Dysthyroid optic neuropathy: a clinical diagnosis or a definable entity?
- 1Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, Bristol, UK
- 2Department of Ophthalmology, Royal Victoria Infirmary, Newcastle upon Tyne, UK
- Correspondence to: Dr C M Dayan Dorothy Hodgkin Building, University of Bristol, Whitson St, Bristol BS1 3NY, UK;
The diagnosis of DON should be made correctly; those affected should be treated promptly and those unaffected spared the risks associated with treatment.
Optic neuropathy is the most feared complication of thyroid eye disease (TED). Thankfully, it is rare, affecting perhaps 4–8% of patients with TED,1,2 but when diagnosed requires urgent treatment with medical (eg, high-dose intravenous steroids) or surgical decompression to avoid permanent or progressive visual loss.3 However, both these treatments carry a considerable risk of morbidity. Hence, it is essential that the diagnosis is made correctly in order that those affected are treated promptly and those unaffected are spared the risks associated with treatment.
Several features are used to make the diagnosis of dysthyroid optic neuropathy (DON) (table 1).1,2,4 The assumption is generally made that if any of these features are present in an individual with dysthyroid eye disease and no other explanation of the defect is apparent, then the individual has DON. Unfortunately, alternative causes for visual impairment are often present in TED—estimated at 20% or more of cases.5,6 Several of these may be linked to the TED itself (eg, keratopathy or glaucoma due to increased orbital venous pressure),7 whereas others are coincidental (eg, amblyopia, uncorrected refractive errors or cataracts). This poses a considerable problem: if the alternative causes are not identified, then DON may be inappropriately diagnosed, whereas if alternative causes are present, visual impairment might be inappropriately ascribed to them when in fact DON is present.