*Olga Adriana Caliman-Sturdza and Andrei Cucu*

#### **Abstract**

Hydrocephalus is a frequent complication of tuberculous meningitis. We present the incidence of hydrocephalus in patients diagnosed with tuberculosis of the nervous system, the therapeutic possibilities and the evolution of these patients. A consensus definition for tuberculous meningitis (TBM) stratified the cases as definite, probable and possible. In various studies, radiological investigations (CT, MRI) can be normal in the initial stages of the disease in approximately 30% of cases, but they do not exclude the possibility of a TBM. The most common radiological changes found in TBM are communicating hydrocephalus (up to 80% of cases), increased basal contrast (50%), cerebral tuberculomas (30%) and cerebral infarcts (10–40%). MRI has been shown to be more sensitive than a CT scan for diagnosed TBM. Communicating hydrocephalus is among the short-term complications of TBM (approximately 80% of cases), being more frequent than non-communicating ones. In these cases, the need to perform a ventriculo-peritoneal unit must be taken into account. Long-term complications are cognitive impairment, epilepsy, stroke, hydrocephalus, myelitis, damage to the hypothalamus or the pituitary gland manifested by obesity, growth disorders and diabetes insipidus. Sequels may occur frequently in TBM such as dementia, epilepsy, neurological deficits, behavioral disorders, blindness and deafness.

**Keywords:** hydrocephalus, meningitis, tuberculosis, short-term complications, long-term complications

## **1. Introduction**

Tuberculous meningitis is an infection of the leptomeninge caused by *Mycobacterium tuberculosis* and represents one of the three forms of tuberculosis located in the central nervous system, along with tuberculoma and spinal arachnoiditis [1]. It is estimated that 2 billion of the planet's inhabitants are infected with *Mycobacterium tuberculosis*, and 10% of them develop various forms of active tuberculosis. Tuberculous meningitis (TBM) represents 1% of all forms of tuberculosis and 5% of forms of extrapulmonary tuberculosis (**Figure 1**) [2].

The etiological diagnosis of TBM continues to represent a real challenge for the clinician, despite the progress made in the diagnosis of *M. tuberculosis* infection. Modern diagnostic methods, based on molecular biology techniques and gamma

#### **Figure 1.**

*Axial and coronal contrast-enhanced T1-weighted MRI showing tuberculous meningitis (leptomeningeal enhancement) (courtesy Dr. Bogdan Dobrovat).*

interferon release tests, have substantially improved TBM prognosis, although the gold standard for diagnosis remains cerebrospinal fluid culture on special media.

TBM complicates 0.3% of untreated TB infections in children, is more common between 6 months and 4 years. The clinical progression of TBM can be rapid or gradual. Rapid progression is more common in infants and young children [3]. Occasionally, TBM occurs many years after infection.

People at increased risk of TBM are also patients with immunodeficiency caused by aging, malnutrition, HIV/AIDS infection and cancer, but also patients under treatment with biological therapies, such as tumor necrosis factor alpha (TNFα) antagonists [4].

TBM is the most severe form of extrapulmonary tuberculosis (TB), diagnosis remains difficult, and early recognition is crucial for a better prognosis. The mortality rate is high, and sequelae occur frequently in survivors [5]. The optimal treatment has not yet been well established. The increase in the number of TBM cases is also related to the increase in the number of HIV-seropositive patients.

TBM is associated with a multitude of complications such as optochiasmatic and spinal arachnoiditis, tuberculous mass lesion in the brain, periventricular infarcts or hydrocephalus [5, 6]. Among these, hydrocephalus represents a negative predictive factor [5]. Regarding hydrocephalus in patients with TBM, studies have shown that it is found in approximately 80% of children with TBM [3, 7].

Hydrocephalus is one of the most frequent complications of TBM, and its management represents a real challenge for the clinician [8].
