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DOI 10.1016/j.clinph.2004.11.006

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2004

Comparison of clonidine to sleep deprivation in the potential to induce spike or sharp-wave activity.

Kettenmann B, Feichtinger M, Tilz C, Kaltenhäuser M, Hummel C, Stefan H

Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

OBJECTIVE

This study aimed to investigate previously observed side effects, i.e. increased epileptic activity during clonidine medication. The safety and effectiveness of clonidine as spike inducing agent compared to sleep deprivation were tested.

METHODS

Patients suffering from drug-resistant localization related epilepsy took part in 3 magnetoencephalography (MEG) sessions. One session was recorded without any activating measures. The other two sessions were either performed after sleep deprivation or after medication with clonidine. Target parameter was the number of spikes or sharp-waves during a 30 min recording period.

RESULTS

About 67% of the patients showed increased spike activity after clonidine, whereas sleep deprivation increased the number of spikes in 33%, and 29% of the patients did not show any activation at all. Clonidine was most effective in temporal lobe epilepsy, when the focus was located in the right hemisphere, and when clonidine serum concentrations were ranging between 0.6 and 1.0 ng/ml.

CONCLUSIONS

This study showed for the first time that clonidine can be considered an effective spike or sharp-wave inducing drug that is superior to the potency of sleep deprivation.

SIGNIFICANCE: The administration of clonidine increases the probability of recording ictal and interictal epileptic activity during limited acquisition time.

Для цитирования: Kettenmann B, Feichtinger M, Tilz C, Kaltenhäuser M, Hummel C, Stefan H. Comparison of clonidine to sleep deprivation in the potential to induce spike or sharp-wave activity.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2004. DOI: 10.1016/j.clinph.2004.11.006.

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