Radiological Evidence in Tuberculous Meningitis
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Clinical history:

A 29-year-old patient presented with an altered behavioral pattern on and off for 1 month. She had been treated at another medical facility with antidepressants and anxiolytics. Before she visited our hospital she had had fever and drowsiness for 4 days and had been started on antibiotics. For further management, she was moved to Kauvery hospital. She presented with irrelevant speech, restlessness,  agitation and was not intermittently oriented to time, place or person.  CSF analysis showed: 85 cells, lymphocytes predominant 80%, elevated protein 288, glucose 21 and ADA  positivity.

An MRI showed FLAIR hyperintensity involving the basal cisterns and the bilateral frontoparietal sulcal spaces. Leptomeningeal enhancement involving the basal cisterns and the bilateral frontoparietal cortical sulciwas noted in the post-contrast T1 and FLAIR images. The possibility of acute meningoencephalitis was raised.

Other differential diagnoses could include –

  • Pyogenic meningitis
  • Fungal meningitis
  • Neurosarcoidosis
  • Leptomeningeal carcinomatosis



Tuberculous meningitis is the most common presentation of intracranial tuberculosis.


Tuberculous meningitis is seen in all age groups, but it has a peak incidence in childhood in high prevalence areas. In adolescents and adults, it is more frequently encountered In low prevalence areas.


● Immunosuppression
● Diabetes mellitus
● Alcoholism


Low-grade fever with headache is the prodromal manifestation. The most common clinical presentations are fever, headache, vomiting and neck stiffness. Cranial nerve palsies of the 3rd, 4th and 6th nerves may be seen. Late stages seizures, focal neurological deficits, stupor and coma may also be seen.

CSF analysis shows lymphocytosis, increased protein level and decreased glucose levels.


Tuberculous meningitis is caused by Mycobacterium tuberculosis. The most common spread of infection is hematogenously from a distant focal point, usually from pulmonary tuberculosis. It lodges immediately deep to the pia forming Rich foci. Later these rupture into the subarachnoid space, forming an exudate. This purulent material is primarily located in the basal cisterns.

From the basal cisterns, the infection spreads to interpeduncular cisterns, around optic chiasm and to the pontomesencephalic, ambient and suprasellar cisterns. The exudate can reach the Sylvian fissures, but an extension to the cerebral convexities is not common. Choroid plexitis may be a late manifestation.



● Non-contrast scans may be normal
● Later complications visible:
o Hydrocephalus
o Infarcts due to arteritis

Following contrast administration :

● Basal enhancing exudates
● Leptomeningeal enhancement, along Sylvian fissures, tentorium
● Ependymitis


● T1
o Normal initially
o T1 shortening seen after the progression of the disease.

● T2
o Normal initially
o T2 shortening is seen after the progression of the disease.

T1 C+ (Gd): diffuse basal enhancement with enhancing exudates

● Magnetization transfer (MT) spin echo: Significantly lower MT ratio is seen in tuberculous meningitis as compared to fungal and pyogenic meningitis


● Hydrocephalus
● Arteritis that may result in ischemic infarcts.
● Cranial neuropathies: most affected nerves are the 3rd, 4th and 6th nerves


An anti-tuberculosis regimen is started after diagnosis confirmation.


Dr. Shabna Jasmin K
Radiology Resident
Kauvery Hospital

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