The symptoms may be more intense because a condition caused by prolonged weightlessness is usually quite unfamiliar.Space motion sickness was effectively unknown during the earliest spaceflights because the very cramped conditions of the spacecraft allowed for only minimal bodily motion, especially head motion. Space motion sickness seems to be aggravated by being able to freely move around, and so is more common in larger spacecraft. Around 60% of Space Shuttle astronauts experienced it on their first flight; the first case of space motion sickness is now thought to be the Soviet cosmonaut Gherman Titov, in August 1961 onboard Vostok 2, who reported dizziness, nausea, and vomiting. The first severe cases were in early Apollo flights; Frank Borman on Apollo 8 and Rusty Schweickart on Apollo 9. Both experienced identifiable and quite unpleasant symptoms—in the latter case causing the mission plan to be modified. Screen images
This type of terrestrial motion sickness is particularly prevalent when susceptible people are watching films presented on very large screens such as IMAX, but may also occur in regular format theaters or even when watching TV or playing games. For the sake of novelty, IMAX and other panoramic type theaters often show dramatic motions such as flying over a landscape or riding a roller coaster. This type of motion sickness can be prevented by closing ones eyes during such scenes.In regular-format theaters, an example of a movie that caused motion sickness in many people is The Blair Witch Project. Theaters warned patrons of its possible nauseating effects, cautioning pregnant women in particular.
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.