Magnetic resonance imaging spectrum of intracranial tubercular lesions: one disease, many faces

Abstract

Tuberculosis is a devastating disease and has shown resurgence in recent years with the advent of acquired immunodeficiency syndrome. Central nervous system involvement is the most devastating form of the disease, comprising 10% of all tuberculosis cases. The causative organism, Mycobacterium tuberculosis, incites a granulomatous inflammatory response in the brain, the effects of which can be appreciated on magnetic resonance imaging (MRI), which can thus be used for diagnosis of the same. Neurotuberculosis can present in various patterns, which can be identified on MRI. The meningeal forms include leptomeningitis and pachymeningitis. Parenchymal forms of neurotuberculosis include tuberculoma in its various stages, tubercular cerebritis and abscess, tubercular rhombencephalitis, and tubercular encephalopathy. Each pattern has characteristic MRI appearances and differential diagnoses on imaging. Complications of neurotuberculosis, usually of tubercular meningitis, include hydrocephalus, vasculitis, and infarcts as well as cranial nerve palsies. Various MRI sequences besides the conventional ones can provide additional insight into the disease, help in quantifying the disease load, and help in differentiation of neurotuberculosis from conditions with similar imaging appearances and presentations. These can enable accurate and timely diagnosis by the radiologist and early institution of treatment in order to reduce the likelihood of permanent neurological sequelae.

Keywords: MRI; brain; spectroscopy; tuberculoma; tuberculosis.

Figure 1

Tubercular leptomeningitis. A (T1W axial) and C (T2W axial) show altered signal intensity in the basal cisterns. B (T1WCE axial) and D (T1WCE coronal) show diffuse leptomeningeal enhancement along the basal cisterns and Sylvian fissures with dilated lateral ventricles

Figure 2

Caseating tuberculomas. A (T2W axial) and B (FLAIR axial) show conglomerate hypointense lesions in left frontal region with perilesional oedema, which on C (T1W axial) appear isointense with a hyperintense rim. D (T1WCE axial) shows ring enhancement of the conglomerate tuberculomas

Figure 3

Caseating tuberculoma with liquefaction. A (T2W axial) and B (T2W coronal) show a focal lesion with T2 hypointense rim and central hyperintensity. C (T1WCE coronal) shows ring enhancement of the lesion. D (MR spectroscopy) shows lipid peak at 1.3 ppm

Figure 4

Miliary tuberculomas. A (T1W axial) shows no significant abnormality. B (T2W axial) shows two focal lesions in the right lentiform nucleus and the left caudate nucleus. C (T1WCE axial) and D (T1WCE coronal) show numerous focal homogeneously enhancing lesions in the cerebral parenchyma

Figure 5

Tubercular abscess. A (T1WCE axial) shows an irregular hypointense lesion with a thin rim of peripheral enhancement. B (T1IR axial) shows the lesion to by hypointense. The lesion shows diffusion restriction on C (DWI axial) and appears heterogeneous in signal intensity on D (T2W axial)

Figure 6

Same case as in Figure 5. Magnetic resonance spectroscopy shows large lipid peak at 1.3 ppm

Figure 7

Tubercular rhombencephalitis. A (T2W axial) and B (FLAIR axial) show conglomerate hypointense lesions involving the pons with perilesional oedema. C (T1WCE axial) shows ring enhancement of the lesions s/o conglomerate tuberculomas

Figure 8

Complications of tubercular meningitis. A (T2W axial) shows gross dilatation of the bilateral lateral ventricles indicating hydrocephalus. B (T2W axial) shows multiple infarcts in bilateral gangliocapsular regions

Figure 9

Neurocysticercosis. Magnetic resonance axial images showing multiple ring enhancing lesions with typical eccentric scolex

Figure 10

Metastasis. Magnetic resonance axial images showing multiple ring enhancing lesions with perilesional oedema at grey-white matter junction with choline peak in addition to lipid/lactate peak on spectroscopy