Bilateral abducens nerve palsy has numerous causes, including cerebrovascular diseases, intracranial hypertension, carotid-cavernous fistulas, infection, trauma, Guillain—Barré syndrome, Wernicke—Korsakoff syndrome, and tumours. The condition rarely presents in isolation; when it… Click to show full abstract
Bilateral abducens nerve palsy has numerous causes, including cerebrovascular diseases, intracranial hypertension, carotid-cavernous fistulas, infection, trauma, Guillain—Barré syndrome, Wernicke—Korsakoff syndrome, and tumours. The condition rarely presents in isolation; when it does, presence of a tumour in the clivus should be ruled out. We present a case of bilateral abducens nerve palsy secondary to clival metastasis of prostate cancer. Our patient was a 72-year-old man with 6-year history of prostate adenocarcinoma and bone metastases who visited our emergency department in March 2018 due to diplopia of 2 months’ progression; he was receiving sixth-line treatment with radium-223 and had already completed 4 cycles, showing good tolerance. He initially reported difficulty with left eye abduction, developing difficulty with right eye abduction 2 weeks later. The most recent imaging studies available, performed a month previously, were bone scintigraphy, which revealed bone lesions in multiple sites, including the skull and the left superior maxillary bone (see online supplementary material), and a chest and abdominal axial CT scan, which revealed no visceral anomalies. A week previously, the patient had undergone a brain MRI study, which was initially interpreted as normal; however, a later evaluation of MR images detected contrast uptake in the left abducens nerve (Fig. 1). An electromyography study conducted the previous day had yielded normal results. The neurological examination detected isolated bilateral abducens nerve palsy (Fig. 2). A blood analysis detected no abnormalities; acute-phase reactants were within normal ranges. A head CT bone window study revealed diffuse hyperdensities in the clivus and sphenoid bones, suggestive of bone metastases (Fig. 1). We started outpatient treatment with dexamethasone dosed at 4 mg/24 h, which was later down-titrated, and skull base radiation therapy (total dose of 30 Gy); given the progression of the cancer, treatment was switched to a new line of chemotherapy with cabazitaxel. Diplopia resolved within 4 weeks, and has not reappeared after 6 months of follow-up. No follow-up neuroimages are available.
               
Click one of the above tabs to view related content.