**2.5 Airsickness:**

Definition of airsickness

Predisposing and contributing factors

Symptoms and signs

Performance effects of airsickness

Prevention and treatment

Airsickness is a version of motion sickness, which has plagued travelers
and crew since the first oceangoing vessel -- the Ark\*, as it pitched
in the turbulent waves. Although we are spared the consequences of a
pair of seasick elephants, we are in the business of managing
airsickness in humans. Approximately 10% of all students taking flight
training will become airsick at some point during their first 10
flights; 15-20% of these will have a severe enough form to interfere
with their control of the aircraft.

Motion sickness in flight is called airsickness. It is a constellation
of symptoms that include lethargy, nausea, pallor, cold sweats, and
vomiting, even total incapacitation. Akin to airsickness, there are many
related forms of motion sickness: seasickness, carsickness, roller
coaster ride sickness, simulator sickness, space motion sickness, and
even camel sickness.

The basic etiology that triggers motion sickness in humans arises from
conflicting, or mismatched sensory input. Normally, stimuli from visual,
vestibular and proprioceptive pathways should correlate. If not, the
brain has difficulty integrating the information. Visual inputs may be
distorted by unfamiliar sights combined with the perception of motion,
which may represent the actual aircraft motion or the artificial motion
of a flight simulator. Vection, or the perception of visual motion, is
detected by receptors in the peripheral retina in response to visual
stimuli.

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ANGULAR MOTION STIMULATES THE SEMICIRCULAR CANALS

The vestibular system receives afferent inputs from two types of
receptors: the otoliths and the semicircular canals, located in the
inner ear. The otoliths detect linear motion and acceleration. The
earth's gravity is a linear form of acceleration and is always detected
by the otoliths so long as we remain in Earth's gravity. Any other
motion in a single direction, be it forward, laterally or vertically,
are different forms of linear motion. These directions are referred to
by the vectors Gx (forward), Gy (lateral) and Gz (vertical). Within the
otoliths, small stones (otoconia) are the masses affected by
acceleration forces. The inertial forces exerted upon the otoconia
trigger neurologic signals reflecting the magnitude and direction of
acceleration.

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height="2.920138888888889in"}

**[INNER EAR]{.underline}: VESTIBULAR APPARATUS (SEMICIRCULAR CANALS &
OTOLITHS) AND COCHLEA**

Angular or rotational motion is detected by a set of three structures in
each ear: the semicircular canals. Positioned at 90 degrees to one
another, they detect changes we refer to in aviation as pitch (nose
up/down), roll (rotation about the longitudinal axis), and yaw (nose
right/left).

Angular acceleration and linear acceleration can exist independently of
each other or coupled. An aircraft accelerating for takeoff on a runway
will experience linear acceleration as it picks up speed in a horizontal
direction, but there is no angular acceleration until the aircraft
begins to pitch/nose up and rotate towards takeoff and climb attitude.
However, as long as we are in the earth's gravitational field, we always
experience at least a linear acceleration of earth's gravity. Only in
the weightless environment will there be a true absence of acceleration
and a pure, uncoupled angular acceleration can be experienced.

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height="4.386805555555555in"}

**LOCATIONS OF PROPRIOCEPTORS IN THE HUMAN BODY**

Finally, there is the proprioceptive (body positioning) sense, or to a
pilot, "seat of the pants". Neural input originates from position
sensors in the joints and muscles. Occasionally other senses can provide
a limited degree of motion, such as audio stimuli. A moving sound source
can provide or imply motion as can the Doppler effect.

Pilots are conditioned to experience certain stimuli in their
environment, thus a pilot making a coordinated turn would expect to have
the visual input of an aircraft turning in a partly rolled and banked
condition with a combined vector of linear acceleration and angular
acceleration, producing an increased proprioceptive response. They might
also expect sound changes as in levels of engine and aerodynamic noise,
air pressure changes in ascent or descent, and lighting changes due to
sun position, even in an overcast. A novice entering the same situation
would find an increased sensation of gravity, with angular motion
occurring, potentially resulting in motion sickness. Conversely, in a
simulator, where the acceleration forces, producing both proprioceptive
and angular acceleration information to the vestibular receptors, as
well as sound and pressure alterations may not be present, symptoms can
be evoked in the experienced pilot, but not in the novice. Therefore,
predisposing factors to motion sickness depend to a large degree on the
previous motion experience of the individual. The experienced or
acrobatic pilot is conditioned to withstand abrupt attitude changes that
a passenger or helicopter pilot might not have experienced. This extends
in practice to all forms of

human endeavor, such as the ice skater who can perform rapid spins that
would render the non-skater vertiginous. The unifying theory is the
integration of information that occurs with conditioning and adaptation
to sensory conflicts. The ultimate adaptability of the human brain to
the motion environment speaks to the plasticity of the neurologic
system.

Failure to adapt may also occur.

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Conditioned airsickness may develop as a pathological state if an
individual, having repeatedly experienced airsickness in flight, begins
to experience symptoms even prior to exposure to the motion environment.
Much like Pavlov's dogs, which were conditioned to salivate at the sound
of a bell, these individuals will vomit at the sound of an aircraft
engine. These pilot/patients can benefit from pharmacologic and
behavioral therapy. Continued gradually escalating exposure is the most
common process for facilitating adaptation. Several days and repeated
sessions of flying usually conditions the patient to the new
environment. The approach may be modest, such as mastering coordinated
standard 30^O^ banked turns before attempting full aerobatics. Some
behavioral modification techniques and relaxation practices have been
used to various degrees of success. The traditional method is to turn
over the controls to the symptomatic student pilot. Instructors find
that giving the student the controls of the aircraft allows them to
anticipate motion, as well as to establish more control over their own
environment, resulting in less \_\_\_\_? The student pilot is actively
coordinating their sensory and motor inputs while controlling the
aircraft, causing less sensory conflict.

Student pilots, but not active pilots, can be treated pharmacologically
and continue to fly, albeit with an instructor pilot present. The most
effective medication currently in use is scopolamine, either orally (0.3
to 0.6 mg 30-120 minutes prior to exposure) or transdermally. This may
result in good control and suppression of the symptoms of nausea,
vomiting and sweating, but may be complicated by the side effects of
drowsiness, dry mouth and reduced visual accommodation. Other
anti-motion preparations include "scope-dex", which is a compounded
scopolamine (0.6 mg) and amphetamine (5-10 mg), taken orally 1-2 hours
prior to exposure. Promethazine (25 mg) in combination with ephedrine
(50 mg) taken orally 1 hour prior to exposure, is also useful for flight
crew. Sedating medications may also be used to good effect in
passengers; these include antihistamines such as diphenhydramine and
meclizine. Unfortunately, the newer non-sedating antihistamines, such as
loratadine*,* in failing to penetrate the blood-brain barrier and cause
sedation, also fail to reach the neural brainstem receptors responsible
for motion sickness, and are much less effective. The sedation from
antihistamines is usually so great as to preclude their use in the
individual who must function during the flight sdt is the side effects
of the anti-motion sickness drugs that preclude their use in active
pilots.