

Do you suffer from muscle weakness that worsens with exertion and improves with rest? It might be more than just fatigue... You could be dealing with Myasthenia Gravis (MG) — a rare autoimmune disorder that disrupts communication between nerves and muscles.Symptoms vary and may include drooping eyelids, difficulty speaking or swallowing, and even weakness in the muscles used for breathing.In this comprehensive medical guide by Dalili Medical, we reveal the causes of Myasthenia Gravis, early warning signs, accurate diagnostic methods, and the latest treatment options — both medical and physical therapy. We also answer the most frequently asked questions to help you understand the condition and live with it safely and confidently.
Myasthenia Gravis (MG) is a rare autoimmune disorder in which the immune system attacks acetylcholine receptors at the neuromuscular junctions. This prevents nerve signals from reaching the muscles, leading to progressive muscle weakness.
The condition often affects muscles that control eye movement, facial expression, swallowing, and speech, and in more severe cases, it may involve the limbs or breathing muscles — potentially leading to respiratory failure in critical situations.
✔️ Yes, MG is a chronic condition, but it can be effectively managed with medication and regular medical follow-up. Many patients can live a relatively normal life.
✅ There is currently no permanent cure, but symptoms can be well-controlled. Some patients achieve complete or partial remission, especially with medication or surgical options like thymectomy.
❌ Not directly, but there is a genetic predisposition in families with autoimmune diseases.
⚠️ It can be, especially if untreated. Myasthenic crisis — a condition where breathing muscles are affected — is a medical emergency requiring intensive care.
Yes, but pregnancy should be planned and managed closely by a specialist. Some medications may need adjustment. Newborns may experience neonatal MG, but it usually resolves within weeks.
The first signs often include:
Drooping eyelids (ptosis)
Double vision (diplopia)
Facial weakness or trouble swallowing
These symptoms may gradually spread to other muscle groups.
Yes, but exercises should be moderate and supervised. Avoid strenuous activities that can over-fatigue the muscles.
No. MG only affects voluntary muscles and does not impact the brain or cognitive function.
⚠️ Yes. Some medications can worsen MG symptoms, including:
Certain antibiotics (e.g., aminoglycosides)
Beta-blockers
Some heart and epilepsy drugs
It’s also best to eat soft, easy-to-chew foods to reduce muscle fatigue.
Although MG often has no clear cause, several factors can increase the risk or worsen symptoms:
Women: Most commonly between 20–40 years
Men: More common after age 60
Can also affect children (Juvenile MG)
More common in young women
More common in older men
Risk is higher in people with a personal or family history of conditions like:
Systemic Lupus Erythematosus (SLE)
Rheumatoid Arthritis
Autoimmune thyroid disorders
Multiple Sclerosis (MS)
Thymic enlargement
Thymoma (tumor) — found in a large number of MG patients
While not typically inherited, MG may run in families, especially in pediatric-onset cases.
Certain drugs may trigger or worsen MG, such as:
Antibiotics (e.g., aminoglycosides)
Beta-blockers
Heart and epilepsy medications
Muscle relaxants
Severe emotional stress, infections, surgery, or even childbirth may trigger symptom flare-ups or cause acute myasthenic episodes.
MG is classified into several types based on age of onset, affected muscles, and the type of autoantibodies found. Here are the most common classifications:
The most common form. It affects a wide range of muscles, including:
Facial and eye muscles
Chewing, swallowing, and speech muscles
Limb muscles (arms and legs)
Respiratory muscles in severe cases
Symptoms typically worsen with activity and improve with rest.
Affects only the eye muscles.
Symptoms include:
Drooping eyelids (ptosis)
Double vision (diplopia)
It may remain confined to the eyes or later progress to generalized MG.
Appears before age 50.
More common in women
Often associated with thymic hyperplasia or active thymus gland
Begins after age 50.
More common in men
Usually linked to AChR antibodies (acetylcholine receptor)
Patients have MuSK antibodies instead of AChR antibodies.
Often causes severe weakness in:
Facial muscles
Swallowing and speech muscles
Less responsive to cholinesterase inhibitors, but may respond well to immunosuppressive therapy
Occurs in patients with a tumor in the thymus gland (thymoma).
Can affect all age groups
Thymectomy (surgical removal of the thymus) is often part of treatment
Patients lack detectable AChR or MuSK antibodies.
Diagnosis is based on:
Clinical symptoms
Electrophysiological and neurological testing
Some patients may carry rare antibodies such as LRP4.
Symptoms vary from person to person but are generally due to weakness in voluntary muscles, which worsens with activity and improves with rest.
Progressive muscle weakness: Worsens with exertion and improves with rest
Double vision (Diplopia) or blurry vision
Drooping of the upper eyelid (Ptosis), especially noticeable in the evening
Difficulty chewing or swallowing, especially after eating for a short time
Slurred or nasal speech (Dysarthria) due to weak facial or throat muscles
Weakness in the neck or limbs, causing:
Trouble holding up the head
Difficulty climbing stairs or walking long distances
Facial expression changes due to weakness in facial muscles
Particularly in advanced cases or during a myasthenic crisis, where respiratory muscles become severely weakened.
MG is an autoimmune disorder in which the immune system mistakenly produces antibodies that attack:
Acetylcholine Receptors (AChR): Blocking nerve signals to the muscles.
Or Muscle-Specific Kinase (MuSK): In less common cases.
Result: Impaired nerve-muscle communication, leading to progressive muscle weakness.
The thymus is located behind the sternum and plays a role in immune regulation.
In MG patients, the thymus may be:
Enlarged (thymic hyperplasia)
Or contain a thymoma (a benign or malignant tumor)
These changes stimulate the production of harmful autoantibodies.
MG is not directly inherited.
However, individuals with a family history of autoimmune diseases (e.g., lupus, autoimmune thyroiditis) have a higher risk of developing MG.
Certain medications may trigger or worsen MG symptoms, including:
Antibiotics (e.g., aminoglycosides)
Heart medications (beta-blockers, calcium channel blockers)
Antiepileptic drugs
Muscle relaxants and some anesthetics
While not direct causes, the following can aggravate MG:
Infections
Emotional or physical stress
Fever or high body temperature
Pregnancy or menstruation
Sleep deprivation or general fatigue
Diagnosing MG involves a combination of clinical evaluation, laboratory tests, and neurophysiological/imaging studies to confirm impaired nerve-muscle communication.
Usually the first step in diagnosis. It includes:
Evaluating muscle strength before and after exertion
Observing improvement after rest
Examining the muscles of:
Eyes (ptosis, double vision)
Face
Neck
Arms and legs
Used to detect autoantibodies that interfere with neuromuscular signaling:
Anti-AChR antibodies: Found in 80–85% of MG cases
Anti-MuSK antibodies: Present in some AChR-negative patients
LRP4 antibodies: Rare, but found in certain seronegative cases
A short-acting drug (edrophonium) is injected, temporarily improving muscle strength.
Immediate improvement in ptosis or double vision suggests MG.
⚠️ No longer widely used due to potential side effects.
Measures muscle response to repeated nerve stimulation.
A progressive decline in electrical response is typical in MG.
The most sensitive test for diagnosing MG.
Detects abnormal delay in nerve signal transmission to muscles.
Especially useful in unclear or mild cases.
Used to assess the thymus gland behind the sternum.
May reveal:
Thymic enlargement
Or a thymoma (thymus tumor)
Crucial for treatment planning, especially if thymectomy is being considered.
Evaluate the function of respiratory muscles, especially in severe or chronic cases.
Helps predict the risk of myasthenic crisis.
A trial dose of pyridostigmine (Mestinon) is administered.
Rapid symptom improvement supports a diagnosis of MG.
Treatment depends on the severity, type of antibodies, and individual response to therapy. It is typically divided into four main pillars:
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Common drug: Pyridostigmine – Brand name: Mestinon®
Mechanism: Increases the level of acetylcholine at neuromuscular junctions, temporarily enhancing muscle contraction.
Use: Effective in mild to moderate cases.
Effect: Begins working within 30–60 minutes and lasts for several hours.
Common drug: Prednisone
Function: Suppresses the overactive immune response attacking the neuromuscular junction.
Warning: Must be taken under strict medical supervision due to side effects such as:
Osteoporosis
High blood pressure
Diabetes
Used if corticosteroids alone are insufficient or to reduce their required dose:
Azathioprine
Mycophenolate mofetil
Cyclosporine
These drugs take weeks to months to show effectiveness but are beneficial long-term.
Administered intravenously.
Mechanism: Modulates the immune system by saturating it with healthy antibodies.
Uses:
During acute crises
Before surgical procedures
When standard medications fail
Mechanism: Filters out harmful autoantibodies from the blood and replaces plasma with substitute fluids.
Result: Rapid, temporary improvement.
Indications:
Myasthenic crises
Preoperative preparation
Presence of thymoma (benign or malignant tumor)
Even without a tumor in certain generalized MG cases
Reduce antibody production
Long-term improvement in symptoms
Studies have shown that surgery:
Reduces symptom severity
May allow reduction of medication dosage
Regular rest: To avoid muscle fatigue
Avoid heat: High temperatures worsen muscle weakness
Meal planning:
Eat when muscles are at their strongest
Small, soft meals to reduce effort in chewing/swallowing
Medication review: Avoid drugs that worsen neuromuscular transmission such as:
Some antibiotics
Cardiac medications
Antiepileptics
Myasthenia Gravis is a chronic autoimmune disease. Though long-term, it is highly manageable with proper treatment.
Thanks to medical advances, most patients can control their symptoms and live a normal or near-normal life.
The thymus is a butterfly-shaped gland behind the breastbone, playing a key role in immune function:
Matures T-cells (a type of white blood cell)
Secretes thymosin (a hormone stimulating immune cell development)
In MG patients, the thymus may abnormally contribute to autoantibody production that targets neuromuscular junctions.
Recommended in:
Presence of a thymoma
Generalized MG not responsive to drugs
Young adults with MG even without tumors
A landmark 2016 study showed that patients undergoing thymectomy:
Required lower corticosteroid doses
Showed faster improvement
Experienced fewer side effects
Open Surgery (Median Sternotomy):
Large chest incision, splitting the breastbone
Suitable for large tumors
More pain, longer recovery (5–7 days)
Multi-port VATS (Video-Assisted Thoracoscopic Surgery):
3–4 small incisions between ribs
Less pain, shorter hospital stay (1–3 days)
Uniportal VATS (Single-Incision):
Only one small cut (3–4 cm)
Less pain, best cosmetic outcome
Requires highly skilled surgeons
Surgical Technique | Incisions | Post-op Pain | Hospital Stay | Cosmetic Impact |
---|---|---|---|---|
Open Surgery | Large | High | 5–7 days | Prominent scar |
Multi-port VATS | 3–4 | Moderate | 1–3 days | Small incisions |
Uniportal VATS | 1 | Minimal | 1–2 days | Excellent appearance |
Since MG is a chronic condition, patient commitment is crucial in controlling symptoms and preventing complications.
Key responsibilities:
Adherence to medications: Never stop or adjust dosage without medical advice.
Routine check-ups: Regular follow-ups with neurologists or immunologists.
Healthy lifestyle: Rest, balanced nutrition, and stress management.
Recognizing warning signs: Seek help immediately if experiencing breathing or swallowing difficulties.