A 4-year-old boy presented with high grade fever, headache and vomiting for 20 days’ duration. The patient had been treated elsewhere with multiple intravenous antibiotics for 2 weeks. There was no history of contact with tuberculosis (TB). The systemic examination was normal apart from papilloedema. Cerebrospinal fluid showed 440/mm3 cells (60% polymorphs), glucose 9 mg/dl, protein 368 mg/dl and polymerase chain reaction PCR) for TB was negative. A computed tomography scan of the head was normal. The patient was commenced on intravenous antibiotics and showed clinical improvement. However, repeat lumbar puncture after 7 days showed persistent hypoglycorrhachia (glucose 10 mg/dl) and elevated protein. Subsequently, the child had a recurrence of his headache. Magnetic resonance imaging (MRI) of the brain revealed multiple ring/disc enhancing lesions with T2W hypointense core and hyperintense rim scattered in the cerebrum, cerebellum, brainstem and intramedullary region of cervical cord at the C3/4 level, along with spinal cord arachnoiditis and basal exudates (fig 1). Neurocysticercosis serology, Mantoux test and chest x-ray were negative. Magnetic resonance spectroscopy (MRS) showed a high peak of lipids, increased choline, low N-acetylaspartate and creatine with choline/creatine ratio >1. Thus, a diagnosis of central nervous system TB was established. The patient was started on standard four drug antitubercular therapy and he subsequently had a satisfactory clinical recovery.
Intramedullary tuberculoma (IT) is rare, the incidence being about 2/100 000 cases of TB.1 Simultaneous occurrence of intracranial tuberculoma and IT is exceedingly rare with only two published reports involving children.1 The combination of these with intracerebellar tuberculomas in children has been reported only once.2 The index case had a unique concordance of brainstem, cerebellum and IT with spinal cord arachnoiditis and tubercular meningitis without any focal deficits.
The most common site of IT is the thoracic spinal cord. IT occurs by haematogenous spread from a pulmonary focus, although occasionally an extrapulmonary focus may be found.1 However, a detailed work up in our case failed to identify the primary focus. The literature suggests a male preponderance (M:F, 1.5:1) in IT.3 The clinical symptoms may be variable with subacute spinal cord compression, focal neurologic deficits or totally asymptomatic as in our case.
MRI/MRS have enabled the accurate diagnosis of IT, obviating the need for biopsy. Controversy exists regarding the management options of IT. There are reports of excellent response to conservative treatment alone with antituberculous drugs. Authors also suggest a combination of microsurgical resection and antituberculous therapy in symptomatic cases.1,3 Our patient showed a gratifying response to antituberculous therapy alone. Surgical intervention may be indicated if there is no response to chemotherapy, the diagnosis is in doubt, or there is a rapid deterioration in neurological function.