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Effects of Psychotropic Drugs on Seizure Threshold during Electroconvulsive Therapy

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      To analyze the relationship between seizure threshold (ST) and psychotropic drugs in patients treated with ECT.


      We examined clinical data from 43 patients. ST was titrated at each treatment session. We examined associations between ST and psychotropic drugs using multivariate correlation analyses. Data are presented as initial ST, the difference in ST between the first and 10th sessions (ΔST 10th), and the mean difference in ST between the first and last sessions (mean ΔST last).


      Multivariate regression analyses showed associations between initial ST and the total chlorpromazine-equivalent dose of antipsychotics (β=0.363, p<0.05). The total fluoxetine-equivalent dose of antidepressants was associated with ΔST 10th (β=0.486, p<0.01) and mean ΔST last (β=0.472, p<0.01).


      Our study elucidated possible effects of psychotropic drugs on ST shifts. Larger doses of antipsychotics were associated with higher initial ST, whereas higher doses of antidepressants were associated with stronger shifts in ST.

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      Most cited references 74

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      Several clinical and research applications require an estimation of therapeutic dose equivalence across antipsychotic medications. Since the advent of the newer atypical antipsychotics, new dose equivalent estimations have been needed. The reported minimum effective dose was identified for each newer atypical antipsychotic medication and for haloperidol across all available fixed-dose placebo-controlled studies. Reported minimum effective dose equivalence ratios to haloperidol were then converted to chlorpromazine equivalents using the "2 mg of haloperidol equals 100 mg of chlorpromazine" convention. To identify the fixed-dose studies, the following sources were searched until June 2002: MEDLINE, the bibliographies of identified reports, published meta-analyses and reviews, Cochrane reviews, Freedom of Information Act material available from the Food and Drug Administration, and abstracts from several scientific meetings from 1997 to 2002. Doses equivalent to 100 mg/day of chlorpromazine were 2 mg/day for risperidone, 5 mg/day for olanzapine, 75 mg/day for quetiapine, 60 mg/day for ziprasidone, and 7.5 mg/day for aripiprazole. These equivalency estimates may be useful for clinical and research purposes. The source of the dose equivalency estimation is evidence-based and consistent across medication.
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        The ketogenic diet (KD) is a broadly effective treatment for medically refractory epilepsy. Despite nearly a century of use, the mechanisms underlying its clinical efficacy remain unknown. In this review, we present one intersecting view of how the KD may exert its anticonvulsant activity against the backdrop of several seemingly disparate mechanistic theories. We summarize key insights gleaned from experimental and clinical studies of the KD, and focus particular attention on the role that ketone bodies, fatty acids, and limited glucose may play in seizure control. Chronic ketosis is anticipated to modify the tricarboxcylic acid cycle to increase GABA synthesis in brain, limit reactive oxygen species (ROS) generation, and boost energy production in brain tissue. Among several direct neuro-inhibitory actions, polyunsaturated fatty acids increased after KD induce the expression of neuronal uncoupling proteins (UCPs), a collective up-regulation of numerous energy metabolism genes, and mitochondrial biogenesis. These effects further limit ROS generation and increase energy production. As a result of limited glucose and enhanced oxidative phosphorylation, reduced glycolytic flux is hypothesized to activate metabolic K(ATP) channels and hyperpolarize neurons and/or glia. Although it is unlikely that a single mechanism, however well substantiated, will explain all of the diet's clinical benefits, these diverse, coordinated changes seem poised to stabilize synaptic function and increase the resistance to seizures throughout the brain.
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          Dopamine regulates the activity of neural networks in the prefrontal cortex that process working memory information, but its precise biophysical actions are poorly understood. The present study characterized the effects of dopamine on GABAergic inputs to prefrontal pyramidal neurons using whole-cell patch-clamp recordings in vitro. In most pyramidal cells, dopamine had a temporally biphasic effect on evoked IPSCs, producing an initial abrupt decrease in amplitude followed by a delayed increase in IPSC amplitude. Using receptor subtype-specific agonists and antagonists, we found that the initial abrupt reduction was D2 receptor-mediated, whereas the late, slower developing enhancement was D1 receptor-mediated. Linearly combining the effects of the two agonists could reproduce the biphasic dopamine effect. Because D1 agonists enhanced spontaneous (sIPSCs) but did not affect miniature (mIPSCs) IPSCs, it appears that D1 agonists caused larger evoked IPSCs by increasing the intrinsic excitability of interneurons and their axons. In contrast, D2 agonists had no effects on sIPSCs but did produce a significant reduction in mIPSCs, suggestive of a decrease in GABA release probability. In addition, D2 agonists reduced the postsynaptic response to a GABA(A) agonist. D1 and D2 receptors therefore regulated GABAergic activity in opposite manners and through different mechanisms in prefrontal cortex (PFC) pyramidal cells. This bidirectional modulation could have important implications for the computational properties of active PFC networks.

            Author and article information

            [1 ]Department of Psychiatry, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Republic of Korea.
            [2 ]Korea University Research Institute of Mental Health, Seoul, Republic of Korea.
            [3 ]Department of Biomedical Science, Korea University Graduate School, Seoul, Republic of Korea.
            [4 ]Seoul Metropolitan Enpyeong Hospital, Seoul, Republic of Korea.
            Author notes
            Correspondence: Hyun-Ghang Jeong, MD, PhD. Department of Psychiatry, Korea University Guro Hospital, Korea University College of Medicine, 148 Gurodong-ro, Guro-gu, Seoul 08308, Republic of Korea. Tel: +82-2-2626-3164, Fax: +82-2-852-1937, parapraxis@
            Psychiatry Investig
            Psychiatry Investig
            Psychiatry Investigation
            Korean Neuropsychiatric Association
            September 2017
            11 September 2017
            : 14
            : 5
            : 647-655
            Copyright © 2017 Korean Neuropsychiatric Association

            This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

            Funded by: Korea University, CrossRef;
            Award ID: K1512631
            Original Article


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