Myasthenia gravis
Myasthenia Gravis
The normal neuromuscular junction releases acetylcholine (ACh) from the motor nerve terminal in discrete packages.The ACh quanta diffuse across the synaptic cleft and bind to receptors on the folded muscle end-plate membrane. Stimulation of the motor nerve releases many ACh quanta that depolarize the muscle end-plate region and then the muscle membrane causing muscle contraction. In acquired myasthenia gravis, the post-synaptic muscle membrane is distorted and simplified, having lost its normal folded shape. The concentration of ACh receptors on the muscle end-plate membrane is reduced, and antibodies are attached to the membrane. ACh is released normally, but its effect on the post-synaptic membrane is reduced. The post-junctional membrane is less sensitive to applied ACh, and the probability that any nerve impulse will cause a muscle action potential is reduced.
Treatment:-
There is no cure for myasthenia gravis, but treatment with immunosuppressants or cholinesterase inhibitors can help control symptoms.
Many patients find that with treatment, and adequate sleep and rest, they can carry on with their normal routine.
Medications include:
Cholinesterase inhibitors: These improve communication between nerves and muscles, and are effective in patients with mild symptoms of MG.
Steroids, such as prednisolone, or immunosuppressants, such as azathioprine, may alter the body’s immune system so that it produces fewer of the antibodies that cause MG.
It usually takes about 4 weeks for steroids to take effect. Azathioprine may take from 3 to 6 months, but it brings about a significant reduction or complete removal of symptoms.
The normal neuromuscular junction releases acetylcholine (ACh) from the motor nerve terminal in discrete packages.The ACh quanta diffuse across the synaptic cleft and bind to receptors on the folded muscle end-plate membrane. Stimulation of the motor nerve releases many ACh quanta that depolarize the muscle end-plate region and then the muscle membrane causing muscle contraction. In acquired myasthenia gravis, the post-synaptic muscle membrane is distorted and simplified, having lost its normal folded shape. The concentration of ACh receptors on the muscle end-plate membrane is reduced, and antibodies are attached to the membrane. ACh is released normally, but its effect on the post-synaptic membrane is reduced. The post-junctional membrane is less sensitive to applied ACh, and the probability that any nerve impulse will cause a muscle action potential is reduced.
Treatment:-
There is no cure for myasthenia gravis, but treatment with immunosuppressants or cholinesterase inhibitors can help control symptoms.
Many patients find that with treatment, and adequate sleep and rest, they can carry on with their normal routine.
Medications include:
Cholinesterase inhibitors: These improve communication between nerves and muscles, and are effective in patients with mild symptoms of MG.
Steroids, such as prednisolone, or immunosuppressants, such as azathioprine, may alter the body’s immune system so that it produces fewer of the antibodies that cause MG.
It usually takes about 4 weeks for steroids to take effect. Azathioprine may take from 3 to 6 months, but it brings about a significant reduction or complete removal of symptoms.
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