Okada T
Niigata University
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Featured researches published by Okada T.
Clinical Eeg and Neuroscience | 1994
Yoshihiro Naganuma; Tohru Konishi; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Shiniti Yagi; Okada T
To clarify the relationship between cognitive function and CBZ therapy, auditory event-related potentials (P300) were examined in 23 patients with Benign Childhood Epilepsy with Centrotemporal Spike (BCECT) compared with 54 normal controls. The results were 1) the mean P300 latency in BCECT (368 +/- 29 msec) was significantly prolonged compared with that in normal controls (349 +/- 30 msec), but most individual patients showed normal values. 2) The prolongation of P300 latency was greatest during the course of therapy. 3) On repeated examination of P300, P300 latency was found to gradually become shorter with age in spite of continuous CBZ therapy. At initiation of CBZ therapy, the P300 latency became shorter; on the other hand, P300 latency became shorter with the discontinuation of CBZ. 4) The age-corrected P300 latency showed a significant positive correlation with the serum concentration of CBZ. Our results suggest that CBZ therapy has both an undesirable effect (chronic impairment) and a desirable effect (improvement of underlying dysfunction caused by epileptogenesis) on cognitive function.
Clinical Eeg and Neuroscience | 1995
Tohru Konishi; Yoshihiro Naganuma; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Okada T
The effects of antiepileptic drugs (AED) on EEG background activity were evaluated in 37 newly treated children with epilepsy, compared with 46 age-matched healthy controls. Before AED therapy, the children with epilepsy, both partial (treated with carbamazepine, CBZ group) and generalized seizures (treated with valproic acid, VPA group), already exhibited significant slowing of EEG with increased delta and decreased alpha power. Following 3 to 6 months of AED therapy, this EEG slowing was enhanced in the CBZ group and reduced in the VPA group. Following 1 year of AED therapy, an increase in frequency was recognized in the CBZ group. These results suggest that 1) most children with epilepsy already exhibit slowing of the EEG at the onset of seizures, which may reflect CNS developmental deficit, 2) the short-term effects on EEG are different between CBZ and VPA, and 3) EEG development with age continues under continuous AED administration. The EEG background activity in children with epilepsy is affected by many factors, which include the underlying CNS dysfunction of the epilepsy itself and also AED therapy (type of AEDs, duration of therapy, etc).
Brain & Development | 1997
Yoshihiro Naganuma; Tohru Konishi; Kazuhisa Hongou; Okada T; Jun Tohyama; Makoto Uchiyama
To clarify the relationship between the cognitive function and EEG activity, auditory event-related potentials (P300) were examined in 72 patients with partial epilepsy. Twenty-six patients (67 trials) had idiopathic partial epilepsies (IPE), and 46 (118 trials) symptomatic or cryptogenic partial epilepsies (SPE). For this study, patients undergoing carbamazepine monotherapy with a dose of less than 16 mg/kg/day were selected to rule out the effects of anti-epileptic drugs. The results were as follows: (1) The P300 latency tended to be prolonged in association with the EEG slowing in both epileptic groups. (2) There was no clear relationship between the frequency of paroxysmal discharges and the P300 latency. (3) The P300 latency was slightly prolonged in the patients with temporal foci compared with that in ones with extra-temporal foci. (4) There was no significant relationship between the generalization of focal paroxysmal discharges and the P300 latency. These results suggested that the influence of EEG abnormalities (particularly paroxysmal discharges) on the P300 latency is relatively little, and the cognitive dysfunction in partial epilepsies mainly originates from other factors such as the epileptogenic lesion itself.
Psychiatry and Clinical Neurosciences | 1992
Kazuhisa Hongou; Tohru Konishi; Yoshihiro Naganuma; Miyako Murakami; Miwa Yamatani; Okada T
The subjects were 66 epileptic children with monopharmacy (CBZ; 39 cases and VPA; 21 cases). The EEG was recorded every 6 months in each patient from the onset (before administration of AED) to one year after discontinuation of AED. The mean ages at starting medication were 8.3f3.0 in the CBZ group and 11.3f2.9 in the VPA group, and those at the final seizure attack was 8.3k2.7 in the CBZ group and 11.0k3.4 in the VPA group, and those at discontinuation of AED was 11.5+2.5 in the CBZ group and 11.8f4.2 in the VPA group. The EEG was taken applying the 10-20 system of electrode placement. The bandpass filters were set at 60 Hz. The EEG was additionally recorded on magnetic tape. Out of 3 min of recording with eyes closed, the EEG sample for an analysis was chosen free of artifacts and paroxysmal judged by inspection. The computerized spectral analysis was done by the record of 0 1 derivations, using Fast Fourier Transformation. Digital conversion was undertaken with 64 Hz. The record was divided into 16 epochs of an 8-sec duration. The spectral analysis resulted in 200 values within 0.5-25 Hz and calculated total power, mean frequency and relative powers in delta (0.5-3.85 Hz), theta (47.85 Hz), alphal (8-9.85 Hz), alpha2 (1012.85 Hz), beta1 (13-19.85 Hz), beat 2 (2025 Hz). The log(X) for both relative band power and total power were evaluated. The changes in the EEG background activity were compared between before and after starting administration of AED, between before and after discontinuation of AED, using the paired t-test. The changes from 6 to 30 months after the final seizure attack was analyzed by 2 way ANOVA in a patient who had not any seizures for at least 30 months.
Brain & Development | 1995
Tohru Konishi; Yoshihiro Naganuma; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Shinichi Yagi; Okada T
(group A). The results were compared with in the case of febrile Conclusion. A long-term EEG abnormality in the course of FS did convulsions with other etiologies (group B). Group A consisted of 12 not always mean the development of epilepsy, and such an EEG patients, who were followed for 3 to 20 years (average, 9 years and 8 abnormality also changes in the course of FS age-dependently. months). Group B consisted of 600 cases, who were followed for 3 to However, in some patients, these may be related to the risk of later 20 years and 6 months (average, 10 years and 6 months). subsequent epilepsy. Results. The sex ratio, positive family history of febrile convulsions among first degree relatives, cases with mental retardation and total seizure number were not different between the two groups. No patient in group A had a family history of epilepsy, but 20 cases (3.3%) in group B had one. The body temperature at the time of convulsions was higher in group A than group B. Hemiconvulsions, prolonged seizures over 60 minutes and recurrent convulsions were significantly more frequent in group A. The time from the onset of fever to the convulsions tended to be longer in group A, but the difference was not significant. The epileptic discharges appearing before 1 year and 2 months of age were compared between the two groups. In group A epileptic discharges were not noted in any case, but in group B they were noted in 10 cases (16.7%1, all being focal spikes. Single afebrile seizures were not noted in group A, but were noted in 37 cases (6.2%) in group B. One patient in group B (5.7%) suffered from later epilepsy (more than 2 afebrile seizures following febrile convulsions). However, the difference was not significant. Conclusion. Thus, the prognosis of febrile convulsions during exanthema subitum is not so poor, except for some clinical differences from febrile convulsions with other etiologies. Keywords; Febrile convulsion; Exanthema subitum; Epilepsy
No to hattatsu. Brain and development | 1993
Yoshihiro Naganuma; Tohru Konishi; Mié Matsui; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Okada T
No to hattatsu. Brain and development | 1990
Yoshihiro Naganuma; Tohru Konishi; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Okada T
No to hattatsu. Brain and development | 1991
Yoshihiro Naganuma; Tohru Konishi; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Okada T
NO TO HATTATSU | 1991
Yoshihiro Naganuma; Tohru Konishi; Kazuhisa Hongou; Miyako Murakami; Miwa Yamatani; Okada T
No to hattatsu. Brain and development | 1987
Miwa Yamatani; Miyako Murakami; Konda M; Tohru Konishi; Suzuki Y; Okada T; Honma K