Tuberculosis – the master masquerader – presenting as posterior fossa mass lesions

Clinical History

A 2-year-old boy presented with nausea, vomiting and convulsion for the past seven days. Physical and neurological examinations revealed no abnormality. MRI brain showed lesions in the posterior fossa. Occipital craniotomy was done followed by exicisional biopsy which showed partially calcified tuberculomas. The patient received AKT with antiepileptic drugs and has improved till date.

Imaging Findings

MRI brain shows an approximately 23 x 50 x 27 mm (AP x TR x CC) sized well-defined lobulated altered signal intensity lesion involving posterior lobes of bilateral cerebellar hemispheres and lower part of cerebellar vermis, which appears mildly hyperintense on T1W images and heterogeneously hypointense on T2W and T2W FLAIR images with whorled or striped appearance.
The lesion shows ring enhancement on post-contrast study.
Abnormal T2 hyperintensity is seen surrounding the lesion, a possibility of vasogenic oedema.
On MR Spectroscopy elevated lipid-lactate peak is seen at 1.3 ppm and reduced NAA/Cr measuring 0.14.
The lesion shows mass effect in the form of compression of fourth ventricle with resultant proximal dilatation of bilateral lateral and third ventricles, suggestive of obstructive hydrocephalus.

Discussion

Tuberculosis remains a major public health issue in developing countries. The most common form of tubercular infection is primary lung infection. Other organ systems may be affected either primarily or in disseminated disease. CNS involvement is thought to represent 1 % of patients with tuberculosis [1] and up to 15% [2, 3] of those with AIDS-related tuberculosis. The route of infection is either haematological dissemination or direct extension via craniofacial infections. It is a disease of all age groups but children and young adults are most commonly involved [2]. Risk factors for tuberculous CNS involvement include young age (children>adults), immunocompromised status and malnutrition.
Most common intracranial presentation is basilar meningitis with hydrocephalus [3]. The most frequent form of parenchymal TB is tuberculoma. Other presentations are tubercular pseudo abscesses, focal cerebritis, microinfarctions and encephalopathy. CNS tuberculoma accounts for 5–10% of intracranial space-occupying lesions in the developing world. Cerebellar involvement is slightly more common in children (6 months to 6 years). Radiological evaluation plays an important role in the diagnosis, monitoring of the response to drug therapy and for assessment of complications [3].
On CT scan, tuberculomas appear as small ring or nodular-enhancing lesions with surrounding mild oedema and mass effect. Old healed granulomatous lesions may appear as calcified lesions. MRI appearance depends on the stage of maturation. On MRI, classical tuberculoma appears as T2-weighted hypointense lesion with a peripheral rim enhancement on post-contrast images. Multiple conglomerated ring enhancing lesions are classical of tuberculomas. As the disease progresses, pseudoabscesses may form that appear as T2W hyperintense lesions with central complete restriction on diffusion-weighted images. They are known as pseudoabscesses as they do not contain neutrophils seen in classical pyogenic abscesses. Tubercular bacilli may cause microvascular obstruction with resultant infarcts which show restriction on DWI in acute stage [4]. On MR spectroscopy, the lesions show decreased NAA/Cr ratio, slight decrease in NAA/Cho ratio and elevated lipid-lactate peaks. Newer techniques like magnetisation transfer ratio (MTR) may be helpful in conflicting cases which shows greater reduction in cases of neurocysticercosis [5]. Efforts should be made to find extracranial focus of infection in all patients with CNS TB as it may help in diagnosis and treatment. The outcome in patients with CNS TB depends on the clinical stage and on the age of the patient. Diagnosing CNS tuberculosis is of prime importance as timely initiation of therapy can lead to reduced morbidity and mortality.

Differential Diagnosis List

Final Diagnosis

Cerebellar tuberculosis

URL:	https://eurorad.org/case/14877
DOI:	10.1594/EURORAD/CASE.14877
ISSN:	1563-4086