Nausea: a review of pathophysiology and therapeutics

Abstract

The sensation of nausea is a common occurrence with diverse causes and a significant disease burden. Nausea is considered to function as a protective mechanism, warning the organism to avoid potential toxic ingestion. Less adaptive circumstances are also associated with nausea, including post-operative nausea, chemotherapy-induced nausea, and motion sickness. A common definition of nausea identifies the symptom as a precursor to the act of vomiting. The interaction, though present, does not appear to be a simple relationship. Nausea is unfortunately the 'neglected symptom', with current accepted therapy generally directed at improving gastrointestinal motility or acting to relieve emesis. Improved understanding of the pathophysiological basis of nausea has important implications for exploiting novel mechanisms or developing novel therapies for nausea relief.

Keywords: autonomic nervous system; central nervous system; diagnostics; nausea; neuroendocrine; pathogenesis; therapeutics; vomiting.

Figure 1.

Pathogenesis of nausea. Central and peripheral pathways involved in pathogenesis of nausea. Afferent information from various stimuli are relayed to nucleus tractus solitarius via four pathways: vestibular and cerebellar, cerebral cortex and limbic system, area postrema and gastrointestinal tract via vagus nerve.* *Once any of these neural pathways are activated, it culminates into sensation of nausea with or without vomiting. The efferent information from nucleus tractus solitarius is also responsible for activation of autonomic nervous response via vagal pathways. Nausea is also associated with gastric dysrhythmia and release of vasopressin. However, the cause–effect relationship of this triad is not very well understood and warrants further studying.