An evolving case of headaches and strokes.

A 51-year-old man was admitted to the emergency department with a 10 week history of gradually worsening frontal headaches and fl uctuating confusion. At the same time, he complained of nausea and vomiting, bilateral facial pain, an unpleasant taste in his mouth and mucoid discharge from both nostrils. He had presented to a nearby district general hospital on two occasions during the fortnight prior to his admission where he had been treated with oral antibiotics for presumed sinusitis. He had lost 1.5 stone in weight in 2 months. On initial assessment he was afebrile, and general examination was unremarkable. Glasgow Coma Score was 15, cranial nerves were normal, there was no focal neurological defi cit in the limbs but he did have bilateral papilloedema. Revised Addenbrooke’s Cognitive Examination Score was 76/100. Past medical history included nephrectomy (for live organ donation to his son), type II diabetes mellitus, hypertension and hypercholesterolaemia. He was an ex-smoker with a 90 pack-year history. His regular daily medications were simvastatin 40 mg and ramipril 10 mg. There was no relevant family or travel history. Admission bloods showed a slightly raised white cell count of 14.4×109/l (neutrophil count 11.2×109/l). The rest of his full blood count was normal. Renal and liver function tests were normal. C reactive protein was 7 mg/l and erythrocyte sedimentation rate (ESR) was 41 mm/h. Urine microscopy showed a trace of protein but no red cells. CT brain was normal. CT scan of his sinuses showed mild mucosal thickening of the sphenoid, ethmoid and frontal sinuses, with bilateral nasal polyposis. Lumbar puncture revealed an opening pressure of 36 cm of CSF which contained 84 white cells/mm3 (74 lymphocytes, 10 neutrophils), 188 red cells, protein 0.71 g/l (normal range 0.15–0.45 g/l) and glucose 3.1 mmol/l (paired plasma glucose 5.0 mmol/l). No organisms were detected on Gram stain, culture or viral PCR. No oligoclonal bands were present in the CSF or serum. CSF cytology revealed large numbers of small mature lymphocytes. He was admitted to the neurology ward and started on intravenous aciclovir 10 mg/kg three times a day and intravenous ceftriaxone 2 g twice a day, based on a working diagnosis of meningitis secondary to sinusitis. Sinusitis can lead to a lymphocytic meningitis because infection adjacent to the meninges induces a sympathetic infl ammatory response without the bacteria being present. In some cases— especially when the thin walled sphenoid sinus is involved—sinusitis can also lead to bacterial meningitis by direct penetration through the sinus wall, retrograde extension along the valveless diploic veins, or systemic bacteraemia and subsequent penetration of the blood– brain barrier. Three days into the admission, he developed photophobia and mild neck stiffness. MR brain scan showed a recent right lacunar infarct (fi gure 1). 1Academic Foundation Trainee in Neurosciences, Department of Clinical Neurosciences, Addenbrooke’s Hospital, Cambridge, UK