Wernicke encephalopathy is an easily missed but highly treatable condition, as the case by Drs. Fujikawa and Sogabe reminds us.1 In addition to typical features of nystagmus, ophthalmoplegia, ataxia and mental status changes, their patient had optic disc edema, which the authors felt was due to optic neuropathy unrelated to Wernicke encephalopathy. However, optic neuropathy has been described in the literature as a manifestation of thiamine deficiency, albeit uncommon, with optic disc edema present in most of these cases.2–8 This edema seems to range from peripapillary retinal nerve fibre layer thickening with retinal hemorrhage2 to marked optic disc swelling with peripapillary hemorrhage3 to pale edema.4 In some cases, the vision loss has been severe, including loss of light perception; however, substantial visual improvement as well as resolution of edema has been reported following thiamine replacement.8 Therefore, it may be unnecessary to consider another etiology when encountering optic disc edema in a patient with Wernicke encephalopathy, particularly in the absence of other concerning neurologic or neuroimaging findings or exposures. That being said, patients with certain genetic conditions, such as Leber hereditary optic neuropathy (Leber being less likely in Drs. Fujikawa’s and Sogabe’s female patient), appear more vulnerable to having their optic neuropathy triggered or exacerbated by nutritional deficiencies.9
Footnotes
Competing interests: None declared.
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