Serotonin syndrome is a potentially deadly reaction that occurs as a result of: therapeutic use of medicament, as a consequence of drugs’ interaction or intentional overdosing with medicaments that influence on the serotonin metabolism.

In this paper the authors presented brief theoretical consideration of etiological causes for clinical onset of serotonin syndrome, clinical features of serotonin syndrome and difficulties in discovering the same in clinical practice. Furthermore, diagnostic criteria, differential diagnoses, treatment and prevention of serotonin syndrome were presented.

Authors presented the case report of female inpatient treated in Psychiatry Clinic in Tuzla University Clinical Centre, whose state of somatic deterioration understood originally within the clinical features of basic diseases. Correspondingly, the dose of pro-serotoninergic antidepressant was increased. Subsequently, and timely recognition of serotonin syndrome, and therapeutic corrections of medication, were of great importance in the course of patients’ recovery.

We report three cases in which toxic serotonin syndrome developed in relation to three different selective serotonin reuptake inhibitors (SSRI) (ie, fluoxetine, sertraline, paroxetine), and which all responded to the discontinuation of the SSRI and also to an additional propranolol treatment.

This case report describes a patient on tranylcypromine who erroneously received a single dose of imipramine and subsequently developed a fatal serotonin syndrome. Both the clinical features and the pathophysiology of the serotonin syndrome are discussed.

Treatment-resistant depression (TRD) may be implicated in 33–57% of depression cases. The currently available effective treatments include electroconvulsive therapy (ECT) or augmentation of serotonin selective reuptake inhibitors (SSRIs) with antipsychotics. ECT and antipsychotics are both associated with safety and tolerability concerns. Depression is hypothesized to result from a dysregulation of monoamine neurotransmitters, although the source of the dysregulation has been unclear. However, recent studies have revealed that an enzyme that degrades the neurotransmitters, known as monamine oxidase-A (MAO-A), may be overactive in patients with depression. Thus, treatments for depression that modulate MAO-A could act upstream relative to current antidepressant treatments. Monoamine oxidase inhibitors (MAOIs) can be highly effective therapeutic agents for depression and some anxiety disorders. Some evidence suggests that MAOIs may act by reversing excessive neurotransmitter depletion within the neuron and the synapse. MAOIs tend to be underutilized in clinical practice, due in part to misinformation and mythology about their dietary and drug interactions. The new class of reversible monoamine oxidase inhibitors (RIMAs) has shown efficacy in depression, with safety and tolerability comparable to SSRIs. This article discusses recent progress in RIMAs toward the treatment of TRD. Dietary and drug interactions of MAOIs will be covered, as well as guidelines for integrating these agents into clinical practice.

Antidepressant treatments, including selective serotonin reuptake inhibitors, are associated in older adults with an increased risk of adverse effects compared to younger adults. This is partly explained by multiple drug use causing drug–drug interactions. In the present report, we describe a case of serotonin syndrome in an 88-year-old woman receiving a low dose of escitalopram. The onset of this episode could have been induced by a drug–drug interaction with an acute treatment by miconazole gingival adhesive tablets. The lack of pharmacokinetic data in the elderly population should prompt us to be especially cautious about prescription of this new formulation of miconazole in association with drugs metabolized by cytochromes P450 isoenzymes.

The serotonin syndrome is a potential side-effect of serotonin-enhancing drugs, including antidepressants such as selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs). We recently reported a genetic mouse model for the serotonin syndrome, as serotonin transporter (SERT)-deficient mice have exaggerated serotonin syndrome behavioural responses to the MAOI tranylcypromine and the serotonin precursor 5-hydroxy-l-tryptophan (5-HTP). As numerous case reports implicate the atypical opioids tramadol and meperidine in the development of the human serotonin syndrome, we examined tramadol and meperidine as possible causative drugs in the rodent model of the serotonin syndrome in SERT wild-type (+/+), heterozygous (+/−) and knockout (−/−) mice. Comparisons were made with SERT mice treated with either vehicle or morphine, an opioid not implicated in the serotonin syndrome in humans. Here we show that tramadol and meperidine, but not morphine, induce serotonin syndrome-like behaviours in mice, and we show that this response is exaggerated in mice lacking one or two copies of SERT. The exaggerated response to tramadol in SERT−/− mice was blocked by pretreatment with the 5-HT1A antagonist WAY 100635. Further, we show that morphine-, meperidine- and tramadol-induced analgesia is markedly decreased in SERT−/− mice. These studies suggest that caution seems warranted in prescribing or not warning patients receiving SSRIs or MAOIs that dangerous side-effects may occur during concurrent use of tramadol and similar agents. These findings suggest that it is conceivable that there might be increased vulnerability in individuals with SERT polymorphisms that may reduce SERT by more than 50%, the level in SERT+/− mice.

We describe a 63 year old male with serotonin syndrome, presenting with choreoathetosis. Differentiating this syndrome from neuroleptic malignant syndrome remains a challenge. It is important to be aware of drugs that can potentially precipitate this syndrome.

Neuroleptic malignant syndrome (NMS) is a potentially life-threatening condition that has been associated with antipsychotic use. Most diagnostic criteria include fever and muscle rigidity, although NMS may present without either. Diagnostic uncertainty in such cases may result in delays in diagnosis and management, leading to adverse consequences for these patients. The differential diagnosis of NMS is broad and includes a number of neurological, medical and psychiatric conditions as well as substance and medication-induced disorders. A case is described that illustrates an atypical presentation of NMS and demonstrates some of the challenges in its diagnosis. Limitations of current NMS criteria are also examined, and suggestions for future criteria are presented.

Serotonin syndrome, a triad of autonomic instability, altered mental status and neuromuscular abnormalities, is usually attributed to serotonergic overdoses. Moclobemide is a new selective monoamine oxidase inhibitor (MAOI) that generally causes mild, self-limited gastrointestinal and central nervous system effects after ingestion. We present a case of serotonin syndrome that occurred after moclobemide overdose, and discuss the recognition and treatment of this important condition. Serotonin syndrome may become increasingly common because of the liberal use of selective serotonin reuptake inhibitors, new MAOIs and other agents such as codeine and meperidine, which have the potential for harmful interaction.