MySsiCase.com
Brought to you by
The Social Security Disability Law Office of
Stephanie O. Joy, Esq.

Making Your Social Security Disability Claim
the
Only Priority
Phone:  (201) 317-0610    Fax:  (888) 550-7517    Email:  stephaniejoy@myssicase.com      URL:  http://MySsiCase.com

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, and hopefully, recover.  It is our understanding that this Disability Firm
is one of the first to proactively assist MG patients obtain SSD benefit, having a
keen understanding of the condition and its varying symptoms.  

Start by filling out the FREE online
Social Security Disability Claim Evaluation Form,
calling me at 201-317-0610
or emailing me at
stephaniejoy@myssicase.com
Myasthenia Gravis, You
Also called: MG

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 individuals with myasthenia gravis, life expectancy is not lessened by the
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.



















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.

Clinical depression  
Click here for a free evaluation of your situation for benefits purposes.
About Myasthenia Gravis
& Social Security Disability
Attorney Stephanie Joy (c.2011)
"Combining the practice of SS law with
Compassion and Communication"
TM


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-Neurol
ogical-Adult.htm#11_12