Tuberculous meningitis

Clinical History

1-year-old girl presented with seizures and fever. Her medical history was unremarkable. Physical examination revealed right haemiparesis. CSF study showed low levels of glucose and lymphocytic pleocytosis. Mantoux test was positive. Serum testing for HIV was negative. Culture of gastric aspirates confirmed diagnosis. She improved with medical management.

Imaging Findings

Frontal chest radiograph showed diffuse 2-3 mm nodules in a random distribution (typically seen in miliary tuberculosis) and segmental atelectasis involving the anterior segment of upper right lobe.
Emergent unenhanced CT of the brain demonstrated ischaemic infarcts within the left basal ganglia (left middle cerebral artery territory) exerting a mass effect and isointense exudates filled basal cisterns. Contrast-enhanced CT showed “contrast filling the cisterns”. There is gross filling and obliteration of the basal cisterns, CFS spaces and left Sylvian sulci. Complicated tuberculous meningitis was suspected.
MR was performed within 2 weeks of initial imaging. It revealed abnormally increased leptomeningeal enhancement and dilatation of all ventricles (communicating hydrocephalus secondary to arachnoiditis). Infarction in left basal ganglia evolved into atrophy.

Discussion

Primary tuberculosis (TB) is seen in patients not previously exposed to Mycobacterium tuberculosis. At radiology, primary TB may progress to miliary TB. It is usually observed in infants and immunocompromised persons, manifesting within 6 months of initial exposure.
CNS involvement is seen in approximately 5% of patients with TB and it does result from haematogenous dissemination. Tuberculous meningitis (TBM) is more closely associated with miliary TB than other varieties of disseminated TB [1].
TBM is caused by a granulomatous hypersensitivity response to the presence of TB bacilli. This leads to a gelatinous exudate which forms and accumulates with predilection for the basal cisterns, covering arteries. The sequelae are due to obliterative endarteritis with resultant infarctions, and impairment of CSF flow dynamics with resultant hydrocephalus [1]. Communicating hydrocephalus can result from the exudates blocking the arachnoid granulations.
Clinical presentation of TBM is often a subacute febrile illness with generalised neurological syndrome.
CT is a well-established tool for making the diagnosis of TBM in children. In the clinical setting, the CT triad of marked contrast enhancement outlining the basal cisterns (not reported with viral and pyogenic infections), hydrocephalus and infarction strongly suggests TB as a likely diagnosis [2]. Basal meningeal enhancement has been shown to be associated with a poorer prognosis [3].
MR is excellent for delineate extent and complications.
Growth of the organism from cultures, for definitive diagnosis, takes between 2 and 6 weeks and has a very low yield [4].
Early diagnosis and specific anti-TB treatment are essential for prevention of permanent sequelae or a fatal outcome in TBM. Mortality is 25-30%; higher in AIDS.
The most common complication of TBM is hydrocephalus. Its management can include medical therapy for patients in good grades and those with communicating hydrocephalus [5].
Other common complication is development of vasculitis and stroke.
So, TBM is the most common manifestation of CNS tuberculosis, early diagnosis is important to reduce morbidity and mortality. Imaging findings may assist the diagnostic, therapeutic and prognostic process while cultures are awaited. The triad of abnormal enhancement, hydrocephalus and infarction has a high specificity for the diagnosis of TBM.

Differential Diagnosis List

Final Diagnosis

Tuberculous meningitis and pulmonary miliary tuberculosis.

URL:	https://www.eurorad.org/case/9833
DOI:	10.1594/EURORAD/CASE.9833
ISSN:	1563-4086