scholarly journals Serotonin syndrome

1999 ◽  
Vol 23 (12) ◽  
pp. 742-747 ◽  
Author(s):  
Shameem Mir ◽  
David Taylor
Keyword(s):  
Monoamine Oxidase ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Syndrome ◽  
Case Reports ◽  
Individual Case ◽  
Drug Combinations ◽  
Clinical Implications ◽  
Review Of Literature ◽  
Long Acting

Aims and methodTo define serotonin syndrome and its symptoms and to discover which drugs or drug combinations are likely to cause it. A review of literature (including case reports) relating to serotonin syndrome collated from searches of MedLine and Micromedex covering the period January 1991 to July 1998.ResultsMost of the data found were either individual case reports or reviews of case reports. Reports of serotonin syndrome seem to be growing, certainly since the introduction of selective serotonin reuptake inhibitors. Particular combinations seem most likely to induce serotonin syndrome. Awareness of this syndrome as a distinct clinical entity seems to be growing.Clinical implicationsSerotonin syndrome is more likely to occur with drug combinations, especially those involving monoamine oxidase inhibitors. It can also occur when swapping antidepressant therapy, especially If changing from a long acting antidepressant such as fluoxetine. Caution is needed when changing antidepressants and particularly when they are used in combination.

scholarly journals Interaction between Monoamine Oxidase B Inhibitors and Selective Serotonin Reuptake Inhibitors

2018 ◽  
Vol 71 (3) ◽  
Author(s):  
Abdullah Aboukarr ◽  
Mirella Giudice
Keyword(s):  
Monoamine Oxidase ◽  
Parkinson Disease ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Syndrome ◽  
Case Reports ◽  
Potential Interaction ◽  
Monoamine Oxidase B ◽  
Study Group ◽  
Maladie De Parkinson ◽  
Mao B

<p>ABSTRACT</p><p>Background: Monoamine oxidase B (MAO-B) inhibitors are used to treat the motor symptoms of Parkinson disease. Depression is commonly associated with Parkinson disease, and selective serotonin reuptake inhibitors (SSRIs) are often used for its management. Tertiary sources warn that the combination of MAO-B inhibitors and SSRIs can result in increased serotonergic effects, leading to serotonin syndrome.</p><p>Objective:To explore the mechanism, clinical significance, and management of this potential drug interaction through a review of the supporting evidence.</p><p>Data Sources: PubMed, MEDLINE (1946 forward), Embase (1947 forward), PsycINFO (1806 forward), and International Pharmaceutical Abstracts (1970 forward) were searched on February 4, 2017. Study Selection and Data Extraction: Studies and case reports describing aspects of the potential interaction between MAO-B inhibitors and SSRIs in patients with Parkinson disease and published in English were identified by both title and abstract.</p><p>Data Synthesis: The search identified 8 studies evaluating the potential interaction between SSRIs and the MAO-B inhibitors selegiline and rasagiline. The largest, a retrospective cohort study of 1504 patients with Parkinson disease, found no cases of serotonin syndrome with coadministration of rasagiline and an SSRI. A survey of 63 investigators in the Parkinson Study Group identified 11 potential cases of serotonin syndrome among 4568 patients treated with the combination of selegiline and antidepressants (including SSRIs). In addition, 17 case reports describing the onset of serotonin syndrome with coadministration of an SSRI and either selegiline or rasagiline were identified. Following discontinuation or dose reduction of one or both of the agents, the symptoms of serotonin syndrome gradually resolved in most cases, with none being fatal.</p><p>Conclusions: According to the literature, serotonin syndrome occurs rarely, and the combination of SSRI and MAO-B inhibitor is well tolerated. Therefore, SSRIs and MAO-B inhibitors can be coadministered, provided that their recommended doses are not exceeded and the SSRI dose is kept at the lower end of the therapeutic range. Among the SSRIs, citalopram and sertraline may be preferred.</p><p>RÉSUMÉ</p><p>Contexte : Les inhibiteurs de la monoamine oxydase B (MAO-B) sont employés dans le traitement des symptômes moteurs de la maladie de Parkinson, maladie à laquelle la dépression est souvent associée et fréquemment traitée à l’aide d’inhibiteurs sélectifs de la recapture de la sérotonine (ISRS). Des sources tertiaires mettent en garde contre la combinaison d’inhibiteurs de la MAO-B et d’ISRS car elle peut mener à une augmentation des effets sérotoninergiques, dégénérant en un syndrome sérotoninergique.</p><p>Objectif : Chercher à connaître le mécanisme, la signification clinique et la prise en charge de cette potentielle interaction médicamenteuse en procédant à une revue des preuves à l’appui.</p><p>Sources des données : Les bases de données PubMed, MEDLINE (depuis 1946), Embase (depuis 1947), PscyINFO (depuis 1806), et International Pharmaceutical Abstracts (depuis 1970) ont été interrogées le 4 février 2017.</p><p>Sélection des études et extraction des données : Des études et des observations cliniques, publiées en anglais, portant sur des aspects de la potentielle interaction entre les inhibiteurs de la MAO-B et les ISRS chez les patients atteints de la maladie de Parkinson ont été repérées par une recherche ciblant les titres et les résumés.</p><p>Synthèse des données : La recherche a permis de trouver 8 études analysant la potentielle interaction entre les ISRS et deux inhibiteurs de la MAO-B : la sélégiline et la rasagiline. La plus importante d’entre elles, une étude de cohorte rétrospective sur 1504 patients atteints de la maladie de Parkinson, n’a relevé aucun cas de syndrome sérotoninergique en présence d’une prise concomitante de rasagiline et d’un ISRS. Une enquête auprès de 63 chercheurs dans le Parkinson Study Group a permis de relever 11 potentiels cas de syndrome sérotoninergique chez 4568 patients traités avec une combinaison de sélégiline et d’antidépresseurs (notamment des ISRS). De plus, 17 observations cliniques qui décrivaient un début de syndrome sérotoninergique en présence d’une prise concomitante d’un ISRS et de sélégiline ou de rasagiline ont été recensées. Suivant la réduction de la posologie ou l’interruption d’un ou des deux médicaments, les symptômes du syndrome sérotoninergique se sont graduellement résolus dans la plupart des cas, et il n’y a eu aucune mortalité.</p><p>Conclusions : Selon la documentation, le syndrome sérotoninergique est rare et la combinaison d’ISRS et d’inhibiteurs de la MAO-B est bien tolérée. Ainsi, les deux types d’inhibiteurs peuvent être administrés conjointement pourvu que l’on ne dépasse pas la posologie recommandée et que la dose d’ISRS demeure dans le bas de l’intervalle thérapeutique. Parmi les ISRS, il peut être préférable d’employer le citalopram ou la sertraline.</p>

scholarly journals Sexual adverse effects with new antidepressants

1998 ◽  
Vol 22 (7) ◽  
pp. 438-441 ◽  
Author(s):  
Shameem Mir ◽  
David Taylor
Keyword(s):  
Adverse Effect ◽  
Sexual Dysfunction ◽  
Adverse Effects ◽  
Monoamine Oxidase ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Case Reports ◽  
Depressive Illness ◽  
Serotonin Reuptake Inhibitors ◽  
Psychotropic Agents

Sexual dysfunction is a widely recognised adverse effect of many psychotropic agents. Older antidepressants such as monoamine oxidase inhibitors and tricycles, particularly clomipramine, are known to engender sexual adverse effects. In depression, this problem is exacerbated by the occurrence of impotence and lowered libido as part of depressive illness itself. We examined evidence relating to more recently introduced antidepressants: selective serotonin reuptake inhibitors, moclobemide, venlafaxine, nefazodone, mirtazapine and reboxetine. We reviewed published trials and case reports collated from searches of Medline, PsychLit and Micromedex from 1985 to December 1997, and contacted manufacturers of new antidepressants and requested information from them.

Neurobehavioral Consequences Associated with Long Term Tramadol Utilization and Pathological Mechanisms

2020 ◽  
Vol 18 (10) ◽  
pp. 758-768 ◽  
Author(s):  
Khadga Raj ◽  
Pooja Chawla ◽  
Shamsher Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Syndrome ◽  
Dopamine Synthesis ◽  
Synthetic Analog

: Tramadol is a synthetic analog of codeine used to treat pain of moderate to severe intensity and is reported to have neurotoxic potential. At therapeutic dose, tramadol does not cause major side effects in comparison to other opioid analgesics, and is useful for the management of neurological problems like anxiety and depression. Long term utilization of tramadol is associated with various neurological disorders like seizures, serotonin syndrome, Alzheimer’s disease and Parkinson’s disease. Tramadol produces seizures through inhibition of nitric oxide, serotonin reuptake and inhibitory effects on GABA receptors. Extensive tramadol intake alters redox balance through elevating lipid peroxidation and free radical leading to neurotoxicity and produces neurobehavioral deficits. During Alzheimer’s disease progression, low level of intracellular signalling molecules like cGMP, cAMP, PKC and PKA affect both learning and memory. Pharmacologically tramadol produces actions similar to Selective Serotonin Reuptake Inhibitors (SSRIs), increasing the concentration of serotonin, which causes serotonin syndrome. In addition, tramadol also inhibits GABAA receptors in the CNS has been evidenced to interfere with dopamine synthesis and release, responsible for motor symptoms. The reduced level of dopamine may produce bradykinesia and tremors which are chief motor abnormalities in Parkinson’s Disease (PD).

Pharmacotherapy for obessive-compulsive disorder

1998 ◽  
Vol 173 (S35) ◽  
pp. 64-70 ◽  
Author(s):  
John H. Greist ◽  
James W. Jefferson
Keyword(s):  
Monoamine Oxidase ◽  
Effective Treatment ◽  
Serotonin Reuptake ◽  
Randomised Controlled Trials ◽  
Case Reports ◽  
Controlled Trials ◽  
Behaviour Therapy ◽  
Obsessive Compulsive ◽  
Compulsive Disorder ◽  
Randomised Controlled

Background Pharmacotherapy for obsessive-compulsive disorder (OCD) was seldom beneficial before clomipramine, a potent selective serotonin reuptake inhibitor (SSRI), became available. Subsequent progress in pharmacotherapy for OCD has increased the possibility of effective treatment for most sufferers.Method Randomised controlled trials of pharmacotherapy for OCD were reviewed, as well as reports of beneficial pharmacotherapy found in open trials and case reports.Results SSRIs are well-tolerated by patients with OCD, even in large doses. Prose roto n erg i c augmentation is seldom helpful but antipsychotic augmentations seem beneficial for many OCD patients with comorbid tics.Conclusions Potent SSRIs are the pharmacotherapy of choice for OCD, with a more limited role reserved for monoamine oxidase inhibitors. If one SSRI is ineffective, others may be beneficial. Non-drug therapies are also important in OCD: behaviour therapy is frequently helpful but infrequently available and neurosurgery is sometimes helpful when all other treatments have failed.

Selective serotonin reuptake inhibitors in affective disorders — I. Basic pharmacology

1998 ◽  
Vol 12 (4_suppl) ◽  
pp. 5-S20 ◽  
Author(s):  
Paul J. Goodnick ◽  
Burton J. Goldstein
Keyword(s):  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Reuptake Inhibitors ◽  
Selective Serotonin ◽  
Principal Mechanism ◽  
Reuptake Inhibition ◽  
Racemic Mixtures ◽  
Dopamine Reuptake ◽  
Long Acting ◽  
Pharmacologically Active

The selective serotonin reuptake inhibitors (SSRIs), citalopram, fluoxetine, fluvoxamine, paroxetine and sertraline, are the result of rational research to find drugs that were as effective as the tricyclic antidepressants but with fewer safety and tolerability problems. The SSRIs selectively and powerfully inhibit serotonin reuptake and result in a potentiation of serotonergic neurotransmission. The property of potent serotonin reuptake appears to give a broad spectrum of therapeutic activity in depression, anxiety, obsessional and impulse control disorders. However, despite the sharing of the same principal mechanism of action, SSRIs are structurally diverse with clear variations in their pharmacodynamic and pharmacokinetic profiles. The potency for serotonin reuptake inhibition varies amongst this group, as does the selectivity for serotonin relative to noradrenaline and dopamine reuptake inhibition. The relative potency of sertraline for dopamine reuptake inhibition differentiates it pharmacologically from other SSRIs. Affinity for neuroreceptors, such as sigma1, muscarinic and 5-HT 2c, also differs widely. Furthermore, the inhibition of nitric oxide synthetase by paroxetine, and possibly other SSRIs, may have significant pharmacodynamic effects. Citalopram and fluoxetine are racemic mixtures of different chiral forms that possess varying pharmacokinetic and pharmacological profiles. Fluoxetine has a long acting and pharmacologically active metabolite. There are important clinical differences among the SSRIs in their pharmacokinetic characteristics. These include differences in their half-lives, linear versus non-linear pharmacokinetics, effect of age on their clearance and their potential to inhibit drug metabolising cytochrome P450 (CYP) isoenzymes. These pharmacological and pharmacokinetic differences underly the increasingly apparent important clinical differences amongst the SSRIs.

Non-Fatal Intoxication with a High Dose of Citalopram in a Suicidal 14-Year-Old Girl

2019 ◽  
Vol 47 (2) ◽  
pp. 168-170 ◽  
Author(s):  
Johannes Weigl ◽  
Timo Vloet ◽  
Karin Egberts ◽  
Wolfgang Briegel ◽  
Julia Kratz ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Syndrome ◽  
Reference Range ◽  
Cardiac Toxicity ◽  
Case Reports ◽  
High Dose ◽  
Cardiac Safety ◽  
Good Tolerability ◽  
Off Label

Abstract. The use of selective serotonin reuptake inhibitors (SSRIs) like citalopram in the clinical treatment of depressive symptoms in children and adolescents has become increasingly common, although application is mostly off-label. The increasing number of prescriptions is not only due to their good efficacy, but also due to their good tolerability and the comparatively low risk in cases of intoxication. However, there is discussion about the cardiac safety of overdose ingestion of citalopram. Here, we report in detail on an adolescent with depressive symptoms who used 800 mg of citalopram in order to attempt suicide. In contrast to other case reports in adults, our patient showed only mild neurological symptoms and no cardiac toxicity or symptoms of a serotonin syndrome, despite a high citalopram blood concentration measured about two hours following ingestion of citalopram (633 ng/ml; therapeutic reference range for adults 50–110 ng/ml).

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