Thyroid Eye Disease (TED) is a complex autoimmune condition that causes inflammation and swelling of the tissues and muscles surrounding the eyes. Although often called Graves’ ophthalmopathy, it most commonly occurs in people with Graves’ disease. Specialized testing is necessary because TED symptoms, such as eye bulging, redness, and double vision, can easily be mistaken for other eye disorders. A comprehensive diagnostic approach is required to confirm the presence of TED, assess its severity, and determine the optimal treatment strategy.
Clinical Examination and Symptom Assessment
The initial step in diagnosing Thyroid Eye Disease involves a detailed clinical examination performed by an ophthalmologist. This assessment focuses on quantifying the physical changes and the impact of the disease on visual function.
Proptosis, or the forward bulging of the eye, is measured using a Hertel exophthalmometer. This device rests on the lateral orbital rims and measures the distance from the corneal apex to the rim. A reading greater than 20 millimeters or an asymmetry between the eyes of more than two millimeters is generally considered significant for proptosis.
The doctor also assesses for signs of inflammation and disease activity using the Clinical Activity Score (CAS). This score is typically based on seven specific signs of active inflammation, including spontaneous orbital pain, pain on attempted eye movement, redness of the eyelids, and swelling of the conjunctiva. A score of three or higher is often used to define active, inflammatory disease, which helps guide the decision for anti-inflammatory treatment.
Eyelid retraction is another common sign, often presenting as a visible white area (scleral show) above or below the iris. The physician meticulously evaluates eye movement, as the swelling of extraocular muscles can restrict movement, leading to diplopia, or double vision. This double vision is restrictive, meaning the eye cannot physically move in certain directions due to the enlarged muscles, differentiating it from other neurological causes of diplopia.
Laboratory Testing for Autoimmune Status
While the clinical examination detects physical effects, blood tests are essential to confirm the underlying autoimmune driver. Standard thyroid function tests measure the levels of Thyroid Stimulating Hormone (TSH), Free T3, and Free T4. In most cases, a person with active TED will have suppressed TSH and elevated Free T3 and Free T4, indicative of hyperthyroidism associated with Graves’ disease.
The most definitive markers are the Thyroid Receptor Antibodies (TRAb), and specifically the Thyroid Stimulating Immunoglobulin (TSI). These antibodies mistakenly bind to the TSH receptors found on both the thyroid gland and the orbital tissues. The presence of elevated TRAb or TSI confirms the diagnosis of Graves’ disease and is highly correlated with the development and severity of TED.
Testing for these antibodies is important because TED can occur even when TSH, T3, and T4 levels are normal, a condition known as euthyroid Graves’ ophthalmopathy. In these cases, TED is confirmed not by hormone imbalance, but by the presence of high levels of the specific autoantibodies attacking the eye tissues. Serial measurement of TRAb can also monitor the activity and progression of the autoimmune process.
Structural Confirmation Through Advanced Imaging
Advanced imaging techniques are mandatory to visualize the internal structures of the orbit and confirm the extent of tissue damage. Computed Tomography (CT) scans and Magnetic Resonance Imaging (MRI) are the primary tools used, each offering unique advantages. CT scans provide excellent detail of the bony orbit and are often used when surgical decompression is considered, while MRI is superior for showing soft tissue and assessing active inflammation.
The characteristic finding in TED is the enlargement of the extraocular muscle bellies, described as “tendon-sparing.” This means the muscle tissue swells, but the distal tendon connecting the muscle to the eyeball remains normal in size. This distinctive pattern helps differentiate TED from other inflammatory orbital disorders where the entire muscle, including the tendon, is enlarged.
The extraocular muscles are typically involved in a specific order, with the inferior rectus and medial rectus muscles being the most frequently affected. Imaging is crucial for detecting orbital apical crowding, which is the compression of the optic nerve at the narrowest part of the eye socket. This occurs when the massively enlarged muscles and surrounding fat tissue reduce the space available for the optic nerve, representing a sight-threatening complication that demands immediate intervention. MRI, especially with specialized sequences, can identify active inflammation within these muscles, helping determine if the disease is still in its active, treatable phase.