Involvement of the eyes can be an unpredictable accompaniment of thyroid disorders, producing a spectrum of symptoms ranging from eye irritation, swelling, light sensitivity, and a staring appearance to the less frequent but more severe problems of double vision, cornea erosion, and optic nerve compromise. The initial symptoms are common and annoying. The more advanced symptoms can evolve into permanent eye changes and threaten vision, but these occur in only a small percentage of people with thyroid disorders.
To understand the answers to these questions, one needs some information about the autoimmune basis of the disorder, the several degrees of eye changes, and the expected disease course.
Eye problems developing with hyperthyroidism were described over 160 years ago by Dr. Robert Graves of Dublin. That is why it is called Graves' disease. It is now known to be an autoimmune disorder. By "autoimmune," we mean that the body's immune system produces a reaction to its own tissues -- in the case of Graves' disease react not only against thyroid cells, but also commonly react against tissues behind the eyes (muscles and fat) and rarely react against skin tissues of the legs and hands. The reasons for this autoimmune reactivity to several tissues is not fully understood, but probably relates to similar tissue antigens in these areas, or perhaps to neighboring genetic locations for these tissues.
The eye involvement, like the thyroid disorder, is mediated in part by white blood cells (lymphocytes) that accumulate in the targeted tissues. These cells produce the antibodies that cause local tissue inflammation and fluid accumulation, resulting in abnormal functioning of the affected tissues.
Connective tissue cells (fibroblasts) also react by releasing complex proteins.
For the thyroid gland, this usually causes overactivity and increased release of thyroid hormones. For the eyes, the immune reaction causes swelling of muscles and fat behind the eyes (orbital tissues), resulting in retraction of the eyelids, forward protrusion of the eyes (proptosis or exophthalmos), and sometimes dysfunction of the eye muscles and optic nerve.
Most of the eye problems develop, if they are going to occur at all, within eighteen months of the hyperthyroidism. Since the autoimmune process may selectively affect the thyroid gland, the eyes, or the skin, variants of Graves' disease are seen in which one, two, or all three of these tissues are affected. Thus, the thyroid may be overactive while the eyes and skin remain normal. Alternatively, eyes or skin may be affected while the thyroid continues to release normal amounts of thyroid hormone.
While most people with overactive thyroid due to Graves' disease probably have some mild eye changes that do not cause them any symptoms, about three per cent of them with more severe disease will require some form of treatment. Although clinicians speculate that the type of treatment given to control thyroid overactivity may influence the development of eye problems, there is as yet not clear consensus that one form of treatment is superior in preventing the later emergence of eye involvement.
Although the fundamental cause of Graves' eye disease remains unknown, we do understand the immediate cause of the symptoms and findings that patients experience. The eye socket is a cone and the globe of the eye sits in it like a scoop of ice cream. The walls of the cone are made of bone that resists expansion. The muscles that move the eyes partially fill the space in the cone behind the globe and the rest of that space is filled with vessels and loose connective tissue. Through this space runs the optic nerve.
In Graves' eye disease the eye muscles and connective tissue swell for reasons that are still not fully understood. Regardless of why they swell however they increase the pressure in the space behind the globe of the eye and force the globe forward in the orbital cone. As the globe moves forward more of the sensitive cornea is exposed. The eyes become red and congested and the eyelids fail to cover the protruding globe. If the pressure behind the eye is high enough the function of the optic nerve may be impaired and this can cause blurring of vision and loss of color vision. The swollen eye muscles move sluggishly and when they do not move in concert the patient experiences double vision. Thus one can accurately state that ALL the clinically apparent manifestations of Graves' eye disease stem from either swelling in the space behind the globe of the eye or from restriction of the motion of the muscles that move the globe of the eye. It follows that effective treatment for Graves eyes will either reduce the swelling, expand the space, or improve the range or coordinate the movement of the eye muscles.
For many years cortisone derivatives such as prednisone or prednisolone have been used to reduce the swelling and congestion in Graves' eyes. These agents are effective but when used long term or in high dosage they evoke undesirable side effects such as weight gain, high blood sugar and thin bones. Other immunosuppressive agents such as azathioprine have been tried but have not been widely accepted as being both safe and effective. External beam radiotherapy has been employed for the same purpose but its usefulness has recently been challenged and its place in the treatment of Graves' eyes is currently being reassessed.
Treatments that expand the orbital space include many varieties of orbital decompression which vary only in where the incision is made, from which orbital wall bone is removed and how much new space is actually created. Different medical centers tend to specialize in different procedures so it is wise to ask your surgeon for the information that supports the choice you have been offered.
Treatments that affect the movement of the eye muscles are almost entirely surgical. There may be some role for exercises intended to strengthen the eye muscles. Some patients are very much benefited by the addition of prisms to their glasses. These prisms can correct for minor degrees of double vision. Severe degrees of double vision require repositioning the shortened swollen eye muscles so they can at least keep the eye straight in the resting position and while reading.
In approaching surgical treatment of Graves' eye disease the desired sequence is to first perform orbital decompression if it is needed. Eye muscle surgery is next and surgery that is intended to improve eyelid position is done last. As is true of most surgical procedures the training, skill and experience of your surgeon are important determinants of outcome.
Your thyroid gland tells every cell in your body the rate at which it should function.