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  Muscular and Bone


What Is Myasthenia 
  Gravis (MG)

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  What Is Myasthenia Gravis      

What Is Myasthenia Gravis?
Myasthenia gravis is a chronic disorder characterized by weakness and rapid 
fatigue of any muscles under your voluntary control. It results from a breakdown 
in the normal communication between nerves and muscles.

The disorder leaves your nerves and muscles healthy, and the muscle weakness 
you experience improves with rest. In moderate to severe cases, 
myasthenia gravis may cause difficulties with speech, chewing, swallowing 
and breathing, as well as weakness of your limbs.

Myasthenia gravis is rare but affects both children and adults. It's most common 
in women younger than age 40 and in men older than age 60. Treatments can't 
cure myasthenia gravis, but they can relieve symptoms

Signs and Symptoms
Myasthenia gravis may affect any of the muscles that you voluntarily control. 
It more commonly affects certain muscles, including those of the face, eyes, arms 
and legs, and those involved in chewing, swallowing and breathing. Signs and 
symptoms may include:

Facial muscle weakness, including drooping eyelids 
Double vision 
Difficulty in breathing, talking, chewing or swallowing 
Muscle weakness in the arms or legs 
Fatigue brought on by repetitive motions 

The more a muscle action is repeated, the worse the weakness becomes. 
In myasthenia gravis, good days alternate with bad. Remissions may occur, 
however, and may last for months. In rare cases, breathing or swallowing 
problems worsen, requiring emergency medical care.

Causes
When your nervous system is functioning normally, the chemical acetylcholine 
transmits nerve impulses to your muscles. At specialized areas of your muscles, 
called neuromuscular junctions, receptor sites receive impulses and signal your 
muscles to contract in daily movements, such as raising a spoon to your mouth.

In myasthenia gravis, there's a breakdown in communication between your nerves 
and muscles. The culprit is your immune system. For unknown reasons, 
myasthenia gravis causes your immune system to produce antibodies that block 
or destroy many of your receptor sites — up to 80 percent of them. With fewer 
receptor sites, your muscles receive fewer nerve signals, causing the weakness.

It's believed that the thymus gland, a part of your immune system located in the 
upper chest beneath the breastbone, may trigger or maintain the production of 
these antibodies. Large in infancy, the gland shrinks in healthy adults. However, 
some people with myasthenia gravis have abnormally large thymus glands. 
About 15 percent develop tumors of the thymus.

Some factors can make myasthenia gravis worse, including illnesses such as a 
cold, stress and overexerting yourself

When To Seek Medical Advice
If you experience muscle weakness or have difficulty controlling the muscles of 
your eyes, face and mouth, difficulty breathing or fluctuating weakness in your 
arms and legs, see your doctor. These could be indications of myasthenia gravis. 
Although there's no cure for myasthenia gravis, the outlook for managing its 
symptoms is good. The sooner you see your doctor, the sooner treatments can 
help you improve your muscle strength and the sooner you can learn about 
strategies that can help you use your energy in the most efficient ways.

Screening And Diagnosis
The key symptom that points to the possibility of myasthenia gravis is muscle 
weakness that improves with rest. Tests to confirm the diagnosis may include:

Neurologic examination. This may include testing of your reflexes, muscle 
strength, muscle tone, senses of touch and sight, gait, posture, coordination, 
balance and mental skills. 
Electromyography. During the first part of this test, a small electrical impulse is 
applied to your skin to stimulate your nerves to test the strength of your muscle 
contraction. In the second part, a thin-needle electrode inserted into one of your 
muscles helps measure patterns of electrical activity in your muscle at rest and 
with slight muscle contraction. 
Blood analysis. A blood test may reveal the presence of abnormal antibodies 
that disrupt the receptor sites where nerve impulses signal your muscles to move. 
Edrophonium chloride test. Injection of the chemical edrophonium chloride 
(Tensilon) may result in a sudden, although temporary, improvement in your 
muscle strength, an indication that you may have myasthenia gravis. 
Edrophonium chloride acts to block an enzyme that inhibits the transmission of 
signals from your nerve endings to your muscle receptor sites. 

Treatment
There is no cure for myasthenia gravis. But these treatments, alone or in 
combination, relieve symptoms for many people:

Medications. Several drugs, called cholinesterase inhibitors, enhance 
communication between nerves and muscles. These drugs don't treat the 
underlying problem, but they do improve muscle contraction. Corticosteroids 
inhibit the immune system, limiting antibody production. Prolonged use of 
corticosteroids can lead to serious side effects, such as bone thinning, 
weight gain, diabetes, increased risk of some infections and a redistribution 
of body fat. 
Surgery. Removal of the thymus gland brings marked relief to about half the 
people with severe myasthenia gravis, but the effect is often delayed for many 
years and the response is more dramatic in younger people. 
Plasmapheresis (plaz-muh-fuh-RE-sis). This procedure can remedy 
life-threatening stages of myasthenia gravis. Plasmapheresis involves removal 
of antibodies from your blood that block transmission of signals from your nerve 
endings to your muscle's receptor sites. Blood is taken from your body, passed 
through a filter that removes the specific antibodies and then is returned to your 
body. This approach is expensive and time-consuming. Also, other forms of 
therapy are necessary for long-term restoration of muscle strength. Otherwise, 
the immune system soon makes new antibodies to replace those that have been 
removed. 

As part of your treatment, your doctor may suggest physical therapy and 
occupational therapy to help you adjust to tasks you need to do around the house 
and in your job.

Coping Skills
Supplementing your medical care with these approaches may help you make the 
most of your energy and cope with the symptoms of myasthenia gravis:


Adjust your eating routine. Try to eat when you have good muscle strength, 
possibly an hour after taking your medication. Also, take your time eating and 
rest between bites. Try soft foods and avoid sticky foods. 
Use safety precautions at home. Install grab bars or railings in places where you 
may need support, such as when you're getting out of the tub. Keep the floors and 
halls in your house clear of clutter, cords and loose rugs. Outside your home, keep
the steps, sidewalk and path to your car clear. 
Use electric appliances and power tools. Save your energy in the bathroom, in the
 kitchen or at the workbench by using electric appliances such as toothbrushes, 
can openers and screwdrivers. 
Wear an eye patch. Using an eye patch can relieve double vision if you suffer 
from this effect. Wear the patch while you read or watch television. To avoid 
eyestrain, occasionally switch the patch from one eye to the other. 
Plan ahead. If you have a chore to do around the house, shopping to do or an 
errand to run, plan the activity to coincide with when your medication provides 
your peak energy level. If you're working on a project at home, gather everything 
you need for the project at one time, to eliminate extra trips that may drain your 
energy. 
Ask for help. Depending on your energy level, you may not be able to do 
everything you planned around the house or run every errand that you need to. 
Ask family members and friends to lend a hand. 
Manage stress. Because emotional stress can make myasthenia gravis worse, 
look for ways to reduce stress. These may include relaxation techniques such as 
biofeedback and meditation. 




Safety and Myasthenia Gravis
Studies show that most accidents with injuries occur in the home. 
The Myasthenia Gravis patient who may have double vision, trouble walking, and 
general muscle weakness is at greater risk for injury. 
To assist the myasthenia gravis patient, following are suggestions for safety in the 
home. 

In the Bathroom
Put grab bars by the tub or shower. 
Use a shower chair with rubber grips in the tub or shower. 
An elevated toilet seat and/or rails may be helpful. 
Put non-slip strips or a mat in the tub or shower. 
Use a hand-held shower head to make it easier to check the water temperature 
and to help in bathing and rinsing off. 
If unsure of yourself in the bath or shower, have someone on stand-by for help. 
Be sure to mop up any water on the floor and have bath mats and rugs secured to the floor with tape or a rubber gripper under the rug. 
Other Rooms


Remove area throw rugs. 
Tape down edges of large rugs. 
Have rails on both sides of staircases and check any rugs on the stairs to make 
sure they are securely attached to the stairs. 
Do not wax floors. 
Pad sharp corners on shelves and furniture by taping a small towel on the corners. 
Put furniture along walls and do not change the arrangement of furniture, if possible
 Repair holes and rough spots in floors and steps 
Keep clutter, toys, and any small items off the floor. 
Move electrical and telephone cords out of walkways. 
Mop up spills on the floor immediately. 
Provide bright lighting throughout the house. 
Keep small night lights on, especially in the bedroom, bathroom, stairs, and kitchen. 
Have emergency lighting, such as flash lights, in a convenient location in case of power outages. 
Remove wheels or casters from bed or chairs. 
Place the bed within easy reach of telephone. lights, and bathroom. 
Place a bell or whistle by the bed to use to call for help. 
Wear low heeled shoes with non-slip soles. Bare feet are safer than socks or soft slippers. 
If you must hold onto furniture or walls, obtain a cane or walker and arrange to have a therapist provide training on how to use the equipment. 
Have smoke alarms on each floor of the house and make sure they work. 
Have emergency numbers and a fire extinguisher readily available. 


Outside the Home
Keep sidewalks and driveways repaired. 
Walk on hard surfaces where you can see possible dangers such as holes or toys. 
If possible, have hand rails on both sides of stairs. 
If stairs are a problem to climb, a ramp can be used or built for easy access. 
Have toys, tools, lawn equipment and other obstacles off the walk area. 
In icy or snow conditions, have all walk-ways and steps clear. Avoid trying to do it 
yourself. Apply cat litter or sand on the area to provide traction. 
If your mailbox is far from the house, ask the post office to deliver your mail to the 
door. 
Other services, such as trash pick-up, newspaper delivery, and recycling pick-up, 
can be contacted to pick-up at the house instead of curb side.
Reviewed/compiled by:
Tina M. Vassar, RN, MSN, CS

This publication has been approved by the National Medical Advisory Board.
Myasthenia Gravis Foundation, 1996.


Diagnosis/Symptoms 
The Creatine Kinase Test
Almost everyone with a neuromuscular disorder has had, or will have, a 
creatine kinase test. But what exactly is creatine kinase (CK), and why are its levels
measured in neuromuscular diseases?

CK, also known as phosphocreatine kinase, or CPK, is a type of protein called an 
enzyme. It catalyzes, or "encourages," a biochemical reaction to occur. The 
normal function of CK in our cells is to add a phosphate group to creatine, turning 
it into the high-energy molecule phosphocreatine. Phosphocreatine is burned as a
quick source of energy by our cells.

However, the normal function of CK isn't as relevant, in this case, as what happens 
to CK when muscle is damaged. During the process of muscle degeneration, 
muscle cells break open and their contents find their way into the bloodstream. 
Because most of the CK in the body normally exists in muscle, a rise in the amount 
of CK in the blood indicates that muscle damage has occurred, or is occurring.

To measure CK levels, a blood sample is taken and separated into fractions that 
contain cells and a fraction that doesn't — the serum. The amount of CK in the 
serum is reported in units (U) of enzyme activity per liter (L) of serum. In a healthy 
adult, the serum CK level varies with a number of factors (gender, race and activity),
 but normal range is 22 to 198 U/L (units per liter).
Higher amounts of serum CK can indicate muscle damage due to chronic disease
or acute muscle injury. For this reason, if you're scheduled to have blood drawn 
for a CK test to diagnose a potential muscle disorder, you should limit your 
exercise to normal activities before the test.

CK tests are used to evaluate neuromuscular diseases in five basic ways:
To confirm a suspected muscle problem before other symptoms occur
To determine whether symptoms of muscle weakness are caused by a muscle 
or a nerve problem
To differentiate between some types of disorders such as dystrophies versus 
congenital myopathies
To detect "carriers" of neuromuscular disorders, particularly in Duchenne 
muscular dystrophy. A carrier has a genetic defect, but doesn't get the full-blown 
disease. A carrier's child may have the full disease.
To follow the course of a disease that fluctuates (primarily the inflammatory 
myopathies), or to document episodes of acute muscle injury, as might occur in 
some metabolic myopathies.


Because elevated CK levels indicate muscle damage, many parents wonder 
why their children with Duchenne muscular dystrophy (DMD) had higher CK levels 
when they were younger and had more muscle function. This seeming paradox 
occurs because muscle degeneration is more rapid at the earlier stages and, 
possibly, because there's more muscle bulk available to release CK into the 
circulation at this time.

CK levels can be slightly elevated (500 U/L) in nerve disorders like 
Charcot-Marie-Tooth disease, amyotrophic lateral sclerosis or spinal muscular 
atrophy, or grossly elevated (3,000 to 3,500 U/L) in DMD or inflammatory 
myopathies.

During episodes of acute muscle breakdown (rhabdomyolysis), CK levels can 
temporarily go off the scale, topping out at 50,000 to 200,000 U/L. At the same time, 
some neuromuscular disorders, such as the congenital myopathies (nemaline, 
central core disease and others) and myasthenia gravis, may not trigger any 
elevation of CK levels. CK levels don't always reflect the level of functional impact 
on the individual. 

Electromyography and Nerve Conduction Velocities
Diagnosis of neuromuscular disease hinges on a doctor's ability to identify a 
specific defect of neuromuscular function. Sometimes, a doctor can infer this 
functional defect - and the disease associated with it - by giving a physical exam, 
doing a blood test or looking at the anatomy of nerves and muscles.

But other times, the doctor may have to directly evaluate the functions of nerves 
and muscles and the connections between them by using two complementary 
techniques - nerve conduction velocity testing (NCVs) and electromyography 
(EMGs).

 
Action Potentials
Both NCV and EMG rely on the fact that the activity of nerves and muscles 
produces electrical signals called action potentials. A nerve is actually a bundle 
of axons, cables that conduct action potentials from one end of a nerve cell (or 
neuron) to the other. 

In motor neurons (neurons that connect to muscle), these action potentials travel 
toward the muscle, where they cause release of a chemical called acetylcholine. 
Acetylcholine opens tiny pores in the muscle, and the flow of sodium and 
potassium ions through these pores creates action potentials in the muscle, 
leading to contraction. 

In NCV and EMG, these tiny electrical events are amplified electronically, then 
visualized on a TV-like monitor called an oscilloscope and even heard using 
audio equipment.

NCV and Axons
NCV measures action potentials conducted by axons, so doctors use it for 
diagnosing diseases that primarily affect nerve function, such as different forms of 
Charcot-Marie-Tooth disease (CMT). 

It's done by placing surface electrodes (similar to those used for electrocardiograms)
on the skin at various points over a nerve. One electrode delivers a mild electrical 
shock to the nerve, stimulating it to generate an action potential. The other 
electrodes record the action potential as it's conducted through the nerve.

Doctors often use NCV to determine the speed of nerve conduction (hence, its 
name). Conduction speed is influenced by a coating around axons, called myelin.
Myelin insulates each axon and normally forces action potentials to "jump" quickly
 from one end of the axon to the other. If the myelin breaks down (as in CMT1), the 
action potential travels more slowly.

NCV also can measure the strength of the action potential in the nerve, which is 
proportional to the number of axons that contribute to it. If axons degenerate (as in 
amyotrophic lateral sclerosis) or become clogged with debris (as in CMT2), the 
action potential becomes smaller.

EMG and Muscle
An electromyogram measures the action potentials produced by muscles, and is 
therefore useful for diagnosing diseases that primarily affect muscle function, 
including the muscular dystrophies. Also, some EMG data can reveal defects in 
nerve function.

In EMG, the doctor inserts a needlelike electrode into a muscle. The electrode 
records action potentials that occur when the muscle is at rest and during voluntary
contractions directed by the doctor.

While a healthy muscle appears quiet at rest, spontaneous action potentials are 
seen in damaged muscles or muscles that have lost input from nerve cells (as in 
ALS or myasthenia gravis). During voluntary contraction, dystrophic (wasted) 
muscles show very small action potentials, and myotonic (stiff) muscles show 
prolonged trains of action potentials. Altered patterns of muscle action potentials 
can indicate defects in nerve function.

A Little Discomfort
Though NCVs and EMGs are valuable tools for doctors, they can be distressing 
for patients. Some people find the electric shocks of the NCV or the needle 
penetration of the EMG uncomfortable or even painful. Young children might 
struggle during the tests, making it difficult for doctors to carefully monitor nerve 
and muscle activity. To ease discomfort, topical anesthetic can be applied to the 
skin - but it won't prevent muscle pain during the EMG. Sometimes sedating 
medications are needed to keep a child calm. 

Partly because of these factors, NCVs and EMGs are generally used when it's not 
possible to gather the right information from other diagnostic tests. Muscle biopsy 
(excising and examining muscle tissue; see Quest, vol. 7, no. 4) can reveal 
hallmark anatomical features of some neuromuscular diseases, making EMG 
and NCV unnecessary. Genetic tests are now available for diagnosing some 
diseases, and in those cases, EMG and NCV usually can be bypassed.

Nonetheless, NCV and EMG remain the gold standards for evaluating the function 
of nerve and muscle. So, when a doctor suspects that a patient has a 
neuromuscular disease that isn't clearly associated with anatomical or genetic 
defects (like some types of CMT, or myasthenia gravis), NCV and EMG are 
among the most valuable diagnostic tools

Common Questions Patients 
Ask About
Thymectomy Surgery In Myasthenia Gravis

Myasthenia Gravis is often associated with enlargement of the thymus gland; 
about 10% of MG patients have a tumor of the gland (thymoma). Since the 1940s, 
MG has been treated with surgical removal of the thymus gland (thymectomy), 
with the observation that most patients improve a year or so following surgery. 
In general, a thymectomy is performed in patients under the age of 60, in those 
with moderate or severe symptoms and in those suspected of having a thymoma.

The thymus gland is located in the upper chest under the breastbone. It is 
composed of two main lobes and is shaped somewhat like a butterfly lying over 
the windpipe. The exact role of the thymus in Myasthenia Gravis is not completely 
understood.

When a thymectomy is being considered by the physician and patient, the referral 
is made to a surgeon who has experience performing this type of surgery.

The surgeon then examines the patient and reviews the various medical records, 
tests and x-rays. After learning about the surgery, including the preparation and 
any possible complications, the patient and the surgeon make a decision on 
whether or not to proceed with the surgery. In general, the patient should not 
undergo thymectomy or any other surgery unless his or her physical condition is 
good. Sometimes intravenous immune globulin (IVIg) or plasmapheresis can be 
used to prepare a myasthenic for surgery.

A thymectomy is performed to improve the long-term clinical course of MG. 
The response to thymectomy is variable; about 30% eventually experience 
complete drug-free remission, and another 50% experience significant 
improvement. 

The following are some of the most common questions asked by a myasthenic 
who is considering thymectomy surgery. Since each patient’s situation is unique, 
it is essential to discuss these and all questions about this surgery with the 
Myasthenia Gravis physician and surgeon.

How is surgery performed?
The surgery can be performed several ways. The first is the transsternal incision 
in which the incision is made lengthwise on the chest and the breastbone (sternum)
is opened. This technique is the most widely used because it allows the surgeon 
to be as certain as possible about the complete removal of the thymus. A second 
type of incision is the transcervical, which is a smaller horizontal incision across 
the lower part of the neck. A third type, video assisted or thorascopic surgery is 
recent; data on its outcome for myasthenia is scarce. It is the least painful, and the 
recovery time is shorter. With the thorascopic technique, surgeons only need to 
make a small incision as well as small holes in to which to insert instruments. 
The thorascopic contains a miniature camera; and surgeons watch what they are 
doing on a video monitor. The surgeon will determine the optimal surgical 
procedure, which may be based upon the position or number of lobes of the 
thymus, as well as on experience and outcome data.

Intravenous Immunoglobulins
Common Questions Patients Ask About
IVIg Therapy In Myasthenia Gravis

 What is IVIg?
IVIg is intravenous immune globulin. It is also known as pooled human gamma 
globulin or simply, gamma globulin. IVIg has been used for decades in modern 
medicine in the treatment of a variety of infectious or inflammatory diseases. 
In patients who are lacking in the antibodies necessary to fight infection, 
IVIg replaces those lost antibodies. 

IVIg is used also in the treatment of a variety of autoimmune disorders. Over the 
past two decades, IVIg has been used extensively in the treatment of some 
autoimmune neurological disorders, including myasthenia gravis (MG). There are
indications that IVIg is an effective treatment for some patients with autoimmune 
myasthenia gravis.

How does IVIg work?
IVIg seems to affect the function or the production of antibodies in the immune 
system. The exact mechanism of how IVIg works in successfully treating 
myasthenia gravis and other autoimmune disorders is not entirely understood.

Since IVIg is a blood product, is it safe?
IVIg is felt to be very safe with regard to exposure to infection or viruses. Donors 
are screened. The processing of IVIg inactivates such infections as HIV, Hepatitis 
B and C. Nonetheless, it is a human blood product that comes from multiple 
donors.

Are there adverse effects that occur with IVIg treatments?
For the most part, IVIg is considered quite safe. However, there are several 
adverse effects that may occur on occasion. Some patients develop headache, 
chills, and aches during the infusion. Slowing the infusion and using medicines to 
relieve these symptoms may be helpful. 

Some patients will experience fatigue, fever, or nausea that may persist up to 
24 hours after the infusion. Some patients may have migraine headaches, 
aseptic meningitis, skin reactions or a more severe allergic type reaction. 
Because IVIg is a highly concentrated protein, it can sometimes interfere with 
blood flow and clotting.

Myasthenia Gravis Medication Information Card
(Drugs to be Avoided or Used with Caution in MG)
2000-2001

D-penicillamine and alpha-interferon should not be used in myasthenic patients, 
as it they can cause MG. Botulinum toxin should be avoided. 
Increased weakness in a significant number of MG patients has been reported 
with the following drugs. Use only with caution and monitor for exacerbation of MG 
symptoms: ? Neuromuscular blocking agents such as succinylcholine and 
vecuronium- should only be used by an anesthesiologist familiar with MG

? Quinine, quinidine, or procainamide- avoid 

? Selected antibiotics, particularly aminoglycosides and ciprofloxacin. Note: Many other antibiotics have been reported to increase MG weakness in occasional patients.

? Beta-blockers: propranolol, timolol maleate eyedrops

? Calcium channel blockers 

? Iodinated contrast agents (a form of X-ray dye)



       

 

    


 






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