Tuberculous ventriculitis as a relapse following central nervous system tuberculoma.

Abstract

A 74-year-old female patient was admitted with complaints of memory loss, nausea, loss of balance, and urinary incontinence, all of which started approximately 2 months earlier and increased gradually. These symptoms were so severe that she could no longer take care of herself, and her children had begun to assist her. Her medical history included a diagnosis of central nervous system (CNS) tuberculoma and tuberculous lymphadenitis 3 years prior, which were diagnosed upon complaints of severe headache and treated with isoniazid (300 mg/day), rifampicin (600 mg/day), ethambutol (1,500 mg/day) and pyrazinamide (2,000 mg/day) for 1 year. Cranial MR imaging (MRI) at diagnosis of CNS tuberculoma revealed an intense gadolinium-enhanced mass lesion with lobulated contour in the left basal ganglia (Fig 1), and thoracic computed tomography (TCT) identified paratracheal and subcarinal lymphadenopathies. The diagnosis of tuberculosis was confirmed by biopsy of the mediastinum. Following anti-tuberculosis treatment applied during that period, the patient’s ability to walk and her cognitive capacities recovered, and MRI revealed complete elimination of the tuberculoma. Due to the complaints mentioned above, the patient was hospitalized in the neurology service, where her vital signs and systemic physical examination remained normal. Neurological examination revealed an increased tendency to sleep and limited cooperation, even though she could comply with verbal directions, and her visual orientation was intact. No signs of motor deficit, cranial nerve palsy, or meningeal irritation were observed. DTRs and fundus examination were normal. Laboratory analysis indicated normal complete blood counts, biochemical parameters, thyroid function, and vitamin B12 levels, and an erythrocyte sedimentation rate of 25 mm/h. MRI identified a large ependymal contrast enhancement on the ventricular walls of the third, fourth, and lateral ventricles (Fig 2a–c). Lumbar puncture led to the following findings: protein 2,165 mg/L (150–450), glucose 43 mg/dL (simultaneous blood glucose level was 110 mg/dL), cell count 70 leukocyte/mm (all lymphocytes) and a positive Pandy’s test. A cerebrospinal fluid (CSF) smear showed large numbers of lymphocytes, few plasmocytes, degenerated cells and giant cells similar to Langhans type 1–2, and areas resembling eosinophilic small necroses, which led to a diagnosis of tuberculous meningitis (TBM). The CSF culture was negative. We evaluated albumin and IgG in serum and CSF, and found the patient’s IgG index to be 0.70, indicative of intrathecal IgG synthesis. TCT showed no evidence of tuberculous infection. After initiation of fourdrug antituberculosis treatment (isoniazid 300 mg/day, rifampicin 600 mg/day, ethambutol 1,500 mg/day, and pyrazinamide 2,000 mg/day and dexamethasone 2 mg/ day), she was referred to the Infectious Diseases Clinic where she was treated for 2 months. Upon discharge, the patient had full cognitive function; she could easily follow directions and was well-oriented to her surroundings. Control cranial MRI revealed a decrease in ependymal contrast uptake (Fig 2d–f). S. K. Guler (&) N. Gunes B. G. Cokal T. Yoldas Department of Neurology, Ankara Training and Research Hospital, Şukriye district, Ulucanlar Avenue, No: 89, 06340 Ankara, Altindag, Turkey e-mail: keskinselda@gmail.com