A 46-year-old previously healthy female developed an insidious onset severe persistent headache, most prominent in the occipital region lasting for 10 days. Six days after the onset, she experienced dysarthria and a difficulty in moving her tongue within the mouth with a difficulty in eating and drinking. She did not complain of nasal regurgitation of food or nasal quality of speech. After admission, she was found to have a high-grade fever. She was otherwise healthy and denied symptoms of cough, decreased appetite, weight loss, or past history of tuberculosis. On admission, she was found to be ill with elicitable neck stiffness. Neurological examination revealed bilateral hypoglossal nerve palsy with marked tongue atrophy, more prominent in the left side (Figure 1) with tongue fasciculations and without other cranial nerve palsies or pyramidal weakness. Her eye movements were saccadic with a broad-based ataxic gait without other signs of cerebellar involvement.
Her blood tests revealed a haemoglobin of 12.5g/dl with a neutrophil leukocytosis (19,000/microL; 92.2% of neutrophils) with elevated ESR (100 1st Hr) and CRP (195 u/L). Her blood cultures were negative. Noncontrast CT brain did not reveal any abnormality. Cerebrospinal fluid (CSF) biochemistry revealed significant elevation of protein (111 mg/dL) with 59 polymorphs and 8 lymphocytes per cubic millimetre with reduced CSF glucose (29 mg/dL). CSF for GeneXpert for tuberculosis and staining for acid-fast bacillus (AFB) and fungal and atypical cells were negative. Pyogenic, mycobacterial, and fungal CSF cultures were negative and CSF for Meningococcus, Haemophilus, and Pneumococcus antigens were also negative. Her chest radiograph did not reveal any changes suggestive of pulmonary tuberculosis or sarcoidosis. Syphilis (VDRL & THPA), HIV serology, and autoimmune markers for vasculitis (rheumatoid factor, ANA (IF), and p & c-ANCA) were negative.
We initiated her on empirical treatment as for pyogenic meningitis with ceftriaxone and vancomycin for which she had a gradual improvement of general status with improvement of fever, meningism, gaze, and gait abnormalities while tongue weakness and atrophy persisted. Since we considered tuberculous meningitis as a possibility, we deferred treatment with steroids. Her rapid recovery in the absence of steroids or antituberculous drugs further supported our presumed diagnosis of pyogenic meningitis. Subsequently, she underwent MRI of brain and brainstem, which revealed a posteromedial infarction in the lower part of the medulla oblongata without leptomeningeal enhancement and did not show a significant cerebral oedema (Figure 2). At the end of three weeks of antibiotics, inflammatory markers and repeat CSF analysis reached normal levels. After discharge, we reviewed her at one month and three & six months and she was free of fever with good general condition and had normal inflammatory markers. However, she had persistent tongue atrophy with difficult speech from which she was gradually recovering with the help of physiotherapy.