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It is not fully understood why some patients develop one pattern of tissue involvement while others show a different pattern. However some differences are likely to be due to anatomical variation: the secondary sequelae of GO relate to the interaction between the degree and speed of onset of the inflammation and the anatomical constraints of the orbit, which are at least in part racially determined. It is clear that there is premorbid variation in the relative position of the globe within the orbit and in the laxity of the anterior orbital septum (AOS)(see the section “Can You Give Me a Short Mechanistic Explanation for All These Clinical Manifestations?”).

Extraocular muscles tend to be asymmetrically involved. While most patients show some muscle involvement on imaging, up to 10% of patients show orbital fat expansion with apparently normal muscle dimensions. The latter can still lead to exophthalmos; however, restriction of eye movements is uncommon and when it does occur is diffuse rather than localized to 1 or several muscles. About 1 in 10 patients presents with unilateral exophthalmos of 2 mm or more [29]. Smoking is associated with more severe GO.

Fig. 3. Diagrammatic representation of secondary effects of GO. Secondary effects depend partly on the laxity of the AOS shown in red. a Normal relationships of structure within the orbit. b Gross compression of the nerve (white arrows) caused by increased orbital muscle volume unaccompanied by significant exophthalmos: therefore high intraorbital pressure. c Gross self-decompression. The optic nerve may be compromised by stretching.