Clinical spectrum of muscle weakness in human West Nile virus infection

• Published in: Muscle & nerve 2003-09, Vol.28 (3), p.302-308
• Main Authors: Leis, A. Arturo, Stokic, Dobrivoje S., Webb, Risa M., Slavinski, Sally A., Fratkin, Jonathan
• Format: Article
• Language: English
• Subjects: Acute Disease; Aged; Biological and medical sciences; Causality; Diseases of striated muscles. Neuromuscular diseases; Female; Humans; Immunoglobulin M - blood; Male; Medical sciences; Middle Aged; Motor Neurons - pathology; Motor Neurons - virology; muscle; Muscle Weakness - physiopathology; Muscle Weakness - virology; Muscle, Skeletal - innervation; Muscle, Skeletal - physiopathology; Muscle, Skeletal - virology; Neurology; paralysis; poliomyelitis; Poliomyelitis - physiopathology; Poliomyelitis - virology; Quadriplegia - physiopathology; Quadriplegia - virology; Retrospective Studies; Spinal Cord - pathology; Spinal Cord - physiopathology; Spinal Cord - virology; weakness; West Nile Fever - complications; West Nile Fever - physiopathology; West Nile virus; West Nile virus - immunology; West Nile virus - pathogenicity
• ISSN: 0148-639X; 1097-4598
• DOI: 10.1002/mus.10440

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV‐associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV‐associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment. Muscle Nerve 28: 302–308, 2003