Myasthenia Gravis or MG is a chronic ,autoimmune and neuromuscular disorder caused by blockage of neuromuscular transmission resulting in weakness and tiredness of skeletal muscles. The autoimmune attack occurs when autoantibodies from against the nicotinic acetylcholine postsynaptic receptors at the neuromuscular junction of skeletal muscles.
SYMPTOMS : Difficulty in Swallowing (Dysphagia) , Shortness of breath (Dyspnea), Impaired speech ( Dysarthria ) , Chronic fatigue ( Myalgia Encephalomyelitis ) , Drooping eyelids ( Ptosis) ,Weakness in arms and legs ( Asthenia ).
TREATMENT : Mestinon (pyridostigmine bromide) Orally administrated with tablets or syrups . Mestinon boosts the effect acetylcholine , improving nerve muscle communication and enhancing muscle strength.
Soliris ( eculizumab ) , administrated intravenously. It binds to complement protein C5, blocking complement system activation.
Ultomiris ( ravulizumab ) , administrated intravenously , binds to complement protein C5, blocking complement system activation .
Zilbrysq (zilucoplan), administrated subcutaneously, binds to complement protein C5, blocking complement system activation.
Efgartigimod formulations , administrated both subcutaneously and intravenously , blocks FcRn, increasing the rate at which MG self reactive antibodies are destroyed .
Rystiggo ( rozanolixizumab ), subcutaneously administrated , blocks FcRn , increasing the rate at which MG self reactive antibodies are destroyed.
Monoclonal antibodies , these proteins suppress an overactive immune system .
Plasma exchange ( plasmapheresis ) removes harmful antibodies from plasma and replaces them with donor plasma .
Surgery ; Thymectomy ( removal of thymus gland ).
MEDICATION:
Cholinesterase inhibitors ( anticholinesterase) Immunosuppressants ( corticosteroids ) Prednisone
CAUSES:
1 Autoimmunity 2 Thymus gland ( enlarged) 3 Certain medications 4 Stress 5 Surgery 6 Illness 7 Infection 8 Pregnancy 9 Menstrual Period
DIAGNOSIS :
Blood test
The blood test is conducted to detect a specific antibody that obstructs the transmission of signals between nerves and muscles . Typically an elevated level of these antibodies indicates the presence pf MG in person . However ,it is not necessary that all individuals with this condition will manifest high levels of antibodies ,chiefly if it primarily affects the extraocular ( eye) muscles. In cases where symptoms persist despite a normal blood test result , the test may be repeated at a later time .
Nerve tests
The single fiber electromyography is used with the patient of MG during voluntary activation .The sweep is triggered on the first potential and increased fit of nerve is seen in the second potential. The electrical recordings can show whether the signals sent from the nerves to the muscles are being disrupted, which may be a sign of myasthenia gravis.
Scans
Thymus is a small gland which produces immune cells and makes immunity in the body to see thymoma imaging scans are done .In several cases brain MRI is done to ensure that MG hasn't affected the brain .
Edrophonium test/ Tensilon test
It is given intravenously through injection which contains a medicine known as edrophonium chloride. If the condition temporary improves in muscle strength after the injection in 10 min , then person may likely have myasthenia gravis. If the condition worsen in 10 min , then person may likely have cholinergic crisis.
CONCLUSION
Myasthenia gravis is an autoimmune disease that can be effectively treated. While a few patients with myasthenia gravis experience spontaneous remission or respond well to treatment with AChE inhibitors , the majority require corticosteroids and /or cortisteroid sparing drugs.
Comments
There are no comments for this story
Be the first to respond and start the conversation.