電撃痙攣、電撃けいれん

English Journal

[Evidence-based treatments in therapy-resistant bipolar depression].

Sienaert P1, Lambrichts L, Dols A, De Fruyt J.Author information 1*Dit onderzoek werd eerder gepubliceerd in Bipolar Disorders (2013;15:61-9)met als titel 'Evidence-based treatment strategies for treatment-resistant bipolar depression: a systematic review'. Afgedrukt met toestemming.AbstractOBJECTIVE: To present an overview of all available randomized trials on treatment strategies in patients with medication-resistant bipolar depression, a common clinical problem.
Nederlands tijdschrift voor geneeskunde.Ned Tijdschr Geneeskd.2013;157(38):A6075.
OBJECTIVE: To present an overview of all available randomized trials on treatment strategies in patients with medication-resistant bipolar depression, a common clinical problem.DESIGN: Systematic review.METHOD: We carried out a Medline search for publications from 1966 to 2012 using the search terms
PMID 24330789

Nefopam enhances the protective activity of antiepileptics against maximal electroshock-induced convulsions in mice.

Czuczwar M1, Czuczwar K, Cięszczyk J, Kiś J, Saran T, Łuszczki JJ, Turski WA.Author information 1Department of Anesthesiology and Intensive Care, Medical University, Staszica 16, PL 20-081 Lublin, Poland. czuczwarm@gmail.comAbstractNefopam is a centrally acting non-opioid analgesic with a mechanism of action that is not completely understood. Adverse effects associated with the therapeutic use and overdose of nefopam are mainly associated with the central nervous system, such as hallucinations, cerebral edema and convulsions. The aim of this study was to assess the effect of nefopam on the electrical threshold and its influence on the protective activity of antiepileptic drugs in the maximal electroshock test in mice. A 5 mg/kg dose of nefopam significantly elevated the electric seizure threshold, while a dose of 1 mg/kg failed to protect mice against electroconvulsion. At a subthreshold dose of 1 mg/kg, nefopam significantly enhanced the anticonvulsant activity of valproate against electroconvulsions. The protective activity of phenobarbital and phenytoin was significantly enhanced by co-administration of nefopam at the 5 mg/kg dose, but this same dose of nefopam failed to affect the protective activity of carbamazepine. In conclusion, nefopam exerts an anticonvulsive effect when given alone and significantly enhances the protective activity of certain antiepileptic agents against electroconvulsions induced in mice.
Pharmacological reports : PR.Pharmacol Rep.2011;63(3):690-6.
Nefopam is a centrally acting non-opioid analgesic with a mechanism of action that is not completely understood. Adverse effects associated with the therapeutic use and overdose of nefopam are mainly associated with the central nervous system, such as hallucinations, cerebral edema and convulsions.
PMID 21857079

Phenylbutyric acid prevents rats from electroconvulsion-induced memory deficit with alterations of memory-related proteins and tau hyperphosphorylation.

Yao Z1, Guo Z, Yang C, Tian Q, Gong CX, Liu G, Wang JZ.Author information 1Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Hangkong Road 13#, Wuhan 430030, PR China.AbstractElectroconvulsive therapy has been commonly applied in the treatment of refractory depression, but its cognitive side effects are noticed and restrict its application. The molecular mechanisms underlying the side effects remain elusive, and there is no efficient prevention. By employing a recognized electroconvulsive shock (ECS) rat model, we found in the present study that ECS induced spatial memory deficits with simultaneous decreases in synaptic proteins of N-methyl-D-aspartate receptor 2A/B (NR2A/B) and postsynaptic density 95 (PSD95), the immediate early gene c-Fos and cAMP response element binding (CREB) proteins, all of which are memory-related proteins. ECS also caused tau hyperphosphorylation at multiple Alzheimer-related phosphorylation sites with activation of glycogen synthase kinase-3beta (GSK-3beta), Akt and phospho-PKR-like endoreticulum (PERK), and inhibition of protein phosphatase-2A (PP)-2A. Intraperitoneal injection of phenylbutyric acid (PBA), an aromatic short chain fatty acid with the functions of molecule chaperon, prevented rats from the ECS-induced memory deficits, alterations of the memory-associated proteins, and tau hyperphosphorylation. Our data suggest that PBA may be potentially used for attenuating the side effects caused by electroconvulsive therapy.
Neuroscience.Neuroscience.2010 Jun 30;168(2):405-15. doi: 10.1016/j.neuroscience.2010.03.060. Epub 2010 Apr 3.
Electroconvulsive therapy has been commonly applied in the treatment of refractory depression, but its cognitive side effects are noticed and restrict its application. The molecular mechanisms underlying the side effects remain elusive, and there is no efficient prevention. By employing a recognized
PMID 20371270

Japanese Journal

難治性うつ病に対するm-ECT (特集難治性うつ病)

平田豊明
日本精神科病院協会雑誌 30(2), 95-99, 2011-02
NAID 40018724536

Influences of Histamine H_1 Receptor Antagonists on Maximal Electroshock Seizure in Infant Rats(Pharmacology)

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Biological & pharmaceutical bulletin 30(3), 477-480, 2007-03-01
… In this study, electroconvulsion was induced by stimulating rats using ear-clip electrodes, and the durations of electroencephalogram (EEG) seizure, tonic extensor (TE) seizure and clonic (CL) seizure induced by maximal electroshock were measured. …
NAID 110006239188