16.02.4 Motion Sickness and Drugs for

Figure 16.4 Motion sickness (Copyright QUT, Sheila Doggrell)

Thus, drugs that act at histamine H1 receptors or muscarinic receptor can modify motion sickness. The histamine H1-receptor antagonist promethazine crosses the blood-brain barrier to act at cerebellum histamine H1-receptors to inhibit motion sickness. Promethazine also act as an antagonist at the cholinergic muscarinic receptors, which may contribute to effectiveness in preventing motion sickness.

The muscarinic receptor antagonist scopolamine is non-selective. Scopolamine crosses blood-brain barrier to act at the cerebellum M-receptor to inhibit motion sickness. Scopolamine is used as a transdermal patch to prevent motion sickness.

Drugs that are effective in the treatment of cytotoxic-induced emesis are not effective in motion sickness, indicating a different pathway is involved. Motion is monitored by the inner ear (the vestibular system), which has an input into the cerebellum, where histamine H1-receptors and muscarinic M receptors are involved in controlling nausea and vomiting (Figure 16.4).