Leptomeningeal tuberculosis

A 32-year-old male patient with a clinical history of 4 months of asthenia, adynamia, fever, cough, and headache of intensity 10/10. Rx of thorax revealed lobar pneumonia.

Gadolinium-enhanced images demonstrate extensive linear leptomeningeal enhancement within the sulcal spaces on both cerebral hemispheres and cerebellar hemispheres and the extent to the interpeduncular cistern, basal cistern and the Sylvian fissure (Figs 1, 2, 3).

Tuberculosis is the first cause of morbidity and mortality among people living with HIV worldwide, with 390, 000 deaths in 2014. [1]
A total of 5 to 9% of patients with AIDS develop tuberculosis, and, of these, 2% to 18% have CNS involvement [2]. The clinically active disease can develop after exposure to Mycobacterium tuberculosis organisms or after reactivation of latent infection. Basal meningitis is the most common intracranial manifestation of tuberculosis [2].
The onset of tuberculous meningitis is insidious, and the symptoms are non-specific such as: fever, malaise, headache, nausea, neck stiffness, photophobia, or confusion[2]. It affects basal cisterns, Sylvian fissures and rarely, leptomeninges over cerebral convexities [3]. The exudate in the basal cisterns can obstruct cerebrospinal fluid flow, causing hydrocephalus, and cranial nerve palsies, especially of third, fourth and sixth nerves [2, 3].
The isolation of Mycobacterium tuberculosis for the definitive diagnosis from the tissue on smear or culture is possible only in a few patients. Culture takes 6 to 8 weeks for the result. So, the diagnosis is a challenge, and the imaging could support the diagnosis in a congruent epidemiological and clinical context.
In the case of tuberculous meningitis, there is a triad that includes: abnormal meningeal enhancement predominantly in the basal regions of the brain and Sylvian fissures on postcontrast images, hydrocephalus, and infarcts [3]. The appearance of focal and diffuse pachymeningitis on MR imaging is non-specific and may be seen in many inflammatory and non-inflammatory conditions [2]. However, specificity and sensitivity of basal enhancement for the diagnosis of tuberculous meningitis have been reported as 100% and 89% [4].
Enhancement over the convexities can be seen in late-stage tuberculous meningitis, and tentorial and cerebellar meningeal involvement is less common. In our patient, we found typical and atypical findings, maybe, associated with the advanced AIDS disease without treatment.
It is important to diagnosis tuberculous meningitis because it responds well to antitubercular treatment. The standard regimen begins with isoniazid, pyrazinamide, ethambutol, and rifampicin for two months. After this initial phase, isoniazid and rifampicin or rifabutin are continued for at least 9–12 months [1].
Mortality from HIV-associated tuberculous meningitis often exceeds 50%, which is roughly double the rate compared to patients without HIV [5].
In Colombia, tuberculous meningitis is a frequent opportunistic neuroinfection in immunosuppressed patients. Although the diagnosis difficulties, magnetic resonance can support the diagnosis and allow the timely treatment.