An unusual cause of diplopia

Excerpt

We here report the case of a 51-year-old man who was admitted in our neurology unit to explore a sudden onset of diplopia. Upon clinical examination, the patient showed signs of intrinsic and extrinsic right third nerve palsy, which had developed over a couple of days, without any associated pain or visual acuity loss. Clinical examination was otherwise normal. Angio-CT scanner, brain MRI and MRA were normal, as was the neck Doppler. MRI included high-resolution sequences, and no meningeal or third nerve enhancement was observed after Gadolinium contrast medium injection (Fig. 1). Peripheral blood counts were normal. Due to a strong history of autoimmune disorders (pericarditis, uveitis, Grave-Basedow thyroiditis, vitiligo), biological signs of active inflammatory disorders were looked for but there was none, with the exception of slightly increased sedimentation rate (28 mm/h) and C-reactive protein (14.6 mg/L). The patient was under Acenocoumarol for a recent pulmonary embolism, and l-Thyroxin. Past treatment included corticosteroids, colchicine, and radioiodine ablation of the thyroid. Analysis of the cerebrospinal fluid (CSF) showed a moderate increase in protein levels, and increased numbers of white blood cells (23/mm³). Those cells were identified as 92 % of myeloid blasts (Fig. 2). A bone marrow biopsy revealed an infiltration by 29 % of myeloblasts, confirming the diagnosis of acute myeloid leukaemia (AML). Cytogenetic and molecular analyses revealed a t(9;11)(p22;q23) rearrangement of MLL(KMT2A/MLLT3) gene, as well as trisomy 3 (EVI1, 3q26). An ¹⁸F-fluorodeoxyglucose PET-CT was performed and did not reveal any other extra medullary localisation.

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