MANAGEMENT OF THYROID OPTIC NEUROPATHY

Thyroid ophthalmopathy is the most common orbital disorder of adults. Synonymous terms include Graves' orbitopathy, thyroid-related immune o rbitopathy, and dysthyroid ophthalmopathy. Thyroid orbitopathy most co mmonly occurs in patients with active or treated Graves' disease, typi cally within 1 year of development of hyperthyroidism. Patients with t hyroid orbitopathy, however, may be euthyroid or hypothyroid. The diso rder usually affects women in the fourth and fifth decades, the female -to-male ratio being approximately 4:1. Thyroid orbitopathy is clinica lly apparent to some extent in nearly half of all patients with Graves ' disease. The incidence of Graves' disease in the United States is ap proximately 0.4%. The clinical manifestations of thyroid ophthalmopath y include eyelid retraction, proptosis, restrictive myopathy (most com monly involving the medial or inferior rectus muscles), conjunctival c ongestion, exposure keratopathy, elevated intraocular pressure, and op tic neuropathy. Thyroid orbitopathy is considered to be of autoimmune etiology, but the specific pathophysiology is poorly understood. Both humoral and cell-mediated mechanisms have been invoked, although their exact roles are not yet defined. The stimulation of orbital fibroblas ts to produce excess glycosaminoglycans and direct autoimmune damage t o orbital tissues have been postulated as general mechanisms for the o rbitopathy. The myriad immunological findings and experimental results attempting to pinpoint the pathophysiology of thyroid orbitopathy are beyond the scope of this discussion.