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Vestibuloocular Reflex Testing
Manali S Amin, MD, Consulting Staff, Department of Otolaryngology, Children's Hospital in
Boston, Brigham and Women's Hospital
Horst Konrad, MD, Professor Emeritus, Department of Surgery, Division of Otolaryngology,
Southern Illinois University School of Medicine
Updated: Mar 12, 2008
Introduction
A physician with bilateral, peripheral vestibular dysfunction described the classic example of the
vestibuloocular reflex (VOR) and its functional significance. The physician noticed that he was
unable to read street signs while walking. However, if he stood still, objects became clear, and he
was able to read again. This description of bilateral, vestibular dysfunction highlights the role of
the vestibuloocular reflex in the stabilization of objects on the retina during brief head
movements. When walking, vibrations from heel strike are transmitted to the head. A
combination of the vestibuloocular reflex and the vestibulocollic reflex (VCR) stabilize visual
acuity. Compensatory neck movements mediate the vestibulocollic reflex while head movements
mediate the vestibuloocular reflex. Without the stabilizing effect of the vestibuloocular reflex,
head perturbations as little as 2 Hz or 80° can result in retinal slip, which significantly alters
visual acuity.
Separate studies by Jacobs and Carpenter show that visual acuity declines by 50% at a point 2°
from the center of the fovea.[1,2 ]The fovea is that part of the retina where photoreceptor density is
greatest and visual acuity is highest. Thus, the main purpose of the vestibuloocular reflex is to
maintain objects on the fovea, which thereby allows a person to visualize objects clearly during
brief head movements.
When the head moves, the vestibuloocular reflex responds with an eye movement that is equal in
magnitude but opposite in direction. Head movements, rotational and translational, stimulate the
vestibuloocular reflex. With a rotational movement, the head moves relative to the body.
Examples of this include turning the head back and forth, nodding, and bringing the ear in
contact with the shoulder. Translational movements occur when the entire body (including the
head) is moved in tandem. Translational movements may occur when an individual stands on a
moving sidewalk. Thus, rotational vestibuloocular reflex (r-VOR) responds to angular motion of
the head and results from stimulation of the semicircular canals, whereas translational
vestibuloocular reflex (t-VOR) responds to linear motion of the head and results from
stimulation of the otolithic organs. Some head movements may involve a combination of both
translational vestibuloocular reflex and rotational vestibuloocular reflex.
Vestibuloocular reflex anatomy and physiology
A simplistic view of the vestibuloocular reflex (VOR) involves a 3-neuron arc that consists of
the vestibular ganglion, vestibular nuclei, and oculomotor nuclei. Although this arc provides a
basic framework, the pathways involved in the generation of the vestibuloocular reflex are much
more complex.

Rotational vestibuloocular reflex
o During rotational movements of the head, the endolymphatic fluid within the
semicircular canals shifts because of its inertia, which deflects the cupula.
Endolymphatic flow toward the ampulla is excitatory in the horizontal canals,
while flow away from the ampulla is excitatory in the superior and posterior
canals. Afferent nerves from the ampulla carry both excitatory and inhibitory
signals to the 4 major vestibular nuclei: medial vestibular nucleus, lateral
vestibular nucleus, inferior or descending vestibular nucleus, and superior
vestibular nucleus. Different regions within each of the nuclei project to the
oculomotor nuclei (cranial nerves III, IV, and VI). Efferent signals from these
nuclei then result in contraction and relaxation of the appropriate ocular muscles.
o Excitation of the superior canal results in contraction of the ipsilateral superior
rectus and contralateral inferior oblique muscles and relaxation of the ipsilateral
inferior rectus and contralateral superior oblique muscles, which results in an
upward torsional eye movement. Excitation of the posterior canal results in
contraction of the ipsilateral superior oblique and contralateral inferior rectus
muscles and relaxation of the ipsilateral inferior oblique and contralateral superior
rectus muscles. This results in a downward torsional eye movement. Finally,
excitation of the lateral canal results in contraction of the ipsilateral medial rectus
and contralateral lateral rectus muscles and relaxation of the contralateral medial
rectus and ipsilateral lateral rectus muscles. This results in a horizontal eye
movement toward the opposite ear.
o The vestibulocerebellum compares input from visual and vestibular sensors and
mediates changes in the vestibuloocular reflex after vestibular injury or change in
visual function.
o In addition to oculomotor projections, the vestibular nuclei send fibers to the
vestibulocerebellum, the nucleus prepositus hypoglossi, and the cells within the
paramedian tracts. The nucleus prepositus hypoglossi is crucial for the
maintenance of a steady gaze, while the cells within the paramedian tracts are
responsible for relaying information to the vestibulocerebellum, specifically the
flocculus. Reciprocal projections to and from the cerebellum assist in fine motor
control of eye movements. The latency of action of the rotational vestibuloocular
reflex (r-VOR) is 7-15 milliseconds, which is the time required for the eyes to
respond in an equal, but opposite, manner to the motion of the head. This time is


remarkably fast compared with the latency for visually mediated eye movements,
which is longer than 75 milliseconds.
o Finally, recent studies suggest that cerebral function may also be responsible for
the modification of the vestibuloocular reflex and the ability to suppress the
vestibuloocular reflex. Specifically, injuries to the parietal vestibular cortex and
the ocular gyrus appear to interfere with visual suppression of the vestibuloocular
reflex. In particular, the right temporoparietal cortex is believed to be involved in
the modulation of the VOR. This region has been shown to be sensitive to the
effects of sleep deprivation, particularly with respect to VOR gain during step
testing.[3 ]
Translational vestibuloocular reflex
o The translational vestibuloocular reflex (t-VOR) pathways are activated in
response to stimulation of the otolithic organs. The utricle responds to lateral
translation stimuli, whereas the saccule responds to vertical translations.
Translational vestibuloocular reflex pathways have not been studied as
extensively as the pathways for the rotational vestibuloocular reflex.
o However, translational vestibuloocular reflex pathways also appear to be
mediated by projections to the ocular motor nuclei via projections from the
vestibular nuclei. Specifically, excitation of the utricular macula results in
contraction of the ipsilateral superior oblique, superior rectus, and medial rectus
muscles and relaxation of the contralateral inferior oblique, inferior rectus, and
lateral rectus muscles.
Other vestibular reflexes
o Finally, note that the vestibuloocular reflex (VOR) is only one of 3 vestibular
reflexes. The vestibulospinal and vestibulocollic reflexes also contribute to
stability. The vestibulospinal reflex can be tested with the use of computerized
dynamic posturography. The reader is referred to eMedicine articles Vestibular
Rehabilitation and Inner Ear, Evaluation of Dizziness for additional information.
o Of the 3 vestibular reflexes, the vestibulocollic reflex is the least understood. The
vestibulocollic reflex is indicative of otolithic (saccular) function and can be
elicited by direct (intraoperative) stimulation of the inferior vestibular nerve,
acoustic stimuli, mechanical stimulation of the forehead, and galvanic stimulation.
The response can be measured as a myogenic potential in the ipsilateral
sternocleidomastoid and trapezius muscles. The test used, a vestibular evoked
myogenic potential (VEMP) test, continues to involve in its clinical application.
For more information on VEMP testing, the reader is referred to eMedicine article
Inner Ear, Evaluation of Dizziness.
Vestibuloocular reflex dysfunction

Similar to all other systems in the body, most individuals are not aware of the presence of
the vestibuloocular reflex (VOR) until it malfunctions. Acute vestibuloocular reflex
dysfunction may manifest in several different ways, depending on the anatomical location
of the lesion or lesions, and may result from labyrinthine disorders or disorders of the
central vestibular system. See the table at the end of this section details.




Studies have shown that patients with a unilateral peripheral vestibular lesion may exhibit
asymmetric responses to rotation. On the other hand, patients with a compensated
unilateral lesion show a characteristic pattern of decreased gain and increased phase lead
at low-frequency stimulation.
Bilateral peripheral vestibular lesions are characterized by low gain and phase lag as
determined by sinusoidal testing. These patients commonly report oscillopsia, a sensation
of vertical or horizontal motion of the environment, or persistent unsteadiness, especially
in the dark. Rotational chair testing is ideal in the assessment of these patients because,
unlike caloric testing, higher frequencies are tested and both labyrinths are
simultaneously stimulated. This allows for an accurate determination of remaining
vestibular function, which is important for determining a course of treatment.
Central vestibular deficits may also affect the vestibuloocular reflex. Thurston et al have
shown that gains may be increased in some individuals with cerebellar deficits.
Cerebellar atrophy, on the other hand, may result in a disorganized nystagmus pattern
with beat-to-beat variabilities in the amplitude. As previously mentioned, lesions within
the parietal vestibular cortex and the ocular gyrus may interfere with the ability to
suppress vestibuloocular reflex visually.
Although an impaired VOR is generally the result of an injury to the vestibular system,
note that VOR may be affected by systemic disease processes such as migraines,
depression, and anxiety disorders. With migraine vestibulopathy, one may see an elevated
gain with visually enhanced VOR (VVOR), a testing paradigm where the VOR rotation
stimulus is done in a lighted (ie, visually enhanced) environment rather than in the
traditional dark booth. Patients who experience anxiety disorders may have an increased
vestibular sensitivity resulting in significantly higher VOR gains and shorter time
constants.[4 ]Finally, those patients with major depression have been shown to have
hypoactive vestibular nuclei, resulting in a decrease in the slow phase of the nystagmus.
All of these disorders should be screened for and considered when testing an individual
with vestibular dysfunction.
Table 1. Manifestations of Vestibuloocular Reflex Dysfunction
Lesion or
Disorder
Unilateral
peripheral
lesion, acute
Unilateral
peripheral
lesion,
compensated
Bilateral
peripheral
lesion, acute
Bilateral
peripheral
Clinical Signs and
Gain
Phase (Time
Symptoms
Constant)
Nystagmus in plane of Decreased
Decreased
the affected canal;
toward side of vestibuloocular
spontaneous nystagmus lesion
reflex time constant
...
Still
Time constant rises
decreased (but slightly compared
closer to 1)
with acute
Oscillopsia, visual
impairment
...
Some oscillopsia with Near normal
rapid head movement
Symmetry
Asymmetric
(directional
preponderance)
Asymmetric
Vestibuloocular
...
reflex time constant
<6 s
Decreased time
...
constant
lesion,
compensated
Cerebellar
Central
vestibular
dysfunction
Oscillopsia, down-beat Little change
nystagmus
(increased or
decreased)
Oscillopsia, purely
Decreased or
vertical or torsional
increased
nystagmus, balance
(variable)
disorders, spontaneous
nystagmus
...
Asymmetric
Prolonged or
shortened time
constant (variable)
Asymmetric
Technique
Evaluation of the vestibuloocular reflex
As in the evaluation of all patients, the history and physical examination are the primary
determinants of further assessment with laboratory, radiologic, and other ancillary testing. If a
patient reports true vertigo, this is suggestive of a dysfunction in the semicircular canals, its
central projections, or both. If a patient reports body or room tilt, this implies dysfunction within
the otolithic system. Oscillopsia is a symptom reported by patients with vestibuloocular reflex
(VOR) dysfunction. Patients with these and other vestibular symptoms often undergo a series of
tests for diagnosis and localization of a lesion.

Evaluation of rotational vestibuloocular reflex
o The rotational vestibuloocular reflex is analyzed for 3 parameters: gain, phase,
and symmetry. Gain is the ratio of the amplitude of eye movement to the
amplitude of the head movement (stimulus). Phase is a parameter that describes
the timing relationship between head movement and the reflexive eye response.
When the head and eyes move at exactly the same velocity in opposite directions,
they are said to be completely out of phase, or 180°. If the reflex eye movement
leads the head movement, a phase lead is present. Likewise, if the compensatory
eye movement trails the head movement, a phase lag is present. Finally, testing is
analyzed for symmetry. Symmetry is a comparison of the slow component of the
nystagmus when the head is rotated to the right compared with rotation to the left.
Each of these parameters is useful in the diagnosis and localization of vestibular
lesions.
o The simplest way to analyze rotational vestibuloocular reflex is to have a patient
read a target such as an index card while the examiner passively rotates the
patient's head in a horizontal plane at a frequency of 2 Hz. If the patient's gain is
decreased, visual acuity deteriorates and corrective saccades may be noted.
However, the patient's visual acuity should not deteriorate with shoulder-to-ear
head movements; therefore, this test can be used to help identify patients who are
malingering.
o A second method of analyzing rotational vestibuloocular reflex gain is with an
ophthalmoscope. The patient is asked to view a distant target while shaking his or
o
o
o
o
o
her head at a frequency of higher than 2 Hz. The examiner then views the optic
vessels and disc. Because the eye movement is equal but opposite to the head
movement, the vessels and disc should appear stationary. This corresponds to a
gain of 1. If the eyes appear to move in the opposite direction of the head, the gain
is hypoactive, or less than 1. If the eyes appear to move in the same direction as
the head, the gain is hyperactive, or greater than 1.
Although the 2 previously mentioned tests are useful for a quick bedside clinical
assessment, the results of both tests are subjective. In addition, phase and
symmetry are difficult to assess with these methods. The most commonly used
tests for quantifying rotational vestibuloocular reflex abnormalities are caloric
testing, rotational chair testing, and head autorotation tests. Caloric testing
provides information on the horizontal canals at nonphysiologic frequencies and
is described in greater detail in Inner Ear, Evaluation of Dizziness. Rotational
chair testing provides a detailed analysis of an individual's gain, phase, and
symmetry at various rotational frequencies. Rotational chair testing and its
interpretation and applications are described in detail in Rotary Chair Testing.
A second method of objectively testing the rotational vestibuloocular reflex is
with head autorotation. This technique tests the high-frequency (2-6 Hz)
rotational vestibuloocular reflex. One method of testing head autorotation is with
standard electrooculography techniques. Electrodes are placed on the face in the
standard fashion and are then connected to a computer, which records the
impulses from the electrodes. Patients are then asked to rotate their head while
focusing on a light, as with other electronystagmography testing. Audible signals
that instruct patients to turn their head are given.
Alternatively, head autorotation testing may be conducted with the use of a
special headband with rotational sensors. The headband contains an
electrooculography amplifier and a calibrated rotational head velocity sensor. This
equipment is then connected to a computer, and patients are again presented with
auditory cues to rotate their head. The auditory cues start at a frequency of
approximately 2 Hz and increase to 6 Hz. One of 2 testing paradigms may be
used. Patients may be asked to focus on an object while rotating the head, or their
vision may be suppressed with a visor.
The rotational vestibuloocular reflex is analyzed for gain and phase with the use
of the head autorotation. Head autorotation with a visor yields results
indistinguishable from those of the rotational chair in a dark room. Unlike
rotational chair testing, however, autorotation can test rotational vestibuloocular
reflex frequencies higher than 1 Hz and can be used for both horizontal and
vertical rotational vestibuloocular reflex testing. High-frequency head rotation
testing from 2-6 Hz is important because many daily activities involve head
movements in these ranges. Head autorotation offers additional advantages over
traditional rotational vestibuloocular reflex testing. While providing quantitative
data, head autorotation requires less time to run than caloric or rotational chair
testing, costs less, and is portable.
Newer methods of testing vestibuloocular reflex continue to be studied. One study
has shown that whole-body rotation with the use of a standard swivel chair and

passive head rotation also yields results similar to those of the rotational chair, up
to a frequency of 1 Hz.
Translational vestibuloocular rotation
o The translational vestibuloocular rotation (t-VOR) and interaction of the otolithocular responses are not routinely tested in most laboratories. These tests are
mostly considered experimental and often involve sophisticated, expensive
equipment such as a linear sled cart, off-vertical axis rotation, or a platform
suspended from the ceiling (ie, parallel swing).
o Newer, less expensive techniques in development include manual translational
heaves and a head sled that, unlike the linear sled, moves only the head.
Additionally, the clinical significance of translational vestibuloocular reflex
continues to be studied. These studies may elucidate the mechanism behind
motion sickness and may have a future role in bedside monitoring of patients with
unilateral vestibular dysfunction.
Rehabilitation


Acute vestibuloocular reflex dysfunction, whether peripheral or central, is disturbing to a
patient. However, as patients begin to compensate, the dysfunction becomes less
debilitating and noticeable in situations that require complex interaction of the 2 systems.
Patients can actively promote compensation through a series of rehabilitation exercises.
Vestibuloocular reflex disturbances are treated with different forms of rehabilitation
exercises. For example, patients are asked to hold an index card 1 foot from their eyes
and to focus on a word or object on the index card as they rotate their head. Refer to
eMedicine article Vestibular Rehabilitation for more detail. Rehabilitation is adversely
affected by vestibulosuppressive medications.
Impact of Age on the Vestibuloocular Reflex



In recent years, studying the natural maturational and aging effects on the vestibuloocular
reflex (VOR) have been of particular interest.[5,6,7 ]Studies have shown that the VOR may
be present as early as 3 months of age. Furthermore, the absence of VOR by the age of 10
months may be an abnormal finding. Even in premature infants, the VOR is expected to
be equivalent to a full term child's by around the age of 9 months.
In one study, children (<11 y) were shown to have higher gains and phase lead at 0.08 Hz
when compared with adults. However, at a higher frequency (0.5 Hz), no difference was
found in the data obtained in children relative to adult normative data. A second study
also suggests that at higher rotational frequencies (0.5 Hz and 2 Hz), VOR may be mature
as early as 8 years of age. These studies show that maturational differences are found in
the VOR, and adult normative data may not be appropriate when testing children.[7 ]
At the other extreme, adult normative data may also be inappropriate when testing the
elderly, on whom the natural process of aging may impact the gain of translational VOR.
In one study, healthy subjects over the age of 60 were shown to have significantly
reduced gains with translational VOR testing when compared with adults younger than
40.[6 ]This was felt to be the effects of normal aging.

A second study examined the effects of aging on rotational VOR through a 5-year
longitudinal study of adults over the age of 75. Healthy subjects were tested annually for
5 years. With sinusoidal rotation, rotational VOR gains and phase leads both increased
with age when rotated at a low frequency (0.05 Hz) and high peak velocities (120°/s and
240°/sec). At higher frequencies and lower peak velocities, no significant change was
seen. These studies and several others show that the natural maturational and aging
processes affect the vestibular system and must be accounted for when testing patients
with vestibular symptoms.
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Keywords
VOR testing, VOR, vestibulo-ocular reflex testing, vestibulo-ocular reflex, peripheral vestibular
dysfunction, vestibular dysfunction, visual acuity testing, vision disturbance, vision difficulty,
vision testing, rotational VOR, r-VOR, translational VOR, t-VOR, oscillopsia, vestibular lesion,
VOR dysfunction, vestibulo-ocular reflex dysfunction, vestibuloocular reflex dysfunction,
labyrinthine disorder, central vestibular deficit, central vestibular disorder, vestibuloocular reflex
testing, translational vestibuloocular reflex testing, rotational vestibuloocular reflex testing,
nystagmus, head autorotation, caloric testing, vestibuloocular reflex
Contributor Information and Disclosures
Author
Manali S Amin, MD, Consulting Staff, Department of Otolaryngology, Children's Hospital in
Boston, Brigham and Women's Hospital
Manali S Amin, MD is a member of the following medical societies: American Academy of
Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American
College of Surgeons, American Rhinologic Society, and Triological Society
Disclosure: Nothing to disclose.
Coauthor(s)
Horst Konrad, MD, Professor Emeritus, Department of Surgery, Division of Otolaryngology,
Southern Illinois University School of Medicine
Horst Konrad, MD is a member of the following medical societies: American
Bronchoesophagological Association, American College of Surgeons, American Medical
Association, American Neurological Association, American Otological Society, American
Society for Head and Neck Surgery, California Medical Association, North American Skull Base
Society, and Society of University Otolaryngologists-Head and Neck Surgeons
Disclosure: Nothing to disclose.
Medical Editor
Robert A Battista, MD, FACS, Assistant Professor of Otolaryngology, Northwestern
University Medical School; Physician, Ear Institute of Chicago, LLC
Robert A Battista, MD, FACS is a member of the following medical societies: American
Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American
Neurotology Society, and Illinois State Medical Society
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Managing Editor
Peter S Roland, MD, Professor, Department of Neurological Surgery, Professor and Chairman,
Department of Otolaryngology-Head and Neck Surgery, Director of Clinical Center for
Auditory, Vestibular and Facial Nerve Disorders, Chief of Pediatric Otology, University of
Texas Southwestern Medical Center; Adjunct Professor of Communicative Disorders, University
of Texas School of Human Development
Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha,
American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and
Neck Surgery, American Auditory Society, American Laryngological Rhinological and
Otological Society, American Neurotology Society, American Otological Society, North
American Skull Base Society, and Society of University Otolaryngologists-Head and Neck
Surgeons
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Disclosure: Nothing to disclose.
Chief Editor
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Surgery, University of Colorado School of Medicine
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