Tuberculous meningitis
General description
Tuberculous meningitis is meningitis caused by Mycobacterium tuberculosis and occurs secondary to primary or activated tuberculosis, resulting in tuberculosis bacteremia and seeding of the brain and meninges like miliary tuberculosis foci.
Headache, irritability, vomiting, fever, rigidity of the neck, convulsions, focal neurological symptoms, impaired consciousness, and lethargy may occur. These symptoms develop more slowly than aseptic meningitis in the acute phase and resemble those of the common cold, but their long-term persistence is what differentiates them from aseptic meningitis.
Tuberculoma
Cerebral tuberculoma is thought to be the result of hematogenous spread of Mycobacterium tuberculosis, and symptoms such as paralysis and increased intracranial pressure due to parenchymal drainage are the main features of the disease. Cerebellar tuberculomas are most common in children, and in adults, in the frontal and parietal lobes..
Basal leptomeningitis
Tuberculous meningitis is typically observed in the basal portion of the pia mater, though the lesions can be diffusely distributed.
Ventriculomegaly
An accumulation of CSF in the brain, is commonly associated with tuberculous meningitis. It occurs because the inflammation can block the flow of CSF, leading to increased pressure and swelling.
Tuberculous myelitis
Tuberculous myelitis typically exhibits transverse T2WI hyperintensity with swellings that extend longitudinally, defined as the involvement of three or more contiguous vertebral segments.
Gravitation abscess
MRI occasionally reveals an encapsulated fluid collection extending extra-axially, known as a gravitation abscess. T2WI demonstrates hyperintensity with peripheral contrast enhancement, indicating encapsulation.
Tuberculoma (Non-caseating granuloma)
Non-caseating granulomas appear as iso- to hypointense on T1WI and hyperintense on T2WI and FLAIR. DWI/ADC sequences show no restricted diffusion. Following contrast administration with gadolinium, there is homogeneous enhancement.
Tuberculoma (Caseating granuloma)
T1WI shows iso- to hypointensity with a hyperintense rim. T2WI displays hypointensity, representing gliosis and abundant monocyte infiltration, surrounded by vasogenic edema. DWI/ADC sequences indicate no restricted diffusion. After gadolinium administration, there is either homogeneous or ring enhancement.
Tuberculoma (Caseating granuloma with central liquefaction)
Caseating granuloma with central liquefaction appears as iso- to hypointense with a hyperintense rim on T1WI. On T2WI, it shows a hypointense rim with central hyperintensity, surrounded by vasogenic edema. DWI/ADC sequences exhibit variable diffusion restriction. Following contrast administration with gadolinium, there is ring enhancement.
Calcified granuloma
Calcified granuloma is characterized by calcified attenuation on CT scans. On T1WI, it appears iso- to hypointense, and on T2WI, it is hypointense. FLAIR sequences show no suppression. DWI/ADC sequences indicate no restriction in diffusion. After contrast administration with gadolinium, there is no enhancement.