Evolving cerebral infarction in a patient with tuberculous meningitis

Background: Tuberculosis (TB) is a major contributor of global morbidity and mortality worldwide. In 2018, 10 million people were infected with tuberculosis and 1.5 million died from the disease. On the other hand, tuberculous meningitis (TBM) is the most severe form of extra pulmonary tuberculosis with high mortality without treatment. Cerebral infarctions are common complications in patient with TBM with 15–57% patients affected. Here, we reported a case of TBM with evolving cerebral infarctions. Case Description: A 37 y old previously healthy man presented with fever for 1 w with chills and rigors. He also complained of persistent severe headache with occasional vomiting. Otherwise, he denied cough, difficulty in breathing, abdominal pain or diarrhoea. There was reduced appetite and weight loss for past 1week. On examination, his blood pressure was 110/60 mmHg, pulse rate was 105bpm, temperature 38.1. He was alert and conscious. Neurological examination showed reactive pupils and power of 5/5 in both limbs. He was admitted for suspected meningitis. A computed tomography of brain was done which showed ill-defined hypodensity at left head of caudate nucleus and internal capsule. There was leptomeningeal enhancement upon contrast. His CSF examination showed 100TWBC (90% lymphocytes), protein 5 g/l, glucose ratio of 0.33. CSF Genexpert and cryptococcal antigen were negative. He was then started on anti-tuberculous therapy with dexamethasone. 2d into anti-TB treatment, patient was noted to have slow in response. Repeated CT brain showed more prominent hypodensities. 2 d later, patient developed right sided body weakness with power of 3/5. A repeated CT brain showed worsening cerebral grey white matter edema. His condition subsequently stabilized with treatment. Discussion: Cerebral infarction is common in TBM. Commonly involved area is “TB zone” supplied by lenticulostriate, anterior choroidal and thalamogeniculate arteries. Several mechanisms have been proposed for development of infarctions in TBM. Basal exudates are responsible for ischemia. These inflammatory exudates will then lead to vasculitis, thrombosis and vasospasm of vessels. Area prone for infarctions include basal ganglia, internal capsule and thalamus. Conclusion: TBM is important cause of mortality worldwide. Recognising the area of infarction can facilitate early diagnosis and management of complications.