Spatial Disorientation and Its Implication of Vertigo and Vertigo-Induced Vomiting

Abstract

Histamine H₁ receptors are involved in the development of the symptoms and signs of motion sickness and vertigo-induced vomiting. In the development of motion sickness and vertigo-induced vomiting, a neural mismatch signal encoding spatial disorientation activates the histaminergic neuron system in the hypothalamus, and the histaminergic descending impulse stimulates H₁ receptors in the emetic center of the brainstem. The histaminergic input to the emetic center through H₁ receptors is independent of the dopaminergic emetic inputs through dopamine D₂ receptors in the chemoreceptor trigger zone of the area postrema or the serotoninergic emetic inputs through serotonin 5HT₃ receptors in the visceral afferents. Antihistamines block the emetic H₁ receptors to prevent motion sickness and vertigo-induced vomiting. Central post-synaptic H₁, but not H₂ or peripheral H₁ receptors, play an important role in the development of motion sickness. Therefore, BBB-penetrating and sedating H₁ receptor blockers, but not non-BBB-penetrating and non-sedating H₁ receptor blockers or H₂ receptor blockers, prevent motion sickness and vertigo-induced emesis.