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(DON), and as they may not be volunteered, they should be specifically elicited from all patients with progressive or otherwise symptomatic disease as detecting subtle evidence of DON is crucial. If DON is significantly asymmetrical (30%), then an afferent pupil defect will also be apparent [13].

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      Older patients are also more likely to have unilateral or very asymmetrical disease and are more likely to be euthyroid or hypothyroid at the time of presentation [5].

      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?”).

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