Two cases of acute encephalopathy in young children clearly showed evidence of influenza A virus infection and bilateral thalamic lesions. Influenza-associated encephalopathy with bilateral thalamic lesions has mostly been reported in Japan; it differs from Reye's syndrome in several respects. Other factors in addition to influenza virus infection may have contributed to the etiology of encephalopathy in our case patients.

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We treated 27 children with idiopathic epilepsy with zonisamide monotherapy over a period of 2 years and observed behaviour disturbances in a prospective study. In all cases, seizure control was excellent; however, two cases (7.4%) had behaviour disturbances. The first (Case 1) was a 14-year-old girl with partial epilepsy which began at age 4 years. Zonisamide was administered at age 6 years, which was effective against her seizures, but selective mutism, violent behaviour, and lack of concentration developed at age 10 years. The second (Case 2) was a 15-year-old girl with generalized tonic-clonic seizures which began at age 10 years. Zonisamide was also effective against her seizures, but obsessive compulsive disorders (OCD) developed at age 13 years. The patients have had no other physical or mental problems and decreasing the dosage of zonisamide reduced the problems. There are few reports of behaviour disturbances provoked by zonisamide monotherapy in epileptic children who are neither physically nor mentally disturbed. While problems can develop several years later, in the present study, decreasing the zonisamide dosage maintained adequate prevention of seizures and eliminated the behaviour disturbances. Zonisamide is still a useful anticonvulsant for epileptic seizures, but physicians should be wary of its adverse behavioural side effects, which may arise several years later.

A three-year old girl was hospitalized in a semi-conscious state following a febrile convulsion. She did not recover despite treatment and died 16 days after admission. Influenza A virus (H3N2) was detected from a throat swab from the patient, and serum hemagglutinin-inhibiting antibodies to the virus elevated from less than 8 to 256. Brain CT revealed bilateral thalamic hemorrhage and peripheral low density. Subarachnoid hemorrhage was also observed thereafter. Based on clinical manifestations and neuroimaging, this patient was diagnosed as an atypical case of acute necrotizing encephalopathy associated with influenza A virus infection. Such rapid progressive encephalopathies may occur due to intracranial vascular injury including vasculitis or spasms. Although it is clear that influenza A virus triggered this case, we cannot confirm that it was a pathogen. Also, it might be advisable to consider other possible contributing factors such as drugs administered before hospitalization.

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