Purpose of review: Although acute flaccid paralysis (AFP) is more frequently seen in the tropics than in temperate regions, recent outbreaks of West Nile virus (WNV) in North America have drawn attention to this important presentation. Starting with anatomical and neurophysiological considerations, this article examines data on AFP caused by WNV, and considers recent data on paralysis caused by enteroviruses, and Guillain-Barré syndrome (GBS).
Recent findings: Neurophysiological, radiological and pathological studies suggest WNV causes AFP by damaging anterior horn cells in the spinal cord. The clinical presentation is probably best described as a 'poliomyelitis-like illness', and the disease as 'WNV myelitis'. Other findings during the recent outbreaks include increasing recognition of a Parkinson's-disease like presentation, and descriptions of virus transmission in blood transfusions and transplanted organs. GBS is now recognized as several disorders characterized by immune-mediated attack on peripheral nerves: in acute inflammatory demyelinating polyneuropathy the myelin sheath and Schwann cell of sensory and motor nerves are targeted; acute motor axonal and acute motor and sensory axonal neuropathy often follow Campylobacter jejuni enteritis and are associated with antibodies against the ganglioside component of the nerve axolemmal membrane. In Asia-Pacific, enterovirus 71 has caused outbreaks of neurological diseases with AFP and encephalitis, but no single genogroup of virus appears responsible for severe disease.
Summary: Despite the near eradication of poliomyelitis, AFP caused by viruses remains an important clinical presentation. Distinguishing direct viral causes from GBS is important for public health reasons, and to avoid inappropriate therapies.