Enterovirus D68 (EV-D68) has emerged worldwide as an important cause of respiratory disease. Between mid-August 2014 and January 15, 2015, the Centers for Disease Control and Prevention confirmed 1153 cases of EV-D68–associated respiratory illness originating from 49 states. With this outbreak, there have been at least 107 cases of children presenting with acute flaccid myelitis associated with lesions identified on magnetic resonance imaging that were largely restricted to the spinal gray matter.1-4 Children with this syndrome typically present with an acute febrile respiratory syndrome followed within 2 weeks by the development of acute flaccid myelitis, characterized by motor weakness, decreased tone and reflexes, and relatively preserved sensation. Weakness is of acute onset, preferentially affects upper limbs, and is often asymmetric. Cranial nerve involvement, including facial weakness, dysarthria, or dysphagia, may occur. Findings from the electrodiagnostic and magnetic resonance imaging studies are consistent with involvement of spinal cord motor neurons. Most patients have an associated cerebrospinal fluid pleocytosis. Paralysis has typically been prolonged and recovery incomplete. The exact role of EV-D68 in this syndrome has not been conclusively established, but approximately 50% of affected children have polymerase chain reaction–amplifiable EV-D68 RNA in nasopharyngeal or other upper respiratory tract secretions but not, to date, in cerebrospinal fluid.1,2,4
Tyler KL. Rationale for the Evaluation of Fluoxetine in the Treatment of Enterovirus D68-Associated Acute Flaccid Myelitis. JAMA Neurol. 2015;72(5):493–494. doi:10.1001/jamaneurol.2014.4625
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