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Acute necrotizing encephalopathy (ANE) is a rare disease, which is characterised by the rapid development of multiple, symmetrical brain lesions. These lesions affect the thalamus bilaterally, the brainstem tegmentum and the cerebellar medulla. The clinical picture consists of a rapidly deteriorating encephalopathy that develops 1–3 days after a prodromal febrile illness. Indeed, ANE has been related to influenza A virus infection, but to date it has also been associated with other viruses and mycoplasma.1
We report a case of ANE, characterized by a combination of unusual features.
In July 2001, a 17-year-old previously healthy Italian boy was admitted to his local hospital due to a state of deep unconsciousness, with a sudden onset, after 1 day of high fever and cough. He had not been given any aspirin. Neurological examination revealed no pupil abnormalities, no abnormal postures or focal and lateralising signs, no Babinski sign and no signs of meningeal irritation. Computed tomography (CT) of the brain was normal. An electroencephalogram (EEG) showed generalised slow-wave activity. Urinalysis, and all biochemical and haematological parameters were normal. Cerebrospinal fluid (CSF) showed normal pressure, no increase in cells, normal glucose levels and an increase in proteins (55 mg/dl, normal values 20–40). CSF cultures showed no bacterial growth; immunoelectrofocusing for oligoclonal bands revealed a normal pattern. Serum antibody titres against common viruses …