Abstract

To the Editors: A 5-year-old male patient presented with 3 months of vomiting, headache, mood change, and 3 days of fever. He was conscious, oriented, cooperative. Basal biochemical, hematologic parameters, and acute phase reactants were normal. On craniospinal magnetic resonance imaging (MRI), leptomeningeal enhancement in the frontobasal region, and basal cisterns was identified, suggesting tuberculous meningitis (TBM). Microscopic examination of cerebrospinal fluid (CSF) revealed lymphocytosis (120/mm3), an elevated protein (152 mg/dL), low glucose (37 mg/dL), and a normal chloride (124 mmol/L) with no malignant cells on cytological examination. The CSF culture revealed no bacterial growth. Ehrlich-Ziehl-Neelsen staining and PCR of Mycobacterium tuberculosis of CSF were negative. On follow-up, seizure-like movements in the form of lip-licking were observed. The patient was started on quadruple antituberculosis therapy and steroid with the presumptive diagnosis of TBM. Mycobacterial culture revealed no growth. A biopsy could not be performed due to the proximity of the lesions to Wernicke’s area. In the fourth month of the treatment, the patient presented with a focal tonic seizure. Repeated MRI revealed aggravation of leptomeningeal enhancement compared with previous imaging and emerging multiple dural-leptomeningeal enhancing nodules along the spinal cord. A spinal biopsy was performed. The pathological diagnosis was diffuse leptomeningeal glioneuronal tumor (DLGNT). Diagnosis of TBM is difficult for clinicians due to its similarity to other forms of meningitis and malignancies in clinical aspects and the limitation of diagnostic methods. Diffuse leptomeningeal glioneuronal tumor is a rare and recently recognized neoplasm of the central nervous system described in the 2016 World Health Organization classification of brain tumor.1 Most tumors seem to show slow progress, and some aggressive cases have also been reported.1 The typical radiological finding on MRI is a leptomeningeal enhancement, usually involving the spinal cord and basal cisterns.1 Due to the similarity in clinical and radiological findings, DLGNT can often be misdiagnosed as chronic infections of the central nervous system including tuberculosis.1 Current diagnostic methods for TBM are limited in sensitivity and hence, large volumes of CSF that are impractical especially in children are required. The sensitivity of acid-fast bacilli microscopy in TBM is about 20%–40%.2 Mycobacterial culture which is the standard for diagnosis, is positive in only about 40% of cases.2 The sensitivity of PCR testing of CSF is reported to be 56%.2 Hence, negative laboratory results do not always rule out TBM. Radiographic findings are characterized by abnormal meningeal enhancement mostly in basal cisterns and posterior fossa, and along the spinal cord.1 Tuberculosis endemicity in Turkey and a rarity of DLGNT caused the radiological findings to be interpreted primarily in favor of tuberculosis. Another cause for delay in diagnosis was the negative CSF cytology for malignancy. CSF cytology of DLGNT is usually negative, which leads to challenges for diagnosis. In this case, as there was no microbiological evidence of tuberculosis, a meningeal biopsy was performed and played a key role in the management of the patient.

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