The role of influenza A and influenza B in acute childhood encephalitis and encephalopathy (ACE) was evaluated prospectively in all children admitted to the Hospital for Sick Children, Toronto, Canada, during an 11-year period from Jan 1994- Dec 2004. Influenza infection was defined by detection in the nasopharynx by immunofluorescence microscopy or viral culture and/or by a 4-fold or greater rise in complement fixation titer. In 311 children with ACE, influenza infection was detected in 22 (7%); 11 were <5 years of age. Fourteen fulfilled criteria for ACE. Influenza A was detected in 13 of 14 cases, and influenza B in 1 case. Neurologic manifestations developed within 5 days of onset of respiratory symptoms in 64%. These included seizures, cranial nerve abnormalities, focal motor deficits, gait abnormalities, meningismus, torticollis, hyperreflexia and opisthotonus. Two presented with status epilepticus, and 2 had hemiparesis. CSF pleocytosis occurred in 3 patients, and elevated protein in 4. Neuroimaging abnormalities noted in 8 of 14 tested were more common in children <2 years of age. Neurologic sequelae occurred in 8 patients (in 5 <2 years of age), and included seizures, hemiparesis, ataxia, and speech disorder. EEGs were abnormal in all 8 of those with neurologic sequelae and in 4 of 6 without sequelae. An acute rather than a postinfectious process was suggested by the briefness of the respiratory prodrome. [1]

COMMENT. Influenza virus infection is associated with 5% of cases of acute childhood encephalitis/encephalopathy in Canada. The younger children <5 years of age are most susceptible, and children <2 years of age are most likely to have neurologic sequelae.

A Japanese study of prognostic factors in influenza-associated encephalopathy evaluated 442 cases retrospectively [2]. Type A influenza was detected in 84% and type B in 9.5%. Fifty-four cases (22%) had a history of febrile convulsions. Significant factors for a poor prognosis and death in 35(19%) of 184 cases were an elevated transaminase, hyperglycemia, hematuria or proteinuria, and use of diclofenac sodium for fever during the infection. Factors showing a trend toward poor prognosis were elevated body temperature (>41C), low platelets, and low blood sugar. The occurrence of these signs should prompt admission to intensive care.