Winning Abstracts from the 2013 Medical Student Abstract Competition: West Nile Virus Associated Flaccid Paralysis
Dan Isaac, Edward Via Virginia College of Osteopathic Medicine, Class of 2013
This year over 4,000 cases of West Nile virus have been confirmed in the United States, with over 200 reported deaths. Neuroinvasive West Nile Virus (WNV) is responsible for almost 200 deaths this year alone. Acute flaccid paralysis is a rare neurological manifestation of WNV infection and the pathophysiological mechanism is yet to be elicited. The clinical and diagnostic studies outlined in this report may support previously hypothesized mechanisms by which WNV leads to acute paralysis.
A 54- year-old homeless male with unknown past medical history was admitted to the hospital with bilateral lower extremity paraplegia, after being found by emergency medical services. The patient was disoriented with disorganized thoughts and tangential speech. Examination revealed a thin, unkempt male with lower extremity muscular atrophy. Examination revealed decreased motor function in bilateral lower extremities, more pronounced on the left compared to the right. Sensation, noxious stimulus testing, proprioception and vibratory sensations were preserved. Patellar reflexes were absent and Babinksi testing was negative. Upper extremity neurological testing revealed no deficits. Imaging studies were negative and electromyogram showed decreased amplitude of compound muscle action potentials but no evidence of denervation. However, given the patient's clinical symptoms and albuminocytologic dissociation on lumbar puncture it was determined the patient's symptoms were consistent with Guillain-Barre Syndrome. Plasmapheresis was initiated; however, no clinical improvement was noted. Additional laboratory work-up revealed positive IgM and IgG serum titers for WNV. The final diagnosis was paraplegia likely secondary to WNV infection. The patient was transferred to outpatient rehabilitation and his status remains unchanged.
Neuroinvasive disease, including meningitis and encephalitis, accounts for approximately 51% of documented cases of WNV infection; however, flaccid paralysis is a much less common manifestation. Clinical manifestations including areflexia, asymmetric weakness and preserved sensory functions, as documented in this report, suggest that the pathological mechanism involves viral infiltration of the anterior horn cells leading to a poliomyelitis-like syndrome (Sejvar et al 2003, Morrey et al 2008). In addition, electrodiagnostic studies show decreased amplitudes of muscle action potentials with preserved sensory function, as documented in the presented case, also suggests anterior horn cell dysfunction (Sejvar et al, 2003). Although this patient did not become overtly enchephalopathic, he did present with altered mental status and disorganized thought which may have been related to neuroinvasive disease. No significant improvement has been noted in the patient's functional status; however, long-term follow-up studies done by Sevjar (2006) indicate that clinical improvement is most notable at four months and may even take up to one year to be evident. This report underscores the importance of including WNV infection in future assessment of patients presenting with paraplegia of unknown etiology, particularly throughout periods of increasing incidence in the community.