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A 37-year-old man of Pakistani origin gave a 2-week history of worsening headache, confusion and seizures. He had recently returned from a trip to Pakistan. His only previous medical history was retinitis pigmentosa. On initial examination, he was feverish and photophobic, with no focal neurological deficit.
An initial CT scan of head showed basal ganglia calcification but no other parenchymal changes. Cerebrospinal fluid (CSF) showed raised protein (0.97 g/L), low glucose (2.8 mmol/L compared with plasma glucose of 8.1 mmol/L) and a lymphocytic pleocytosis of 138×106/L. CSF opening pressure was not documented.
Question 1: What is the most likely diagnosis and how should he be managed?
Acutely altered mental state, headache, fever and seizures should raise suspicion for central nervous system (CNS) infection, in particular meningoencephalitis. The CSF findings, ethnic origin and travel history strongly suggest tuberculous (TB) meningitis; we started rifampicin, isoniazid, pyrazinamide and moxifloxacin, together with dexamethasone, initially 24 mg/day according to British Infection Society guidelines. His seizures settled with levetiracetam. His baseline chest radiograph was normal. MRI scan of brain showed non-enhancing high T2 signal lesions in the left mesial frontal lobe and right parieto-occipital region (figure 1).
Question 2: What is the differential diagnosis of his MR brain appearances?
Infective causes are the most likely at this stage, including TB meningoencephalitis and viral encephalitis. The initial imaging does not show the meningeal enhancement or tuberculomas that can occur in TB meningitis. Neoplastic causes such as CNS lymphoma are possible, although the subacute presentation is atypical and there would usually be contrast enhancement. Neuroinflammatory causes are also in the differential diagnosis, with many potential causes.
We continued anti-TB treatment and gradually reduced the dexamethasone dose. Five days later, his CSF had improved, …
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