Severe Cysticercal Meningitis: Clinical and Imaging Characteristics

Graciela Cárdenas Department of Neuropsychopharmacology, Department of Neurochemistry, Department of Clinical Research, and Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico

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Helgi Jung Department of Neuropsychopharmacology, Department of Neurochemistry, Department of Clinical Research, and Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico

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Camilo Ríos Department of Neuropsychopharmacology, Department of Neurochemistry, Department of Clinical Research, and Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico

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Agnes Fleury Department of Neuropsychopharmacology, Department of Neurochemistry, Department of Clinical Research, and Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico

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José Luís Soto-Hernández Department of Neuropsychopharmacology, Department of Neurochemistry, Department of Clinical Research, and Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico

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In disease-endemic areas, severe cysticercal meningitis (SCM) is characterized by intense inflammatory cerebrospinal fluid (CSF) and negative bacterial and fungal cultures. There have been no systematic studies of SCM. We characterized patients with SCM and compare them with neurocysticercosis (NC) patients with mild CSF abnormalities by conducting a nine-year retrospective review at a neurological referral center. Two groups of patients were compared: group A, those with severe CSF pleocytosis > 1,000 cells/mm3 (n = 12), and group B, those with CSF pleocytosis ≤ 1,000 cells/mm3 (n = 126). All patients had positive CSF results in an enzyme-linked immunosorbent assay for cysticercal antigens and negative CSF cultures for bacteria, fungi, and mycobacteria. Intracranial hypertension, meningeal signs, CSF hypoglycorrachia, and a longer clinical course of NC were more frequently seen in group A. It is likely that SCM often goes unrecognized. Its correct identification may reduce morbidity and risks of unnecessary surgery in patients with chronic NC and CSF shunts.

Author Notes

*Address correspondence to Graciela Cárdenas, Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez Insurgentes Sur 3877, Tlalpan CP 14269, Mexico City, DF, Mexico. E-mail: grace_goker@yahoo.de

Authors' addresses: Graciela Cárdenas, Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico, E-mail: grace_goker@yahoo.de. Helgi Jung, Department of Neuropsychopharmacology, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico, E-mail: helgijung@yahoo.com.mx. Camilo Ríos, Department of Neurochemistry, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico, E-mail: crios@cueyatl.uam.mx. Agnes Fleury, Department of Clinical Research, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico, E-mail: afleury@correo.biomedicas.unam.mx. José Luís Soto-Hernández, Department of Neuroinfectology, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico, E-mail: joseluis_sotohernandez@yahoo.com.

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