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GRAVES` DISEASE
Symptoms and Signs
History
Epidemiology
Etiology
Ocular signs
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Etiology

Most people with thyroid eye disease had, do have or will subsequently develop an overactive thyroid gland. Although associated with thyroid dysfunction, or hyperthyroidism, in 10–15% of cases the condition occurs without clinical or biochemical evidence of thyroid disease. Occasionally people have a normally functioning thyroid gland but have abnormal antibodies against their thyroid gland. In 40% thyroid eye disease occurs while the thyroid is overactive and in 40% can occur years after the overactive thyroid has been treated successfully. A minority of patients are even hypothyroid at the time their eye disease occurs.

Overactivity of the thyroid gland is usually caused by an «autoimmune condition». This means that cells which normally protect the body from infection develop a "fault" and begin to recognise the thyroid gland as foreign material and attack it. This stimulates the thyroid gland to produce extra thyroid hormones. The attacking process may spill over to the tissues (fat and muscles) in the orbit causing them to swell. It is not yet known why cells develop the fault that causes them to attack the thyroid gland or why only a fraction of patients with overactivity of the thyroid develop thyroid eye disease. Thyroid eye disease does appear to be more common and more severe in smokers.

It is not clear, how or why the immune system attacks the orbital tissues. The result is enlargement of the fat volume and the extraocular muscles. As the muscles get larger, 3 things can happen. The eyeball gets pushed forward, the muscles themselves become stiff (the eye may not move normally), or the muscles may press on the optic nerve. The medial and inferior rectus muscles tend to be more often affected than others. When they becomes stiff, the globe cannot move normally. This often results in double vision with one image seen on top of the other. If the optic nerve is compressed, the patient is usually aware of blurred, dark or dim vision. There may be blurring or distortion related to surface problems due to the exposure and drying. It is important for the physician to sort out whether or not there is any evidence of optic nerve dysfunction. This is detected by carefully checking vision, pupillary reactivity, visual fields, colour vision, visual evoked potentials and the appearance of the optic nerve head.

Although Graves` Orbitopathy is usually preceded by thyroid abnormalities sometimes the eye symptoms may come first or the thyroid may appear to be normal. The connection between the eyes and the thyroid is through the immune system. The same conditions that lead to the immune system attacking the eye muscles often precedes an attack on the thyroid gland. Most frequently this makes the thyroid gland produce thyroid hormone inn excess that in turn can lead to tremors, shakes, weight loss, rapid heart beat or palpitations, nervousness, and sensitivity to heat. Less commonly the attack on the thyroid gland leads to low thyroid production or even normal thyroid levels.