In thyroid eye disease, autoimmune inflammation of orbital musculature and fat increases the bulk of the orbital contents. Orbital tension rises and patients stratify according to the ease with which their globes can proptose. Restriction of proptosis is associated with optic nerve compression and visual loss; exophthalmos, with corneal damage. Ocular motility is affected, initially by muscle inflammation; late in the disease, by fibrosis. Extraocular factors, including thyroid endocrine disturbance, antigen release, infections, malignancies, and smoking, may trigger and drive the orbital myopathy. The management of thyroid eye disease by the identification and treatment of drives, followed by immunomodulatory therapy, is discussed. Fourteen patients with compressive optic neuropathy were treated with immunomodulation using intravenous methylprednisolone, oral prednisolone, and cyclosporin A, and followed up for a minimum of three years. All recovered their pre-morbid visual acuities and visual fields in both eyes. Severe disturbances of ocular motility also recovered in 30 patients, treated with the same regime. In one subject, ocular motility normalised with intravenous steroids and cyclosporin A, but no oral prednisolone. Morbidity from the treatment was low. Immunomodulation is a rational and successful method for managing optic nerve compression and disordered motility in this condition.