How to Get Rid of Serotonin syndrome?

Serotonin syndrome is characterized by changes in autonomic, neuromotor, and cognitive-behavioral function triggered by increased serotonergic stimulation. It typically results from pharmacodynamic and/or pharmacokinetic interactions between drugs that increase serotonin activity.

The serotonin syndrome is a hypersotonergic state which is a very dangerous and a potentially fatal side effect of serotonergic enhancing drugs which can have multiple psychiatric and non-psychiatric symptoms. Serotonin syndrome has been reported as a result of interactions between MAOIs-including selegiline and reversible MAO-A inhibitors (RIMAs)-and various serotonergic compounds.

It is a condition which has been on the rise since the 1960's when we began using more and more drugs which directly affect serotonin. This is a toxic condition which requires heightened clinical awareness in order to prevent, recognize, and treat the condition promptly. Promptness is vital because, as we just mentioned, the serotonin syndrome can be fatal and death from this side effect can come very rapidly. This syndrome is a toxic hyperserotonergic state whose rate of incidence is unknown, but is on the rise. The suspected cause of that increase is the introduction of the new selective serotonergic enhancing agents in clinical practice - the SSRIs. This disorder, brought on by excessive levels of serotonin, is difficult to distinguish from the neuroleptic malignant syndrome because the symptoms are so similar. The neuroleptic malignant syndrome is a serious condition brought on by the use of the neuroleptic drugs.

Serotonin syndrome is caused by drug induced excess of intrasynaptic 5-hydroxytryptamine. The clinical manifestations are mediated by the action of 5-hydroxytryptamine on various subtypes of serotonin receptors. There is no effective drug treatment established. The history of the treatment of serotonin syndrome with 5-hydroxytryptamine blocking drugs is reviewed. A literature search was undertaken using both Medline and a manual search of the older literature. Reports of cases treated with the 5-HT2 blockers cyproheptadine and chlorpromazine were identified and analysed. There is some evidence suggesting the efficacy of chlorpromazine and cyproheptadine in the treatment of serotonin syndrome. The evidence for cyproheptadine is less substantial, perhaps because the dose of cyproheptadine necessary to ensure blockade of brain 5-HT2 receptors is 20-30 mg, which is higher than that used in the cases reported to date (4-16 mg).

In Bio-Psychiatry it is a common thought that SSRI's are believed to have their effect by inhibiting the re-uptake of serotonin (downregulation of transporters) and thereby gradually increasing serotonin outside the tissue cell wall (extracellular) in the synaptic gap between brain cells (neurons) in the brain. In this important study, Zoloft (Lustral, sertraline) was given to monkeys for 4 weeks to establish how long it would take before Zoloft would have it's effect on serotonergic neurons and thus elevation of serotonin. In contrast with the commonly accepted SSRI theory, it was observed that serotonin levels raised NOT gradually, but rapidly and dramatically and kept on raising during these 4 weeks, an effect that can NOT be ascribed solely to a "re-uptake inhibition" of serotonin.

Treatment of Serotonin syndrome

supportive therapy
removal of precipitating agent
case reports suggest that non-specific serotonin antagonists (eg chlorpromazine, methysergide, cyproheptadine or propranolol) may be beneficial in severe cases.

Also find out Serotonin Syndrome Symptom

Selective Serotonin Reuptake Inhibitors and MAOIs

How does SSRI antidepressant work and SSRIs antidepressant uses?

Monoamines

Antidepressant-like profile and effects of rolipram (selective inhibitor of cyclic AMP) in the central nervous system.

What are the side effects of MAOIs (Monoamine oxidase inhibitors)?

Tricyclic Antidepressant