Dr Balaji Anvekar FRCR: CNS tuberculosis neuroradiology

MRI Axial T1 post contrast images show intensely enhancing basal exudates with multilocularity on left side of mid brain which is very typical of tuberculosis.

An associated diffuse lepto meningeal enhancement and an associated hydrocephalus.

The same Mycobacterium tuberculosis, from distant source commonly the pulmonary tuberculosis, the infection may spreads haematogeneously to CNS, in brain gets lodged deep to the pia. These foci then rupture into subarachnoid space forming basal exudates.
These basal exudates are hyperdense on CT and hyperintense on MRI FLAIR, often located in basal cisterns obliterating the normal Csf density or csf signal intensity from cisternal spaces.
Among basal cisterns commonly includes suprasellar cistern, supra chiasmatic cistern and interpeduncular cistern, posteriorly in pre pontine and ambient cistern. Laterally on anteromedial surfaces of temporal lobes, along sylvian fissures and along hemispheric cortical sulci, anteriorly along inter hemispheric fissure and on inferomedial surface of frontal lobes. Ependymal lining of lateral ventricles and choroid plexus involvement is uncommon.
The adjacent brain parenchyma may show variable degrees of edema, MRI Flair sequence is most sensitive for this.
Following contrast administration additional features like intense enhancement along these basal exudates, its multilocularity, leptomeningeal enhancement focal or diffuse along sylvian fissures, tentorium and cerebral convexities. Ependymitis may be visible.
Among complications includes Vasculitis induced infarcts for which MRI Diffusion is most sensitive and Hydrocephalus which may seen even on CT but whether it is compensated or non compensated hydrocephalus that is best demonstrated on MRI FLAIR by T2 hyperintense peri ventricular ooz of csf.
The basal exudates are a purulent material, thick and gelatinous, result from cell mediated immune response. This may be the reason the typical imaging finding of tubercular meningitis like enhancing basal exudates and lepto meningeal enhancement may not be seen in elderly patient due to age related reduced capacitance of cell mediated immunity (reference : Clinicoradiological features of tuberculous meningitis in patients over 50 years of age S G Srikanth, A B Taly, K Nagarajan)

Involvement of CNS seen in approximately 5% of total patients of tuberculosis.
With greater prevalence immunocompromised patients, CNS involvement is seen in up to 15% of cases of acquired immunodeficiency syndrome – related tuberculosis.
CNS involvement usually results from hematogenous spread.
CNS tuberculosis various common forms include tuberculous meningitis, tuberculoma, Calcified tubercular granuloma, Abscesses, and in spine osseous involvement is more common than non osseous spinal cord and spinal meningeal involvement.

Classification of Brain and Spine tuberculosis:
In brain

Tubercular Meningitis and its complications
Basal exudates.
Diffuse or focal lepto meningeal enhancement.
Patchy meningitis.
Hydrocephalus.
Vasculitis causing infarction
Cranial Neuropathies
Parenchymal Tuberculosis
Tuberculomas.
Tubercular abscesses.
Miliary Tuberculomas.
Focal Cerebritis.
Tubercular Encephalopathy.
Tuberculoma en plaque.
Tubercular Hypophysitis.
Tuberculosis of Calvarium and skull base.
Orbital Tuberculosis
Otitis Media and temporal bone tuberculosis
In spine and spinal cord

Discitis.
Spondylodiscitis
Vertebral osteomyelitis.

Non osseous spinal tuberculomas.
Arachnoiditis.
Myelitis.

Tuberculous Meningitis
The most common manifestation of CNS tuberculosis across all age groups.
Early diagnosis is important to reduce morbidity and mortality.
Usually due to hematogenous spread but can also be secondary to rupture of a parenchymal focus or direct extension from cerebrospinal fluid.
Imaging finding include exudates most pronounced in the basal cisterns seen as hyper density on CT and hyperintensity on MRI Flair. Abnormal enhancement of exudates particularly in basal cisterns, sometimes along meninges within the cortical sulci over the cerebral convexities and in the sylvian fissures. These findings are better seen at contrast enhanced MRI than CT. This appearance is nonspecific and has a wide differential diagnosis that includes meningitis from other infective agents; non infective inflammatory diseases such as sarcoidosis, patchy meningitis; and neoplastic causes, both primary and secondary. In subtle cases or milder and initial stages a non specific faint hyperintensity in the region of cortical sulci on FLAIR may be be the only finding.
Common complication of tuberculous meningitis include:
A) communicating hydrocephalus, caused by blockage of the basal cisterns or arachnoid granulations by inflammatory exudates.
B) Occasionally, non-communicating hydrocephalus occurs due to the mass effect of a tuberculoma particularly at aqueduct or foramen of monro.
C) Vasculitis induced Infarcts, also a common complication, in ~ 30% of patients, mostly within the basal ganglia, resulting from vasculitis of perforators, rarely direct vascular compression. Carries bad prognosis and seen multi drug resistant cases.
D) Cranial nerve involvement , occurs in 17%–70% of cases, most commonly affecting the second, third, fourth, and seventh cranial nerves. Seen as abnormal enhancement along the nerve.

Parenchymal Tuberculosis
Tuberculoma (tuberculous granuloma), the most common CNS parenchymal lesion of tuberculosis.
This lesion may be solitary, multiple, multi locular or military.
May be seen anywhere within the brain parenchyma, most commonly frontal and parietal lobes.
Tuberculomas can exist in conjunction with tuberculous meningitis, although not a consistent combination.
At CT, tuberculomas appear as round or lobulated lesion with low or high attenuation, homogeneous or ring enhancement, irregular walls of varying thickness. One-third of patients demonstrate the “target sign” (ie, central calcification or punctate enhancement with surrounding hypoattenuation and ring enhancement). This finding is suggestive of, but not pathognomonic for, tuberculosis.
The MR imaging findings depend on whether the tuberculoma is caseating, and if so, whether the center is liquid or solid. It is thought that there is a progression from noncaseating to caseating and then from a solid to a liquid center. A noncaseating tuberculoma is hypointense relative to gray matter on T1-weighted images and hyperintense on T2-weighted images, with homogeneous gadolinium enhancement.
Caseating tuberculomas with a solid center are isointense to hypointense on both T1- and T2-weighted MR images. They usually have a variable amount of surrounding edema, which is hyperintense on T2-weighted images. Caseating tuberculomas with a liquid center are hypointense on T1-weighted images and centrally hyperintense on T2-weighted images, with a peripheral hypointense rim on T2-weighted images that represents the capsule. Rim enhancement is usually seen at gadolinium-enhanced MR imaging.
Calcified tuberculoma or tubercular granuloma, after treatment, tuberculomas can completely resolve; however, calcification is seen in up to one-fourth of cases and is identified most clearly at CT as faint to dense nodular calcification with or without perilesional odema.
Miliary CNS tuberculosis, usually associated with tuberculous meningitis, pathogenetic relationship is suspected. At MR imaging appears as multiple tiny (<2-mm), hyperintense T2 foci with nodular or ring enhancement.
Tuberculous abscesses, are rarely seen and can be similar in appearance to liquid-centered caseating tuberculomas, although they tend to be larger and are more often multiloculated. At CT, these abscesses appear as hypoattenuating lesions with surrounding edema, mass effect, and peripheral geographic enhancement.
Tuberculous cerebritis, occurs very rarely.

Spinal tuberculous Meningitis
The MRI is must for imaging. Findings ranges from CSF loculation, matting of the nerve roots of cauda equina or patchy dural or cord enhancement. Chronic lesions may not enhance. Syringomyelia as a complication of arachnoiditis.

Image gallery of CNS TB:

Axial FLAIR show effacement of cortical sulci in dependent portions of brain with hyperintensity in the region of cortical sulci, needs Csf analysis to rule out meningitis.