Pacific CE Motion Sickness

To begin this review of motion sickness, recall the children's story of several blind men who encounter an elephant and try to determine what it is by feeling various parts of its anatomy. In one version of the story, each of the men has recently become blind and each had a trade before being blinded. One man, a former firefighter, feels the elephant's trunk and concludes that the object is a fire hose. Another, a former soldier, feels the tip of a tusk and decides that the object is a giant spear. The third, an ex-logger, feels a leg and determines that the object is a tree.

Each person made a conclusion based on limited information and his own personal background. Motion sickness is something like an elephant in this context. Optometrists often conclude that motion sickness results from a binocular imbalance that can be remedied by the prescription of lenses, prisms, or therapy. Some ear, nose, and throat physicians regard motion sickness as a symptom of vestibular malfunction and prescribe drugs to sedate the inner ear. Physical therapists sometimes view motion distress as a "lack of adaptation to motion" problem and provide exercises that help patients adapt to the sensations of motion. Some psychologists and psychiatrists view motion sickness as an over-reaction to the normal sensation of motion that everyone feels and prescribe anxiety reduction procedures such as hypnosis, biofeedback, or tranquilizers.

Just as the blind men who tried to analyze the elephant based on limited sampling and personal backgrounds, health care providers often do not see motion sickness as a condition with interacting visual, vestibular, and psychological components that typically requires a multi-disciplinary, team oriented approach.

Mother Nature has given humans several sensory systems to detect the effects of gravity and to allow us to remain upright when we move through the environment. These symptoms include the proprioceptive or somatosensory system (muscle and tendon senses), the vestibular system, and the visual system - specifically the part of the visual system that senses the periphery. For most of us, these systems work well together and allow us to engage in tasks ranging from simply sitting in a chair without falling over, to skiing at high speed. The systems help us to know "where we are in space," which is somewhat the same concept as "where we are with respect to the pull of gravity."

Unfortunately, sometimes these systems deliver information that is in conflict with reality or information that is not internally consistent between systems. For example, in an airplane the vestibular and proprioceptive systems might indicate that you are moving up and down, tipping over, hitting severe turbulence, etc., but at the same time your visual system says that the walls of the airplane are not moving and neither is the seat in front of you. This sets up a conflict, which can result in dizziness, motion sickness, vertigo, nausea, panic, and other unpleasant sensations.

In an aircraft, we can understand why these sensations occur, but for some patients, the sensations occur during their daily activities either continuously or episodically without an apparent external cause. Because conflicts typically involve visual system information as part of the conflict (even though vision might be contributing normal information), sensory conflicts are of interest to vision care specialists.

This course will demonstrate that mismatches must occur between visual, vestibular, and/or proprioceptive inputs (or stored memories of these inputs) for a person to experience motion sickness. In turn, mismatches produce symptoms that can be aggravated by patient anxiety, and significant, sometimes debilitating motion sickness can occur.

Motion sickness has gained increasing interest in recent years because of the difficulties encountered by military aircraft pilots who are subjected to unusual acceleratory forces (1) and by astronauts who must function under conditions of weightlessness. (2)

Although motion sickness can result in disaster for fighter pilots and astronauts (approximately 50% of whom experience space sickness), it also causes trouble for the more typical patients who might be seen in an optometric practice.

Motion sickness is a term applied to a group of unpleasant symptoms that characteristically accompany motion. The eliciting motion is usually experienced in a vehicle such as a car, train, ship, or airplane. However, motion sickness can also be produced by only the appearance of motion such as might be experienced in a Cinerama or flight simulator.

Signs and symptoms of motion distress include irritability; vertigo (also known as vection), a false sense of self-motion with respect to the world or of the world; oscillopsia, a false sense of object-motion; dizziness; and autonomic nervous system activity (e.g., sweating, salivation, nausea, and vomiting). Early symptoms can also include fatigue, which in severe or prolonged cases can progress to depression and even a professed desire to die. There are psychological symptoms associated with severe motion sickness that can be life threatening in some individuals.

Susceptibility to motion sickness under conditions of normal driving, flying, or boating varies widely in the population. Females tend to be more susceptible than males (2-6) and persons of intermediate age are more susceptible than very young infants or elderly persons. (2,5,7,8) Although the exact incidence of motion sickness in the general population is not known, given a proper combination of provocative stimuli, every normal individual is susceptible to this condition. (9)

Before exploring current theories regarding the etiology of motion sickness, it is helpful to have an historical perspective. Reason and Brand have reviewed several theories of motion sickness, (9) and a sampling of these theories is presented here beginning with some early theories of seasickness.

Most nineteenth century authorities agreed that seasickness was caused by motion and not by the damp sea air or other malevolent entities as previously suspected. A key question was what part of the anatomy tended to be disrupted by motion, and the answers were varied. The most popular theories might be termed the “blood” and the “guts” theories. Respectively, these theories proposed that motion disrupted vascular circulation and/or caused the viscera to shift, thus triggering nausea and vomiting.

The “guts shift” theories varied with regard to the mechanism thought to mediate vomiting. The simplest theory proposed that vomiting was a reflex response to irritation of the gastric mucosa. A more complex variation suggested that movements of the viscera caused abdominal contractions and over-stimulated the Pacinian corpuscles (encapsulated sensory nerve endings), consequently producing nausea and vomiting. Other theories proposed that visceral movements battered the liver, which consequently released too much bile into the small intestine and eventually caused emesis (vomiting). Variations of these “gut shift” theories abounded.

Vascular theories fell into two categories: those that proposed a lack of blood flow to the brain (cerebral anemia) and those that proposed too much blood going to the brain (cerebral hyperemia). One theory suggested that vascular deficiency was due to the irritation of the eyes by perceived motion, which, by reflex action, produced spasm in the cerebral capillaries causing giddiness and vomiting. Other vascular theories argued that motion produced cerebral hyperemia, which destabilized brain cells in the vomiting center of the medulla oblongata.

Additional theories were proposed including one that considered motion sickness to be a direct consequence of disturbed vision. This eyestrain theory rested on clinical evidence that other forms of eyestrain commonly produced gastric symptoms, headache, and dizziness. Passengers aboard ships attempting to fixate on the swirling waves and other moving objects were said to suffer eye muscle fatigue. This created ocular imbalance manifested by horizontal nystagmus, dizziness, headache, and eventually nausea and vomiting. (5,8)

Another theory of motion sickness etiology was proposed in 1881. Having noted the similar symptoms of seasickness and Meniere’s disease, Irwin and de Champeaux published independent papers attributing seasickness to a disturbance of the vestibular apparatus.

As evidence accumulated, involvement of the vestibular apparatus became the common theme in most theories of motion sickness. Despite the eyestrain theory and a few other surviving hypotheses, vestibular theories have dominated recent motion sickness research activities.

An often-asked question regarding motion sickness concerns which neural pathways are necessary for the signs and symptoms to occur. In addressing this question, it is convenient to think in terms of the peripheral afferent nerves and the central structures that might be involved.

The gut shift theories implicated visceral afferents in the motion sickness syndrome. Swing sickness susceptibility experiments in which humans or animals were literally swung in a swing have been performed using dogs that had undergone abdominal sympathectomy (cutting part of the sympathetic nervous system) and/or abdominal vagotomy (cutting the vagus nerve). In most cases these dogs demonstrated increased resistance to swing sickness, but, in a third of the animals, there was no change in resistance to the swing sickness. This indicates that visceral afferents from the gastrointestinal tract may heighten susceptibility, but do not play a major role in causing motion sickness. (10)

Investigators have demonstrated motion sickness susceptibility in blind individuals and in normally sighted people who have their eyes covered. (14) This indicates that direct visual afferents may not form an essential link in the motion sickness pathway. Extraocular eye muscle afferents have also been shown to be unnecessary for motion sickness to occur. In dogs, afferents from the external eye muscles were blocked with Xylocaine and no subsequent change in swing sickness susceptibility occurred. (15)

On the other hand, bilateral section of the vestibular nerve (CN VIII) in animals seems to confer immunity to motion sickness. (11,12) Bilateral labyrinthectomy is equally effective in preventing motion distress, thus indicating the essential role of these structures in motion sickness. (11,12,13)

Because the vestibular system seems to be one of the key players in producing motion sickness, an understanding of this system is essential. The main function of the vestibular system is to furnish information on head position and motion with respect to gravity. Vestibular information is transmitted into the brain via the VIIIth (auditory) Cranial Nerve from which it flows to many nuclei for processing and analysis.

The vestibular system is composed of two sets of organs, together less than the size of a quarter, that are located within the inner ear on either side of the head. Components of the vestibular system are the semicircular canals and the otolith organs. These are contained in a fluid-filled, bony labyrinthine structure.

The semicircular canals respond to angular acceleration. Each canal is structured like a tube within a tube: the inner membranous portion of the canal separates endolymph from perilymph fluid. Perilymph is similar to cerebral spinal fluid, but endolymph has a unique concentration of ions and is not merely a filtrate of the perilymph.

When a canal is rotated in its appropriate plane, the endolymph wants to rotate in the opposite direction. (Imagine a hula-hoop filled with water; when the hoop rotates, the water attempts to flow in the opposite direction.) Each canal contains a structure known as an ampulla containing a cupula, which stretches across the canal and prevents actual flow of the endolymph.

Nonetheless, motion produces a force on the cupula, which deflects it slightly. Hair cell neurons at the base of the cupula change their firing rate depending on the deflection of the cupula, and this signals information relevant to head acceleration.

In addition to the ampulla, there are two orthogonal otolith organs on each side of the head: the utricle and the saccule. These organs form out-pouchings of the semicircular canals. When the head is held upright, the utricles lie in a roughly horizontal plane; and the saccules are oriented in an approximately vertical plane. The utricles respond primarily to horizontal (front-to-back and side-to side) linear movements, and the saccules respond primarily to vertical linear movements.

The otolith organs respond to linear acceleration, such as experienced in an airplane during take-off or landing, or at the beginning of a ride on an elevator. The otolith organs respond to gravity, and can provide a rough idea of where we are with reference to the earth, even with a lack of visual, tactile, or other cues.

Each otolith organ contains a macula comprised of about 20,000 to 30,000 hair cells. The tips of the hairs protrude into a gelatinous membrane suspended in the perilymph above the macula. Atop the membrane lie the otoconia, which are calcium carbonate crystals also known as "ear-rocks." Like the hair cells of the semicircular canals, the otolith hair cells respond with increased (excitatory) or decreased (inhibitory) firing rates, depending on the direction of deflection caused by movement of the otoconia.

Nerve fibers from the semicircular canals and otolith organs, along with fibers from the cochlea (the hearing portion of the inner ear), form the VIIIth Cranial Nerve. The afferent fibers terminate at the vestibular nuclei in the brainstem. There are connections between the vestibular nuclei and the nuclei of the IIIrd, IVth, and VIth Cranial Nerves, as well as the cerebellum.

(It is important to rule out vestibular pathologies as causes of motion sickness, so a description of the more common vestibular pathologies is included as an Appendix to this course.)

Because the vestibular system seems necessary for motion sickness to occur, the vestibular nuclei where most vestibular nerve fibers terminate are probably also necessary for motion sickness to occur. (15) Other vital structures include the nodulus and uvula of the cerebellum. Ablation of these structures in dogs has been effective in eliminating emetic responses that characteristically follow long exposures to swinging motion. (13)

In an experiment using dogs, Wang and Chinn investigated an area located in the superficial region of the medulla dorsolateral to the vagal nuclei. (16) This area, referred to as the chemoceptive emetic trigger zone (CCTZ), is the receptor site for certain central emetic agents. Although there is controversy regarding the role of the CCTZ in humans, it seems likely that the trigger zone is an integral part of the motion sickness pathway. (9,15,17,18)

There is another interesting entity referred to in the literature as the “vomiting center.” The center may or may not be morphologically distinct, but there are certain neural mechanisms responsible for the coordinated muscular contractions necessary for vomiting. (15) Borison and Wang produced vomiting by electrical stimulation of the reticular formation in decerebrate cats. (19) This localization of the vomiting center is particularly interesting because of the proximity of several key centers including those responsible for respiration, salivation, and balance, all of which are involved in the vomiting response. (20)

The final central structure to be considered here is the cerebrum. Evidence from animal studies indicates that the cerebrum is not essential for the development of motion sickness caused by certain provocative stimuli. (9) Motion sickness has been reported to occur in a decorticate humans, lending support to this view. (21)

In summary, the following structures appear to be vital links in the neural pathway responsible for motion sickness:

Notably, there is no evidence indicating that visceral afferents, visual afferents, or extra-ocular muscle afferents are necessary for motion sickness to occur.

As an aside, it is interesting to speculate about why nausea, vomiting, and other autonomic nervous system problems should be triggered by the largely sensory phenomenon of motion sickness. There are several unproven and highly speculative theories to explain this. One suggests that control centers for processing balance information and for regulating the autonomic nervous system are located physically next to each other in the brain and that there is electrical or chemical "overflow" of activity from one center to the other.

A second theory is based on the concept that certain poisons create vestibular disturbances and the body has evolved a means to clear ingested poisons by vomiting when the vestibular system signals an upset. As an example of how this might work, consider what happens when a person drinks enough alcohol to upset the vestibular system.

A third theory suggests that anxiety results from the brain's sensory confusion during abnormal motion and this anxiety triggers an autonomic nervous system reaction. For example, a positive feedback loop could develop in which a person feels a little queasy during airplane turbulence and gets anxious about feeling queasy. This creates more anxiety, and a positive feedback loop is established that produces an autonomic nervous system over-action.

On the basis of the physiological evidence available, one might be led to believe that vision plays no significant role in motion sickness. The evidence cited thus far indicates that the vestibular apparatus must be intact for motion sickness to occur, but the visual system seems, at best, to be of peripheral importance. However, it is also known that motion sickness can occur in situations involving only provocative visual stimuli and no appreciable vestibular stimulation. (22-24) This is the case when a patient reports sickness while watching a movie with rapid, graphic motion. Helicopter simulators, (25) car simulators, (9) tilting rooms, (26) and rotating rooms (27) can also cause motion distress by exclusively visual means.

A significant characteristic of any provocative stimulus (whether it is visual, vestibular, or a combination of both) is that it seems to become less provocative after long and/or repeated exposure. This is a very important phenomenon because several therapy procedures, e.g., Gillilan's See Sick Syndrome therapy, involve repeated exposure to provocative visual stimuli. (This therapy is described in another Pacific University On-Line CE course.)

Adaptation of this nature has been studied in slowly rotating rooms. (28) When returned to the stationary environment, subjects who have successfully adapted to the slow rotation experience after-effects similar to the symptoms of motion sickness that occurred during the initial exposure. (9)

Theories that implicate over-stimulation of the vestibular apparatus as the fundamental sensory trigger of motion sickness do not adequately explain visually-induced motion sickness and the phenomenon of adaptation.

In a search for a more complete explanation of motion sickness, a different approach must be taken to discover the common relationship between the sensory triggers that are associated with motion sickness. Thus far, the vestibular apparatus and the visual system have been implicated as primary triggers of motion distress. In addition, non-vestibular proprioceptors are implicated because they converge in a summative relationship with vestibular neurons at the level of the vestibular nuclei. (29) When all three of these systems are considered, it becomes apparent that the common element among them is that they act together to indicate spatial orientation.

Upon further examination, a functional relationship between the spatial receptors is evident. The vestibular apparatus, the proprioceptors of the neck, and the visual system are functionally related to make it possible to fixate a target while standing still and turning the head. While looking at a target, any movement of the head is compensated by a corresponding movement of the eyes in the opposite direction. In a similar fashion, spatial receptors are functionally correlated to maintain normal posture and appropriate control of body movement.

It is proposed that functional relationships such as these are remembered, preserved, or “traced” in the brain. Traces of the sensory relationships, which correspond to habitual tasks are stored as part of an “exposure history” of the individual, and the concept of exposure history has become an integral part of current theory concerning motion sickness.

“Sensory rearrangement” is another fundamental concept of current theories. Sensory rearrangement is a phrase used to describe any situation in which the information from one set of spatial receptors is distorted in a way that is incompatible with information from functionally related receptors.

A classic example of sensory rearrangement may be observed by distorting the visual input with optical devices that both reverse and invert the visual field, e.g., yoked prisms. Such distortion involving one set of receptor inputs disrupts the functional correlation between head and eye movements and causes an apparent movement of the visual field when the head is turned. This illusion occurs because the sensory rearrangement temporarily makes it impossible to coordinate eye and head movements and can produce a condition similar to motion sickness.

The sensory conflict theory, as expounded by Reason and Brand (9,30), suggests that when sensory rearrangement occurs, the total pattern of sensory input conflicts with the pattern expected on the basis of exposure history. This conflict or “neural mismatch” between the stored brain pattern and the new trace is theorized to be the cause of motion sickness.

Again, referring to the example of visual distortion, it has been reported that dizziness, nausea, and other prodromal symptoms are associated with head movements made while wearing a distorting optical device, just as the sensory conflict theory predicts.

Situations that provoke motion sickness can be analyzed by examining various sensory rearrangements that commonly cause neural mismatch. To facilitate this analysis, sensory rearrangements can be classified into two general categories: visual-inertial rearrangements and otolith-semicircular canal rearrangements.

The term “inertial” in this context refers to input from both vestibular and nonvestibular proprioceptors; i.e., inertial stimulation involves the semicircular canals (which respond to angular accelerations of the head), the otolith receptors (which respond to linear accelerations and gravity), and the somatosensory proprioceptors (which sense relative body position). (In physics, “acceleration” is defined as a change in velocity (speed) or direction of movement. Gravity is a linear acceleration that acts in a downward direction, even when an object is “at rest” – the fact that the object is not moving means that some other force is counteracting the effect of gravity. For example, pick up a heavy weight and hold it above your head for a while; eventually, the muscles in your arm will tire (i.e., they can no longer fight the gravitational pull), and the weight comes crashing down to the floor. As the weight falls, it moves faster and faster, hence, the change in velocity.) In each category of sensory rearrangement, three types of sensory conflict can develop. Examples of each type are shown in Table I.

Type 1 sensory conflict occurs when two spatial receptors, A and B, (e.g., visual and vestibular) each signal motion that is uncorrelated with the other or matched in some unfamiliar way. Type 1 visual-inertial conflicts occur in many common situations, e.g., when watching waves from a moving ship. Inertial stimulation is provided by movement of the ship, while unrelated visual stimulation is provided by waves, which move independently of the ship. The unusual combination of these stimuli can cause a neural mismatch and bring on motion sickness.

A similar situation occurs when looking out the side windows of an automobile at the passing scenery. The moving vehicle provides inertial stimulation, which is correlated in an unexpected manner with visual information from the rapidly changing scenery. This type of conflict is probably the source of patient carsickness complaints during travel on straight roads.

Patients with significant changes in their spectacle prescriptions or who are wearing bifocals for the first time, experience changes in visual perception that may cause type 1 sensory conflicts, especially when they move their heads rapidly. For some patients, adaptation to such conflicts can take an extended period and patients who fail to adapt often report complaints of dizziness, nausea, and headache. (9,31,32)

An example of type 1 canal-otolith conflict occurs as a result of cross-coupled angular acceleration. This is experienced when head movements are made about some axis other than the axis of body rotation. This type of motion has been studied in detail with subjects who initiate tilting head movements while sitting on a rotation platform. (9,28) Typical experiences that may elicit this type of sensory conflict include riding in a car on a winding road or flying in a circling airplane. Conflicts of this nature have been shown to be very provocative of motion sickness. (9)

Type 2 sensory conflict occurs when motion is signaled from input A in the absence of expected motion indications from input B (refer to Table 1). Type 2 sensory conflicts include exceptional situations such as space sickness, in which stimulation of the otolith receptors is essentially absent because of reduced gravity. Although few people have experienced space sickness, many can identify with the person who gets a queasy feeling in the pit of the stomach while watching a chase scene photographed from a moving vehicle.

In terms of sensory conflict theory, this phenomenon is explained by pointing out that visual information in the chase scene is usually associated with corresponding inertial stimulation. In the absence of the inertial stimulation, a neural mismatch results.

It is important to note that the cause of the motion distress in this situation is not the visual stimulation per se. This is supported by the observation that people susceptible to motion sickness while watching a film shown in the forward direction are unaffected when the same film is shown in reverse. (33,34) The visual information from the reversed film has no previous association with inertial stimulation, so no conflict is created with stored neural traces, i.e., neural mismatch does not occur.

Type 3 sensory conflict occurs when motion is signaled from input B in the absence of expected motion signals from input A. The patient who reports motion sickness while reading in a car moving along a straight road is likely to be experiencing a type 3 conflict of the visual-inertial variety. This common complaint arises from the neural mismatch caused by the perception of inertial movement without a corresponding visual sensation of movement.

A type 3 conflict of the canal-otolith category occurs during rotation about an earth-horizontal axis. The typical rolling motion associated with ships would be expected to produce this provocative sensory conflict.

From this analysis it is evident that the sensory conflict theory explains those situations in which one sensory input apparently triggers motion sickness without obvious involvement of other sensory inputs; earlier theories did not adequately explain such occurrences.

The sensory conflict theory also explains adaptation. In situations that commonly produce sensory rearrangement and motion sickness, our brains presumably store appropriate traces and make the sensory rearrangement part of our exposure history. Once this occurs, there is no conflict between our expectations and the sensory information being received. As a result, we find relief from motion sickness after a period of adaptation to the provocative situation. Many therapies for motion sickness rely on this concept and repeatedly expose patients to provoking stimuli until the stimuli lose their ability to create symptoms. Re-adaptation after-effects may then occur when the original sensory arrangement is restored and may continue until the original brain patterns have been reestablished.

The visual system has been implicated in the etiology of motion sickness for some patients, but it has not yet become clear what aspect(s) of the system are typically at fault.

For purposes of this discussion, the visual system can be considered to have four major components: the extraocular muscles and their control systems; the central visual system consisting of foveal retinal receptors and the parvocellular pathway; the peripheral visual system consisting of non-central retinal receptors and the magnocellular pathway; and the perceptual system, which is responsible for image formation/interpretation.

In general, the parvocellular pathway carries information about color, high spatial frequency (fine detail), and high contrast stimuli that are imaged on the fovea. The relatively small axons from this system pass through the upper layers of the lateral geniculate nucleus on their way to the visual cortex.

The magnocellular pathway carries information about movement, lower spatial frequencies, and lower contrast stimuli that are imaged in the periphery of the retina. The relatively large axons from this system pass through the lower layers of the lateral geniculate nucleus on their way to the visual cortex.

Although no direct evidence is known to exist regarding the relative contribution of each of these visual system components to motion sickness, each may contribute to different degrees in different situations. Some inferences can be made about their relative contributions by considering situations that provoke motion sickness and clinical techniques that have been found to provide relief.

In the absence of other stimuli, reading, which involves foveal vision and eye movements, does not seem to provoke full-fledged motion sickness in some patients, although it can produce fatigue and headaches, which are early motion sickness symptoms. Clinically, it is believed that slightly under-minusing motion sickness patients can be beneficial, and this would have a significant effect on the foveal vision pathway.

Other lens-related factors that have been reported clinically to affect motion sickness susceptibility include changing cylindrical lens powers, changing lens base curves, and prescribing monovision lenses. Monovision prescriptions are interesting because some anecdotal reports indicate an increase in motion sickness susceptibility, some reports indicate a decrease, and others indicate no change.

Binocular vision problems are significantly related to motion sickness susceptibility, with vertical and exo deviations increasing the probability that the patient will have motion sickness problems. In the case of significant deviations, it is likely that the foveal region of the deviating eye is being suppressed, which suggests that the peripheral vision system is related to the motion sickness. The peripheral system is also believed to be responsible for telling the brain where the person is with respect to gravity, so this component of the visual system would be the most likely conflict with vestibular and/or somatosensory information.

Decreasing light input to the eyes by prescription of tints or sunglasses is recommended as a way of decreasing motion sickness and this may selectively affect the peripheral vision pathway and make it less sensitive to flicker and rapidly changing stimuli. The peripheral visual pathway is also implicated in Cinerama-induced motion sickness because viewing motion on a large Cinerama screen seems to create more sickness than viewing the same material on a small screen, e.g., a television set. (Possible this is also because larger eye movements are required when viewing the Cinerama screen.)

Visual perceptual processes also seem to play a role in motion sickness susceptibility. This is indicated by the example presented previously in which a movie of a car chase provoked motion sickness, but only when it was played in the proper direction. No motion sickness was provoked when the movie was played backwards, which demonstrates the necessity for previous visual learning or memories for comparison to the actual scene being viewed.

Other brain processes can also be implicated in motion sickness susceptibility. Some patients can imagine motion and become ill, and others may have exaggerated responses to motion cues.

The role of visual system components in creating motion sickness may be quite complex. For the optometrist considering how vision can cause motion sickness, it becomes apparent that fully half of the provocative situations represented in Table 1 involve vision. Of course, the converse is also true, indicating that the vision care specialist is limited in the extent to which any form of vision-oriented therapy can alleviate all types of motion sickness.

A patient complaining of carsickness might seek help from an optometrist and may receive some relief through vision therapy or might be given instructions regarding how to position the head and/or eyes when riding. However, the causes of his or her motion sickness are not likely to be confined to visual-inertial sensory conflicts. They might also include canal-otolith conflicts that are outside of the realm of vision. In this case, another approach is in order and the solution may be as simple as having the patient place his or her head against a rest to avoid movement while traveling.

The previous example illustrates the complexity involved in trying to treat a person with motion sickness. Often the provocative stimulus produces several sensory conflicts, (9) which have additive effects that act together to cause motion distress. Any single preventative measure taken against motion sickness will likely meet with partial success, depending on the type and number of sensory conflicts that are involved. This means that treatment may need to be approached using several different strategies, as evidenced by the multiplicity of therapies available.

A frequently discussed source of sensory conflict problems is binocular imbalance, especially unresolved vertical imbalance. It has been said that vertical imbalances are somewhat like hyperopia in that a portion of the imbalance is manifest and easy to detect whereas another portion is latent so special techniques must be used to reveal it.

Roy has advocated the use of vertical prisms to relieve motion distress and related symptoms for some patients. His prism prescription is based on a prolonged monocular occlusion paradigm (3 days per eye) in which latent vertical deviations are revealed. (54) Other doctors prescribe prism to correct the associated phoria as measured using fixation disparity testing.

It has been suggested that some vertical deviations are the end result of vestibular problems. The vestibular system signals that the head is tilted when it is really straight, and the visual system compensates with a vertical deviation in response to the aberrant vestibular input. Whether this is true or not is unclear, and more evidence will be required to support the possibility.

Many patients with susceptibility to motion sickness also have horizontal imbalances, especially exo deviations, which can be treated with training or prisms.

In light of the sensory rearrangement theory, it seems reasonable that patients with binocularity problems would be highly susceptible to motion sickness. Difficulties with fusion would introduce incongruous images that may cause a neural mismatch in situations that are not commonly provocative of motion sickness in normal individuals.

Gillilan proposed a method of treatment for what he has termed the “Gillilan See Sick Syndrome (SSS),” which is characterized by headaches, nausea, dizziness, and photophobia. (51)

Clinical diagnosis of Gillilan SSS is made on the basis of a history of high susceptibility to motion sickness and a simple Marsden ball demonstration. Key questions asked in taking the history include, “Do you ever get car sick on a straight road, such as a freeway, when riding in the back seat or looking out the side window?” "Are you supersensitive to light?" (If the patient does not report significant photophobia, Gillilan does not make a diagnosis of SSS.) And, “Do you get car sick when you read in a car?” An affirmative answer to these questions would reveal susceptibility to visual-inertial conflicts.

Confirmation of susceptibility to the See Sick Syndrome can be demonstrated by having the patient watch a Marsden ball swinging laterally or in a circle at a distance of about 40 cm. According to Gillilan, it is only a matter of seconds before the SSS patient will become dizzy, nauseous, or both, in addition to experiencing eye discomfort. Again, assuming the patient maintains a constant head position, this demonstration would produce a visual-inertial conflict, rather than a canal-otolith conflict, thus indicating the patient’s susceptibility to motion sickness in atypical visual environments. (Gillilan has noted that there are a small number of delayed SSS reactors who will not react to the swinging ball immediately but will develop symptoms up to 30 minutes later.)

Gillilan treats the SSS with a regimen of eye motility exercises including Marsden ball techniques and pencil pushups. Eye discomfort, headaches, and nausea are common during and immediately after the first training sessions. However, in some cases treatment produces little discomfort by the end of the second week. Following this routine, most patients report alleviation of their symptoms and are able to perform everyday tasks without developing the characteristic headaches, nausea, and dizziness formerly associated with the tasks.

Kaplan has described an accommodative convergence problem that produces a set of symptoms call the “Kaplan Syndrome.” Among the symptoms cited is motion sickness. Kaplan therapy involves application of yoked prisms in a base-down or base-up configuration. (52,53)

Based on the assumption that peripheral vision plays a role in motion sickness, lenses that block or partially occlude the periphery have been prescribed with occasional success. As with many motion sickness therapies, there are insufficient cases in which this technique has been used to assess its success or the specific types of patients who might benefit from it.

When the head turns, the eyes also turn to compensate for the movement. This reflex, called the Vestibulo-Ocular Reflex (VOR), forms part of the gaze stabilization mechanism that the brain uses to hold visual fixation as the head moves. The vestibular system senses head motion and commands the eye muscles to move in compensation. Failure of this mechanism can cause oscillopsia or bouncing vision when a patient walks or otherwise moves the head.

To operate properly, the ratio (sometimes called the gain) of vestibular movement signal versus the amount of compensating eye movement must be correct. If, because of faulty vestibular function, the eyes move too much or too little (or too fast or too slow in the case of a pursuit movement) in response to a head movement, sensory conflict results and the patient experiences signs and symptoms very much like those of motion sickness.

There is strong clinical evidence that many patients with motion sickness will be made worse by the prescription of progressive addition lenses. This is probably due to the peripheral distortions inherent in the lens design and the possibility of anismetropia with resulting anisekonia if one lens is positioned slightly higher than the other. Many doctors only prescribe multiple pairs of single vision lenses for their presbyopic patients who are susceptible to motion sickness.

A specialist once said that you do not have to be crazy to have sensory conflict problems and motion sickness, but these problems can certainly make you feel crazy. A bit of an over-statement perhaps, but there is a kernel of truth in it. Patients who cannot trust their sensory systems can become quite neurotic and often work very hard at avoiding situations (e.g., flying, riding in the backseats of automobiles, etc.) that provoke symptoms.

It is also the case that many patients experiencing conflict problems wonder if the problem is really just all just in their heads. In fact, motion sickness susceptibility is physiological in addition to psychological. Being reassured of this is typically comforting to the patient.

Many patients with severe motion sickness can become quite neurotic and experience panic attacks that might be set off by sensory conflicts. Sometimes the psychological problems that result from motion sickness can greatly outlast the physiological problems causing the sickness, and, even if therapies designed to remove the causative factors are effective, the patient will still be symptomatic.

Various forms of psychological therapy including biofeedback have been used successfully in the treatment of motion sickness. The aim of biofeedback training is to reduce anxiety and enable the patient to suppress or disregard the symptoms of impending sickness, e.g., cold sweating, pallor, and nausea, before the onset of frank motion sickness occurs. (1,56,57)

Although often not as effective as the manipulation of factors such as posture, field of vision, and head movement restraint, the proper use of drugs is a common treatment for motion sickness. (3) Drug therapy can involve use of antihistamines such as dimenhydrinate (Dramamine®), cyclizine hydrochloride (Marazine®), and meclizine hydrochloride (Antivert®, Bonine®) that sedate the inner ear and reduce its output. (46,2) A problem with these drugs is that they also sedate the whole patient and can make driving or doing mental work difficult.

Some patients use Transderm scopolamine patches that deliver drug slowly through the skin, and anti-nausea medications such as promethazine (Phenergan®) can also be prescribed.

The table below presents information on some of the more commonly prescribed motion sickness drugs. Note that several of the drugs have visual side-effects and/or are contraindicated for glaucoma patients.

Because head movements do not appear to be the determining factor, the possibility of head position, and more specifically, of semicircular canal position as the critical factor is raised. To illustrate this, some sailors have found that lying on the back with the head elevated 20 to 30 degrees can reduce susceptibility to sea sickness. In any case, it seems clear that adopting the supine position in some fashion eliminates certain sensory conflicts, thus reducing the incidence of motion sickness.

Watch the Horizon

In most situations, it has been found that visual information that conflicts with other sensory information promotes motion sickness. Conversely, visual information that reinforces other sensory information tends to suppress sickness. (3) For example, the incidence of experimental swing sickness can be reduced by more than ten times when visual information corresponding to the swing motion is provided. (41)

Persons suffering from seasickness or carsickness are often advised to watch the distant horizon. (9,39,40,41) When this advice is followed, a fixed central visual field and a moving peripheral visual field are seen. This combination of stimuli is perceived as motion of the observer with respect to a stationary environment (42) and reinforces indications of motion received from the vestibular apparatus. This reduces visual-inertial sensory conflicts. (2)

Canal-otolith conflicts may also be reduced because fewer erratic head movements are made when the horizon or some other visual reference is viewed. (35,41)

In some cases, a practical solution for youngsters suffering from carsickness is to seat them in a raised car seat that will enable them to see the horizon out the front window. (43,44) (Obviously, caution is required when selecting a raised infant seat to ensure that it meets accident protection standards.)

When it is impossible to look at the horizon and visual-inertial conflict is inevitable, it is advisable to close the eyes. If this is impractical, some advantage might be gained by wearing an optical device that restricts peripheral vision while allowing central vision. (2) This is because central vision is believed to contribute little to spatial orientation and therefore would presumably have little effect on the development of motion sickness. (42,45)

Accupressure

Several products are available that use elastic wrist straps with metal buttons to press on the P6 acupuncture point on the insides of the wrists. There are variations of this device made with magnetic buttons and buttons that deliver a low-level electric current.

Typical treatment is absolute bed rest for several weeks in the hope that the fistula will heal itself. If bed rest is not successful, surgery to seal the leak can be attempted.

Meniere's disease and endolymphatic hydrops are related problems of inner ear fluid chemistry. Meniere's patients experience episodes of intense vertigo, nausea, nystagmus, and hearing loss extending over periods ranging from 30 min to 24 hours (or occasionally longer). The cause of Meniere's is unknown but some speculate that an allergy is involved. Others suggest that an ototoxicity possibly caused by aspirin or an aminoglycoside may play a role.

Endolymphatic hydrops is considered by some to be a chronic form of Meniere's. In hydrops, there is elevated pressure in the endolymphatic fluid of the inner ear. Hydrops patients experience vertigo, nausea, and other symptoms, but the symptoms are chronic and less intense than those experienced by Meniere's patients. The cause of hydrops can be malabsorption of endolymph in the endolymphatic sac or excessive fluid production.

Treatment of Meniere's and hydrops is similar and consists of avoiding things like alcohol, caffeine, sugar, and salt that change the fluid osmolarity of the endolymph. Drugs like acetazolamide (Diamox®) can also be used to reduce fluid production. Antihistamines to quiet the inner ear and diuretics to stabilize the inner ear fluids can be used. If the problems are severe enough, surgery can be used to section part of the VIIIth nerve or portions of the inner ear can be killed with graded doses of streptomycin. Some surgeons also implant very tiny drainage tubes in the endolymphatic sac to reduce fluid pressure.

In some ways, hydrops is a vestibular analog to ocular glaucoma. Because the fluid pressure is too high, drugs can be used to lower it, but, if treatment is not successful, cell death results. In the case of the visual system, field loss results, whereas in the case of hydrops, hearing and balance losses occur.

Summary It is not reasonable for vision care specialists to treat patents with specific inner ear diseases but they do need to recognize the signs and symptoms associated with these problems. Sometimes patients will describe a hearing loss along with complaints of vertigo, motion sickness, or dizziness, and the patient might even have nystagmus. Proper referral (usually not to a general physician or an audiologist and perhaps not even to and ear nose and throat specialist) to a tertiary level specialist (typically a neuro-otologist) can help these patients immensely.

Support for patients with vestibular problems is available from the Vestibular Disorders Association (VEDA) (http://www.vestibular.org/). VEDA maintains an extensive Web site and provides useful material for patients and doctors who want to know more about this subject.

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Some of the material presented in this course was derived from presentations made by Drs. Bradley Coffey, Hannu Laukkanen, and Karl Citek at Pacific University College of Optometry. Other material was derived from a paper published in the Journal of the American Optometric Association by J. Randall Pitman, OD, and Robert L. Yolton, PhD, OD.

Contact this editor:
Robert L. Yolton, PhD, OD
Padicif University College of Optometry
2043 College Way
Forest Grove OR 97116
yoltonr@pacificu.edu

Pacific University College of Optometry provides On-Line CE as a service to optometrists. The college does not endorse or recommend any products, equipment, or services that might be discussed in the courses. Courses are prepared by individuals believed to be experts in their areas of specialization who are compensated for their efforts. The College relies on their expertise to produce accurate and timely courses. Questions or concerns about courses should be directed to the individual authors and/or the Continuing Education Department at the College of Optometry at kundart@pacificu.edu .

	Visual (A) versus Inertial (B)	Canal (A) versus Otolith (B)
Type 1 conflicts (Input A and input B both signal motion)	Watching waves from moving ship; Looking out side windows of car; Significant change in refractive correction	Cross-coupled angular acceleration; Riding in a car on a winding road, or flying in a circling airplane
Type 2 conflicts (Input A signals motion in absence of expected input B)	Cinerama sickness; Helicopter and automobile stimulator sickness	Space sickness under conditions of micro-gravity which produces abnormal vestibular activity
Type 3 conflicts (Input B signals motion in absence of expected input A)	Reading in a car by looking down at a book	Rotation about a non-vertical or an earth horizontal axis

Medication	Dose	Contra-indications	Adverse Effects	Comments
Scopolamine	Patch: Change every 72 hours. Apply to hairless area behind ear. Oral: 0.4 to 0.8 mg every 6 to 8 hours.	Gastrointestinal or bladder neck obstruction (e.g., prostatic hypertrophy), liver or kidney disease, risk for acute-angle closure glaucoma.	Dry mouth, bradycardia, blurred vision (especially in hyperopic persons), decreased memory for new information, decreased attention and alertness.	Useful for longer journeys. Do not touch eyes after applying patch. Contraindicated in children.
Dimenhydrinate	Adults: 25 to 50 mg up to 4 times per day. Children: 1.25 mg/kg, up to 25 mg. Can be repeated every 6 hours.	Use with caution in persons with asthma, cardiac arrhythmias, pyloric or bladder neck obstruction, narrow-angle glaucoma.	Drowsiness, thickened respiratory secretions, dry mouth, blurred vision, paradoxical excitement in children.
Diphenhydramine	Adults: 25 to 50 mg up to 4 times per day. Children: 1.0 mg/kg, up to 25 mg	As for dimenhydrinate.	As for dimenhydrinate.
Promethazine	Adults: 25 to 50 mg up to 4 time per day.	As for dimenhydrinate.	As for dimenhydrinate; hypertension, abnormal movements.	May be combined with ephedrine to help maintain alertness. Primarily controls nausea. Not recommended for children.
Meclizine	25 to 50 mg daily.	Asthma, narrow-angle glaucoma, bladder neck obstruction.	Drowsiness, dry mouth, occasional blurred vision.	Not recommended for children.

Etiology and Management of Motion Sickness: A Review of Optometric Considerations