Article Text
Statistics from Altmetric.com
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).
MR scan of brain at presentation. (A, B) Axial T2-weighted images showing high signal in the mesial frontal regions. Coronal FLAIR image showing high signal in mesial frontal (C) and right parieto-occipital region (D). FLAIR, fluid-attenuated inversion recovery
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, …
Footnotes
Contributors CK: conception; acquisition of data; writing of first draft and subsequent versions; review and critique. EM: acquisition of data; writing of first draft; review and critique. TB: acquisition of data; review and critique. RS: acquisition of data; review and critique. DHM: conception; acquisition of data; review and critique.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Obtained.
Provenance and peer review Commissioned. Externally peer reviewed by Ben Turner, London, UK.
Read the full text or download the PDF:
Other content recommended for you
- Infectious encephalitis: mimics and chameleons
- Diagnosis and treatment of viral encephalitis
- Central nervous system infections in patients with systemic lupus erythematosus: a systematic review and meta-analysis
- Thymoma associated paraneoplastic encephalitis (TAPE), a potential cause of limbic encephalitis
- Viral encephalitis: a clinician’s guide
- The management of infants and children treated with aciclovir for suspected viral encephalitis
- Early autoimmunity and outcome in virus encephalitis: a retrospective study based on tissue-based assay
- Rhomboencephalitis
- Rapidly progressive dementia and ataxia in an elderly man
- Paediatric autoimmune encephalopathies: clinical features, laboratory investigations and outcomes in patients with or without antibodies to known central nervous system autoantigens