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Myasthenia Gravis

Myasthenia Gravis. Disease of the neuromuscular junction characterized by fluctuating weakness of certain skeletal muscle groups. Myasthenia Gravis(MG). Acetycholine (ACh) is an important neurotransmitter that stimulates muscle tissue to contract.

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Myasthenia Gravis

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  1. Myasthenia Gravis • Disease of the neuromuscular junction characterized by fluctuating weakness of certain skeletal muscle groups. Neurology Chapter of IAP

  2. Myasthenia Gravis(MG) • Acetycholine (ACh) is an important neurotransmitter that stimulates muscle tissue to contract. • MG is an autoimmune disease in which antibodies are formed against ACh and a reduction in ACh receptor sites at the neuromuscular junction. Neurology Chapter of IAP

  3. Neurology Chapter of IAP

  4. Pathophysiology • Loss of muscle strength. • There is no single cause identified, however, thymic tumors and viral infections have been found in a certain number of patients. Neurology Chapter of IAP

  5. Clinical manifestations • Primary s/s= easy fatigability of skeletal muscle during activity. • Muscles involved: eyes and eyelids, chewing, swallowing, speaking, and breathing. • Fluctuating weakness: usually strong in the a.m., progressively weaker with activity. Neurology Chapter of IAP

  6. Clinical Manifestations • 90% of patients have eye involvement • Facial mobility may be impaired • Muscles of limb and trunk less often affected. • No sensory or reflex loss; muscle atrophy is rare. Neurology Chapter of IAP

  7. Clinical manifestations • Variable course • May be precipitated by emotional stress, pregnancy, menses, secondary illness, trauma, temperature extremes, hypokalemia, ingestion of drugs with neuromuscular blocking agents, surgery. Neurology Chapter of IAP

  8. Complications • Aspiration, respiratory insufficiency, and respiratory infection • Acute exacerbation called myasthenic crisis. • The opposite of this is a cholinergic crisis and results from overdose of cholinergic drugs. Neurology Chapter of IAP

  9. Diagnostic studies • Assessment: • Have pt look up for 2-3 minutes; if MG, patient will have increased droop of eyelids. • EMG may show muscle fatigue • Tensilon test- in MG reveal improved muscle contractility after IV anticholinesterase agent edrophonium chloride (tensilon) • Also diagnosis cholinergic crisis- muscle weakness gets worse • Keep atropine on hand to counteract effects of tensilon Neurology Chapter of IAP

  10. Therapeutic management • Anticholinesterase inhibitors-prevents anticholinestersase from breaking down ACh; helps neurotransmission. Monitor dose! • Mestinon, Prostigmine Corticosteroids- decrease immune response Prednisone Plasmapheresis- removes ACh antibodies and short-term improvement. Neurology Chapter of IAP

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