Tuberculous Granulomatous Meningitis

Clinical Features

Tuberculous meningitis may occur at any age. In children, it is often part of a disseminated miliary tuberculosis. Unlike purulent meningitis, the symptoms evolve over several weeks. Cranial nerve signs, often ocular nerve palsies, are common. Increased intracranial pressure develops after a few weeks due to obstructive hydrocephalus.

The CSF shows pleocytosis with PNLs and lymphocytes; this changes after a few days to predominantly lymphocytes, high protein levels, and low glucose and chloride levels. The demonstration of the bacilli in CSF sediment is often difficult, and their growth in culture requires several weeks. Contrast-enhanced CT scan and MRI demonstrate the basal exudate, hydrocephalus, tuberculomas, and infarcts.


The primary infection, commonly in the lungs or lymph nodes, may be active or latent, although, in some cases, no clinical evidence of an extraneural infectious focus is found. The microorganisms reach the meninges or the vessel wall via the bloodstream and produce a small tubercle. From here, the microorganisms invade the sub-arachnoid space and evoke a granulomatous meningeal reaction. Grossly, this reaction is characterized by multiple small meningeal tubercles and a thick gelatinous exudate. The exudate is typically confined to the basal cisterns and subarachnoid space, extending into the spinal subarachnoid space (Fig. 6.5).

The histology is characterized by: (a) meningeal tubercles composed of lymphocytes, plasma cells, epi-thelioid cells, Langhan's-type multinucleated giant cells, and areas of caseation necrosis; and (b) subarachnoid exudate containing fibrin and massive perivascular and diffuse infiltrations with mononuclear cells and caseations (Fig. 6.5). The inflammation usually involves the vascular walls and the cranial nerve roots. It may extend into the parenchyma, where it produces a granuloma-tous meningoencephalitis.

Late complications of tuberculous meningitis are infarction due to thrombotic occlusion of inflamed vascular walls and hydrocephalus due to fibrotic obliteration of the subarachnoid space and obstruction to CSF circulation.

Tuberculoma. Microtubercles may develop into large granulomas, which produce mass effect and raised intracranial pressure (Fig. 6.6).

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