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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.
June 2013 Issue of IMpact