A number of medications used for nausea such as ondansetron and metoclopramide are not effective in motion sickness.Scopolamine is the most effective medication. Evidence is best for when it is used preventatively. It is available as a skin patch. Side effects may include blurry vision.Other effective first generation antihistamines include doxylamine, diphenhydramine, promethazine, meclizine, cyclizine, and cinnarizine. In pregnancy meclizine, dimenhydrinate and doxylamine are generally felt to be safe. Side effects include sleepiness. Second generation antihistamines have not been found to be useful.Dextroamphetamine may be used together with an antihistamine or an antimuscarinic. Concerns include their addictive potential.Those involved in high-risk activities, such as SCUBA diving, should evaluate the risks versus the benefits of medications. Promethazine combined with ephedrine to counteract the sedation is known as "the Coast Guard cocktail". Alternative medicine
Alternative treatments include acupuncture and ginger although their effectiveness against motion sickness is variable. Providing smells does not appear to have a significant effect on the rate of motion sickness. Epidemiology
Roughly one-third of people are highly susceptible to motion sickness, and most of the rest get motion sick under extreme conditions. Around 80% of the general population is susceptible to cases of medium to high motion sickness. The rates of space motion sickness have been estimated at between forty and eighty percent of those who enter weightless orbit. Several factors influence susceptibility to motion sickness, including sleep deprivation and the cubic footage allocated to each space traveler.
Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherringtons Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherringtons Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, tenth nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherringtons Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.A recent theory  argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals (nauseogenic) vs. otolith organs (anti-nauseogenic). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., in free fall) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic). Diagnosis
The diagnosis is based on symptoms.