Myasthenia gravis is an autoimmune disorder in which antibodies target the neuromuscular junction, and fatigable weakness that worsens with use and improves with rest is the hallmark feature. The most common initial presentation is ocular, with ptosis and diplopia, and approximately 85% of ocular MG patients progress to generalized disease within 2 years. There is a well-recognized autoimmune association with Graves disease and other autoimmune conditions. The ice test is a useful bedside maneuver that improves ptosis by slowing acetylcholinesterase activity through cooling. Anti-acetylcholine receptor antibodies are positive in approximately 85% of generalized cases, and seronegative patients may have anti-MuSK or anti-LRP4 antibodies. Repetitive nerve stimulation showing a decremental response greater than 10% at low-frequency stimulation confirms the neuromuscular junction defect. Chest imaging should always be obtained because approximately 15% of patients have a thymoma and approximately 65% have thymic hyperplasia. Treatment includes pyridostigmine for symptomatic relief, immunosuppression with corticosteroids or steroid-sparing agents, thymectomy, and IVIG or plasmapheresis for myasthenic crisis. Myasthenic crisis with respiratory failure is the most dangerous complication, and forced vital capacity should be monitored closely in patients with worsening bulbar or respiratory symptoms. Medications that can exacerbate MG and must be used with caution include aminoglycosides, fluoroquinolones, beta-blockers, and magnesium.