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Case Report |
1 Department of Radiology, Ochsner Clinic Foundation, 1516 Jefferson Hwy., New
Orleans, LA 70121.
2 Department of Infectious Diseases, Ochsner Clinic Foundation, New Orleans, LA
70121.
Received October 18, 2002;
accepted after revision January 16, 2003.
Address correspondence to A. D. Olsan.
Introduction
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Historically, signs and symptoms of the disease include the sudden onset of fever, headache, malaise, anorexia, nausea, vomiting, eye pain, myalgia, rash, and lymphadenopathy. Acute flaccid paralysis that may be confused with Guillain-Barré syndrome has also been described [3]. Recent outbreaks of West Nile infection appear to be associated with increased morbidity and mortality as well as an occasional severe neurologic disease [4]. Chowers et al. [5], in their study of a 2002 outbreak in Israel with 417 confirmed cases, reported altered levels of consciousness in 109 patients. The New York City epidemic in 1999 involved 59 hospitalized patients, in six of whom flaccid paralysis was reported [1].
Most reported imaging findings associated with the West Nile virus have been limited to studies of the brain. In these cases, most CT examinations have revealed no evidence of acute disease [1, 5, 6], but MR imaging has revealed enhancement of the leptomeninges, periventricular areas, or both in roughly one third of cases investigated by the Centers for Disease Control and Prevention. Additionally, researchers at the National Institutes of Health have reported hyperintensity in the thalamus, deep gray nuclei, and dentate nuclei using a fast FLAIR MR imaging protocol.
Two recent cases of acute flaccid paralysis syndrome and associated enhancement of the cauda equina in patients with West Nile virus infection have been reported [3]. We report details of one case of leptomeningeal enhancement of the conus medullaris and nerve roots of the cauda equina in a patient with confirmed West Nile virus infection and acute flaccid paralysis.
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The patient was treated empirically for bacterial meningitis with vancomycin and ceftriaxone spodium. He then underwent CT of the head, and findings were normal. A lumbar puncture revealed a WBC of 329 x 103/µL with 54% granulocytes, 42% lymphocytes, and 4% monocytes. Protein level was slightly elevated at 75 mg/dL (normal range, 12–60 mg/dL), and glucose level was normal. Results of a bacterial antigen panel were negative. Cerebral spinal fluid and serum were transported to the Louisiana State Department of Health for antibody testing for arboviruses, including West Nile virus.
The patient was admitted to the intensive care unit and administered antibiotics and IV immunoglobulin for presumed Guillain-Barré syndrome while awaiting serologic testing. The fever and headache resolved over the next few days, but the lower extremity weakness worsened. MR imaging of the brain on hospital day 4 revealed subtle increased vascular enhancement. By hospital day 6, the leg weakness had not resolved and MR imaging of the lumbar spine was ordered. This study revealed sheetlike enhancement of the distal conus medullaris and along the nerve roots of the cauda equina (Fig. 1A, 1B, 1C).
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West Nile IgM antibodies were subsequently found to be strongly positive in the cerebral spinal fluid and serum by enzyme-linked immunosorbent assay testing. In the short term, the paralysis did not improve, and the patient was transferred to the rehabilitation unit. Follow-up MR imaging of the lumbar spine revealed leptomeningeal enhancement of the conus medullaris and cauda equina that was similar in distribution and extent to that seen on previous examinations. MR imaging of the cervical and thoracic spine revealed no abnormalities of the spinal cord and minimal degenerative change of the cervical spine.
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