Health Information
Comprehensive undefined information and treatment options at Healers Clinic Dubai.
"You are not alone in this journey."
Understanding This Symptom
Medical Definition
Subject Matter Expert Verified
Myasthenia Gravis (MG) is a chronic autoimmune neuromuscular disorder characterized by autoantibodies attacking components of the neuromuscular junction, most commonly the acetylcholine receptors (AChR antibodies) on skeletal muscle cells.
This antibody-mediated attack disrupts normal nerve-to-muscle communication, causing fluctuating muscle weakness that worsens with activity and improves with rest.
The condition affects voluntary muscles, particularly those controlling eye movements (causing ptosis and diplopia), facial expressions, swallowing (bulbar weakness), speech, and breathing.
Affects approximately 20 per 100,000 people globally, with women typically developing MG earlier (20s-30s) and men later (60s-70s).
Quick Facts
What Optimal Health Looks Like
Understanding how your body functions when healthy helps identify dysfunction
In a healthy neuromuscular system, motor neurons transmit signals to skeletal muscles through the neuromuscular junction.
When a nerve impulse arrives at the nerve terminal, it triggers the release of acetylcholine (ACh) into the synaptic cleft.
Acetylcholine binds to nicotinic acetylcholine receptors (AChR) on the muscle membrane, causing sodium channels to open and depolarizing the muscle fiber.
This generates an action potential that initiates muscle contraction.
Healthy Function
Your body is designed to maintain balance and self-regulate
How This Develops
Autoantibody production - In
Complement-mediated damage - AChR antibodies activate the classical complement pathway, leading to membrane attack complex (MAC) formation that destroys the postsynaptic membrane folds and reduces receptor density by
Receptor blockade - Antibodies physically block the binding sites where acetylcholine normally attaches, preventing normal nerve signal transmission
Receptor modulation - Antibody cross-linking accelerates AChR internalization and degradation, further reducing receptor numbers
In anti-MuSK MG (
In anti-LRP
Thymic abnormalities -
Presynaptic dysfunction - Some antibodies may affect voltage-gated calcium channels, further impairing acetylcholine release
Fatigue mechanism - With repeated stimulation, the limited remaining receptors cannot sustain adequate depolarization, causing progressive weakness with activity that improves with rest
Myasthenic crisis - Severe disease can cause respiratory muscle failure requiring mechanical ventilation, triggered by infection, surgery, medication, or stress
Understanding the mechanism helps us target the root cause rather than just treating symptoms.
What Happens If Left Untreated
Understanding the consequences helps you make informed decisions about your health
Short-Term Consequences
Days to weeks
- [object Object] | [object Object] | [object Object]
Time Matters
Don't wait for symptoms to worsen. Early intervention leads to better outcomes.