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Nucleus (VI)
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LR LRMR MR
J. Spratley et al.
Oculomotor
Nucleus (III)
Trochlear
Nucleus (IV)
Abducens
IR
IO
SR
MR
MLF
ATD
S
SG
L
Inhibitory neuron
Excitatory neuron
Fig. 2.8 Direct pathways of the horizontal semicircular canal vestibular–ocular reex (adapted
from Baloh 2001 [20]). SC scarpa ganglion, S superior nucleus, L lateral nucleus, M medial
nucleus, I inferior nucleus, MLF medial longitudinal fasciculus, ASD ascending tract of Deiters, IR
inferior rectus, IO inferior oblique, SR superior rectus, MR medial rectus, LR lateral rectus
M
Vestibular
I
Nuclei
horizontal eye movements. Torsional eye movements are essentially controlled by
the vertical SCCs as well as by the utricle (Table2.1).
The rst afferent neuron synapsis is in the respective vestibular nuclei associated
with a particular SCC (Table2.1). In the specic case of the lateral SCC, this occurs
in the lateral vestibular nuclei.
Specically, when the head turns (accelerates) to the right (clockwise), on the
precise plane of the horizontal SCC (Fig.2.9), an ampullopetal endolymphatic ow
occurs on the right side and an ampuloffugal ow on the left. As acknowledged, this
action originates a deection of the cupula and the cilia in the crista ampullaris of
the right SCC towards the kinocilium and, consequently, the opening of mechanosensory K+ and voltage-gated Ca2+ channels, initiating an inux of both these ions
into the cell with a subsequent depolarization. The previously described spontaneous basal activity of these sensory organs at rest also allows a status of hyperpolarization and inhibition on the left side, as the exact opposite motion occurs as a
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Table 2.1
SCC semicircular canal
Fig. 2.9 Horizontal
vestibular-–ocular reex
neuronal’s drift overview
Vestibular organs and oculomotor Ipsilateral and contralateral activation
Vestibular
organ
Anterior
SCC
Lateral
SCC
Posterior
SCC
Utricle Lateral Interstitial nucleus of Cajal
Saccule Lateral Vestibulospinal pathways
Vestibular
nucleus
Superior Superior rectus Superior
Medial Medial rectus Lateral rectus Conjugate deviation of
Medial Superior obliquus Inferior rectus Downward and
Ipsilateral oculomotor
muscle
and from there to the
oculomotor and trochlear
nuclei
Contralateral
oculomotor
muscle Ocular motion
obliquus
Upward and
contradirectional
torsional
the eyes to the
opposite side
contradirectional
torsional
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consequence of the reverse orientation of the cilia in the crista ampullaris on this
side. During physiological rotatory stimulation, it has been revealed that the change
in frequency of action potentials is roughly proportional to the deviation of the
cupula [21].
This asymmetric information reaches the vestibular nuclei in the brainstem,
mainly in the medial vestibular nuclei, where different connections mediate the
VOR from the SCC to the oculomotor muscles (Fig.2.9). In the situation presented,
the vestibular nuclei interpret the discharge rates’ difference between left and right
SCCs as movement to the right and therefore trigger the oculomotor nuclei to drive
the eyes to the left to maintain gaze.
The eye response to a head rotation resides in a slow phase until the eye reaches
the edge of the outer canthus and a fast phase as a reset to the initial position. This
pattern repeats itself as long as the stimulus continues, and these two types of
repeated movements, as a saw-tooth pattern, characterize the vestibular nystagmus
variety. The direction of the nystagmus is denominated by the fast phase, as it is the
easiest to perceive. These movements can also be identied and characterized by
vestibular testing procedures such as conventional videonystagmography.
J. Spratley et al.
Vestibulo-spinal andVestibulo-colic Reexes
While the extraocular muscles are responsible for the compensatory ocular response
to movement, through the VOR, the extensor muscles of the neck, trunk, and limbs
are accountable for the body response through the vestibulo-colic and vestibulospinal reexes.
These reexes trigger automatic compensatory movement of the head/trunk in
very much the same way as with the VOR, controlling and balancing the extensor
and exor muscle tonus. These operate in coordination to achieve an appropriate
balance, either in static or dynamic conditions. Gravity, as detected by the otolith
system, acts as an additional driving input. Furthermore, proprioceptive and visual
information concur to provide the correct body position, as gravity is only detected
in the head, regardless of the position of the trunk and lower body.
Two functional categories of vestibulo-spinal reexes can be distinguished: those
acting on the limb muscles, which stabilize the position of the trunk in space, and
those acting on the neck muscles (vestibulo-colic reexes), which stabilize the position of the head in space [22].
The two most important vestibular descending pathways involve the lateral
vestibulo- spinal tract (LVST) and the medial vestibulo-spinal tract (MVST).
Reexive control of head and neck muscles arises through the neurons in the
MVST. These neurons comprise the rapid vestibulo-colic reex, whose role is to
stabilize the head in space and to participate in gaze control [23]. Yet, the MVST
neurons receive input from both the vestibule and the cerebellum, as well as somatosensory information from the spinal cord. These neurons carry both excitatory and
inhibitory signals to innervate neck exor and extensor motor neurons in the spinal
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cord, which clinically may be detected by the cervical vestibular evoked myogenic
potentials (cVEMP).
Last but not least, the LVST receives input from the cerebellum, the vestibule,
and the proprioceptive sensors of the spinal cord. These same LVST bers project
ipsilaterally to many levels of motor neurons in the spinal cord to ultimately provide
coordination of different muscle groups for postural control [24].
References
1. Brandt T, Schautzer F, Hamilton DA, Bruning R, Markowitsch HJ, Kalla R, etal. Vestibular
loss causes hippocampal atrophy and impaired spatial memory in humans. Brain. 2005;128(Pt
11):2732–41.
2. Lopez C. The vestibular system: balancing more than just the body. Curr Opin Neurol.
2016;29(1):74–83.
3. Wiener-Vacher SR, Hamilton DA, Wiener SI.Vestibular activity and cognitive development in
children: perspectives. Front Integr Neurosci. 2013;7:92.
4. Gray O.A brief survey of the phylogenesis of the labyrinth. J Laryngol Otol. 1955;69(3):151–79.
5. Engstrom H.Microscopic anatomy of the inner ear. Acta Otolaryngol. 1951;40(1–2):5–22.
6. Anthwal N, Thompson H.The development of the mammalian outer and middle ear. J Anat.
2016;228(2):217–32.
7. Moore KL, Persaud TVN.The developing human: clinically oriented embryology. 10th ed.
Elseivier Ltd; 2016.
8. Baloh R, Kerber KA. Clinical neurophysiology of the vestibular system. 4th ed. Oxford
Univesity Press; 2011.
9. Morsli H, Choo D, Ryan A, Johnson R, Wu DK.Development of the mouse inner ear and
origin of its sensory organs. J Neurosci. 1998;18(9):3327–35.
10. Rouvière H, Delmas A.Anatomía Humana: Descriptiva, Topográca Y Funciona. 11th ed.
Elsevier; 2005.
11. Corrales CE, Mudry A.History of the endolymphatic sac: from anatomy to surgery. Otol
Neurotol. 2017;38(1):152–6.
12. Biedron S, Westhofen M, Ilgner J.On the number of turns in human cochleae. Otol Neurotol.
2009;30(3):414–7.
13. Ewald JR. Physiologische Untersuchungen ueber das Endorgan des Nervus octavus.
Bergmann; 1892.
14. Spoendlin HH.Organization of the sensory hairs in the gravity receptors in utricule and saccule of the squirrel monkey. Z Zellforsch Mikrosk Anat. 1964;62(5):701–16.
15. Engstrom H, Bergstrom B, Ades HW.Macula utriculi and macula sacculi in the squirrel monkey. Acta Otolaryngol Suppl. 1972;301:75–1.
16. Brandt T.In: Brandt T, editor. Vertigo: it’s multisensory syndromes. 2nd ed. London: SpringerVerlag; 2003.
17. Wilson VJ, Maeda M.Connections between semicircular canals and neck motorneurons in the
cat. J Neurophysiol. 1974;37(2):346–57.
18. Ito M, Nisimaru N, Yamamoto M.Pathways for the vestibulo-ocular reex excitation arising
from semicircular canals of rabbits. Exp Brain Res. 1976;24:257–71.
19. Baloh RW, Kerber K.Baloh and Honrubia’s clinical neurophysiology of the vestibular system.
NewYork: Oxford University Press, Inc.; 2010.
20. Baloh RW, Honrubia V.Clinical neurophysiology of the vestibular system. 3rd ed. NewYork:
Oxford University Press, Inc; 2001.
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21. Goldberg JM, Fernandez C.Physiology of peripheral neurons innervating semicircular canals
of the squirrel monkey. 1. Resting discharge and response to constant angular accelerations. J
Neurophysiol. 1971;34:635.
22. Wilson VJ, Jones GM.Mammalian vestibular physiology. NewYork: Plenum Press; 1979.
23. Peterson BW, Goldberg J, Bilotto G, Fuller JH.Cervicocollic reex: its dynamic properties
and interaction with vestibular reexes. J Neurophysiol. 1985;54(1):90–109.
24. Shinoda Y, Sugiuchi Y, Futami T, Ando N, Kawasaki T.Input patterns and pathways from the
six semicircular canals to motoneurons of neck muscles. I.The multidus muscle group. J
Neurophysiol. 1994;72(6):2691–702.
J. Spratley et al.
Chapter 3
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Tests toEvaluate theVestibular System
AlexanderChern andLawrenceLustig
Introduction
Maintaining balance involves a complex interplay of the vestibular system, visual
system (eyes and related anatomy), and proprioceptive system. Indeed, the etiology
of “dizziness” can often be multifactorial and a challenging diagnosis. The thorough
evaluation of a dizzy patient should always begin with a thorough history and physical exam, which are often sufcient to obtain a reasonable diagnosis explaining the
patient’s symptoms [1]. However, although the majority of vestibular disorders may
be elucidated from a thorough history and physical exam, appropriate vestibular
tests can help rene the diagnosis and inform management decisions in specic
situations. This chapter will focus on clinical and vestibular laboratory tests for the
evaluation of the dizzy patient.
Physical Exam andBedside Vestibular Evaluation
A bedside vestibular evaluation is an important adjunct to a thorough otolaryngologic examination. It is important to conduct a detailed neurotologic examination,
including a cranial nerve examination, evaluation for nystagmus and oculomotor
function, positional tests, and postural tests.
A physical examination should include evaluation of spontaneous, gaze-evoked,
and headshake nystagmus. Spontaneous and gaze-evoked nystagmus may help
A. Chern · L. Lustig (*)
Department of Otolaryngology—Head and Neck Surgery, NewYork-Presbyterian/Columbia
University Irving Medical Center and Columbia University Vagelos College of Physicians
and Surgeons, New York, NY, USA
e-mail: lrl2125@cumc.columbia.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
B. T. Crane et al. (eds.), Disorders of the Vestibular System,
https://doi.org/10.1007/978-3-031-40524-2_3
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A. Chern and L. Lustig
localize the lesion in a patient with a suspected vestibular disorder [2]. Peripheral
vestibular nystagmus is often suppressed by visual xation but may be seen during
funduscopic examination in the dark. Frenzel goggles have 10× diopter lenses that
prevent visual xation and may also help accentuate nystagmus.
Skew deviation and a head tilt may suggest a unilateral disturbance of the
vestibulo- ocular pathways. Shortly after the unilateral vestibular loss, patients perceive the vertical as being tilted 10–30° toward the lesioned side. Although this
distortion usually diminishes over time, in some cases it may be present even after
vestibular compensation has taken place [3].
Several bedside tests are useful for detecting unilateral vestibular defects. The
head impulse test (HIT; also known as the head thrust test, as described by Halmagyi
[4]) is a passive head movement test where the examiner suddenly turns the patient’s
head rapidly to the right or left along a horizontal plane (yaw plane) while the
patient maintains gaze on the examiner. If the vestibulo-ocular reex (VOR) is normal, the eyes remain xed on the target. Patients with vestibular hypofunction may
generate a “catch-up” saccade (known as the head thrust sign) when the head is
rapidly turned toward the side of the lesion—this is considered a positive HIT.The
head shake test is an active movement test—the patient turns his or her head vigorously back and forth with eyes closed for about 30s to “charge” the brainstem’s
velocity storage mechanism. Upon stopping and opening the eyes, nystagmus usually beats away from the pathologic side; head-shaking nystagmus is typically
absent in normal subjects. “Tapping the head” [5] or application of a 60Hz vibration stimulus to the mastoid bone [6] may also evoke horizontal beating nystagmus
beating away from the side of vestibular hypofunction.
Dynamic visual acuity testing is useful for patients suspected of having bilateral
vestibular loss [7]. These abnormalities usually correlate with oscillopsia, as gaze
stabilization during high-velocity head movements is facilitated by the VOR, which
produces compensatory eye movements to stabilize images on the retina. Peripheral
vestibular lesions decrease the gain of the VOR and increase retinal image slip during head movements. Worsening visual acuity by at least three lines on a visual
acuity chart (i.e., Snellen chart) during head impulses turning from side to side at
1Hz or more is abnormal. Hyperventilation is known to accentuate downbeating
nystagmus in patients with cerebellar lesions [8] and may induce nystagmus toward
the side of the vestibular schwannomas [9].
Subjective visual horizontal (SVH) and subjective visual vertical (SVV) are
valuable clinical tests to measure otolith function, particularly utricular function
[10, 11]. The gravitational input from otoliths usually dominates the patient’s perception of verticality or horizontality. To assess SVH or SVV, the patient is asked to
sit with his or her head xed in an upright position while looking at an illuminated
line (i.e., on a computer display or projector) in complex darkness. The patient is
asked to adjust the line several times from starting positions at different angles to his
SVV or SVH. In acute peripheral vestibulopathy, there is usually a deviation of
SVV or SVH by several degrees toward the affected side. Central compensation will
facilitate the gradual improvement of the patient’s tilt perception.
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Positional (or static positional) tests are discussed in the electronystagmography
(ENG) and videonystagmography (VNG) portions of this chapter. Positioning (or
dynamic positional) tests are also useful. These include the Dix-Hallpike maneuver
and the roll test. The Dix–Hallpike maneuver is done to assess for BPPV of the
vertical (posterior or anterior) semicircular canals (SCCs). To perform this test, the
patient sits upright on the examination table with the head rotated 45° from the
sagittal plane to the side. The patient is quickly lowered by the clinician such that
the patient’s head hangs off of the table. If rotational or torsional nystagmus is
observed, then the patient has BPPV of the posterior SCC ipsilateral to the side the
head is turned toward or the anterior SCC contralateral to the side the head is turned
toward. This is repeated with the head turned 45° to the other side. The roll test is
used to evaluate for BPPV of the horizontal SCCs. With the roll test, the patient is
placed in the supine position with the head raised 30° by the clinician. The patient’s
head is rotated to both sides for 30s, watching for horizontal geotropic or apogeotropic nystagmus. The laterality of the lesion is determined by the intensity of the
evoked horizontal nystagmus. If geotropic nystagmus is observed, the lesion side is
the side on which head movement evokes more intense nystagmus. If ageotropic
nystagmus occurs, the lesion side is the side on which head movement evokes less
intense nystagmus. Of note, BPPV most commonly occurs in the posterior
SCC.Frenzel goggles may be useful for monitoring nystagmus during positioning
tests by suppressing xation.
Other bedside tests include postural control tests, such as the Romberg test, tandem gait test, Fukuda stepping test, and past-pointing test. With the Romberg test,
the patient is asked to stand erect with feet together and eyes closed. Increased sway
or a fall toward either side is considered a positive (abnormal) sign. The basis of the
test stems from the thought that balance comes from the combination of proprioception, vestibular input, and vision. If two of these systems are working, the patient
should be able to maintain a fair degree of balance. By removing visual input, two
of the systems remain, and if there is a vestibular or sensory (i.e., proprioceptive)
disorder, the patient is more unbalanced. The tandem gait test has the patient walk
in a straight line with one foot placed immediately in front of the other, arms down
by their sides, and closed eyes. Healthy individuals can take 10 steps without deviation, while patients with vestibular dysfunction fail this test. The Fukuda stepping
test has the patient march in place with eyes closed. After 50–100 steps, the patient
is asked to open his or her eyes. A rotation greater than 30° toward one side is considered abnormal. With the past-pointing test, the clinician is facing the patient. The
clinician extends his or her arms and points straight ahead with index ngers 6in.
apart. The patient is asked to lift both arms overhead while pointing with both index
ngers and then to bring down both arms and touch the clinician’s index ngers
while keeping arms extended. This is repeated with the patient’s eyes closed. A
deviation to one side is considered a positive or abnormal test.
Although the sophistication of the clinical examination of the vestibular patient
continues to evolve [12], the clinician may need to quantify vestibular function for
validation, prognostication, and treatment planning. Moreover, a vestibular abnormality that is not evident by clinical evaluation may be diagnosed using quantitative
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vestibular testing [13]. Objective evaluations of vestibular function may be useful in
facilitating diagnostic renement and informing management strategies in specic
clinical scenarios.
A. Chern and L. Lustig
Indications for Vestibular Testing
Vestibular tests are tests of function whose purpose is to establish if there are abnormalities in the vestibular portion of the inner ear. If no inner ear abnormality is
found, dizziness may be due to central nervous system (CNS) disorders (e.g.,
migraine, cerebrovascular disease), systematic disorders (e.g., dehydration, peripheral neuropathies), vascular disorders (e.g., hypotension), or psychological problems (e.g., anxiety). Studies suggest that vestibular testing is more accurate than
clinical assessment in identifying inner ear disorders [13]. Auditory pathway tests
(i.e., audiometry, auditory brainstem response test, and electrocochleography) can
also be ordered similarly and are frequently ordered in conjunction with vestibular
testing. One analysis demonstrated that hearing evaluation followed by either posturography or ENG was cost-effective [14].
Vestibular tests are also useful in detecting central vestibular disorders. One
study demonstrated that internuclear ophthalmoplegia (central eye movement disorder) is missed by 71% of physicians without quantitative oculomotor testing [15].
Vestibular tests can help determine if more expensive tests (e.g., magnetic resonance imaging) are needed—they are more accurate than clinical ndings in predicting abnormalities in neurology [16]. Finally, they may be useful to document
peripheral vestibular disorders such as benign paroxysmal positional vertigo
(BPPV), vestibular neuronitis, and gentamycin ototoxicity.
ENG andVNG
ENG or VNG is the rst step in vestibular testing. The traditional ENG utilizes
electric potentials to detect eye movements, while the newer VNG relies on video
analysis of eye motion through infrared cameras. Both rely on the VOR and its ability to generate efcient eye movements to keep the environment steady during head
movements. ENG and VNG are useful for detecting any abnormality along that
pathway—the peripheral vestibular system or the nerves that connect it to the brain
and the eye muscles. These tests have four components: (1) oculomotor tests, (2)
positional tests, (3) positioning tests, and (4) caloric tests, which will be
detailed below.
Equipment
Standard ENG equipment consists of the following components [17]: (1) an amplier of corneoretinal potentials that occur following eye movements, (2) band-pass
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and notch lters for ltering out undesignated muscle activity around the eyes and
electrical noise in the room, (3) a signal recorder, (4) a printer, (5) a linear array, and
(6) water and air caloric stimulators. The most common techniques used to record
eye movements are electrooculography (EOG) for ENG and videooculography
(VOG) for VNG.EOG is a simple, inexpensive test that measures the change in
corneoretinal potential by measuring the direction and velocity of eye movements
using electrodes typically placed above, below, and to the side of the eyes, along
with a ground electrode in the forehead [18]. Infrared VOG is an alternative method
of recording eye movements utilizing infrared cameras that measure the eye in the
dark for VNG [19]. Torsional eye movements are not recorded with EOG but can be
seen with infrared video recordings. VNG may be more accurate and consistent
compared to the traditional ENG because it is less sensitive to artifacts (i.e., lid
movement artifacts and electrical noise generated by muscle).
Clinical Application
VNG/ENG is helpful in diagnosing vestibular pathology—since each ear is stimulated separately, the laterality of the disease can be determined. Data from VNG/
ENG can support the diagnosis of pathologies like BBPV, vestibular neuritis,
Meniere’s disease, labyrinthitis, and ototoxicity, as well as brainstem and cerebellar
diseases affecting oculomotor control mechanisms. With vestibular schwannomas,
it may be helpful to predict the nerve from which the tumor originates; caloric
weakness may be associated with tumors originating from the superior vestibular
nerve. VNG/ENG may also predict whether the patient will experience vertigo after
vestibular schwannoma removal. However, sole reliance on VNG/ENG to identify
lesions of the CNS is not appropriate—abnormal ndings do not necessarily indicate a CNS lesion [20, 21]. See Table3.1 for comparisons of components of the
bedside vestibular examination with subtests of standard VNG/ENG.
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Oculomotor Tests
Oculomotor tests assess the accuracy, latency, and velocity of eye movements for a
given stimulus. The oculomotor test battery includes saccade tests, smooth pursuit
tests, optokinetic nystagmus (OKN) testing, gaze-evoked testing, and xation suppression testing—all of which assess accuracy, latency, and velocity of eye movements for a given stimulus. Abnormalities in oculomotor testing suggest a central
neurologic etiology, as these tested eye movements originate in the cerebellum [22].
Saccade Tests
Saccades are rapid, ballistic eye movements that abruptly change the point of xation to bring an object of interest from the periphery of the visual eld into the
center of the line of sight. Saccades are controlled by the occipitoparietal cortex,
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