**2. Pathogenesis**

Tuberculosis of the central nervous system in adults is almost always secondary to a latent tuberculosis focus or active pulmonary tuberculosis. In children, TBM is secondary to the primary complex, which disseminates hematogenously in the early stage of evolution, the maximum number of illnesses being recorded in the age group of 1–3 years.

#### *Hydrocephalus in Tuberculous Meningitis DOI: http://dx.doi.org/10.5772/intechopen.110251*

In adults, extraneural tuberculosis foci are represented by miliary, bone, urogenital or serous tuberculosis [9]. The main defensive mechanism of the host that intervenes at the beginning against Mycobacterium tuberculosis is the alternative pathway of complement activation, but once it reaches the CSF the bacteria has every chance to survive because the humoral defense is absent at this level. Two important mechanisms are involved in the immunopathogenesis of tuberculous meningitis: activation of the monocyte/macrophage system and T lymphocytes with the release of cytokines in the CSF; temporary and reversible depression of cellular immunity by decreasing the number of CD4 T lymphocytes, especially in severe forms, independent of immunodeficiency induced by other causes (including HIV infection) [10].

Tuberculous meningitis is a granulomatous meningitis whose main morphopathological aspects are meningeal inflammation with fibrinous exudate and small disseminated tubercles predominantly in the basal cisterns; inflammation of the choroid plexuses and the ventricular and ependymal epithelium (**Figure 2**); inflammation of the cerebral arteries, with the possibility of their secondary thrombosis and the appearance of cerebral microinfarcts. Infarction of small arteries causes symptoms similar to encephalitis; cerebral tuberculomas, with more frequent localization in the brain stem, thalamus and cerebral hemispheres; they behave as expansive intracerebral processes; cerebral edema, of variable degree and extent [9, 10].

In severe forms, severe disorders of CSF hydrodynamics occur, with the consequent appearance of hydrocephalus, both by blocking the aqueduct of Sylvius and the foramen of Lushka, and by decreasing CSF resorption at the level of Pachionii granulations [8, 9]. Due to the accumulation of a large amount of serofibrinous exudate at the base of the brain, compression of the cerebral arteries is also found at this level. The lesions of the choroid plexuses are morphologically identical to those observed in the meninges: fibrin deposits, specific perivascular follicles, obliteration, their fibrous organization leading to cloazonation. One of the consequences of choroid plexites is liquid hypersecretion, the direct consequence of specific exudation. This exudate, as well as the cloazonation, favors the occurrence of internal hydrocephalus, which

#### **Figure 2.**

*Axial contrast-enhanced T1-weighted MRI showing tuberculous meningitis (first image). Coronal FLAIR MRI sequence showing postoperative images of an external ventricular drainage in case of tuberculous hydrocephalus. The red arrow marks the place where the external catheter was inserted into the lateral ventricle (the second image) (courtesy Dr. Bogdan Dobrovat).*

mainly affects the frontal, temporal and occipital extensions of the ventricles. Arachnoid lesions are mainly located in the basal optochiasmatic region, being responsible for eventual blindness from TBM [9].
