Thyroid ophthalmopathy (Graves orbitopathy) is an autoimmune orbital inflammatory disease associated with Graves' disease and is one of the most common causes of orbital masses in adults. Autoimmune antibodies against the TSH receptor activate fibroblasts in extraocular muscles and orbital fat tissue, causing inflammation, edema, and fibrosis. Bilateral involvement is typical but may be asymmetric; unilateral presentation occurs in 5-10% of cases. The characteristic finding is extraocular muscle thickening with tendon sparing — inferior rectus > medial rectus > superior rectus > lateral rectus pattern ('I'M SLow' mnemonic). Increased orbital fat tissue (lipogenesis) contributes to proptosis. In severe cases, optic nerve compression (dysthyroid optic neuropathy) can cause vision loss.
Age Range
25-65
Peak Age
45
Gender
Female predominant
Prevalence
Common
Thyroid ophthalmopathy begins with autoimmune antibodies against the TSH receptor (TRAb) activating orbital fibroblasts. Orbital fibroblasts are present in both extraocular muscles and orbital fat tissue, expressing TSH receptor and IGF-1 receptor. Antibody activation leads to glycosaminoglycan (especially hyaluronic acid) production and adipogenesis by fibroblasts; hyaluronic acid draws water through its strong hydrophilic structure, increasing extraocular muscle volume — reflected as muscle thickening on MRI/CT. Tendon sparing results from the much lower fibroblast density in tendon tissue compared to muscle belly — autoimmune targeting is concentrated in the muscle belly. The 'I'M SLow' pattern reflects the relatively higher fibroblast content of inferior and medial rectus muscles. In the chronic phase, inflammation converts to fibrosis and muscle stiffness/restriction develops. When increased orbital content (swollen muscles + expanded fat) is confined by the bony orbital walls, anterior displacement occurs (proptosis); crowding at the orbital apex can compress the optic nerve, developing dysthyroid optic neuropathy.
On coronal CT reformats, bilateral thickened medial and lateral rectus muscles appear as an expanded 'bottle body' in the mid-orbit, while thinning toward normal tendon insertion at the orbital apex appears as a narrow 'bottle neck' — this image resembles a Coca-Cola bottle. This sign is a characteristic coronal CT finding for thyroid ophthalmopathy and summarizes bilateral extraocular muscle thickening with tendon sparing in a single image. Muscle involvement pattern (I'M SLow: inferior > medial > superior > lateral) is also evaluated on the same coronal sections.
CT demonstrates bilateral extraocular muscle thickening; tendon insertion sites are preserved at normal thickness and thickening is concentrated in the muscle belly — fusiform enlargement pattern. 'Coca-Cola bottle' appearance is created on coronal reformats: thickened medial and lateral rectus muscles represent the bottle body, while normal orbital apex represents the bottle neck. Involvement pattern typically follows inferior rectus > medial rectus > superior rectus > lateral rectus. Increased orbital fat volume accompanies and contributes to proptosis. Bilateral but asymmetric involvement is typical.
Report Sentence
Bilateral fusiform thickening of extraocular muscles is identified in both orbits with preserved tendon insertions — a finding consistent with thyroid ophthalmopathy.
On T2-weighted sequences in the active inflammation phase, extraocular muscles show increased signal (hyperintensity) — indicating edema and inflammatory infiltration. Muscle edema becomes more prominent on fat-suppressed T2 (STIR/TIRM) sequences. T2 signal increase is prominent in the acute/active phase, while signal normalizes or decreases in the chronic/fibrotic phase — this T2 signal change is critical for disease activity assessment and guides treatment planning. Orbital fat increase is also seen as expansion of orbital fat compartments on T2 STIR.
Report Sentence
Increased signal in extraocular muscles of both orbits is identified on T2-weighted STIR sequences, consistent with active inflammatory process.
On contrast-enhanced MRI, thickened extraocular muscles show enhancement in the active inflammation phase — reflecting inflammatory hypervascularity and capillary permeability increase. Enhancement is concentrated in the muscle belly, tendon insertion site does not enhance (tendon-sparing). In the chronic/fibrotic phase, enhancement decreases or disappears. Fat-suppressed T1 post-contrast sequence shows muscle enhancement most clearly by separating it from orbital fat. Lacrimal gland enhancement may accompany.
Report Sentence
Increased enhancement of thickened extraocular muscles is identified on contrast-enhanced fat-suppressed series, consistent with active thyroid ophthalmopathy.
Coronal CT demonstrates thickened extraocular muscles surrounding and compressing the optic nerve at the orbital apex — 'apical crowding' finding. This finding indicates risk of dysthyroid optic neuropathy and suggests need for urgent treatment (high-dose steroids or surgical decompression). Narrowing of subarachnoid space around the optic nerve sheath and prominence of optic nerve sheath may accompany. May be bilateral but asymmetric — more severe unilateral involvement correlates with vision loss risk.
Report Sentence
Coronal images demonstrate thickened extraocular muscles surrounding and compressing the optic nerve at the orbital apex ('apical crowding'), indicating risk of dysthyroid optic neuropathy.
B-mode ultrasonography can measure increased extraocular muscle thickness — while normal muscle thickness is 3-5 mm, it can reach 7-12+ mm in thyroid ophthalmopathy. Muscle echogenicity decreases in the acute phase (edema, hypoechoic) and increases in the chronic phase (fibrosis, hyperechoic). Tendon sparing can be demonstrated by decreased thickening at the muscle-tendon junction. Orbital fat increase may be seen as echogenicity changes in retrobulbar fat. On A-mode ultrasonography, low internal reflectivity is consistent with acute inflammation, high internal reflectivity with chronic fibrosis.
Report Sentence
Ultrasonography demonstrates increased extraocular muscle thickness in both orbits with low echogenicity consistent with acute inflammatory process.
Criteria
Orbital fat increase is the dominant finding. Extraocular muscles are normal or mildly thickened. Proptosis results from fat expansion. Generally seen in younger patients.
Distinct Features
Orbital fat volume markedly increased on CT, muscles normal. Optic neuropathy risk is low. Medical treatment usually sufficient instead of surgical decompression. Fat decompression (fat removal) is surgical option.
Criteria
Extraocular muscle thickening is the dominant finding. Orbital fat is normal or minimally increased. Generally seen in older patients. Optic neuropathy risk is high (apical crowding).
Distinct Features
Proptosis may not be prominent — muscles expand and fill toward apex, compressing optic nerve. Urgent steroid or surgical decompression may be needed. CAS score and T2 STIR signal increase are activity indicators.
Criteria
Both orbital fat increase and extraocular muscle thickening are prominent — most common type. Both proptosis and eye movement restriction are present.
Distinct Features
Combined treatment approach may be needed. Activity assessment is done with MRI. Surgical decompression may include both bone and fat decompression.
Distinguishing Feature
Orbital pseudotumor is usually unilateral, painful, and rapid-onset. Tendon involvement is seen (tendon thickening) — unlike thyroid ophthalmopathy, tendons are not spared. Lacrimal gland and orbital fat infiltration may accompany. Rapid response to steroid therapy is typical. Thyroid function tests are normal.
Distinguishing Feature
Orbital lymphoma shows diffuse orbital infiltration, wrapping around structures with 'moulding' effect. Marked restricted diffusion on DWI (high cellularity). Usually begins unilaterally. Thyroid ophthalmopathy is differentiated by bilateral tendon-sparing muscle thickening. Biopsy is needed for diagnosis.
Distinguishing Feature
IgG4-related orbital disease is characterized by bilateral lacrimal gland enlargement and infraorbital nerve thickening. Extraocular muscle involvement may occur but lacrimal gland involvement is dominant. Elevated serum IgG4 is a diagnostic clue. In thyroid ophthalmopathy, lacrimal gland involvement is secondary and muscle involvement is dominant.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
CAS (Clinical Activity Score) for disease activity. MRI with STIR for muscle edema assessment. Selenium supplementation for mild disease. IV methylprednisolone for moderate-severe active disease. Teprotumumab (IGF-1R inhibitor) as targeted therapy. Orbital decompression for sight-threatening or disfiguring disease.Treatment of thyroid ophthalmopathy is determined by disease activity and severity. Selenium supplementation and tear replacement may be sufficient for mild disease. For moderate-severe active disease, intravenous methylprednisolone (EUGOGO protocol) is first-line treatment. Teprotumumab (anti-IGF-1R antibody) is a new FDA-approved targeted therapy effective in reducing proptosis and diplopia. When dysthyroid optic neuropathy develops, urgent high-dose steroids and surgical decompression (endoscopic medial wall decompression or multi-wall decompression) are required. In the stable/inactive phase, eye muscle surgery (strabismus correction) and orbital decompression (cosmetic) can be planned. Treatment sequence: medical first → surgical decompression → strabismus surgery → eyelid surgery (rehabilitation pyramid). Thyroid function of all patients must be normalized — euthyroid state is critical for orbital disease stabilization.
Steroids or radiotherapy are used in the active inflammatory phase. Optic nerve compression requires urgent decompression. Orbital decompression or strabismus surgery may be considered in the chronic phase.