Abstract
In the past decade, we have learned that Graves' ophthalmopathy is probably part of a multi-organ autoimmune disease in genetically susceptible individuals. The orbital target tissue is the extraocular muscle (EOM), which becomes distended acutely and contracted chronically. The swollen EOMs, especially the medial rectus, may compress and damage the optic nerve at the orbital apex. The external soft tissue signs are identical in Graves' patients with and without optic neuropathy. It is the ductional deficits that identify those with high risk for optic neuropathy, so attention to the motility disturbance is critical.
Judicious use of corticosteroids, x-irradiation and orbital wall removal is effective in preventing and reversing visual loss in a majority of acute cases. Of the newer medical remedies, cyclosporine A holds the greatest promise, but is limited by its toxicity. We still lack information on the comparative efficacy of the various treatments and on the optimal timing of their use.