The term "motion sickness" describes a set of autonomic symptoms caused by incongruent sensory impressions under conditions of motion. Cold sweats, pallor, nausea, and vomiting are caused by a stress reaction to the motion.
Motion or travel sickness is as old as the various types of motion that cause it, whether on land, in the air, or at sea; sea sickness is the most notorious and in the extreme case can affect as many as 60% of even an experienced crew.
Motion sickness is a syndrome that occurs when a patient is exposed to certain types of motion and usually resolves soon after its cessation. It is a common response to motion stimuli during travel. Although nausea is a hallmark symptom, the syndrome includes symptoms ranging from vague malaise to completely incapacitating illness. These symptoms, which can affect the patient's recreation, employment, and personal safety, can occur within minutes of experiencing motion and can last for several hours after its cessation.
Nearly all persons will have symptoms in response to severe motion stimuli, and a history of motion sickness best predicts future symptoms.' Females, children two to 15 years of age, and persons with conditions associated with nausea report increased susceptibility.
A functional vestibular system is a pre-requisite for motion sickness to occur. Subjects with non-functioning labyrinths were immune to motion sickness under all test conditions, even after prolonged exposure to stormy seas. Bilateral vestibular neurectomy and labyrinthine ablation rendered susceptible laboratory animals immune to motion sickness. Vision is not essential to motion sickness, since blind subjects are susceptible. Bilaterally labyrinthine defective subjects would develop only mild symptoms of visually induced sickness, although no direct stimulus of the semicircular canals is practiced during the provoking stimulus. This suggests that visual inputs normally associated with a vestibular stimulus would give rise to a central vestibular activity, even in the absence of vestibular stimulus. Indeed, optokinetic stimulation has been found to induce direction specific modulations of resting discharge in the vestibular nuclei in several species, including the rhesus monkey. If tonic activation of the vestibular nuclei neurons is not maintained by the primary vestibular afferents, no central vestibular response to optokinetic stimulus would take place.
Repeated exposure to the provoking stimuli results in attenuation of symptoms and even their complete disappearance. For most individuals such adaptation occurs by 2 to 3 times of continuous stimulation. Habituation is a learned central process in which the decreased susceptibility to rough sea conditions is maintained, albeit with significant intervals of up to several weeks between sailings. Habituation to motion sickness elicited by optokinetic stimulation was completely retained for 1 month and partially retained for 1 year. Habituation is probably acquired only if exposure to the provoking stimuli is frequently experienced. Experimental evidence indicates that when the exposure is of short duration, the habituation so acquired is highly specific to the prevailing stimulus. However, when the offending motion is extended well beyond the point of adaptation, some degree of generalization to other motion patterns does occur. Recent evidence suggests that preflight exposure to variable virtual orientations is more effective than non-variable training in reducing space motion sickness and spatial disorientation.
Although nausea may be the first recognized symptom of motion sickness, it is almost always preceded by other subtle symptoms such as stomach awareness (i.e., a sensation of fullness in the epigastrium), malaise, drowsiness, and irritability. Failure to attribute early symptoms to motion sickness may lead to delays in diagnosis and treatment. Although mild symptoms are common, severely debilitating symptoms are rare.
Prevention of motion sickness is more effective than treating symptoms after they have occurred. Therefore, patients should learn to identify situations that may lead to motion sickness and be able to initiate behavioral strategies to prevent or minimize symptoms.
All measures that reduce conflicting sensory input, accelerate the process of multi-sensory adaptation, prevent factors that might aggravate nausea, and promote psychological factors which enable the subject to cope with his/her condition can be useful to ameliorate motion sickness. The recommendation to fix vision on a stable reference point such as the horizon is very popular among sailors. This measure could reduce visual sensory conflict especially in sailors and passengers located below the deck where the whole visual environment is moving with them, giving the mistaken visual impression that they are not moving in relation to the outside world. Going to the open bridge and allowing sight of the external world and the horizon will reduce the sensory conflict and alleviate motion sickness. Accordingly, subjects who were exposed to angular motion in a tilting room had less motion sickness symptoms with a reduced decrement in performance when they had a visual reference from the outside world by means of a projected artificial horizon. In a controlled study of the influence of the visual scene on carsickness, the results were non-conclusive. A direct wide or narrow forward view out of the car reduced motion sickness, but the provision of a real time video view of the road ahead did not reduce motion sickness. Very recently, the use of stroboscopic illumination that inhibits retinal slip was reported to reduce experimental motion sickness symptoms.
Medications are most effective when taken prophylactically before traveling, or as soon as possible after the onset of symptoms. Medications are most effective when combined with behavioral strategies. To familiarize themselves with common side effects, patients should first take medications in a comfortable environment before using them for motion sickness during travel.
Scopolamine, an anticholinergic, is a first- line option for preventing motion sickness in persons who wish to maintain wakefulness during travel. A Cochrane review of 14 randomized controlled trials (RCTs) showed that scopolamine is effective for the prevention of motion sickness. A more recent RCT of 76 naval crew members showed that transdermal scopolamine is more effective and has fewer side effects than the antihistamine cinnarizine (not available in the United States). If the recommended dose of scopolamine does not adequately relieve symptoms, the dose may be doubled. Adding a second patch of transdermal scopolamine was well tolerated in a small RCT of 20 sailors.
First-generation antihistamines have been used to treat motion sickness since the 1940s.' They are generally recommended for patients who can tolerate their sedative effects. Benzodiazepines are occasionally administered for severe symptoms of motion sickness and have been proven effective in a single small study. The serotonin agonist reduced motion sickness symptoms in a single RCT of 25 patients with recurrent migraines. The serotonin antagonist Ondansetron (Zofran) is ineffective for the prevention and treatment of motion sickness.
