Correction to: Meningomyeloradiculitis following yellow fever 17D vaccination: a case report.

There was an error in the original article. In the last paragraph of the Case Report section, the sentence "One month later, two plasma exchanges were followed by only slight improvements in upper-limb motor function (Fig. 1)." should have been "One month later, four plasma exchanges were followed.

Meningomyeloradiculitis following yellow fever 17D vaccination: a case report.

The yellow fever 17D vaccine contains live-attenuated virus. Initial efficacy and safety reports were favorable. Recently, however, neurologic and viscerotropic adverse events (AE) were described. We managed a 61-year-old man who experienced meningomyeloradiculitis 18 days after receiving the yellow fever 17D vaccine. The manifestations were atypical. The cerebrospinal fluid contained high titers of anti-yellow fever immunoglobulins M and G and of anti-flavivirus immunoglobulins G. After methylprednisolone (1 g/day for 3 days), intravenous human immunoglobulins (140 g over 5 days), and two plasma exchanges, the symptoms improved only slightly. Neurological adverse events after yellow fever vaccination are rare or underestimated. To our knowledge, this is the first reported case of meningomyeloradiculitis after yellow fever vaccination. A remarkable feature is the intrathecal production of yellow fever antibodies, which probably played a pathogenic role and may have been related to a recent episode of influenza.

Duloxetine-related posterior reversible encephalopathy syndrome: A case report.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) has well-established links with several drugs. Whether a link also exists with serotonin-norepinephrine reuptake inhibitor such as duloxetine is unclear. METHODS: We report on a patient who developed PRES with a coma and myoclonus related to hypertensive encephalopathy a few days after starting duloxetine treatment. Magnetic resonance imaging was performed and catecholamine metabolites assayed. RESULTS: The patient achieved a full recovery after aggressive antihypertensive therapy and intravenous anticonvulsant therapy. CONCLUSIONS: The clinical history, blood and urinary catecholamine and serotonin levels, and response to treatment strongly suggest that PRES was induced by duloxetine. Duloxetine should be added to the list of causes of PRES.