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At least 19 recordsLinked to original sources
PubMed1996

[Depressive stupor--malignant neuroleptic syndrome--serotonin syndrome. A case contribution to a difficult differential diagnosis].

Depressive stupor and malignant neuroleptic syndrome are very well-known problems in clinical psychiatry. The serotonin syndrome, however, a potentially life-threatening side effect of treatment with serotonergic substances, has been included in the clinical differential diagnosis increasingly often in the last few years. The development of new serotonin selective antidepressants and selective reversible inhibitors of monoamine oxidase A has led to the use of more and more substances that can cause these life-threatening complications if they are taken in too high doses or together with other drugs. We present a 61 year old depressed female impatient who developed an abortive malignant neuroleptic syndrome while being treated for depressive stupor. We discuss a possible relation between serotonin syndrome and a highly dosed combination therapy with moclobemide. Owing to the importance of both syndromes, we consider drug monitoring absolutely necessary for patients who are being treated with new antidepressants, and especially for those who develop neurological and psychiatric complications when such preparations are given in combination with other drugs.

Antidepressive Agents, Tricyclic↗
PubMed2006

Lithium and venlafaxine interaction: a case of serotonin syndrome.

Serotonin syndrome, which occurs as a result of enhanced serotonin concentration in the central nervous system, is a well-known adverse effect of serotonin-active medications. The concomitant use of antidepressant drugs associated with lithium as a co-adjuvant seems to increase the risk of this adverse reaction. We report a case of the serotonin syndrome during treatment with lithium and venlafaxine, an antidepressant with a dual selective re-uptake inhibition mechanism, and review the literature for similar cases. A 71-year-old woman developed serotonin syndrome while receiving treatment with moderate doses of lithium and venlafaxine for refractory depression. She had been taking higher doses of venlafaxine during the previous months with no significant secondary effects. Use of the Naranjo adverse drug reaction probability algorithm indicated a probable relationship between serotonin syndrome and treatment with lithium and venlafaxine.

Aged↗
PubMedDate not supplied

Isolated venlafaxine-induced serotonin syndrome.

Serotonin syndrome is a potentially fatal complication of serotonergic drug therapy. Usually, serotonin syndrome occurs with the concomitant use of two serotonergic drugs; this case report describes a patient with a classic presentation of serotonin syndrome induced solely by a venlafaxine overdose. Emergency physicians need to be aware that the serotonin syndrome may occur not only with serotonergic drug combinations but also with overdoses of a single potent serotonergic agent such as venlafaxine.

Adult↗
PubMed1995

Serotonin syndrome.

Serotonin syndrome is a potentially life-threatening complication of psychopharmacologic drug therapy. The syndrome is produced most often by the concurrent use of two or more drugs that increase brainstem serotonin activity and is often unrecognized because of the varied and nonspecific nature of its symptomatology. Serotonin syndrome is characterized by alterations in cognition, behavior, autonomic nervous system function and neuromuscular activity. Patients with serotonin syndrome usually respond to discontinuation of drug therapy and supportive care alone, but they may require treatment with a specific antiserotonergic drug such as cyproheptadine, methysergide and/or propranolol.

Adolescent↗
PubMed1997

Serotonin syndrome.

Serotonin syndrome usually occurs after treatment with monoamine oxydase inhibitors and drugs that enhance serotoninergic transmission. Serotonin agents, such as Proza, are commonly prescribed drugs; therefore, the serotonin syndrome appears more frequently than before. Clinicians must be able to prevent, recognize, and treat this syndrome in their practice. This review summarizes the literature of case reports of patients who developed the serotonin syndrome.

Fluoxetine↗
PubMed2006

Serotonin syndrome.

Serotonin syndrome is a preventable, drug-related complication that results from increased brainstem serotonin activity, usually precipitated by the use of one or more serotonergic drugs. Its clinical presentation consists of autonomic dysfunction, alteration in mental status, and neuromuscular disorder. Early recognition and treatment is important, because this condition is potentially fatal. Management includes withdrawal of causative agents and supportive measures such as hemodynamic stabilization, sedation, temperature control, hydration, and monitoring for complications. Serotonin antagonists, specifically cyproheptadine, have been used, but the documented benefits are purely anecdotal.

Blood Chemical Analysis↗
PubMed1995

Encephalopathy during amitriptyline therapy: are neuroleptic malignant syndrome and serotonin syndrome spectrum disorders?

This report describes a case of encephalopathy developed in the course of amitriptyline therapy, during a remission of unipolar depression. This patient could have been diagnosed as having either neuroleptic malignant syndrome (NMS) or serotonin syndrome (SS). The major determinant of the symptoms may have been dopamine/serotonin imbalance in the central nervous system. The NMS-like encephalopathy that develops in association with the use of antidepressants indicates that NMS and SS are spectrum disorders induced by drugs with both antidopaminergic and serotonergic effects.

Amitriptyline↗
PubMedDate not supplied

Neuroleptic malignant syndrome and serotonin syndrome in the critical care setting: case analysis.

BACKGROUND: Serotonin syndrome (SS) and neuroleptic malignant syndrome (NMS) are medical emergencies associated with psychotropic administration. Differentiation and treatment can be complex, especially when features of both syndromes are present and the patient has taken both serotonergic and neuroleptic agents. METHOD: Case analysis of a poly-drug overdose (venlafaxine, topiramate, divalproex sodium, risperidone, and carbamazepine) presenting with mixed SS/NMS features and whose clinical management suggests a practical algorithm for treatment of undifferentiated SS/NMS in critical care settings. RESULTS: The suggested algorithm includes: 1) Supportive care and withdrawal of all potentially offending agents; 2) Laboratory evaluation with prompt initiation of treatment for both disorders--cyproheptadine for SS and dantrolene for NMS; 3) Do not use bromocriptine (contraindicated in SS) or chlorpromazine (contraindicated in NMS) initially; 4) Add bromocriptine when clinical presentation becomes consistent with NMS (SS can be prolonged if serotonergic agent has long half-life). CONCLUSIONS: Prompt and appropriate identification and intervention are essential for successful management of SS and NMS. The suggested treatment algorithm allows for specific treatment of both disorders and avoids potentially exacerbating either one. The algorithm derived from this case could serve as both a practical guideline and impetus for further investigation in light of increasing psychotropic co-administration.

Adult↗
PubMed2001

The serotonin syndrome: investigation using the Japanese version of the Serotonin Syndrome Scale.

This preliminary study was performed to investigate the prevalence of the serotonin syndrome in a group of Japanese patients in a clinical setting and to test the reliability and value of the Serotonin Syndrome Scale (SSS) as an assessment tool in a Japanese-language version (JSSS). Twenty-three patients, all being treated with serotonin agonists, gave informed consent to participate. Only one patient fulfilled strict diagnostic criteria of the serotonin syndrome and none of the JSSS scores reached the cutoff point of the SSS. Cronbach's alpha coefficient for the JSSS was 0.56. All inter-rater reliability coefficients were in the excellent range, and the JSSS had a high stability over time. The mean dose of fluvoxamine in the subgroup with high scores on the JSSS was significantly larger than that in the subgroup with low scores and there was a positive but non-significant correlation between total JSSS scores and doses of fluvoxamine. This preliminary study indicates that (1) a full serotonin syndrome was a rare phenomenon in a group of Japanese patients in a clinical setting and (2) the JSSS is a simple and reliable scale for evaluating the serotonin syndrome.

Adult↗
PubMed1996

Serotonin syndrome.

Selective serotonin reuptake inhibitors (SSRIs) are replacing tricyclic antidepressants (TCAs) with increasing frequency in the United States. Although SSRI poisoning tends to be less serious that TCA poisoning, the incidence of adverse side effects and drug interactions may be greater. The serotonin syndrome is a potentially severe adverse drug interaction characterized by the triad of altered mental status, autonomic dysfunction, and neuromuscular abnormalities. The serotonin syndrome is similar to the neuroleptic malignant syndrome, leading to misdiagnosis. Although serotonin syndrome may result in death, most patients recover completely with supportive care alone. The main pathophysiologic mechanism appears to be excessive 5-hydroxytryptophan stimulation; this finding is supported by reports of beneficial effects with serotonin-antagonist treatment. The incidence of the serotonin syndrome may increase as SSRIs continue to replace TCAs. Morbidity and costly diagnostic procedures may be avoided if prompt diagnosis and appropriate treatment are provided.

5-Hydroxytryptophan↗
PubMed1987

High-dose clonidine motor syndrome: relationship to serotonin syndrome.

Reciprocal forepaw treading, hindlimb abduction, and Straub tail are some of the abnormal motor behaviors of the classical 'serotonin syndrome,' which results from activation of serotonin (5-HT) receptors. However, we also observed them in the syndrome evoked by the alpha-adrenergic agonist clonidine, at high doses (5-40 mg/kg). Other features of the clonidine syndrome (scored from videotapes) were body and head tremor, forelimb hyperextension, ataxia, vertical jumping, tactile hyperreactivity, and autonomic signs (piloerection, pupillary dilatation, salivation, proptosis). The clonidine syndrome persisted for several hours and was not lethal. Clonidine suppressed locomotor activity (photocell recording) and induced episodes of catalepsy and 5-HT-independent impairment of motor habituation. Single high doses of drugs active at several different neurotransmitter receptors significantly reduced total behavioral score through effects primarily on tremor and autonomic signs, but none prevented the clonidine syndrome. Lesions of monoaminergic neurons [intracisternal 5,7-dihydroxytryptamine (DHT) or 6-hydroxydopamine] or monoamine depletion by intraperitoneal reserpine all failed to prevent this motor syndrome. Co-administration of 5-HTP and clonidine did not exacerbate the clonidine syndrome in naive rats and did not prevent the onset of the serotonergic syndrome in rats with DHT lesions. These data suggest that neither catecholamines nor 5-HT have a major role in the serotonin-like behavioral responses to high doses of clonidine.

Adrenergic alpha-Antagonists↗
PubMed2002

Serotonin syndrome caused by selective serotonin reuptake-inhibitors-metoclopramide interaction.

OBJECTIVE: To report 2 cases of serotonin syndrome with serious extrapyramidal movement disorders occurring when metoclopramide was coadministered with sertraline or venlafaxine. CASE SUMMARY: A 72-year-old white woman was treated with sertraline for depression for 18 months and was then admitted to the hospital with a fractured tibia. She was administered metoclopramide because of nausea and, within 2 hours, developed agitation, dysarthria, diaphoresis, and a movement disorder. These symptoms recurred following 2 subsequent administrations of metoclopramide. Treatment with diazepam led to resolution of symptoms within 6 hours, and there was no recurrence at 6 weeks' follow-up. A 32-year-old white woman with major depression was treated with venlafaxine for 3 years. She was admitted following a fall and, after being given metoclopramide, developed movement disorder and a period of unresponsiveness. After a second dose of metoclopramide, these symptoms recurred and were associated with confusion, agitation, fever, diaphoresis, tachypnea, tachycardia, and hypertension. She improved with administration of diazepam, but needed repetition of this treatment over the next 16 hours. Symptoms resolved within 2 days, and she continued venlafaxine with no further adverse effects. DISCUSSION: Both cases met Stembach's criteria for serotonin syndrome and had serious extrapyramidal movement disorders. The possible pathophysiologic mechanisms for the adverse reactions include a single-drug effect, a pharmacodynamic interaction, and a pharmacokinetic interaction. We believe that a pharmacodynamic interaction is most likely. CONCLUSIONS: Clinicians should be aware of a risk of serotonin syndrome with serious extrapyramidal reactions in patients receiving sertraline or venlafaxine when metoclopramide is coadministered even in a single, conventional dose.

Accidental Falls↗
PubMed2002

[Serotonin syndrome].

The serotonin syndrome is a hyperserotoninergic state resulting from an excess of intrasynaptic 5-hydroxytryptamine, induced by multiple psychotropic agents, but also non psychiatric drugs. It is a potentially dangerous and sometimes lethal condition. The clinical manifestations usually include cognitive, neuromuscular and autonomic features and are mediated by the action of serotonin on various subtypes of receptors. The main differential diagnosis is the neuroleptic malignant syndrome. Treatment is mainly supportive. No pharmacological agent has been definitely demonstrated really effective. However, reports of cases treated with the 5-HT2 blockers, including cyproheptadine or chlorpromazine have suggested that these agents could have some efficacy. Serotonin syndrome is a toxic condition which requires heightened clinical awareness among physicians in order to prevent, recognize, and treat the condition promptly.

Diagnosis, Differential↗
PubMed2005

Gastric pentadecapeptide BPC 157 effective against serotonin syndrome in rats.

Serotonin syndrome commonly follows irreversible monoamine oxidase (MAO)-inhibition and subsequent serotonin (5-HT) substrate (in rats with fore paw treading, hind limbs abduction, wet dog shake, hypothermia followed by hyperthermia). A stable gastric pentadecapeptide BPC 157 with very safe profile (inflammatory bowel disease clinical phase II, PL-10, PLD-116, PL-14736, Pliva) reduced the duration of immobility to a greater extent than imipramine, and, given peripherally, has region specific influence on brain 5-HT synthesis (alpha-[14C]methyl-L-tryptophan autoradiographic measurements) in rats, different from any other serotonergic drug. Thereby, we investigate this peptide (10 microg, 10 ng, 10 pg/kg i.p.) in (i) full serotonin syndrome in rat combining pargyline (irreversible MAO-inhibition; 75 mg/kg i.p.) and subsequent L-tryptophan (5-HT precursor; 100 mg/kg i.p.; BPC 157 as a co-treatment), or (ii, iii) using pargyline or L-tryptophan given separately, as a serotonin-substrate with (ii) pargyline (BPC 157 as a 15-min posttreatment) or as a potential serotonin syndrome inductor with (iii) L-tryptophan (BPC 157 as a 15 min-pretreatment). In all experiments, gastric pentadecapeptide BPC 157 contrasts with serotonin-syndrome either (i) presentation (i.e., particularly counteracted) or (ii) initiation (i.e., neither a serotonin substrate (counteraction of pargyline), nor an inductor for serotonin syndrome (no influence on L-tryptophan challenge)). Indicatively, severe serotonin syndrome in pargyline + L-tryptophan rats is considerably inhibited even by lower pentadecapeptide BPC 157 doses regimens (particularly disturbances such as hyperthermia and wet dog shake thought to be related to stimulation of 5-HT2A receptors), while the highest pentadecapeptide dose counteracts mild disturbances present in pargyline rats (mild hypothermia, feeble hind limbs abduction). Thereby, in severe serotonin syndrome, gastric pentadecapeptide BPC 157 (alone, no behavioral or temperature effect) has a beneficial activity, which is likely, particular, and mostly related to a rather specific counteraction of 5-HT2A receptors phenomena.

Animals↗
PubMed2004

The serotonin syndrome.

The serotonin syndrome is a complex of symptoms that are thought to be largely attributable to changes in sensitivity in the serotonin receptor systems in the brainstem and the spinal cord due to drugs. Severe cases are almost always caused by a combination of two or more 'serotonergic' drugs, of which at least one is a selective serotonin reuptake inhibitor or a monoamine oxidase inhibitor. Usually, the syndrome heals spontaneously after withdrawal of the medication. Cessation of 'serotonergic' medication is the preferred treatment as well as supportive care.

Brain Stem↗
PubMed1999

Antidepressants and the serotonin syndrome in general practice.

BACKGROUND: As a consequence of the greater use of agents affecting the serotonergic system, a syndrome of serotonin hyperstimulation has been recognized more frequently. The serotonin syndrome is characterized by a constellation of symptoms that include mental status changes, agitation, myoclonus, hyperreflexia, sweating, shivering, tremor, diarrhoea, lack of coordination, and fever. Deaths have been reported. AIM: To identify cases of the serotonin syndrome among patients prescribed a new antidepressant in general practice, and to determine doctors' awareness of the syndrome. METHOD: Patients who were dispensed nefazodone in England between 1996 and 1997 were identified using dispensed prescription data. Prescribing doctors were sent questionnaires as part of a post-marketing surveillance study. Patients reported to have experienced two or more features of the serotonin syndrome were identified, and specific questionnaires were sent to their general practitioners. RESULTS: There was a 96.2% return rate of serotonin syndrome questionnaires. Nineteen cases met criteria for the syndrome (incidence = 0.4 cases per 1000 patient-months of treatment with nefazodone). Eight patients developed symptoms while taking nefazodone alone. Serotonergic symptoms were reported to a similar degree with five other antidepressants studied by the same method. In total, 85.4% of responding general practitioners were unaware of the serotonin syndrome. CONCLUSION: Improved awareness of the syndrome is needed within general practice. There is a need to distinguish the relatively minor serotonergic symptoms from those of a severe, life-threatening serotonin syndrome.

Adolescent↗