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      Electroconvulsive therapy and its different indications Translated title: Terapia electroconvulsiva y sus diferentes indicaciones Translated title: L'électroconvulsivothérapie et ses différentes indications

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          Abstract

          In spite of recent developments in the pharmacotherapy of depressive disorders, the delay until clinical improvement can be achieved, and the considerable rate of nonresponse and nonremission, are major problems which remain unresolved. Electroconvulsive therapy (ECT) is a nonpharmacoloqic bioloqical treatment which has been proven to be a highly effective treatment option, predominantly for depression, but also for schizophrenia and other indications. Though there is a lack of controlled investigations on long-term treatments, ECT can also be used for relapse prevention during maintenance therapies. The safety and tolerabitity of electroconvulsive treatment have been enhanced by the use of modified stimulation techniques and by progress in modern anesthesia. Thus, today a safe treatment can also be offered to patients with higher somatic risks, ECT still represents an important option, especially in the therapy of treatmentresistant psychiatric disorders after medication treatment failures. Earlier consideration of ECT may reduce the rate of chronic and difficult-to-treat psychiatric disorders.

          Translated abstract

          A pesar de los recientes progresos en la farmacote-rapia de los trastornos depresivos aun persisten sin resolverse dos importantes problemas: la latencia hasta alcanzar la mejoría clínica, y la alta frecuencia de falta de respuesta y de remisión. La terapia electroconvulsíva (TEC) es un tratamiento biológico no farmacológico que ha probado ser una opción terapéutica altamente efectiva, preferentemente para la depresión, pero también para la esquizofrenia y otras indicaciones. Aunque faltan investigaciones controladas en tratamientos a largo plazo, la TEC también puede ser empleada en prevención de recaídas durante las terapias de mantenimiento. La seguridad y tolerabilídad del tratamiento elec-troconvulsívo han aumentado con el uso de técnicas de estimulación modificadas y por el progreso de la moderna anestesia. De esta manera hoy en día también se puede ofrecer un tratamiento seguro a pacientes que tienen mayores riesgos somáticos. La TEC aun representa una importante opción, especialmente en el manejo de pacientes con trastornos psiquiátricos resistentes al tratamiento después de fallar la terapia medicamentosa. Con las consideraciones anteriores la TEC puede reducir la frecuencia de trastornos psiquiátricos crónicos y difíciles de tratar.

          Translated abstract

          Malgré les récents développements dans le domaine de la pharmacothérapie de la dépression, la latence de survenue de l'amélioration clinique et le taux considérable d'absence de réponse et de rémission sont des problèmes majeurs non résolus à ce jour, L'électroconvulsivothérapie (ECT) est un traitement biologique non pharmacologique qui a prouvé sa grande efficacité thérapeutique surtout dans la dépression mais aussi dans la schizophrénie et d'autres indications. En dépit d'un manque d'études contrôlées sur les traitements à long terme, l'ECTpeut être également utilisé dans la prévention des rechutes au cours des traitements d'entretien. Les progrès de l'anesthésie moderne et les techniques de stimulation dites modifiées ont amélioré la tolérance et la sécurité d'emploi de l'ECT. Aujourd'hui, un traitement sûr peut donc être proposé aux patients à risque somatique plus élevé, L'ECT reste une alternative importante surtout dans le traitement des troubles psychiatriques résistants au traitement en cas d'échec thérapeutique antérieur. Envisager l'ECT de façon précoce pourrait diminuer le taux de troubles psychiatriques chroniques difficiles à traiter.

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          Most cited references130

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          World Health Organization.

          Ala Alwan (2007)
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            Regulation of BDNF and trkB mRNA in rat brain by chronic electroconvulsive seizure and antidepressant drug treatments.

            The influence of chronic electroconvulsive seizure (ECS) or antidepressant drug treatments on expression of brain-derived neurotrophic factor (BDNF) and its receptor, trkB, was examined by in situ hybridization and Northern blot. In frontal cortex, acute ECS increased BDNF mRNA approximately twofold, an effect significantly augmented by a prior course of chronic ECS treatment (10 d). In the hippocampus, the influence of chronic ECS varied between the major subfields. In the dentate gyrus granule cell layer, chronic ECS decreased the acute induction of BDNF and trkB mRNA by approximately 50%, but prolonged their expression: levels remained elevated two- to threefold 18 hr later after the last chronic ECS treatment, but returned to control 18 hr after acute ECS. In CA3 and CA1 pyramidal cell layers, chronic ECS significantly elevated the acute induction of BDNF, and tended to prolong the expression of BDNF and trkB mRNA. A similar effect was observed in layer 2 of the piriform cortex, where chronic ECS significantly increased the acute induction and prolonged the expression of BDNF and trkB mRNA. Chronic (21 d), but not acute (1 d), administration of several different antidepressant drugs, including tranylcypromine, sertraline, desipramine, or mianserin, significantly increased BDNF mRNA and all but mianserin increased trkB mRNA in hippocampus. In contrast, chronic administration of nonantidepressant psychotropic drugs, including morphine, cocaine, or haloperidol, did not increase levels of BDNF mRNA. Furthermore, chronic administration of ECS or antidepressant drugs completely blocked the down-regulation of BDNF mRNA in the hippocampus in response to restraint stress. The enhanced induction and prolonged expression of BDNF in response to chronic ECS and antidepressant drug treatments could promote neuronal survival, and protect neurons from the damaging effects of stress.
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              A molecular and cellular theory of depression.

              Recent studies have begun to characterize the actions of stress and antidepressant treatments beyond the neurotransmitter and receptor level. This work has demonstrated that long-term antidepressant treatments result in the sustained activation of the cyclic adenosine 3',5'-monophosphate system in specific brain regions, including the increased function and expression of the transcription factor cyclic adenosine monophosphate response element-binding protein. The activated cyclic adenosine 3',5'-monophosphate system leads to the regulation of specific target genes, including the increased expression of brain-derived neurotrophic factor in certain populations of neurons in the hippocampus and cerebral cortex. The importance of these changes is highlighted by the discovery that stress can decrease the expression of brain-derived neurotrophic factor and lead to atrophy of these same populations of stress-vulnerable hippocampal neurons. The possibility that the decreased size and impaired function of these neurons may be involved in depression is supported by recent clinical imaging studies, which demonstrate a decreased volume of certain brain structures. These findings constitute the framework for an updated molecular and cellular hypothesis of depression, which posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, neurotrophic factors necessary for the survival and function of particular neurons. This hypothesis also explains how stress and other types of neuronal insult can lead to depression in vulnerable individuals and it outlines novel targets for the rational design of fundamentally new therapeutic agents.
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                Author and article information

                Contributors
                Dept of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Germany
                Dept of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Germany
                Journal
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues in Clinical Neuroscience
                Les Laboratoires Servier (France )
                1294-8322
                1958-5969
                March 2008
                : 10
                : 1
                : 105-117
                Affiliations
                Dept of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Germany
                Dept of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Germany
                Author notes
                Article
                10.31887/DCNS.2008.10.1/tcbaghai
                3181862
                18472488
                d4bbd6ce-c866-4445-a2b1-76fd9446a7c7
                Copyright: © 2008 LLS

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Clinical Research

                Neurosciences
                schizophrenia,depression,treatment resistance,electroconvulsive therapy
                Neurosciences
                schizophrenia, depression, treatment resistance, electroconvulsive therapy

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