Myastenia Gravis can be as unique as people themselves, with symptoms often varying from person to person.(2) Getting to a diagnosis may be a long and difficult journey. When doctors meet with people living with MG and discuss specific concerns or symptoms, they may consider a diagnosis of any of these types of MG:
Our immune systems typically create antibodies to fight diseases. However, in gMG, some antibodies mutate into autoantibodies that attack the body instead of protecting it. This occurs when these autoantibodies target proteins in the neuromuscular junction, disrupting communication between nerves and muscles (3).
Approximately 85% to 90% of people with gMG have specific serotypes identified through antibody testing (4). Serotypes refer to variations of MG characterised by the proteins targeted by autoantibodies. The main serotypes include (1):
These antibodies interfere with the transmission of signals from the brain to the muscles, resulting in symptoms such as muscle weakness, difficulty swallowing, speaking, and other everyday tasks (4). About 80% of people with generalised MG test positive for AChR antibodies.(2)
If a person has generalised MG, including seronegative MG (see below), they typically experience symptoms that impact many areas of their body. Their symptoms might include muscle weakness, trouble chewing and swallowing, and problems with speaking or smiling. They also might have difficulty doing everyday tasks, such as climbing stairs (5).
Other symptoms of generalised MG include5:
Seronegative MG occurs when no identifiable autoantibodies are present. Despite the absence of specific antibodies, individuals experience symptoms like those with gMG, including challenges with breathing, movement, and speaking (5-6).
Some people living with MG experience symptoms exclusive to their eye muscles. This is called ocular Myasthenia Gravis, and it affects about 10% to 40% of MG patients.7 In some people, ocular MG progresses into generalised MG (8).
Common symptoms of ocular MG are diplopia (double vision) and ptosis (drooping eyelids).(8) Often, people living with ocular MG notice that their eye muscles feel weakest at the end of the day.
Why does MG only affect eye muscles for some people? Eye muscles are structured differently than muscles in the arms, stomach, legs and back. They tend to be more vulnerable to attacks from the immune system (9).
This type of MG can occur anytime from birth through early childhood (12). Unlike other types of MG, it’s not an autoimmune disorder. Instead, it stems from a genetic issue.
Symptoms of congenital MG resemble those of generalised MG(13). However, they might be milder if the condition appears later in life (13).
This rare condition usually begins before the age of 18 and lasts throughout life. Symptoms might start gradually and could be hard to notice, so the disease may go undiagnosed for a while. The most common symptoms of juvenile MG are drooping eyelids and double vision. In more generalised forms, patients may experience fatigue and problems with eating and swallowing (10).
Knowing the types of MG might help those living with MG, as well as caregivers, better understand the condition. It may also help loved ones provide more informed support. Healthcare providers may discuss MG types in more detail and provide information about managing symptoms.
This type of MG affects 10% to 20% of babies born to women with Myasthenia Gravis (10). During pregnancy, mothers might pass their autoantibodies to a developing fetus.11 Symptoms, which usually appear in the first 24 hours of a baby’s life, may include (11):
Usually, as the mother’s autoantibodies disappear from the baby’s bloodstream, the baby recovers. It may take a few weeks or months (10).
Living with myasthenia gravis shouldn't stop you from doing the things you love. By talking to your healthcare professional, you can find a management plan that is tailored to your personal goals.
REFERENCES :
1. Kuks JBM. Clinical presentations of myasthenia gravis. In: Kaminski H, Kusner L, eds. Myasthenia Gravis and Related Disorders, Third Ed. Current Clinical Neurology. Humana Press; 2018:85-100.
2. Gilhus N. Lancet Neurol. 2015;14:1023-1036.
3. Hehir M, et al. Neurol Clin. 2018;36:253-260.
4. Gilhus N. N. Engl J Med. 2016;375;26:2570-2581.
5. Gilhus N, et al. Nat Rev Dis Primers. 2019;5:30.
6. Farrugia M, et al. Front Neurol. 2020;11:604.
7. Howard JF. Clinical Overview of MG, MGFA. 2015. https://myasthenia.org/Understanding-MG/Overview-of-MG. Accessed Feb 2022.
8. Deymeer F. Acta Myol. 2020;39:345-352.
9. Nair, et al. Indian J Ophthalmol. 2014;62:985-991.
10. O’Connell K, et al. Front Neurol. 2020;11:743.
11. Gilhus N. Front Neurol. 2020;554(11):1-6.
12. Engel A, et al. Lancet Neurol. 2015;14(4):420-434.