The main cause of myasthenia gravis is the immune system’s production of self-reactive antibodies that target acetylcholine receptors — proteins that are important for nerve-muscle communication. While the exact origin of these antibodies is not well established, it is thought that abnormalities in the thymus gland may be involved in their appearance.
In most cases, myasthenia gravis is caused by the immune system’s production of self-reactive antibodies that disrupt nerve-muscle communication, and thus it is considered an autoimmune disease. In rare cases, individuals may have genetic mutations that affect nerve-muscle communication, which is sometimes considered a heritable form of myasthenia gravis that is not autoimmune in nature.
Although the disease mechanisms of myasthenia gravis are not expected to cause pain, many patients report experiencing this symptom somewhat regularly. It is possible that pain arises secondarily to generalized muscle weakness, which can lead to changes in posture that cause non-specific muscle or joint aches.
Myasthenia gravis is generally not caused by genetic factors, and its symptoms more commonly emerge in adulthood. In rare cases, babies born to mothers with myasthenia gravis also may have the condition, but it is usually temporary and goes away in the first months of life. Individuals with congenital myasthenia gravis are born with mutations that affect nerve-muscle communication, but symptoms may not emerge until later in life.