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Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651
Online ISSN 1827-1855
Murakami M., Kuratsu J.-I-, Takeshima H., Soyama N., Shinojima N., Ushio Y.
Department of Neurosurgery, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto 860, Japan
Background. The spinal seeding from brain tumors sometimes mimicks fungal meningitis on examination of cerebrospinal fluid.
Methods and results. A 19-year-old woman gradually developed increased intracranial hypertension. MRI identified a mass in the right parieto-occipital area. It was totally removed and histologically diagnosed as an anaplastic ependymoma. Radiation- and chemotherapy were administered postoperatively. The patient reported low back pain 5 months after the surgical treatment. MRI disclosed neither spinal dissemination nor tumor recurrence at the primary site. Lumbar puncture was performed and the cerebrospinal fluid (CSF) was found to have an extremely low glucose level (5 mg/dl); no tumor cells were identified. Blood samples were obtained and a relative increase of WBC and CRP was noted. A slight degree of inflammation and low-grade fever were recorded. A tentative diagnosis of fungal meningitis was made and anti-fungal therapy was administered transventricularly and transvenously. However, her neurological condition continued to deteriorate gradually. Sequential CSF studies showed that the glucose level remained extremely low, it even decreased to 0 mg/dl. Eight months after the surgical treatment, MRI with Gd-DTPA revealed marked subarachnoid enhancement in both intracranial and spinal areas. An open biopsy was performed and a histological diagnosis of intracranial and spinal seeding of the anaplastic ependymoma was returned.
Conclusions. We report a patient with intracranial and spinal seeding of an anaplastic ependymoma that mimicked fungal meningitis. We discuss the difficulty of obtaining a differential diagnosis in this case and describe the mechanism of the decreased CSF glucose level.