Strabismus in Thyroid-Associated Orbitopathy

Thyroid associated orbitopathy (TAO) is a frequent cause of single or multiple extraocular muscle enlargement leading to restrictive strabismus. The impairment of ocular motility is caused by inflammation, followed by fibrosis, of the muscles involved. The inferior rectus and medial rectus muscles are most commonly involved, with typical enlargement of the muscle belly and sparing of the muscle tendon. Pathophysiology of TAO involves insulin-like growth factor-1 receptor (IGF-1R) overexpression and activation, with increased release of proinflammatory cytokines, inflammation, and expansion of extraocular muscle and consequent restrictive strabismus. Glucocorticoids are the first-line treatment of active TAO to reduce orbital inflammation to improve extraocular motility, and to reduce diplopia. Orbital radiation therapy (OR) is effective in recent onset ocular motility impairment. Teprotumumab, an insulin-like growth factor-1 receptor inhibitor, has shown remarkable results in reduction of diplopia in multicenter, randomized placebo-controlled trials. In patients with TAO, strabismus surgery should not be carried out until the angle of deviation is stable for at least 4 months, and observation is advisable when diplopia is absent in primary or reading position. Indications, timing and aims of surgical treatment and basic rules of surgical techniques are described and discussed. Under-correction is the most common reported complication of horizontal strabismus correction; late over-correction may occur following inferior rectus recession. Strabismus surgery should be performed after decompression surgery, as decompression can modify the initial deviation or result in new onset strabismus. However, a combined surgical treatment may be proposed in selected patients.