Abstract
Purpose. We wanted to investigate the relative significance of fat and muscle enlargement in the development of dysthyroid optic neuropathy (DON) in Graves' orbitopathy (GO). Methods. Preoperative coronal CT scans of 13 patients with and without DON who subsequently underwent orbital decompression were retrospectively analyzed. Thirteen patients imaged for unilateral orbital fractures served as controls. Results. The retrobulbar muscle volume was 2.1 ± 0.5 cm3 (mean ± SD) in controls, 4.3 ± 1.5 cm3 in GO without DON, and 4.7 ± 1.7 cm3 in GO with DON. The retrobulbar fat volume was 5.4 ± 1.6 cm3 in controls, 8.7 ± 8.0 cm3 in GO without DON, and 9.4 ± 3.1 cm3 in GO with DON. The muscle and fat volumes were higher in patients with GO than in controls (P < 0.001), but the volumes in orbits with and without DON were not significantly different. The volume of the optic nerve were similar in the 3 groups. The number of apical, coronal 2 mm thick slices with no fat was 2.9 ± 0.9 in normal orbits, it was 4.1 ± 1.0 in GO orbits without DON and 5.3 ± 0.8 in GO orbits with DON (P = 0.007). Conclusion. Apical muscle enlargement may be more important than orbital fat enlargement in the development of DON. However, the fact that apical crowding and muscle enlargement also occur in orbits without DON suggests that other factors also play a role in the development of DON.
Highlights
Graves’ disease is an autoimmune disease manifesting in the thyroid, in the dermis, and in orbital connective tissues and muscles [1]
Comparison of normal female and male orbits showed that male orbits had 14% greater orbital muscle volume and female orbits had 10% more orbital fat volume than male orbits
We examined the orbital volumes of retrobulbar muscle, fat, and optic nerve in orbits from patients with Graves’ disease complicated with Graves’ orbitopathy (GO) and compared them with normal orbits
Summary
Graves’ disease is an autoimmune disease manifesting in the thyroid, in the dermis, and in orbital connective tissues and muscles [1]. The time association between GO and thyroid disease varies; GO can occur before, during, or after the onset of hyperthyroidism and, less frequently, in euthyroid or hypothyroid cases. The symptoms and signs of active GO include eye discomfort and watering eyes, double vision, eyelid retraction, proptosis, eyelid edema, strabismus, chemosis, disfigurement, corneal problems, and dysthyroid optic neuropathy (DON) [2, 4]. The latter is the most serious manifestation of GO. DON occurs in 3.4–8% of patients and is thought to be due to optic nerve compression in the orbital apex by enlarged muscles [3,4,5]. The presence of DON can be established by using simple clinical criteria such as reduced visual acuity and the finding of impaired colour vision by using Ishihara colour plates [4]
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