About Myasthenia Gravis

myasthenia

Poor communication can cause all manner of trouble. That’s true not only between people, but even in a single person’s body. When the parts of the muscles responsible for receiving nerve impulses are mistaken by the immune system for disease and destroyed, the nerves can no longer properly communicate with the muscles, and voluntary muscle movements are affected, resulting in a condition called myasthenia gravis. Myasthenia gravis affects about one in 5,000 people. It can strike anyone at any time, but initial onset is most common people between the ages of 50 and 70 and in in women under 40.

It’s not always clear what causes the immune system to attack the muscles. Myasthenia gravis is one of the few autoimmune diseases that does not appear to have a genetic component, but there is probably an inborn predisposition that, in combination with environmental triggers, leads to the condition. People who take certain medications—some types of antibiotics, beta blockers, quinine, or some others—are more likely to develop the condition. Other risk factors involve the thymus gland, where immune antibodies are produced. Occasionally, myasthenia gravis patients have a non-cancerous tumor in the thymus gland. More often, an enlarged thymus exhibits excess activity, producing the undesired antibodies.

Because myasthenia gravis affects the brain’s ability to send impulses to the muscles, it interferes with voluntary muscle movements, though autonomous activity such as the heart beating remain unaffected. That means difficulty taking a breath or speaking—speech becomes soft or hoarse—trouble chewing or swallowing, facial muscle paralysis, double vision and problems looking people in the eye, and a feeling of having to work harder than usual to move, stand from a chair, or climb up stairs. Another symptoms is a diminished sense of smell, even though this doesn’t involve the muscles.

Fortunately, myasthenia gravis generally is easily treated. When there is a tumor involved, removing the tumor, or even all or part of the gland itself, generally clears up the condition. When there is not, a common approach is to flood the body with the neurotransmitter that relays the signal to the muscles, o compensate for the damage to the receptor sites. As with many autoimmune diseases, drugs that suppress the activity of the immune system alleviate the condition.

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