“…ST is characterized by the excessive accumulation of serotonin into the body, which, ultimately, leads to neuromuscular hyperexcitability by the excessive serotonergic agonism of the central and peripheral nervous system, whose clinical findings include agitation, tremor, inducible and ocular clonus, diaphoresis, hyperreflexia, hypertonia, and hyperthermia (over 38 • C) (Boyer and Shannon, 2005). A great number of case reports showed that these events occurred predominantly in mental patients who had been taking serotonergic antidepressant medications including fluoxetine [a selective serotonin reuptake inhibitor (SSRI)] (Martindale and Stedeford, 2003;Kapadia et al, 2016), paroxetine, a SSRI (Bach et al, 2004;Mihai et al, 2007;Ng et al, 2008;Shanmugam et al, 2008;Schwiebert et al, 2009;Wolvetang et al, 2016), venlafaxine [a selective serotonin and norepinephrine reuptake inhibitor (SSNRI)] (Majithia and Stearns, 2006), citalopram, a SSRI (Mathew et al, 2006;Pollack et al, 2009), duloxetine, a SSNRI (Rowley et al, 2009), and clomipramine [a serotonin reuptake inhibitor (SRI)] (Khan et al, 2007), and have been commonly interpreted to be attributed to the reaction of MB as a potent monoamine oxidase A (MAO-A) inhibitor (Gillman, 2011;Top et al, 2014). In effect, MAO has a part in the degradation process of a diversity of monoamines such as serotonin, epinephrine, norepinephrine, dopamine, and histamine (Yeung et al, 2019;Floris et al, 2020).…”