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drifting of eye movement in the opposite direction, thus
stabilizing the binocular fixation point. This pattern of
slow–fast–slow movements is
nystagmus
(Fig. 38-22).
Clinically, the direction of nystagmus is named for the
fast phase of nystagmus.
Spontaneous nystagmus that occurs without head
movement or visual stimuli is always pathologic. It seems
to appear more readily and more severely with fatigue and
to some extent can be influenced by psychological factors.
Nystagmus due to a CNS pathologic process, in contrast
to vestibular end-organ or vestibulocochlear nerve
sources, seldom is accompanied by vertigo. If present, the
vertigo is mild. Nystagmus eye movements can be tested
by caloric stimulation or rotation (to be discussed).
Vertigo
Disorders of vestibular function are characterized by a
condition called
vertigo,
in which an illusion of motion
occurs. With vertigo, the person may be stationary and
the environment in motion (i.e., objective vertigo) or the
person may be in motion and the environment stationary
(i.e., subjective vertigo). Persons with vertigo frequently
describe a sensation of spinning, “to-and-fro” motion,
or falling.
Vertigo should be differentiated from light-headedness,
faintness, or syncope.
74–77
Presyncope, which is character-
ized by a feeling of light-headedness or “blacking out,”
is commonly caused by postural hypotension (see Chapter
18) or a stenotic lesion in the cerebral circulation that
limits blood flow. An inability to maintain normal gait
may be described as dizziness despite the absence of
objective vertigo. The unstable gait may be caused by dis-
orders of sensory input (e.g., proprioception), peripheral
neuropathy, or gait problems, and usually is corrected by
touching a stationary object such as a wall or table.
Vertigo can result from central or peripheral vestibular
disorders. Vertigo due to peripheral vestibular disorders
tends to be severe in intensity and episodic or brief in
duration. In contrast, vertigo due to central vestibular
causes tends to be mild and constant and chronic in
duration.
Motion sickness is a form of normal physiologic
vertigo. It is caused by repeated rhythmic stimulation of
the vestibular system, such as that encountered in car, air,
or boat travel. Vertigo, malaise, nausea, and vomiting
are the principal symptoms. Autonomic signs, including
lowered blood pressure, tachycardia, and excessive
sweating, may occur. Hyperventilation, which commonly
accompanies motion sickness, produces changes in blood
volume and pooling of blood in the lower extremities that
lead to postural hypotension and sometimes to syncope.
Some persons experience a variant of motion sickness,
complaining of sensing the rocking motion of the boat
after returning to ground. This usually resolves after the
vestibular system becomes accustomed to the stationary
influence of being back on land.
Disorders of Peripheral Vestibular
Function
Disorders of peripheral vestibular function occur when
signals from the vestibular apparatus are distorted,
as in benign paroxysmal positional vertigo, or are
unbalanced by unilateral involvement of one of the
vestibular organs, as in Ménière disease. The inner ear
is vulnerable to injury caused by fracture of the petrous
portion of the temporal bones; by infection of nearby
structures, including the middle ear and meninges;
and by blood-borne toxins and infections. Damage to
the vestibular system can occur as an adverse effect of
certain drugs or from allergic reactions to foods. The
aminoglycosides (e.g., streptomycin, gentamicin) have a
specific toxic affinity for the vestibular portion of the
inner ear. Alcohol can cause transient episodes of vertigo.
The cause of peripheral vertigo remains unknown in
approximately half of the cases.
Severe irritation or damage of the vestibular end-
organs or nerves results in severe balance disorders
reflected by instability of posture, ataxia, and falling
Slow
Left ear
Right ear
Fast
Fast
Slow
Horizontal canals
Direction of
spin
Direction of
endolymph
movement
Hair
displacement
Nerve
discharge
Nystagmus
FIGURE 38-22.
Effect of spinning a subject clockwise. On
acceleration, the endolymph in the horizontal ducts will lag
behind with respect to movement of the duct wall.The hairs
of cristae will be displaced to the left. In the left semicircular
duct, hair displacement is away from the kinocilium, leading
to decreased nerve discharges below the resting level. On the
right, hair displacement is toward the kinocilium, leading to
an increase in nerve discharge above the resting level. (From
Sekurt FE. Basic Physiology for the Health Professions. 2nd ed.
Boston, MA: Little, Brown; 1982:140.)
