Simulator sickness is a subset of motion sickness that is typically experienced by pilots who undergo training for extended periods of time in flight simulators. Due to the spatial limitations imposed on these simulators, perceived discrepancies between the motion of the simulator and that of the vehicle can occur and lead to simulator sickness.

It is similar to motion sickness in many ways, but occurs in simulated environments and can be induced without actual motion. Symptoms of simulator sickness include discomfort, apathy, drowsiness, disorientation, fatigue, vomiting, and many more.

These symptoms can reduce the effectiveness of simulators in flight training and result in systematic consequences such as decreased simulator use, compromised training, ground safety, and flight safety. Pilots are less likely to want to repeat the experience in a simulator if they have suffered from simulator sickness and hence can reduce the number of potential users. It can also compromise training in two safety-critical ways:

1. It can distract the pilot during training sessions.

2. It can cause the pilot to adopt certain counterproductive behaviors to prevent symptoms from occurring.

Simulator sickness can also have post-training effects that can compromise safety after the simulator session, such as when the pilots drive away from the facility or fly while experiencing symptoms of simulator sickness.

One common suggestion is to simply look out of the window of the moving vehicle and to gaze towards the horizon in the direction of travel. This helps to re-orient the inner sense of balance by providing a visual reaffirmation of motion.

In the night, or in a ship without windows, it is helpful to simply close one's eyes, or if possible, take a nap. This resolves the input conflict between the eyes and the inner ear. Napping also helps prevent psychogenic effects (i.e. the effect of sickness being magnified by thinking about it).

Fresh, cool air can also relieve motion sickness slightly, although it is likely this is related to avoiding foul odors which can worsen nausea.

While playing computer games, and mainly in first-person shooter games, some cases of simulation sickness can be resolved by changing the field of view in the game. Some games have a default setting which places a player's vision a small distance ahead of the actual object controlled, which will most likely trigger simulation sickness.

Space motion sickness is caused by changes in g-forces, which affect spatial orientation in humans. According to "Science Daily", "Gravity plays a major role in our spatial orientation. Changes in gravitational forces, such as the transition to weightlessness during a space voyage, influence our spatial orientation and require adaptation by many of the physiological processes in which our balance system plays a part. As long as this adaptation is incomplete, this can be coupled to motion sickness (nausea), visual illusions and disorientation."

Modern motion-sickness medications can counter space sickness but are rarely used because it is considered better to allow space travelers to adapt naturally over the first day or two than to suffer the drowsiness and other side effects of medication. However, transdermal dimenhydrinate anti-nausea patches are typically used whenever space suits are worn because vomiting into a space suit could be fatal, as it could obscure vision or block airflow. Space suits are generally worn during launch and landing by NASA crew members and always for extra-vehicular activities (EVAs). EVAs are consequently not usually scheduled for the first days of a mission to allow the crew to adapt, and transdermal dimenhydrinate patches are typically used as an additional backup measure.

The following factors increase some people's susceptibility to airsickness:

- Fatigue, stress, and anxiety, are some factors that can increase susceptibility to motion sickness of any type.

- The use of alcohol, drugs, and medications may also contribute to airsickness.

- Additionally, airsickness is more common in women (especially during menstruation or pregnancy), young children, and individuals prone to other types of motion sickness.

- Although airsickness is uncommon among experienced pilots, it does occur with some frequency in student pilots.

The most common hypothesis for the cause of motion sickness is that it functions as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in a ship with no windows), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the discordance, the brain will come to the conclusion that the individual is hallucinating and further conclude that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.

An alternative theory, also known as the Nystagmus Hypothesis, has been proposed based on stimulation of the vagus nerves resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eye's six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherrington's Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherrington's 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, 10th 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 Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.

Travelers who are susceptible to motion sickness can minimize symptoms by:

- Choosing a window seat with a view of the ground or of lower clouds, such that motion can be detected. This will not work if the plane is flown in the clouds for a long duration.

- Choosing seats with the smoothest ride in regards to pitch (the seats over the wings in an airplane). (This may not be sufficient for sensitive individuals who need to see ground movement)

- Sitting facing forward while focusing on distant objects rather than trying to read or look at something inside the airplane.

- Eating dry crackers, olives or suck on a lemon, to dry out the mouth, lessening nausea.

- Drinking a carbonated beverage.

Space adaptation syndrome (SAS) or space sickness is a condition experienced by around half of space travelers during adaptation to weightlessness. It is related to motion sickness, as the vestibular system adapts to weightlessness.

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual.

Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience.

The following environmental factors have been shown to increase the risk of DCS:

- the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one.

- repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above within similar short periods increase the risk of developing altitude DCS.

- the rate of ascent – the faster the ascent the greater the risk of developing DCS. The US Navy Dive Manual indicates that ascent rates greater than about when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of with the last taking at least one minute. An individual exposed to a rapid decompression (high rate of ascent) above has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.

- the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of and above, carry a greater risk of altitude DCS.

- underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits.

- diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at increase their risk of DCS.

- diving at altitude – diving in water whose surface altitude is above — for example, Lake Titicaca is at — without using versions of decompression tables or dive computers that are modified for high-altitude.

The Simulator Sickness Questionnaire (SSQ) is currently the standard for measuring simulator sickness. The SSQ was developed based upon 1,119 pairs of pre-exposure/post-exposure scores from data that were collected and reported earlier. These data were collected from 10 Navy flight simulators representing both fixed-wing and rotary-wing aircraft. The simulators selected were both 6-DOF motion and fixed-base models, and also represented a variety of visual display technologies. The SSQ was developed and validated with data from pilots who reported to simulator training healthy and fit.

The SSQ is a self-report symptom checklist. It includes 16 symptoms that are associated with simulator sickness. Participants indicate the level of severity of the 16 symptoms that they are experiencing currently. For each of the 16 symptoms there are four levels of severity (none, slight, moderate, severe). The SSQ provides a Total Severity score as well as scores for three subscales (Nausea, Oculomotor, and Disorientation). The Total Severity score is a composite created from the three subscales. It is the best single measure because it provides an index of the overall symptoms. The three subscales provide diagnostic information about particular symptom categories:

- Nausea subscale is made up of symptoms such as increased salivation, sweating, nausea, stomach awareness, and burping.

- Oculomotor subscale includes symptoms such as fatigue, headache, eyestrain, and difficulty focusing.

- Disorientation subscale is composed of symptoms such as vertigo, dizzy (eyes open), dizzy (eyes closed), and blurred vision.

The three subscales are not orthogonal to one another. There is a general factor common to all of them. Nonetheless, the subscales provide differential information about participants' experience of symptoms and are useful for determining the particular pattern of discomfort produced by a given simulator. All scores have as their lowest level a natural zero (no symptoms) and increase with increasing symptoms reported.

Morning sickness may be an evolved trait that protects the baby against toxins ingested by the mother. Evidence in support of this theory includes:

- Morning sickness is very common among pregnant women, which argues in favor of its being a functional adaptation and against the idea that it is a pathology.

- Fetal vulnerability to toxins peaks at around 3 months, which is also the time of peak susceptibility to morning sickness.

- There is a good correlation between toxin concentrations in foods, and the tastes and odors that cause revulsion.

Women who have "no" morning sickness are more likely to miscarry. This may be because such women are more likely to ingest substances that are harmful to the fetus.

In addition to protecting the fetus, morning sickness may also protect the mother. A pregnant woman's immune system is suppressed during pregnancy, presumably to reduce the chances of rejecting tissues of her own offspring. Because of this, animal products containing parasites and harmful bacteria can be especially dangerous to pregnant women. There is evidence that morning sickness is often triggered by animal products including meat and fish.

If morning sickness is a defense mechanism against the ingestion of toxins, the prescribing of anti-nausea medication to pregnant women may have the undesired side effect of causing birth defects or miscarriages by encouraging harmful dietary choices.

The cause of morning sickness is unknown. While some have claimed it to be due to psychological reasons, this is not supported by evidence.

Nausea and vomiting may also occur with molar pregnancy.

A study of certain aspects of motion sickness among medical transport attendants showed that the onset of the sopite syndrome is likely to occur independently of the mode of transportation; little difference was observed in the frequency of sopite symptoms for ground transport compared to air transport. Also, the length of time exposed to vehicular motion did not appear to affect the occurrence (or lack thereof) or severity of the sopite syndrome. No difference was observed in the incidence of the sopite syndrome for men versus women.

The sopite syndrome is likely a cumulative disorder. For instance, when a subject has the flu, a hangover may exacerbate the symptoms of the illness. A subject normally resistant to motion sickness may experience symptoms of motion sickness when also experiencing flu-like (or hangover-like) symptoms.

True acrophobia is uncommon.

A related, milder form of visually triggered fear or anxiety is called visual height intolerance. Up to one-third of people may have some level of visual height intolerance.

Traditionally, acrophobia has been attributed, like other phobias, to conditioning or a traumatic experience. Recent studies have cast doubt on this explanation; a fear of falling, along with a fear of loud noises, is one of the most commonly suggested inborn or "non-associative" fears. The newer non-association theory is that a fear of heights is an evolved adaptation to a world where falls posed a significant danger. The degree of fear varies and the term phobia is reserved for those at the extreme end of the spectrum. Researchers have argued that a fear of heights is an instinct found in many mammals, including domestic animals and humans. Experiments using visual cliffs have shown human infants and toddlers, as well as other animals of various ages, to be reluctant in venturing onto a glass floor with a view of a few meters of apparent fall-space below it. While an innate cautiousness around heights is helpful for survival, an extreme fear can interfere with the activities of everyday life, such as standing on a ladder or chair, or even walking up a flight of stairs.

A possible contributing factor is a dysfunction in maintaining balance. In this case the anxiety is both well founded and secondary. The human balance system integrates proprioceptive, vestibular and nearby visual cues to reckon position and motion. As height increases, visual cues recede and balance becomes poorer even in normal people. However, most people respond by shifting to more reliance on the proprioceptive and vestibular branches of the equilibrium system.

An acrophobic, however, continues to over-rely on visual signals whether because of inadequate vestibular function or incorrect strategy. Locomotion at a high elevation requires more than normal visual processing. The visual cortex becomes overloaded resulting in confusion. Some proponents of the alternative view of acrophobia warn that it may be ill-advised to encourage acrophobics to expose themselves to height without first resolving the vestibular issues. Research is underway at several clinics.

The cause is the most mysterious aspect of the disease. Commentators then and now put much blame on the generally poor sanitation, sewage and contaminated water supplies of the time, which might have harboured the source of infection. The first outbreak at the end of the Wars of the Roses means that it may have been brought over from France by the French mercenaries whom Henry VII used to gain the English throne. However, the "Croyland Chronicle" mentions that Thomas Stanley, 1st Earl of Derby used the "sweating sickness" as an excuse not to join with Richard III's army prior to the Battle of Bosworth.

Relapsing fever has been proposed as a possible cause. This disease, which is spread by ticks and lice, occurs most often during the summer months, as did the original sweating sickness. However, relapsing fever is marked by a prominent black scab at the site of the tick bite and a subsequent skin rash.

Noting symptom overlap with hantavirus pulmonary syndrome, several scientists proposed an unknown hantavirus as the cause. A critique of this hypothesis included the argument that, whereas sweating sickness was thought to be transmitted from human to human, hantaviruses are rarely spread in this way. However, infection via human-to-human contact has been proven in hantavirus outbreaks in Argentina.

The sopite syndrome has been associated with visually-induced and vestibular motion sickness. Other factors associated with drowsiness such as darkness or physical fatigue may intensify the effects of motion-induced sleepiness. The sopite syndrome may occur with little motional stimulus (though the greatest effects tend to be observed in subjects who have been exposed for longer periods of time), and often persists for a time after the motional stimulus has ceased.

Ascending slowly is the best way to avoid altitude sickness. Avoiding strenuous activity such as skiing, hiking, etc. in the first 24 hours at high altitude reduces the symptoms of AMS. Alcohol and sleeping pills are respiratory depressants, and thus slow down the acclimatization process and should be avoided. Alcohol also tends to cause dehydration and exacerbates AMS. Thus, avoiding alcohol consumption in the first 24–48 hours at a higher altitude is optimal.

The symptoms and signs, as described by physician John Caius and others, were as follows: the disease began very suddenly with a sense of apprehension, followed by cold shivers (sometimes very violent), giddiness, headache, and severe pains in the neck, shoulders and limbs, with great exhaustion. After the cold stage, which might last from half an hour to three hours, the hot and sweating stage followed. The characteristic sweat broke out suddenly without any obvious cause. Accompanying the sweat, or after, was a sense of heat, headache, delirium, rapid pulse, and intense thirst. Palpitation and pain in the heart were frequent symptoms. No skin eruptions were noted by observers including Caius. In the final stages, there was either general exhaustion and collapse, or an irresistible urge to sleep, which Caius thought to be fatal if the patient was permitted to give way to it. One attack did not offer immunity, and some people suffered several bouts before dying. The disease tended to occur in summer and early autumn.

Pre-acclimatization is when the body develops tolerance to low oxygen concentrations before ascending to an altitude. It significantly reduces risk because less time has to be spent at altitude to acclimatize in the traditional way. Additionally, because less time has to be spent on the mountain, less food and supplies have to be taken up. Several commercial systems exist that use altitude tents, so called because they mimic altitude by reducing the percentage of oxygen in the air while keeping air pressure constant to the surroundings.

Ghost sickness is a cultural belief among some traditional indigenous peoples in North America, notably the Navajo, and some Muscogee and Plains cultures, as well as among Polynesian peoples. People who are preoccupied and/or consumed by the deceased are believed to suffer from ghost sickness. Reported symptoms can include general weakness, loss of appetite, suffocation feelings, recurring nightmares, and a pervasive feeling of terror. The sickness is attributed to ghosts () or, occasionally, to witches or witchcraft. Children are thought to be especially at risk of being affected because they are not as attached to their new bodies.

Taravana is a disease often found among Polynesian island natives who habitually dive deep without breathing apparatus many times in close succession, usually for food or pearls. These free-divers may make 40 to 60 dives a day, each of 30 or 40 metres (100 to 140 feet).

Taravana seems to be decompression sickness. The usual symptoms are vertigo, nausea, lethargy, paralysis and death. The word "taravana" is Tuamotu Polynesian for "to fall crazily".

Taravana is also used to describe someone who is "crazy because of the sea".

In the Muscogee (Creek) culture, it is believed that everyone is a part of an energy called "Ibofanga". This energy supposedly results from the flow between mind, body, and spirit. Illness can result from this flow being disrupted. Therefore, their "medicine is used to prevent or treat an obstruction and restore the peaceful flow of energy within a person". Purification rituals for mourning "focus on preventing unnatural or prolonged emotional and physical drain."

The grief resolution processes for traditional Native Americans are qualitatively different than those usually seen in mainstream Western cultures. In 1881, there was a federal ban on some of the traditional mourning rituals practised by the Lakota and other tribes. Lakota expert Maria Yellow Horse Brave Heart proposes that the loss of these rituals may have caused the Lakota to be "further predisposed to the development of pathological grief". Some manifestations of unresolved grief include seeking visions of the spirits of deceased relatives, obsessive reminiscing about the deceased, longing for and believing in a reunion with the deceased, fantasies of reappearance of the deceased, and belief in one's ability to project oneself to the past or to the future.

The fear of flying may be created by various other phobias and fears:

- Fear of crashing, which in rare cases will cause death, is the most common reason for the fear of flying.

- Fear of closed in spaces (claustrophobia), such as that of an aircraft cabin

- Fear of heights (hypsophobia)

- Feeling of not being in control

- Fear of vomiting, where a person will be afraid that they'll have motion sickness on board, or encounter someone having motion sickness and have no control over it (such as escaping it)

- Fear of having panic attacks in certain places, where escape would be difficult and/or embarrassing (agoraphobia)

- Fear of hijacking or terrorism

Anticipatory anxiety of being out of control and overwhelmed can prevent a person from planning to travel by air. The thought of an upcoming flight can cause great distress, particularly when compelled to travel by air. The most extreme manifestations can include panic attacks or vomiting at the mere sight or mention of an aircraft or air travel.