scholarly journals Transient Serotonin Syndrome by Concurrent Use of Electroconvulsive Therapy and Selective Serotonin Reuptake Inhibitor: A Case Report and Review of the Literature

2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Nagahisa Okamoto ◽  
Kota Sakamoto ◽  
Maki Yamada

The serotonin syndrome, which is characterized by psychiatric, autonomic nervous and neurological symptoms, is considered to be caused by excessive stimulation of the 5-HT1A and 5-HT2 receptors in the gray matter and spinal cord of the central nervous system, after the start of dosing or increase of the dose of a serotoninergic drug. There have been hardly any reports of induction of serotonin syndrome by electroconvulsive therapy (ECT) in combination with antidepressant. We present the case of a female patient with major depressive disorder (MDD) who developed transient serotonin syndrome soon after the first session of ECT in combination with paroxetine. Paroxetine was discontinued, and her psychiatric, autonomic nervous and neurological symptoms were gradually relieved and disappeared within 2 days. We performed the second ECT session 5 days after the initial session and performed 12 sessions of ECT without any changes in the procedure of ECT and anesthesia, but no symptoms of SS were observed. Finally, her MDD remitted. ECT might cause transiently increased blood-brain barrier (BBB) permeability and enhance the transmissivity of the antidepressant in BBB. Therefore, it is necessary to pay attention to rare side effect of serotonin syndrome by ECT in combination with antidepressant.

Author(s):  
Kevin T. Gobeske ◽  
Eelco F. M. Wijdicks

Serotonin syndrome affects the central nervous system, the autonomic nervous system, and the neuromuscular system and can have acute and potentially life-threatening manifestations. By definition, serotonin syndrome is associated with changes in serotonin exposure and thus might be described more accurately as serotonergic excess or serotonin toxicity. The central nervous system effects of serotonin involve regulation of attention, arousal, mood, learning, appetite, and temperature.


2019 ◽  
Vol 20 (9) ◽  
pp. 2288 ◽  
Author(s):  
James Francescangeli ◽  
Kunal Karamchandani ◽  
Meghan Powell ◽  
Anthony Bonavia

The serotonin syndrome is a medication-induced condition resulting from serotonergic hyperactivity, usually involving antidepressant medications. As the number of patients experiencing medically-treated major depressive disorder increases, so does the population at risk for experiencing serotonin syndrome. Excessive synaptic stimulation of 5-HT2A receptors results in autonomic and neuromuscular aberrations with potentially life-threatening consequences. In this review, we will outline the molecular basis of the disease and describe how pharmacologic agents that are in common clinical use can interfere with normal serotonergic pathways to result in a potentially fatal outcome. Given that serotonin syndrome can imitate other clinical conditions, an understanding of the molecular context of this condition is essential for its detection and in order to prevent rapid clinical deterioration.


1994 ◽  
Vol 165 (4) ◽  
pp. 506-509 ◽  
Author(s):  
Christopher F. Fear ◽  
Carl S. Littlejohns ◽  
Eryl Rouse ◽  
Paul McQuail

BackgroundThe induction agent propofol is known to reduce electroconvulsive therapy (ECT) seizure duration. It is assumed that outcome from depression is adversely affected by this agent. This study compares propofol and methohexitone as induction agents for ECT.MethodIn a prospective, randomised, double-blind study 20 subjects with major depressive disorder (DSM-III-R criteria) received propofol or methohexitone anaesthesia. The Hamilton Depression Rating Scale and Beck Depression Inventory were used to assess depression before therapy, at every third treatment, and at the end of therapy. Seizure duration was measured using the cuff technique.ResultsMean seizure durations (P < 0.01) and mean total seizure duration (P < 0.01) were shorter in the propofol group. There was no difference in outcome.ConclusionsUse of propofol may not adversely affect outcome from depression and it is not necessarily contraindicated as an induction agent for ECT. Our results should be interpreted cautiously, and larger studies are needed.


2018 ◽  
Vol 235 ◽  
pp. 169-175 ◽  
Author(s):  
Erika Martínez-Amorós ◽  
Ximena Goldberg ◽  
Verònica Gálvez ◽  
Aida de Arriba- Arnau ◽  
Virginia Soria ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Arash Mohagheghi ◽  
Asghar Arfaie ◽  
Shahrokh Amiri ◽  
Masoud Nouri ◽  
Salman Abdi ◽  
...  

Introduction and Objective. Despite the effectiveness of electroconvulsive therapy (ECT) in treating major depressive disorder (MDD), its cognitive side effects make it less popular. This study investigated the impact of liothyronine on ECT-induced memory deficit in patients with MDD.Methodology. This is a double-blind clinical trial, in which 60 patients with MDD who were referred for ECT were selected. The diagnosis was based on the criteria of DSM-IV-TR. Patients were divided randomly into two groups to receive either liothyronine (50 mcg every morning) or placebo. After the assessment with Wechsler Memory Scale-Revised (WMS-R) before first session of ECT, posttests were repeated again, two months after the completion of ECT.Findings. By controlling the pretest scores, the mean scores of the experimental group were higher than the control group in delayed recall, verbal memory, visual memory, general memory, and attention/concentration scales (P<0.05).Conclusion. Liothyronine may prevent ECT-induced memory impairment in patients with MDD. This study has been registered in IRCT underIRCT201401122660N2.


In the study of the phenomena of anaphylaxis there are certain points on which some measure of agreement seems to have been attained. In the case of anaphylaxis to soluble proteins, with which alone we are directly concerned in this paper, the majority of investigators probably accept the view that the condition is due to the formation of an antibody of the precipitin type. Concerning the method, however, by which the presence of this antibody causes the specific sensitiveness, the means by which its interaction with the antibody produces the anaphylactic shock, there is a wide divergence of conception. Two main currents of speculation can be discerned. One view, historically rather the earlier, and first put forward by Besredka (1) attributes the anaphylactic condition to the location of the antibody in the body cells. There is not complete unanimity among adherents of this view as to the nature of the antibody concerned, or as to the class of cells containing it which are primarily affected in the anaphylactic shock. Besredka (2) himself has apparently not accepted the identification of the anaphylactic antibody with a precipitin, but regards it as belonging to a special class (sensibilisine). He also regards the cells of the central nervous system as those primarily involved in the anaphylactic shock in the guinea-pig. Others, including one of us (3), have found no adequate reason for rejecting the strong evidence in favour of the precipitin nature of the anaphylactic antibody, produced by Doerr and Russ (4), Weil (5), and others, and have accepted and confirmed the description of the rapid anaphylactic death in the guinea-pig as due to a direct stimulation of the plain-muscle fibres surrounding the bronchioles, causing valve-like obstruction of the lumen, and leading to asphyxia, with the characteristic fixed distension of the lungs, as first described by Auer and Lewis (6), and almost simultaneously by Biedl and Kraus (7). But the fundamental conception of anaphylaxis as due to cellular location of an antibody, and of the reaction as due to the union of antigen and antibody taking place in the protoplasm, is common to a number of workers who thus differ on details.


2009 ◽  
Vol 15 (3) ◽  
pp. 181-191 ◽  
Author(s):  
Niraj Ahuja ◽  
Andrew J. Cole

SummaryPresence of fever in psychiatric patients may signify a number of potentially fatal conditions. Several of these are related to treatments (e.g. neuroleptic malignant syndrome with antipsychotics, serotonin syndrome with serotonergic antidepressants, and malignant hyperpyrexia with anaesthesia used for administration of electroconvulsive therapy) or exacerbated by them (e.g. malignant catatonia with antipsychotics). New classes of drug treatment may be changing the epidemiology of these disorders. We suggest that an initial diagnosis of hyperthermia syndrome is clinically useful as there are some important commonalities in treatment. We outline a systematic approach to identify a particular subtype of hyperthermia syndrome and the indications for more specific treatments where available.


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