[Influenza-associated encephalopathy].

Infection with influenza viruses produces a spectrum of clinical responses, ranging from upper respiratory illness to central nervous system (CNS) involvement. Recently, the number of reports of influenza-associated encephalopathy in Japan has increased. During the winters of 1997-1998 and 1998-1999, when epidemics of type A influenza (H3N2) occurred, many pediatricians reported cases of influenza-associated encephalitis or encephalopathy in children. The prominent indicators of influenza-associated encephalopathy are the abrupt onset of seizures and coma within a few days of developing a high-grade fever. These patients often develop multi-organ failure and have high morbidity and mortality. The pathogenesis of influenza-associated encephalopathy remains unclear. Because not all patients with influenza develop encephalopathy, infection with the influenza vieus is necessary, but not sufficient, for the development of influenza-associated encephalopathy. Viral RNA is rarely detected in the cerebrospinal fluid (CSF), and the presence of viral antigen in the brain has not been proven. Pathological findings, including the lack of detectable viral antigen and inflammatory cells in brain tissues, suggest that direct viral invasion and inflammation are unlikely to be causes of this disease. In influenza-associated encephalopathy, serum and CSF concentrations of several proinflammatory cytokines and cytokine receptors--such as interleukin (IL)-6, IL-1beta, and soluble tumor necrosis factor (TNF) receptor-1 (sTNF-R1)--are elevated and are related to the clinical severity of the disease. Moreover, the damage of vascular endothelial cells has been shown. Using SNPs, molecular analysis of whole genome of the patients are now on going.