3.1 Pathophysiology
Serotonin (5-Hydroxytryptamine, 5-HT) functions as a biochemical mediator both peripherally and centrally.
Its peripheral actions include stimulating vasoconstriction, uterine contraction, bronchoconstriction, gastrointestinal motility, and platelet aggregation. In the central nervous system, serotonin is present in the raphe nuclei of the brainstem, where it inhibits excitatory neurotransmission and modulates wakefulness, attention, mood, appetite, thermoregulation, motor tone, and emesis6,7. Thus, Serotonin is involved in numerous complex physiological processes and many drugs have been developed to manipulate serotonin concentrations 8,9.
Serotonin syndrome arises from an excessive stimulation of serotonin receptors in both the central and peripheral nervous systems, triggered by drugs that elevate synaptic serotonin levels . Serotonin can bind to multiple families of 5-HT receptors. While no single receptor is solely responsible for serotonin syndrome, it is acknowledged in the literature that the subtypes 5-HT1A and 5-HT2A (particularly the latter) play a significant role 2,10.
Serotonin syndrome is by definition a drug-induced syndrome. It is also referred to as ’serotonin toxicity’, which accurately reflects that the syndrome covers a dose-dependent spectrum or a continuum of serotonergic effects from mild adverse effects to life-threatening cases of toxicity1,4,9,11,12.