Myasthenia Gravis (MG) is a chronic, rare neuromuscular disorder that impairs communication between nerves and voluntary muscles. This condition causes fluctuating skeletal muscle weakness that worsens with activity and improves following rest. MG can affect individuals of any age, but it most commonly begins in younger women under 40 and older men over 60.
Is Myasthenia Gravis Contagious
Myasthenia Gravis is not contagious and cannot be transmitted from one person to another. It is impossible to contract MG through physical contact, sharing food or drinks, coughing, or any other means associated with infectious diseases. The disorder is an internal malfunction of the body’s immune system, not an infection caused by an external virus or bacterium.
Family members, caregivers, and friends face no risk of developing the condition from exposure. The disease process is contained within the affected individual’s biological systems and does not involve any transferable pathogens. While a temporary form can rarely occur in newborns if the mother has MG, this is due to the passive transfer of antibodies across the placenta. The infant’s symptoms are temporary, usually resolving within a few weeks to months.
The Autoimmune Mechanism of Myasthenia Gravis
Myasthenia Gravis is classified as an autoimmune disease, meaning the immune system mistakenly attacks healthy cells and tissues. In MG, this attack is directed at the neuromuscular junction, the specialized site where a nerve cell transmits a signal to a muscle cell. This disruption prevents the nerve impulse from successfully triggering a muscle contraction, leading to muscle weakness.
The primary target of this immune assault is the muscle cell’s receptor sites for acetylcholine, a neurotransmitter. Normally, when a nerve fires, it releases acetylcholine, which travels across the junction and binds to these receptors. This binding action initiates the muscle contraction.
In MG, the immune system produces autoantibodies that block, alter, or destroy these acetylcholine receptor sites. By physically occupying or eliminating the receptors, the antibodies prevent the acetylcholine from delivering its message. With fewer functional receptors available, the muscle receives a weaker signal, resulting in the characteristic fluctuating muscle weakness. Some patients also produce antibodies against other proteins, such as MuSK or LRP4, which similarly impair the communication pathway.
Factors Influencing MG Development
Since MG is not contagious, its development is tied to genetic predisposition and other biological factors. While the exact initial cause remains unclear, a personal or family history of other autoimmune conditions, such as lupus or rheumatoid arthritis, can increase an individual’s susceptibility. Certain genetic markers, particularly those involving the human leukocyte antigen (HLA) system, are associated with a greater likelihood of developing the condition.
The thymus gland, an organ located in the upper chest that is part of the immune system, is strongly implicated in the disorder’s onset. In many adults with MG, the thymus gland remains larger than normal, a condition called thymic hyperplasia. Approximately 10% of patients also develop a tumor on the gland, known as a thymoma. Researchers believe the thymus may incorrectly instruct developing immune cells to produce the specific autoantibodies that target the neuromuscular junction.
Environmental factors do not cause MG but can act as triggers that precipitate the onset or worsen symptoms in a person who is already predisposed. These triggers can include infections, such as a respiratory illness, periods of emotional stress, or certain surgeries. Some prescription medications, including certain antibiotics and heart medications, have also been known to exacerbate the muscle weakness associated with the condition.
Common Physical Manifestations
The primary feature of Myasthenia Gravis is muscle weakness that fluctuates in severity, often being mildest in the morning and worsening as the day progresses or after physical exertion. This weakness improves temporarily following periods of rest. In over half of all cases, the initial symptoms are ocular, affecting the muscles controlling eye movement and eyelids.
Common eye symptoms include ptosis (the drooping of one or both eyelids) and diplopia (double vision). This double vision can be horizontal or vertical and often improves when one eye is closed. As the disorder progresses, it frequently involves the muscles of the face and throat, leading to difficulties with speaking and swallowing.
Weakness in the throat muscles can cause speech to sound slurred or nasal (dysarthria), and chewing may become tiring, particularly midway through a meal. Swallowing difficulties (dysphagia) can lead to choking or liquids coming out of the nose. Generalized weakness in the neck and limbs, affecting the ability to hold up the head, raise the arms, or climb stairs, may also occur.