By
Dr. Matthew B Jensen
Corresponding Author Dr. Matthew B Jensen
University of Wisconsin, - United States of America
Submitting Author Dr. Matthew B Jensen
Diplopia, West Nile Virus, Meningitis
Jensen MB. Diplopia Secondary To West Nile Virus Meningitis. WebmedCentral NEUROLOGY 2010;1(9):WMC00580
doi:
10.9754/journal.wmc.2010.00580
No
Abstract
Cranial nerve involvement has been reported with West Nile Virus infection. We report a case of diplopia secondary to West Nile Virus meningitis.
Introduction
Cranial nerve involvement has been reported with West Nile Virus infection. We report a case of diplopia secondary to West Nile Virus meningitis.
Case Report(s)
A 60-year-old right-handed woman presented with two weeks of gradual onset, progressive holocephalic headache. Three days after headache onset she developed horizontal diplopia, fever, new-onset hypertension, and a fine action tremor of both hands. The diplopia was not present on closing either eye. Examination was normal including inspection of ocular motility, however the diplopia worsened on left gaze and right head tilt. All her symptoms resolved in four days except for fever, which lasted two more days.
Routine serum tests were normal and her sedimentation rate was 23. Magnetic resonance imaging was normal except for a six-millimeter cyst lateral to the right basal ganglia and a three millimeter T2 hyperintensity in the right parietal white matter. The cerebrospinal fluid protein was 45 mg/dl, glucose was 65 mg/dl, there were nine red blood cells and 72 white blood cells, of which 35% were neutrophils and 65% were mononuclear cells. Cultures were negative. Serum testing for the West Nile Virus (WNV) was positive for both IgM and IgG.
Discussion
Knowledge of the neurological manifestations of WNV infection is evolving as clinical experience accumulates. Sejvar et al detailed several different syndromes following WNV infection such as encephalitis, meningitis, poliomyelitis-like acute flaccid paralysis, tremor, myoclonus, and Parkinsonism.1 There have been a few reports of cranial nerve involvement during infection. Miller and Liang have reported a patient with fever, headache, and diplopia that had positive WNV laboratory testing.2 Johnston and Chan reported a patient with acute flaccid paralysis who developed bilateral facial weakness and was positive for the WNV.3 Pepperell et al reported the results of 64 patients with WNV infection of whom the three principal types of neurological manifestations were decreased level of consciousness, brainstem and cerebellar signs, and neuromuscular weakness; they list eight patients with “diplopia or opthalmoplegia”.4 Several other cases have been described with ocular motor palsies in association with active WNS infection.5,6 Sampson and Armbrustmacher reported the autopsy results of four patients with WNV, two of who had endoneural mononuclear cell inflammation in the cranial nerve roots.7
Conclusion
This case adds evidence that infection with the WNV can present clinically with disturbance of ocular motility causing diplopia.
Abbreviations(s)
West Nile Virus (WNV)
References
1. Sejvar J, Haddad M, Tierney B, et al. Neurologic manifestations and outcome of West Nile virus infection. JAMA. Jul 2003;290(4):511-515.
2. Miller A, Liang I. Diplopia: a focal neurologic presentation of West Nile meningoencephalitis. Ann Emerg Med. Sep 2003;42(3):413-416.
3. Johnston G, Chan C. Poliomyelitis-like syndrome in a young man with meningoencephalitis: A case report Arch Phys Med Rehabil 2003;84 (9):E35.
4. Pepperell C, Rau N, Krajden S, et al. West Nile virus infection in 2002: morbidity and mortality among patients admitted to hospital in southcentral Ontario. CMAJ. May 2003;168(11):1399-1405.
5. Ross J, Worthington M. Bilateral sixth nerve palsy in West Nile meningoencephalitis. J Neuroophthalmol. Mar 2004;24(1):97-98.
6. Prasad S, Brown M, Galetta S. Transient downbeat nystagmus from West Nile virus encephalomyelitis. Neurology. May 2006;66(10):1599-1600.
7. Sampson B, Armbrustmacher V. West Nile encephalitis: the neuropathology of four fatalities. Ann N Y Acad Sci. Dec 2001;951:172-178.
Source(s) of Funding
Supported by grant 1UL1RR025011 from the Clinical and Translational Science Award (CTSA) program of the National Center for Research Resources (NCRR), National Institute of Health (NIH).
Competing Interests
none
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