The aim of this study was to clarify the difference between influenza and non-influenza cases in clinical symptoms, laboratory and neuroimaging findings, and outcome in children with ANE. We retrospectively studied 22 children with ANE. Eleven of them had virological proof of influenza infection and the other 11 were judged as non-influenza infection. There was no significant difference between influenza and non-influenza cases in sex, antipyretics use and neurological symptoms. Although laboratory data were not different between the two groups, brainstem lesions were relatively more frequent in influenza cases than in non-influenza cases. Outcome was not different between the two groups. The results of our study suggest that the pathogenesis of acute necrotizing encephalopathy will not be dependent on infectious agents.
Key words acute necrotizing encephalopathy, influenza.ANE is a distinct subtype of acute encephalopathy described by . The most prominent feature of ANE is multiple, symmetric brain lesions in both thalami. CT or MRI sometimes reveal lesions in other brain regions including cerebral white matter, internal capsule, putamen, brainstem and cerebellum. The neurological outcome of ANE has been reported to be very poor. The majority of patients with ANE die or survive with moderate or severe neurological sequelae (1).The onset of ANE is triggered by acute febrile diseases, mostly viral infection, among which influenza is the most common prodromal illness (1, 4). However, there have been no reports on differences in clinical symptoms, laboratory and neuroimaging findings, and outcome according to the prodromal illness. We conducted a retrospective study in order to establish whether there are differences in these respects between influenza and non-influenza cases in patients with ANE.
List of Abbreviations:ANE, acute necrotizing encephalopathy; IL-6, interleukin-6; CSF, cerebrospinal fluid; CT, computed tomography; MRI, magnetic resonance imaging; TNF-α, tumor necrosis factor-α.
PATIENTS AND METHODWe recruited 22 children with ANE who had been admitted to 17 hospitals between 1998 and 2005. This cohort was derived from a previous report, whereas the purpose of the present study is quite different (5). The diagnosis of ANE was made on the basis of neuroradiological findings according to the criteria proposed by Mizuguchi et al. (1,2). In this study, we included patients with acute encephalopathy who had multiple focal lesions which were symmetrically distributed in both thalami and other brain regions such as the putamina, cerebral and cerebellar white matter, and brainstem tegmentum (1, 2, 6). CT was the initial neuroimaging performed in 21 patients and MRI in 1. Abnormal findings consistent with ANE were found in the first CT/MRI in all patients. We excluded patients with marked metabolic derangement such as elevated lactate, pyruvate, amino acids, or organic acids levels.