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If you suffer from disabling Myasthenia Gravis 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, and hopefully, recover. My SS work deals in large part with MG, I would be honored to assist you. Start by filling out the FREE online Social Security Disability Claim Evaluation Form, calling me at 201-317-0610 or emailing me at SOJLaw@ptd.net. |
| Myasthenia Gravis |
Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized
by varying degrees of weakness of the skeletal (voluntary) muscles of the body.
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.
If you are undergoing infusion treatments, prescribed Mestinon or similar
prescription medications, and you are still not able to withstand working full time,
you can learn if you may be eligible for disability benefits, at no charge. You may
fill out the MG Disability Benefits Evaluation now by clicking here and Stephanie
will be happy to review it and discuss.
Know also that MG is a Blue Book listing under Social Security disability law. So
while you may feel quite alone, and that few people you know understand
Myasthenia Gravis, or have ever even heard of it, please feel secure that there is
at least a handful of us that practice SS law and are well-studied on MG and how it
can be a disabling condition - ergo, contributing to the SSA making MG one of the
limited, listings in the Blue Book.
m m 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.
by varying degrees of weakness of the skeletal (voluntary) muscles of the body.
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.
If you are undergoing infusion treatments, prescribed Mestinon or similar
prescription medications, and you are still not able to withstand working full time,
you can learn if you may be eligible for disability benefits, at no charge. You may
fill out the MG Disability Benefits Evaluation now by clicking here and Stephanie
will be happy to review it and discuss.
Know also that MG is a Blue Book listing under Social Security disability law. So
while you may feel quite alone, and that few people you know understand
Myasthenia Gravis, or have ever even heard of it, please feel secure that there is
at least a handful of us that practice SS law and are well-studied on MG and how it
can be a disabling condition - ergo, contributing to the SSA making MG one of the
limited, listings in the Blue Book.
m m 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.
| About this medical condition: |
| & Social Security Disability |
| Attorney Stephanie Joy (c.2011) "Combining the practice of SS law with Compassion and Communication" |
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.
http://www.ssa.gov/disability/professionals/bluebook/11.
00-Neurological-Adult.htm#11_12
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.
http://www.ssa.gov/disability/professionals/bluebook/11.
00-Neurological-Adult.htm#11_12
TM