Neurologic symptoms in a previously healthy man spurred a battery of tests to determine the cause. The 51-year-old patient lived alone and was transferred to our intensive care unit from another facility. Emergency medical services personnel first brought him to his local emergency department, where he stated that he had not been feeling well the day before. Then, over a 24-hour period, his level of consciousness decreased, and he developed tetraparesis.
Assessment
On admission to our hospital, the patient’s temperature was normal, and in fact, reached 37.8°C (100°F) only twice during his hospital stay. A neurologic examination showed reduced consciousness with preserved brain stem signs and flaccid tetraparesis with hyporeflexia. A cerebrospinal fluid specimen from a lumbar puncture performed on admission yielded 50 red blood cells/µL, 14 white blood cells/µL, a protein level of 19 mg/dL, and a glucose level of 87 mg/dL.
Results of a urine toxicology screen were unremarkable. The differential diagnosis included infection due to cytomegalovirus, Epstein–Barr virus, herpes simplex virus, syphilis, tuberculosis, toxoplasmosis, or West Nile virus. Enzyme-linked immunosorbent assays of cerebrospinal fluid and blood specimens identified immunoglobulin-M specific for West Nile virus.
Magnetic resonance imaging of the brain, with and without contrast, was obtained on admission. Imaging showed increased signals in the bilateral thalami and globus pallidi, in the substantia nigra, and within the pons, with no diffusion restriction or postcontrast enhancement in these regions due to underlying inflammation (Figure 1, Figure 2).1, 2
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-Meheroz H. Rabadi, M.D. MRCPI, FAAN, FANA
This article originally appeared in the September issue of The American Journal of Medicine.