Teaching Case

A 32-year-old male patient presented with complaints of sudden loss of consciousness and right-sided weakness for the past 2 days. The patient had chronic cough with expectoration, low-grade fever and weight loss for the past 6 months.

Routine blood and serum investigation and sputum microbiological examination was performed, which revealed mycobacterium tuberculosis in the sputum.

Plain MRI scan revealed a lesion involving pons which appeared heterogeneously hypointense on T2 and FLAIR sequence and almost unidentifiable (isointense) on T1. The surrounding area, cerebellar peduncle and part of the cerebellar hemisphere showed hyperintensity on T2 and FLAIR sequence due to peri-lesional oedema. (Fig. 1a-c) The lesion and surrounding oedema caused asymmetrical enlargement of pons with resultant narrowing of fourth ventricle.

The lesion didn't reveal any diffusion restriction. (Fig. 1d)

On post-contrast MRI the lesion showed ring enhancement in T1-weighted images. (Fig. 2)

Spectroscopy revealed lipid lactate peak with increased choline to creatine ratio. (Fig. 3)

CSF examination following lumbar puncture showed raised ADA level, which confirmed the diagnosis of tuberculoma.

The patient was started on Isoniazid, Rifampicin, Pyrazinamide, Ethambutol and Streptomysin therapy and showed symptomatic improvement.

Follow-up MRI has not yet been performed.

Tuberculosis is an endemic disease in many developing countries and is responsible for around eight million deaths worldwide annually. [1, 2] Tuberculosis usually affects the lung but can involve many other organs, and involvement of CNS is the most severe form. [3, 2] CNS tuberculosis usually presents as meningitis, but may cause brain abscess or tuberculoma. [2] Tuberculoma is the space-occupying granulomatous mass resulting from haematogenous spread from distant tuberculous focus. [4] Tuberculomas may be single or multiple, and can occur anywhere in the brain. [2] Histologically, the mature tuberculoma shows a necrotic caseous centre with surrounding fibroblasts, epithelioid cells, Langhans giant cells and lymphocytes. [4]

The patient usually presents with seizures and/or neurological deficit based on the site of the tuberculoma in the brain. [2]

On contrast CT it appears as ring-enhancing lesion, which has to be differentiated from neurocysticercosis. [1]

On MRI tuberculoma appears iso to hypointense with slightly hyperintense rim on T1-weighted images and iso to hypointense with surrounding hyperintense vasogenic oedema on T2 weighted images. [4] Diffusion-weighted imaging in tuberculomas with liquid necrosis shows restricted diffusion, whereas in lesions with solid caseation no diffusion restriction is seen. [2] On post-contrast T1-weighted image it shows ring enhancement. [4]

On MR spectroscopy it shows lipid lactate peak which differentiates it from bacterial abscess. [5] The choline/creatine ratio is also increased in tuberculomas differentiating it from cysticerci. [1]

Other serum, CSF and sputum examinations can help to confirm the diagnosis of tuberculosis. [6]

It responds to AKT containing isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin. In non-responsive cases second line drugs can be used. [7] In patient with neurological deficit surgical intervention is performed. [7] Follow up MRI is done to check the response of therapy. [6]

Take home message: Imaging modality can help to diagnose tuberculoma and to differentiate it from other entities as well as ensure an early treatment start. It also helps to check effectiveness of the treatment given.

Written informed patient consent for publication has been obtained.