Basal exudates in Tuberculous meningitis

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)

Hydrocephalus in Tubercular meningitis

A 22 y o female, known case of tubercular meningitis readmitted to casualty with recent onset headache.
On admission non contrast CT:

This CT study shows diffuse cerebral cortical atrophy – mild but significant for age.

A follow up CT after 1wk:

This CT study shows mild communicating hydrocephalus as a complication of Tubercular Meningitis.

CNS Tuberculosis
Involvement of the CNS is seen in ~y 5% of patients with tuberculosis.
Prevalence is greater in immunocompromised patients.
Tuberculous meningitis is the most common manifestation of CNS tuberculosis.
Communicating hydrocephalus is the most common complication of tuberculous meningitis, often caused by blockage of the basal cisterns by inflammatory exudates. Occasionally, non-communicating hydrocephalus occurs due to the mass effect of a tuberculoma causing the obstruction of CSF flow or ependymal adhesion, the commonest site of obstruction is aqueduct.