s symptoms usually disappear within a few weeks
after birth. Other children develop myasthenia gravis indistinguishable from that seen in
adults. Myasthenia gravis in juveniles is common. As Professor Wilhelm Erb discovered
myasthenia gravis is not directly inherited nor is it contagious. Occasionally, the disease
may occur in more than one member of the same family. Children rarely develop
myasthenia gravis; instead, they may show signs of congenital myasthenia or congenital
myasthenic syndrome. These are not autoimmune disorders, but are caused by defective
genes that control proteins in the acetylcholine receptor or in acetylcholineterase.
More and more research is conducted everyday in search of a cure for myasthenia gravis.
One main contributor to the awareness of this disease is the Myasthenia Gravis
Foundation of America. It is a national volunteer health agency dedicated solely to the
fight against myasthenia gravis. As technology increases, hopefully some one will find a
cure.
Keywords:
word count german medical professor wilhelm other physicians been observing several
cases neuromuscular disease that they believed affecting nerve impulses were transmitted
muscle neuromuscular junction patient experienced quot grave muscular weakness quot
wilhelm named myasthenia gravis through further research physicians discovered
whether affected muscles first created difficulty talking chewing swallowing using arms
legs neither hereditary contagious their discoveries lead more detailed research early
when muscular dystrophy association using snake venom observed that patients with
disease decreased numbers acetylcholine receptors thus discovering that disease affected
acetylcholine receptors skeletal muscles muscular dystrophy association also found
rabbits immune attack against acetylcholine receptors resulted muscle membrane damage
similar seen human myasthenia gravis this rabbit experiment responsible large portion
what scientists know about myasthenia gravis causes progressive abnormally rapid
fatigue voluntary muscles known autoimmune which body generates immune system
attack against skeletal this arises when lymphocytes blood produce antibodies destroy
muscle cell molecules preventing contractions antibodies have been shown decrease
usefulness through accelerated endocytosis blockade receptor endocytosis when
extracellular substances being incorporated into cell vesicles forming inward through
budding plasma membrane researchers have been able demonstrate effect antibodies
receptor using radioactively labeled alpha bungaroo toxin snake poison follow rate
degradation from patients with cause increase rate degradation blockade another form
autoimmune attack from from these patients have shown block binding sites preventing
binding receptor opening channel bind near binding site rather than directly because site
small this case would prevent interfering with molecule moves towards symptoms some
include flattened smile droopy eyes slow pupillary light responses person myasthenic
patient fixed column deformity irregular posture after standing short time period nasal
speech difficulty chewing swallowing dulled facial expression including difficulty
smiling ineffective cough weak expiratory also frequently associated degree weakness
involved varies greatly among however myasthenic patient loss reflexes alteration
sensation coordination generally doesn complain about feelings fatigue instead they
experience localized fatigue specific repeatedly used groups gets occurs ethnic groups
both genders most commonly affects young adult women under older over occur studies
showed women were often affected more than were males more often than females onset
symptoms usually after birth development stages fetus acquire mother generally cases
neonatal temporary child symptoms usually disappear within weeks after birth other
children develop indistinguishable seen adults juveniles common professor wilhelm
discovered directly inherited contagious occasionally occur member same family children
rarely develop instead they show signs congenital congenital myasthenic syndrome these
autoimmune disorders caused defective genes control proteins acetylcholineterase
research conducted everyday search cure main contributor awareness foundation america
national volunteer health agency dedicated solely fight against technology increases
hopefully some will find cure
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