| Myasthenia Gravis and Disability Benefits |
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If you suffer from disabling Myasthenia Gravis (MG) and can no longer
work a full time work week, I would be happy to help you obtain your rightful
Disability Benefits. You may be eligible for Social Security Disability benefits,
even if you will eventually recover.
Start by filling out the FREE online Social Security Disability Claim Evaluation
Form (see Tab, on Left Hand Navigation), calling me at 201-317-0610 or
emailing SsiHelp@ptd.net or sojlaw@ptd.net.
work a full time work week, I would be happy to help you obtain your rightful
Disability Benefits. You may be eligible for Social Security Disability benefits,
even if you will eventually recover.
Start by filling out the FREE online Social Security Disability Claim Evaluation
Form (see Tab, on Left Hand Navigation), calling me at 201-317-0610 or
emailing SsiHelp@ptd.net or sojlaw@ptd.net.
Myasthenia Gravis is a disease characterized by varying degrees of
weakness of the skeletal (voluntary) muscles of the body. The name
myasthenia gravis, which is Latin and Greek in origin, literally means "grave
muscle weakness." With current therapies, however, most cases of majority of
individuals with myasthenia gravis, life expectancy is not lessened by the
disorder. However, if can be disabling, I know. If you find yourself in that
situation, you can see if you may be eligible for disability benefits, at no
charge. You may fill out the MG Disability Benefits Evaluation now by clicking
here.
The hallmark of myasthenia gravis is muscle weakness that increases during
periods of activity and improves after periods of rest. Certain muscles such as
those that control eye and eyelid movement, facial expression, chewing,
talking, and swallowing are often, but not always, involved in the disorder. The
muscles that control breathing and neck and limb movements may also be
affected.
What causes myasthenia gravis?
Myasthenia gravis is caused by a defect in the transmission of nerve impulses
to muscles. It occurs when normal communication between the nerve and
muscle is interrupted at the neuromuscular junction - the place where nerve
cells connect with the muscles they control. Normally when impulses travel
down the nerve, the nerve endings release a neurotransmitter substance
called acetylcholine. Acetylcholine travels through the neuromuscular junction
and binds to acetylcholine receptors which are activated and generate a
muscle contraction. In myasthenia gravis, antibodies block, alter, or destroy
the receptors for acetylcholine at the neuromuscular junction which prevents
the muscle contraction from occurring. These antibodies are produced by the
body's own immune system. Thus, myasthenia gravis is an autoimmune
disease because the immune system - which normally protects the body from
foreign organisms - mistakenly attacks itself.
What is the role of the thymus gland in myasthenia gravis?
The thymus gland, which lies in the upper chest area beneath the breastbone,
plays an important role in the development of the immune system in early life.
Its cells form a part of the body's normal immune system. The gland is
somewhat large in infants, grows gradually until puberty, and then gets
smaller and is replaced by fat with age. In adults with myasthenia gravis, the
thymus gland is abnormal. It contains certain clusters of immune cells
indicative of lymphoid hyperplasia - a condition usually found only in the
spleen individuals with myasthenia gravis develop thymomas or tumors of the
thymus gland. Generally thymomas are benign, but they can become
malignant. The relationship between the thymus gland and myasthenia gravis
is not yet fully understood. Scientists believe the thymus gland may give
incorrect instructions to developing immune cells, ultimately resulting in
autoimmunity and the production of the acetylcholine receptor antibodies,
thereby setting the stage for the attack on neuromuscular transmission.
What are the symptoms of myasthenia gravis?
Although myasthenia gravis may affect any voluntary muscle, muscles that
control eye and eyelid movement, facial expression, and swallowing are most
frequently affected. The onset of the disorder may be sudden. Symptoms
often are not immediately recognized as myasthenia gravis. In most cases, the
first noticeable symptom is weakness of the eye muscles. In others, difficulty in
swallowing and slurred speech may be the first signs. The degree of muscle
weakness involved in myasthenia gravis varies greatly among patients,
ranging from a localized form, limited to eye muscles (ocular myasthenia), to a
severe or generalized form in which many muscles - sometimes including
those that control breathing - are affected. Symptoms, which vary in type and
severity, may include a drooping of one or both eyelids (ptosis), blurred or
double vision (diplopia) due to weakness of the muscles that control eye
movements, unstable or waddling gait, weakness in arms, hands, fingers,
legs, and neck, a change in facial expression, difficulty in swallowing and
shortness of breath, and impaired speech (dysarthria).
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. In neonatal myasthenia, the fetus may acquire
immune proteins (antibodies) from a mother affected with myasthenia gravis.
Generally, cases of neonatal myasthenia gravis are transient (temporary) and
the child's symptoms usually disappear within 2-3 months after birth. Other
children develop myasthenia gravis indistinguishable from adults. Myasthenia
gravis in juveniles is common. Myasthenia gravis is not directly inherited nor is
it contagious. Occasionally, the disease may occur in more than one member
of the same family. Rarely, children may show signs of congenital myasthenia
or congenital myasthenic syndrome. These are not autoimmune disorders, but
are caused by defective genes that produce proteins in the acetylcholine
receptor or in acetylcholinesterase.
How is myasthenia gravis diagnosed?
Unfortunately, a delay in diagnosis of one or two years is not unusual in cases
of myasthenia gravis. Because weakness is a common symptom of many
other disorders, the diagnosis is often missed in people who experience mild
weakness or in those individuals whose weakness is restricted to only a few
muscles. The first steps of diagnosing myasthenia gravis include a review of
the individual's medical history, and physical and neurological examinations.
The signs a physician must look for are impairment of eye movements or
muscle weakness without any changes in the individual's ability to feel things.
If the doctor suspects myasthenia gravis, several tests are available to confirm
the diagnosis. A special blood test can detect the presence of immune
molecules or acetylcholine receptor antibodies. Most patients with myasthenia
gravis have abnormally elevated levels of these antibodies. However,
antibodies may not be detected in patients with only ocular forms of the
disease. Another test is called the edrophonium test. This approach requires
the intravenous administration of edrophonium chloride or Tensilon(r), a drug
that blocks the degradation (breakdown) of acetylcholine and temporarily
increases the levels of acetylcholine at the neuromuscular junction. In people
with myasthenia gravis involving the eye muscles, edrophonium chloride will
briefly relieve weakness. Other methods to confirm the diagnosis include a
version of nerve conduction study which tests for specific muscle "fatigue" by
repetitive nerve stimulation. This test records weakening muscle responses
when the nerves are repetitively stimulated. Repetitive stimulation of a nerve
during a nerve conduction study may demonstrate decrements of the muscle
action potential due to impaired nerve-to-muscle transmission. A different test
called single fiber electromyography (EMG), in which single muscle fibers are
stimulated by electrical impulses, can also detect impaired nerve-to-muscle
transmission. EMG measures the electrical potential of muscle cells. Muscle
fibers in myasthenia gravis, as well as other neuromuscular disorders, do not
respond as well to repeated electrical stimulation compared to muscles from
normal individuals. Computed tomography (CT) may be used to identify an
abnormal thymus gland or the presence of a thymoma. A special examination
called pulmonary function testing - which measures breathing strength - helps
to predict whether respiration may fail and lead to a myasthenic crisis.
How is myasthenia gravis treated?
Today, myasthenia gravis can often be controlled. There are several
therapies available to help reduce and improve muscle weakness.
Medications used to treat the disorder include anticholinesterase agents such
as neostigmine and pyridostigmine, which help improve neuromuscular
transmission and increase muscle strength. Immunosuppressive drugs such
as prednisone, cyclosporine, and azathioprine may also be used. These
medications improve muscle strength by suppressing the production of
abnormal antibodies. They must be used with careful medical followup
because they may cause major side effects.
Thymectomy, the surgical removal of the thymus gland (which often is
abnormal in myasthenia gravis patients), reduces symptoms in more than 70
percent of patients without thymoma and may cure some individuals, possibly
by re-balancing the immune system.
Other therapies used to treat myasthenia gravis include plasmapheresis, a
procedure in which abnormal antibodies are removed from the blood, and
high-dose intravenous immune globulin, which temporarily modifies the
immune system and provides the body with normal antibodies from donated
blood.
These therapies may be used to help individuals during especially difficult
periods of weakness. A neurologist will determine which treatment option is
best for each individual depending on the severity of the weakness, which
muscles are affected, and the individual's age and other associated medical
problems.
What are myasthenic crises?
A myasthenic crisis occurs when the muscles that control breathing weaken to
the point that ventilation is inadequate, creating a medical emergency and
requiring a respirator for assisted ventilation. In patients whose respiratory
muscles are weak, crises - which generally call for immediate medical attention
- may be triggered by infection, fever, or an adverse reaction to medication.
What is the prognosis?
With treatment, the outlook for most patients with myasthenia gravis is bright:
they will have significant improvement of their muscle weakness and they can
expect to lead normal or nearly normal lives. Some cases of myasthenia
gravis may go into remission temporarily and muscle weakness may disappear
completely so that medications can be discontinued. Stable, long-lasting
complete remissions are the goal of thymectomy. In a few cases, the severe
weakness of myasthenia gravis may cause a crisis (respiratory failure), which
requires immediate emergency medical care. (see above).
What research is being done?
Within the Federal Government, the National Institute of Neurological
Disorders and Stroke (NINDS), one of the Federal Government's National
Institutes of Health (NIH), has primary responsibility for conducting and
supporting research on myasthenia gravis. Much has been learned about
myasthenia gravis in recent years. Technological advances have led to more
timely and accurate diagnosis, and new and enhanced therapies have
improved management of the disorder. Much knowledge has been gained
about the structure and function of the neuromuscular junction, the
fundamental aspects of the thymus gland and of autoimmunity, and the
disorder itself. Despite these advances, however, there is still much to learn.
The ultimate goal of myasthenia gravis research is to increase scientific
understanding of the disorder. Researchers are seeking to learn what causes
the autoimmune response in myasthenia gravis, and to better define the
relationship between the thymus gland and myasthenia gravis.
Today's myasthenia gravis research includes a broad spectrum of studies
conducted and supported by NINDS. NINDS scientists are evaluating new and
improving current treatments for the disorder. One such study is testing the
efficacy of intravenous immune globlin in patients with myasthenia gravis. The
goal of the study is to determine whether this treatment safely improves
muscle strength. Another study seeks further understanding of the molecular
basis of synaptic transmission in the nervous system. The objective of this
study is to expand current knowledge of the function of receptors and to apply
this knowledge to the treatment of myasthenia gravis.
weakness of the skeletal (voluntary) muscles of the body. The name
myasthenia gravis, which is Latin and Greek in origin, literally means "grave
muscle weakness." With current therapies, however, most cases of majority of
individuals with myasthenia gravis, life expectancy is not lessened by the
disorder. However, if can be disabling, I know. If you find yourself in that
situation, you can see if you may be eligible for disability benefits, at no
charge. You may fill out the MG Disability Benefits Evaluation now by clicking
here.
The hallmark of myasthenia gravis is muscle weakness that increases during
periods of activity and improves after periods of rest. Certain muscles such as
those that control eye and eyelid movement, facial expression, chewing,
talking, and swallowing are often, but not always, involved in the disorder. The
muscles that control breathing and neck and limb movements may also be
affected.
What causes myasthenia gravis?
Myasthenia gravis is caused by a defect in the transmission of nerve impulses
to muscles. It occurs when normal communication between the nerve and
muscle is interrupted at the neuromuscular junction - the place where nerve
cells connect with the muscles they control. Normally when impulses travel
down the nerve, the nerve endings release a neurotransmitter substance
called acetylcholine. Acetylcholine travels through the neuromuscular junction
and binds to acetylcholine receptors which are activated and generate a
muscle contraction. In myasthenia gravis, antibodies block, alter, or destroy
the receptors for acetylcholine at the neuromuscular junction which prevents
the muscle contraction from occurring. These antibodies are produced by the
body's own immune system. Thus, myasthenia gravis is an autoimmune
disease because the immune system - which normally protects the body from
foreign organisms - mistakenly attacks itself.
What is the role of the thymus gland in myasthenia gravis?
The thymus gland, which lies in the upper chest area beneath the breastbone,
plays an important role in the development of the immune system in early life.
Its cells form a part of the body's normal immune system. The gland is
somewhat large in infants, grows gradually until puberty, and then gets
smaller and is replaced by fat with age. In adults with myasthenia gravis, the
thymus gland is abnormal. It contains certain clusters of immune cells
indicative of lymphoid hyperplasia - a condition usually found only in the
spleen individuals with myasthenia gravis develop thymomas or tumors of the
thymus gland. Generally thymomas are benign, but they can become
malignant. The relationship between the thymus gland and myasthenia gravis
is not yet fully understood. Scientists believe the thymus gland may give
incorrect instructions to developing immune cells, ultimately resulting in
autoimmunity and the production of the acetylcholine receptor antibodies,
thereby setting the stage for the attack on neuromuscular transmission.
What are the symptoms of myasthenia gravis?
Although myasthenia gravis may affect any voluntary muscle, muscles that
control eye and eyelid movement, facial expression, and swallowing are most
frequently affected. The onset of the disorder may be sudden. Symptoms
often are not immediately recognized as myasthenia gravis. In most cases, the
first noticeable symptom is weakness of the eye muscles. In others, difficulty in
swallowing and slurred speech may be the first signs. The degree of muscle
weakness involved in myasthenia gravis varies greatly among patients,
ranging from a localized form, limited to eye muscles (ocular myasthenia), to a
severe or generalized form in which many muscles - sometimes including
those that control breathing - are affected. Symptoms, which vary in type and
severity, may include a drooping of one or both eyelids (ptosis), blurred or
double vision (diplopia) due to weakness of the muscles that control eye
movements, unstable or waddling gait, weakness in arms, hands, fingers,
legs, and neck, a change in facial expression, difficulty in swallowing and
shortness of breath, and impaired speech (dysarthria).
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. In neonatal myasthenia, the fetus may acquire
immune proteins (antibodies) from a mother affected with myasthenia gravis.
Generally, cases of neonatal myasthenia gravis are transient (temporary) and
the child's symptoms usually disappear within 2-3 months after birth. Other
children develop myasthenia gravis indistinguishable from adults. Myasthenia
gravis in juveniles is common. Myasthenia gravis is not directly inherited nor is
it contagious. Occasionally, the disease may occur in more than one member
of the same family. Rarely, children may show signs of congenital myasthenia
or congenital myasthenic syndrome. These are not autoimmune disorders, but
are caused by defective genes that produce proteins in the acetylcholine
receptor or in acetylcholinesterase.
How is myasthenia gravis diagnosed?
Unfortunately, a delay in diagnosis of one or two years is not unusual in cases
of myasthenia gravis. Because weakness is a common symptom of many
other disorders, the diagnosis is often missed in people who experience mild
weakness or in those individuals whose weakness is restricted to only a few
muscles. The first steps of diagnosing myasthenia gravis include a review of
the individual's medical history, and physical and neurological examinations.
The signs a physician must look for are impairment of eye movements or
muscle weakness without any changes in the individual's ability to feel things.
If the doctor suspects myasthenia gravis, several tests are available to confirm
the diagnosis. A special blood test can detect the presence of immune
molecules or acetylcholine receptor antibodies. Most patients with myasthenia
gravis have abnormally elevated levels of these antibodies. However,
antibodies may not be detected in patients with only ocular forms of the
disease. Another test is called the edrophonium test. This approach requires
the intravenous administration of edrophonium chloride or Tensilon(r), a drug
that blocks the degradation (breakdown) of acetylcholine and temporarily
increases the levels of acetylcholine at the neuromuscular junction. In people
with myasthenia gravis involving the eye muscles, edrophonium chloride will
briefly relieve weakness. Other methods to confirm the diagnosis include a
version of nerve conduction study which tests for specific muscle "fatigue" by
repetitive nerve stimulation. This test records weakening muscle responses
when the nerves are repetitively stimulated. Repetitive stimulation of a nerve
during a nerve conduction study may demonstrate decrements of the muscle
action potential due to impaired nerve-to-muscle transmission. A different test
called single fiber electromyography (EMG), in which single muscle fibers are
stimulated by electrical impulses, can also detect impaired nerve-to-muscle
transmission. EMG measures the electrical potential of muscle cells. Muscle
fibers in myasthenia gravis, as well as other neuromuscular disorders, do not
respond as well to repeated electrical stimulation compared to muscles from
normal individuals. Computed tomography (CT) may be used to identify an
abnormal thymus gland or the presence of a thymoma. A special examination
called pulmonary function testing - which measures breathing strength - helps
to predict whether respiration may fail and lead to a myasthenic crisis.
How is myasthenia gravis treated?
Today, myasthenia gravis can often be controlled. There are several
therapies available to help reduce and improve muscle weakness.
Medications used to treat the disorder include anticholinesterase agents such
as neostigmine and pyridostigmine, which help improve neuromuscular
transmission and increase muscle strength. Immunosuppressive drugs such
as prednisone, cyclosporine, and azathioprine may also be used. These
medications improve muscle strength by suppressing the production of
abnormal antibodies. They must be used with careful medical followup
because they may cause major side effects.
Thymectomy, the surgical removal of the thymus gland (which often is
abnormal in myasthenia gravis patients), reduces symptoms in more than 70
percent of patients without thymoma and may cure some individuals, possibly
by re-balancing the immune system.
Other therapies used to treat myasthenia gravis include plasmapheresis, a
procedure in which abnormal antibodies are removed from the blood, and
high-dose intravenous immune globulin, which temporarily modifies the
immune system and provides the body with normal antibodies from donated
blood.
These therapies may be used to help individuals during especially difficult
periods of weakness. A neurologist will determine which treatment option is
best for each individual depending on the severity of the weakness, which
muscles are affected, and the individual's age and other associated medical
problems.
What are myasthenic crises?
A myasthenic crisis occurs when the muscles that control breathing weaken to
the point that ventilation is inadequate, creating a medical emergency and
requiring a respirator for assisted ventilation. In patients whose respiratory
muscles are weak, crises - which generally call for immediate medical attention
- may be triggered by infection, fever, or an adverse reaction to medication.
What is the prognosis?
With treatment, the outlook for most patients with myasthenia gravis is bright:
they will have significant improvement of their muscle weakness and they can
expect to lead normal or nearly normal lives. Some cases of myasthenia
gravis may go into remission temporarily and muscle weakness may disappear
completely so that medications can be discontinued. Stable, long-lasting
complete remissions are the goal of thymectomy. In a few cases, the severe
weakness of myasthenia gravis may cause a crisis (respiratory failure), which
requires immediate emergency medical care. (see above).
What research is being done?
Within the Federal Government, the National Institute of Neurological
Disorders and Stroke (NINDS), one of the Federal Government's National
Institutes of Health (NIH), has primary responsibility for conducting and
supporting research on myasthenia gravis. Much has been learned about
myasthenia gravis in recent years. Technological advances have led to more
timely and accurate diagnosis, and new and enhanced therapies have
improved management of the disorder. Much knowledge has been gained
about the structure and function of the neuromuscular junction, the
fundamental aspects of the thymus gland and of autoimmunity, and the
disorder itself. Despite these advances, however, there is still much to learn.
The ultimate goal of myasthenia gravis research is to increase scientific
understanding of the disorder. Researchers are seeking to learn what causes
the autoimmune response in myasthenia gravis, and to better define the
relationship between the thymus gland and myasthenia gravis.
Today's myasthenia gravis research includes a broad spectrum of studies
conducted and supported by NINDS. NINDS scientists are evaluating new and
improving current treatments for the disorder. One such study is testing the
efficacy of intravenous immune globlin in patients with myasthenia gravis. The
goal of the study is to determine whether this treatment safely improves
muscle strength. Another study seeks further understanding of the molecular
basis of synaptic transmission in the nervous system. The objective of this
study is to expand current knowledge of the function of receptors and to apply
this knowledge to the treatment of myasthenia gravis.
| What is Myasthenia Gravis?? |
| MySsiCase.com |
| Brought to you by the Social Security Disability Law Office of Stephanie O. Joy, Esq. Helping clients, one-on-one, in all 50 U.S. States Ph: 201-317-0610 Email: SsiHelp@ptd.net Fax: 570-424-2384 |
| Myasthenia Gravis is an SSA Bluebook Listing: 11.12 Myasthenia gravis. With: A. Significant difficulty with speaking, swallowing, or breathing while on prescribed therapy; or B. Significant motor weakness of muscles of extremities on repetitive activity against resistance while on prescribed therapy. |
| Wecome Video from Stephanie Joy, Esq. |
