Clinical History
A 55-year-old lady, with a previous history of pulmonary tuberculosis, was presented with fever and lethargy. Lumbar puncture was performed. The cerebrospinal fluid (CSF) showed pleocytosis, elevated protein level, low glucose level and positive acid-fast stain for tuberculous bacilli.
Imaging Findings
Brain MRI revealed hyperintensity on FLAIR images in the subarachnoid space of the basal cisterns and diffuse nodular meningeal enhancement on T1-weighted images after contrast administration (Fig. 1-3). X-ray and CT of the thorax showed right upper lobe consolidation with a cavity lesion and left upper lobe fibrosis associated with postprimary tuberculosis (Fig.4, 5). Six weeks after TB therapy, the follow up brain MRI reveal almost complete resolution of the pathologic meningeal enhancement (Fig.6).
Discussion
Tuberculosis (TB) remains a major global problem and a public health issue of considerable magnitude in recent years. TB has shown resurgence in no endemic populations, a phenomenon that has been attributed to factors such as immigration and the human immunodeficiency virus [1-3]. Tuberculosis is predominantly caused by the organism mycobacterium tuberculosis and encompasses an enormously wide disease spectrum affecting multiple organs and body systems. Although mycobacterium tuberculosis can involve any organ, most commonly the lung, central nervous system (CNS) tuberculosis is the most devastating form of the disease. Approximately 10% of all patients with tuberculosis and up to 20% of patients with AIDS-related tuberculosis have CNS involvement which can result from either haematogenous spread from a distant systemic infection or can be secondary to rupture of a Rich focus or direct extension from CSF infection [3, 4]. Manifestations of the CNS tuberculosis include meningitis, tuberculoma, encephalitis, cerebritis, cerebral abscess and miliary tuberculosis. Tuberculous meningitis is the most common manifestation of CNS tuberculosis across all age groups [4]. Early diagnosis is important to reduce morbidity and mortality [2-3]. MRI with gadolinium administration is the modality of choice and imaging findings include abnormal nodular leptomeningeal enhancement, usually most pronounced in the basal cisterns [1-4]. The most common complication of tuberculous meningitis is communicating hydrocephalus and is caused by blockage of the basal cisterns by inflammatory exudates or sometimes, non-communicating hydrocephalus occurs due to the mass effect of a tuberculoma causing the obstruction of CSF flow [3]. Ischemic infarcts are also a common complication, mostly seen within the basal ganglia or internal capsule regions and resulting from vascular compression and occlusion of small perforating vessels [4]. Cranial nerve involvement occurs in 17%-70% of cases, most commonly affecting the second, third, fourth, and seventh cranial nerves [3-4]. In conclusion, tuberculous meningitis is a major cause of morbidity and mortality. Early diagnosis in tuberculous meningitis may prevent neurologic damage. Imaging studies are an important part of diagnosis and MR imaging should be performed as a first choice of imaging modalities in patients with tuberculous meningitis.
Differential Diagnosis List
Tuberculous meningitis
Brucellosis meningitis
Neuro-sarcoidosis