Treatment of Ocular Myasthenia With Corticosteroids: Yes

摘要: O CULAR findings often represent the first, and sometimes sole manifestation of acquired MG. Ocular MG, with weakness restricted to ocular muscles, is generally considered a mild subtype Nonetheless, diagnosis management purely MG may be particularly challenging frustrating. Diplopia ptosis, resulting from dysfunction neuromuscular junctions (NMJs) extraocular skeletal muscles levator palpebral in impair vision sufficiently interfere work quality life. Whereas symptoms are presenting they also tend most refractory treatment. Response anticholinesterases incomplete, pharmacological suppression NMJ immune attack or thymectomy required for resolution symptoms. The judicious use corticosteroids represents key component individual patients A second consideration that half clinically, reveal decrement on repetitive nerve stimulation extremity muscles. Furthermore, clinical at onset disease develop generalized weakness, especially within first year. This subgroup risk rapid deterioration. Myasthenic crisis better prevented than treated. In this context, treatment warranted electrophysiological evidence third arises recent observations suggesting withholding predispose severe disease. Myasthenia gravis commences 75% patients, susceptibility related antigenic structure and/or reduced safety factor Generalized result increased antibody production expansion molecular targets. Patients treated intervention early course less likely duration initial period an important determinant subsequent severity Correlation occurs other autoimmune conditions, including relapsing experimental encephalomyelitis. It possible unchecked response leads structural changes selfantigens destruction architecture. turn, exposure novel antigens potentiate attack, leading persistence severity. Symptomatic improve but mask ongoing damage. Abrogation would limit end organ damage resultant long-term stimulation,constitutinganadditional reason support treatments selected require close supervision.Optimally, corticosteroidsare used help induce maintain remission. Remission induction requires high oral doses 2 3 months. Potential complications include worsening during weeks therapy, asepticbonenecrosis,hyperglycemia,hypertension,osteoporosis, compromise, psychological disturbance, growth retardation inchildren, cataracts, glaucoma, proximalmyopathy,anddysmorphic soft tissue changes. Complications identified early; best prevented. Ancillary treatmentssuchaselandronatetoprevent osteoporosis useful. Most steroid correlate cumulativedose.Animportantmeans prevent receiving steroids totalsteroiddose.Thismaybeachieved, relapses kept minimum, by dose reduction slow, monitored fashionoverseveralmonths.Alternateday therapy reduces hypothalamicpituitary suppression. Additional strategies need disease, as well azathioprine reduction. differential includes oculopharyngeal dystrophy, mitochondrial disorders, congenital oculomotor neuropathies, brainstem lesions. usual laboratory absent. SeFrom Department Neurology, University California, Davis. CONTROVERSIES IN NEUROLOGY