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.