SS results from the overstimulation of 5-HT1A receptors by selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors, or other serotonergic agents. Clinically, NMS and SS share many features, suggesting different spectrums of a similar disorder. Both syndromes may present with varying degrees of fever, altered mental status, and neuromuscular abnormalities, including leukocytosis, elevated creatinine kinase levels, transaminitis, and low serum bicarbonate levels. Distinctions between the two diagnoses are often difficult to make, having large clinical overlap. However, some authors have suggested that patients with NMS demonstrate higher fevers and more pronounced extrapyramidal effects, while SS patients have lower fevers, myoclonus, and GI dysfunction.3–4 SS secondary to venlafaxine therapy has been well-described in the medical literature.5–9 Clearly, the inclusion of SS in the differential diagnosis of this patient is warranted and may suggest an alternate diagnosis. Fortunately, the treatment for both NMS and SS consists of removing the offending agent and providing supportive care. As stated by the authors,1 there may be a role for both dantrolene and bromocriptine in the treatment of these conditions.