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Диссоциативы и brainwave
Чтобы понять, как эффективно совместить действие веществ и хемисинка, надо хотя бы примерно представлять себе какие изменения в ЭЭГ происходят в течение всего процесса действия вещества и попытаться подстроиться под эти изменения. Вот только боюсь, что научные данные по этому вопросу имеются только в отношении кетамина. Короче говоря, свой энцефалограф нужен. Кроме того, есть большие сомнения относительно линейности процесса, в том плане, что мозг - не стрелка, которая сейчас указывает на бета-волны, а после получаса brainwave - на тета. Все волны присутствуют одновременно, просто у них интенсивность разная.
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Increase in delta- and beta-wave activity of the EEG during rapid opiate detoxification (ROD)-reversal by administration of the non-specific NMDA-antagonist S(+) ketamine-
E. Freyea, Corresponding Author Contact Information, E-mail The Corresponding Author, L.B. Parteckeb and J.V. Levyc
Abstract
Little is known on effects taking place in the CNS during rapid opioid detoxification (ROD) while the patient is under anesthesia. We therefore measured EEG-power spectra in the β, α, Θ, and δ-band in 36 patients undergoing ROD. Measurements were taken before, during steady-state anesthesia and following administration of the antagonist naltrexone. In addition, the non-specific NMDA-antagonist S(+) ketamine was given for reduction of CNS-hyperexcitation, while the efficacy of this adjunct was determined using EEG power spectra analysis. Compared to steady-state anesthesia, EEG power spectra were characterized by a marked decrease of power by 251% in the delta (0.5–3 Hz) and an increase by 209% in the beta- (13–30 Hz) domain when withdrawal was induced with naltrexone. Subsequent administration of S(+)-ketamine induced a reversal of acute abstinence-related EEG power changes: compared to anesthesia with naltrexone on board, power in the EEG increased by 65% in the delta- and decreased by 723% in the beta-band. While sympathetically induced hemodynamic alterations in anesthesia-assisted opioid detoxification can be attenuated by the α2-agonist clonidine and sedation, central nervous sensory activation can be attenuated by the administration of S(+)-ketamine (1.5 mg/kg). Since EEG alterations during acute withdrawal with naltrexone can be controlled by the non-specific NMDA-antagonist S(+)-ketamine, this latter presents a useful adjunct during ROD management.
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Increase in delta- and beta-wave activity of the EEG during rapid opiate detoxification (ROD)-reversal by administration of the non-specific NMDA-antagonist S(+) ketamine-
E. Freyea, Corresponding Author Contact Information, E-mail The Corresponding Author, L.B. Parteckeb and J.V. Levyc
Abstract
Little is known on effects taking place in the CNS during rapid opioid detoxification (ROD) while the patient is under anesthesia. We therefore measured EEG-power spectra in the β, α, Θ, and δ-band in 36 patients undergoing ROD. Measurements were taken before, during steady-state anesthesia and following administration of the antagonist naltrexone. In addition, the non-specific NMDA-antagonist S(+) ketamine was given for reduction of CNS-hyperexcitation, while the efficacy of this adjunct was determined using EEG power spectra analysis. Compared to steady-state anesthesia, EEG power spectra were characterized by a marked decrease of power by 251% in the delta (0.5–3 Hz) and an increase by 209% in the beta- (13–30 Hz) domain when withdrawal was induced with naltrexone. Subsequent administration of S(+)-ketamine induced a reversal of acute abstinence-related EEG power changes: compared to anesthesia with naltrexone on board, power in the EEG increased by 65% in the delta- and decreased by 723% in the beta-band. While sympathetically induced hemodynamic alterations in anesthesia-assisted opioid detoxification can be attenuated by the α2-agonist clonidine and sedation, central nervous sensory activation can be attenuated by the administration of S(+)-ketamine (1.5 mg/kg). Since EEG alterations during acute withdrawal with naltrexone can be controlled by the non-specific NMDA-antagonist S(+)-ketamine, this latter presents a useful adjunct during ROD management.
