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Myasthenia Gravis - Myasthenia Gravis By Robert R Zaid...

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Myasthenia Gravis By Robert R. Zaid Medical Student III February 19, 2004
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Outline Background Anatomy Pathophysiology Epidemiology Clinical Presentation Work-up Treatment Rehabilitation
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Background Acquired autoimmune disorder Clinically characterized by: Weakness of skeletal muscles Fatigability on exertion. First clinical description in 1672 by Thomas Willis
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Anatomy Neuromuscular Junction (NMJ) Components: Presynaptic membrane Postsynaptic membrane Synaptic cleft Presynaptic membrane contains vesicles with Acetylcholine (ACh) which are released into synaptic cleft in a calcium dependent manner ACh attaches to ACh receptors (AChR) on postsynaptic membrane
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Anatomy Neuromuscular Junction (NMJ) The Acetylcholine receptor (AChR) is a sodium channel that opens when bound by ACh There is a partial depolarization of the postsynaptic membrane and this causes an excitatory postsynaptic potential (EPSP) If enough sodium channels open and a threshold potential is reached, a muscle action potential is generated in the postsynaptic membrane
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Pathophysiology In MG, antibodies are directed toward the acetylcholine receptor at the neuromuscular junction of skeletal muscles Results in: Decreased number of nicotinic acetylcholine receptors at the motor end-plate Reduced postsynaptic membrane folds Widened synaptic cleft
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Pathophysiology Anti-AChR antibody is found in 80- 90% of patients with MG Proven with passive transfer experiments MG may be considered a B cell- mediated disease Antibodies
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Pathophysiology T-cell mediated immunity has some influence Thymic hyperplasia and thymomas are recognized in myasthenic patients*
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Epidemiology Frequency Annual incidence in US- 2/1,000,000 (E) Worldwide prevalence 1/10,000 (D) Mortality/morbidity Recent decrease in mortality rate due to advances in treatment 3-4% (as high as 30-40%) Risk factors Age > 40 Short history of disease Thymoma Sex F-M (6:4) Mean age of onset (M-42, F-28) Incidence peaks- M- 6-7 th decade F- 3 rd decade
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Clinical Presentation Fluctuating weakness increased by exertion Weakness increases during the day and improves with rest Extraocular muscle weakness Ptosis is present initially in 50% of patients and during the course of disease in 90% of patients Head extension and flexion weakness Weakness may be worse in proximal muscles
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Clinical presentation Progression of disease Mild to more severe over weeks to months Usually spreads from ocular to facial to bulbar to truncal and limb muscles Often, symptoms may remain limited to EOM and eyelid muscles for years The disease remains ocular in 16% of patients Remissions Spontaneous remissions rare Most remissions with treatment occur within the first three years
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Clinical presentation Basic physical exam findings Muscle strength testing Recognize patients who may develop respiratory failure (i.e. difficult breathing) Sensory examination and DTR’s are normal
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