Ann. N.Y. Acad. Sci.

ISSN 0077-8923

A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S
Issue: Dizziness and Balance Disorders

The bilateral central vestibular system: its pathways,

functions, and disorders
Marianne Dieterich1,2,3 and Thomas Brandt2,4
1
Department of Neurology, Ludwig-Maximilians-University Munich, München, Germany. 2 German Center for Vertigo and
Balance Disorders-IFB, Ludwig-Maximilians-University Munich, München, Germany. 3 Munich Cluster for Systems Neurology
(SyNergy), Munich, Germany. 4 Clinical Neuroscience, Ludwig-Maximilians-University Munich, München, Germany

Address for correspondence: Marianne Dieterich, M.D., F.A.N.A., Department of Neurology, Ludwig-Maximilians-University
Munich, Marchioninistrasse 15, 81377 München, Germany. marianne.dieterich@med.uni-muenchen.de

The bilateral anatomical organization of the vestibular system provides three functional advantages: optimal dif-
ferentiation of head motion and orientation, sensory substitution of a unilateral peripheral failure, and central
compensation of a peripheral or central vestibular tone imbalance. The structure is based on bilaterally ascending
and descending pathways and at least four crossings: three in the brain stem and one in the cortex. The resulting
sensorimotor functions can be subdivided into three major groups: (1) reflexive control of gaze, head, and body in
three spatial planes (yaw, pitch, roll) at the brain stem/cerebellar level; (2) perception of self-motion and control
of voluntary movement and balance at the cortical/subcortical level; and (3) higher vestibular cognitive functions
(e.g., spatial memory and navigation). The bilateral representation of the vestibular system in multiple multisensory
cortical areas and the vestibular dominance of the nondominant hemisphere raise the question of how one global
percept of motion and orientation in space is formed.

Keywords: vertigo; vestibular system; vestibular pathways; vestibular cortex; vestibular disorders; hemispherical
dominance

level; and (3) higher vestibular functions in which

Introduction
The central vestibular system unites ipsilaterally
and contralaterally ascending pathways from the
vestibular nuclei (VN) to the midbrain tegmen-
tum, the thalamus, and the cortex to mediate
perception of self-motion and verticality. It also
provides the sensory input that elicits adequate
descending motor responses to adjust eye, head,
and body to the vertical and to control balance.
Another important part of the system is the
hippocampus/parahippocampus, where cognitive
vestibular functions including spatial memory,
orientation, and navigation are processed. Thus,
the organization of the vestibular system can be
subdivided into three major functional groups: (1)
reflexive sensorimotor control of gaze and balance
at the brain stem/cerebellar level; (2) perception of
self-motion and sensorimotor control of voluntary
movement and balance at the cortical/subcortical
cognition1 or nonvestibular senses come into play,
as occurs in the disorders room-tilt illusion and
spatial hemineglect.2 These three major groups
of function do not operate independently of each
other. For example, reflexive sensorimotor control
of gaze and balance has to be integrated with
voluntary movement and locomotion. Similarly,
the simple perception of position and motion is
always part of higher cognitive functions such as
attention, orientation, and navigation.
The bilateral structure of the peripheral and
central vestibular systems is the key to many of
its sensory, sensorimotor, and cognitive functions
and—most importantly for the clinician—its disor-
ders. An approach that correlates vestibular struc-
ture and function has to take into account the fact
that the vestibular sense is distinct from other sen-
sory modalities and characterized by various special
features:

doi: 10.1111/nyas.12585
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Dieterich & Brandt The bilateral central vestibular system

r All natural vestibular stimuli are multimodal. Sensorimotor brain stem control of
They stimulate multiple senses in order to me- eye–head coordination and postural
diate the perception of body position and self- balance
motion. The central vestibular system is not
Reflexive eye–head coordination via the VOR and
only able to compensate for a unilateral pe-
postural balance via the VSR in the roll, pitch,
ripheral failure but also for central vestibu-
and yaw planes are brain stem functions. A re-
lar tone imbalances (e.g., in Wallenberg’s
cent study of vestibular connectivity using diffusion
syndrome).3,4
r Multiple sensory inputs converge at all levels
tensor imaging (DTI) and combined functional
magnetic resonance imaging (MRI) found a congru-
of the central vestibular system. This system
ent functional and structural link between the VN
is the only one lacking a primary sensory
and the parieto-insular vestibular cortex (PIVC).19
cortex (i.e., all vestibular cortex neurons also
Five separate and distinct pathways were identified:
respond to motion stimulation from other
three run ipsilaterally and two cross at either the
senses).5–9
r The vestibular percept of body position and
pontine or the mesencephalic level. The study con-
firmed findings of earlier electrophysiological and
motion in three-dimensional (3-D) space is
tracer studies in animals and MRI lesion studies in
always exocentric (i.e., it is relative to the sur-
humans20,21 that had examined only certain path-
rounding space). In contrast, the visual and
ways, not the entire system. The tracer studies per-
auditory percepts are always egocentric (i.e.,
formed primarily in the cat and macaque monkey
they are relative to the subject within the
revealed that vestibular pathways travel bilaterally
space).
r Vestibular cortex areas are represented in both
from the VN through at least four ascending tracts—
the medial longitudinal fascicle (MLF),22–24 the as-
hemispheres; however, the ipsilateral input
cending Deiters’ tract (crossed and uncrossed),25 the
from the stimulated end organ is the stronger
crossed ventral tegmental tract,26 and the brachium
input.10 Nevertheless, there is only a single
conjunctivum—to the ocular motor nuclei and the
“global vestibular percept” because one can-
supranuclear integration centers in the rostral mes-
not perceive two different body positions or
encephalic brain stem.27 In its basic version, the
body motions at the same time.11 Information
VOR is a three-neuron arc that links a set of ex-
about the actual sensory input from both sides
traocular eye muscles that are aligned by their pri-
of the head requires interhemispheric callosal
mary direction of pull within the same particular
communication.12,13
r The vestibular system is the only sensory
spatial plane of the horizontal, anterior, or posterior
semicircular canal.17,18 The canals of both labyrinths
modality exhibiting a hemispheric dominance:
form functional pairs in the horizontal and vertical
in right handers it is the right hemisphere, in
working planes: the horizontal right and left pair,
left handers, the left hemisphere.14–16
r Apart from perception, which is mediated in
the vertical anterior of one side along with the pos-
terior canal of the opposite side, and vice versa. The
the cortex, vestibular sensorimotor reflexes—
wiring connecting the two vertical canals diagonally
such as the vestibulo-ocular reflex (VOR) or
to the sagittal plane in the head creates the vertical
the vestibulospinal reflex (VSR)—are medi-
planes of pitch and roll.
ated in the brain stem circuitry but also re-
Structures of a VOR in the horizontal yaw plane
quire integration of the bilateral input from
originate at the lower pontine level and involve
the labyrinths.17,18 This is made possible by
the VN and the paramedian pontine reticular for-
the structural and functional crossings of the
mation, which contains the horizontal velocity-to-
bilateral ascending pathways.19
position integrator for eye movements. Accordingly,
In the following, we will discuss vestibular struc- unilateral vestibular pontine lesions occur at the
tures, functions, and disorders with respect to their critical brain stem site, causing a tone imbalance
bilateral organization in the order in which the sen- in the yaw plane (Fig. 1) with spontaneous nys-
sory input ascends (i.e., from the brain stem to the tagmus, horizontal deviations of perceived straight
thalamus to the cortex). ahead, ipsilateral gait deviation, and falls. Such

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The bilateral central vestibular system
Figure 1. Vestibular syndromes in roll, pitch, and yaw planes
due to a tone imbalance in one of the three major planes of
action of the system. Vestibular disorders in the horizontal yaw
plane are caused by unilateral lesions of the vestibular nuclei
(VN, blue); vestibular disorders in the frontal roll plane are
caused by lesions along the crossed graviceptive pathways from
the VN to the interstitial nucleus of Cajal (INC) (pink); vestibu-
lar disorders in the sagittal pitch plane are caused by bilateral
lesions of vestibular structures (green). The downbeat nystag-
mus syndrome occurs with bilateral cerebellar flocculus lesions
or medullary lesions close to the neurons of the nucleus of
the paramedian tract (dark green). The upbeat nystagmus syn-
drome occurs with bilateral lesions of the MLF at pontomesen-
cephalic level or paramedian in the paramedian tract neurons at
medullary level near the nucleus praepositus hypoglossi. Four
crossings between the bilateral VN pathways and the cortical ar-
eas are represented by red horizontal bars: (1) between VN, (2)
at the lower pontine level, (3) at the midbrain tegmentum, and
(4) transcallosal connections between the parietoinsular
vestibular cortex (PIVC). There is no crossing between the tha-
lamic nuclei (T).
lesions affect the root entry zone of the eighth
nerve28 and may mimic vestibular neuritis. This
disorder, called central vestibular pseudoneuritis,
has also rarely occurred with VN29 and cerebel-
lar infarctions,30 especially of the inferior cerebellar
peduncle and vermis.31 Its immediate clinical dif-
ferentiation from peripheral vestibular neuritis and
central pseudoneuritis must take place in the emer-
gency room before further diagnostic work-up
and management are begun. Skew deviation is the
only specific, but insensitive sign, signaling a cen-
tral vestibular “pseudoneuritis.”32 A normal head-
impulse test in a patient with acute rotational vertigo
12 Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
Dieterich & Brandt
and nystagmus indicates a central lesion.33 These
findings were supported by a prospective study
showing that more than 95% of 100 such patients
had an acute vestibular syndrome with vertigo.34
Unilateral lesions of vestibular pathways above the
level of the VN do not cause a purely vestibular tone
imbalance in the yaw plane.
Mapping of the total vestibular circuitry has re-
vealed that the bilateral vestibular network in its
entirety has a rope-ladder structure extending from
the brain stem to the cortex. Three crossings were
found in the brain stem (VN, pons, midbrain), with
a fourth cortical crossing through the splenium of
the corpus callosum.19 It is important to note that
no crossing has been found at the thalamic level.
Ocular tilt reaction: ascending VOR–OTR
and descending integrator–OTR
The vertical VOR and eye–head coordination in the
roll and pitch planes are integrated in the midbrain
tegmentum within the interstitial nucleus of Cajal
(INC) and the rostral interstitial nucleus of the me-
dial longitudinal fascicle (riMLF).27 This function
can be disturbed not only by unilateral or bilateral
lesions of the INC but also by lesions of the as-
cending graviceptive pathways, which cross at the
pontine level above the VN.35,36 This crossing has
also been confirmed by modern function lesion–
mapping,21,37 and DTI techniques.19 It explains why
unilateral lesions of the VN (e.g., lacunar infarctions
or multiple sclerosis (MS) plaques) cause an ipsiver-
sive synkinesis, the ocular tilt reaction (OTR). OTR
consists of head tilt, skew deviation, and ocular tor-
sion combined with tilts of perceived verticality. It
was first described in monkeys by Westheimer and
Blair.38 In unilateral midbrain lesions of the INC,
the OTR is contraversive owing to this crossing of
the graviceptive pathways in the pons.
Clinical evidence indicates that there are two
types of OTR39 (Fig. 2): the ascending medullary
type and the descending mesencephalic type.
OTR secondary to pontomedullary VN lesions
(Wallenberg’s syndrome) constitutes a tone imbal-
ance of the VOR in roll, whereas OTR due to INC
lesions secondary, for example, to paramedian mid-
brain infarctions may constitute a tone imbalance of
the neural integration center for vertical and rota-
tory eye–head coordination.40,41 The midbrain cen-
ter not only integrates eye and head velocity to po-
sition (for holding the assumed eye–head position
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Dieterich & Brandt The bilateral central vestibular system

Figure 2. Schematic representation of the two different clinically relevant types of ocular tilt reaction (OTR): the pontomedullary
“ipsiversive ascending VOR–OTR” and the mesencephalic “contraversive descending integrator OTR.” The VOR–OTR is induced
by unilateral lesions of the vestibular nuclei (VN). The integrator–OTR is induced by lesions of the interstitial nucleus of Cajal
(INC). Unilateral lesions of the crossing ascending graviceptive pathways of the pontine medial longitudinal fascicle (MLF; rostral
to downward branching of vestibulospinal pathways) cause tilts of perceived vertical and contraversive ocular skew torsion without
head tilt. Unilateral lesions of the vestibular thalamus or cortex cause ipsi- or contraversive perceptual tilts without head tilt or
skew torsion. Body lateropulsion has been described as occurring with unilateral medullary lesions, which affect the vestibulospinal
pathways. The VOR and the neural integrator are two components of a functionally cooperative system mediating eye–head
coordination in pitch and roll. The VOR is specialized on the dynamic reflexive response, whereas the integrator maintains
positions. VOR, vestibulo-ocular reflex.

in space at the end of the movement), but it also
adjusts vestibular reflex responses to voluntary cor-
tical control.39,41 Long descending neurons called
tectoreticulospinal neurons mediate the process.42
They originate in the INC, run through the MLF43 to
the pontine level, and couple eye and head roll mo-
tion by means of excitatory ipsilateral connections
with complex axonal branching. The different man-
ifestations of the ascending VOR type with monocu-
lar or disconjugate ocular torsion of the eyes depend
on whether input from the fibers of the posterior,
anterior, or both semicircular canals are involved
(Fig. 3). If the crossed pontomesencephalic path-
ways are lesioned on one side—rostral to the down-
ward branching of vestibulospinal connections—
tilts of the perceived verticality and ocular skew
torsion occur without head tilt (Fig. 2). Body lat-
eropulsion without components of OTR or other
signs of vestibular dysfunction has been reported to
occur with unilateral medullary lesions, which affect
the descending lateral vestibulospinal tract or the
dorsal spinocerebellar tract.44–47 This isolated symp-
tomatology of lateropulsion must be attributed to
lesions below the ascending fibers of the VOR, which
link the extraocular eye muscles and mediate per-
ception of verticality (Fig. 2).
In summary, the level of the unilateral lesion of
the graviceptive pathways is critical for brain stem
control of the perception of verticality and move-
ment of the eye, head, and body in the roll plane.
It determines the different components of OTR and
lateral postural instability (Fig. 2):
r Lesions in the medulla cause lateropulsion.
r Lesions of the VN cause ipsiversive VOR–OTR.
r Lesions between the VN and the mesen-
cephalic INC cause tilts of the perceived verti-
cality and ocular skew torsion.

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The bilateral central vestibular system
Figure 3. The ascending-VOR type of OTR is characterized
by monocular or dysconjugate skew torsion of the eyes depend-
ing on whether input from fibers of the posterior (PC), anterior
(AC), or both semicircular canals (AC/PC) to the extraocular eye
muscles are affected. An excitatory ascending pathway projects
from the AC to the ipsilateral superior rectus (RS) and the con-
tralateral inferior oblique (OI) muscle. A lesion of this pathway
causes a hypotropia of the ipsilateral eye and an incyclotropia of
the contralateral eye (AC type). An excitatory ascending pathway
is linked from the posterior semicircular canal to the ipsilateral
superior oblique (OS) and the contralateral inferior rectus (RI)
muscle. A lesion of this pathway causes excyclotropia of the
ipsilateral eye and hypertropia of the contralateral eye. A com-
bination of both canals (AC/PC) induces a complete OTR. OTR,
ocular tilt reaction; VOR, vestibulo-ocular reflex; III, oculomo-
tor nucleus; IV, trochlear nucleus; VN, vestibular nucleus; MLF,
medial longitudinal fascicle. Modified from Refs. 36 and 40.
r INC lesions cause contraversive integrator
OTR.
r Lesions above the rostral midbrain tegmen-
tum (i.e., in the thalamus) cause tilts of the
perceived verticality; there are no ocular motor
signs, but rare instances of transient thalamic
astasia occur.
r Cortical lesions cause perceptual tilts and the
pusher syndrome.
14 Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
Dieterich & Brandt
Vestibular tone imbalance in the pitch
plane: switch from unilateral to bilateral
mode of vestibular operation
An additional vestibular pathway for function in
the vertical pitch plane does not appear to be nec-
essary owing to the bilaterality of the graviceptive
pathways. These two pathways provide all of the
information needed: only a switch from unilateral
to bilateral mode of operation is required (“double
roll causes pitch”48 ; Figs. 1 and 4). This is compati-
ble with the clinical experience that vestibular brain
stem disorders in the roll plane always indicate a tone
imbalance due to a unilateral lesion,35,36 while tone
imbalances in the pitch plane, such as downbeat
nystagmus (DBN) and upbeat nystagmus (UBN),
indicate a bilateral lesion.49–52 The latter is clinically
most relevant for patients presenting in the emer-
gency unit. An OTR or lateropulsion is typical, for
example, for a unilateral pontomedullary infarction
in Wallenberg’s syndrome owing to the occlusion
of the posterior inferior cerebellar artery or verte-
bral artery. Unilateral pontomedullary infarctions
do not usually indicate a progressive infratentorial
stroke and therefore do not require invasive treat-
ment such as systemic or local thrombolysis. An
acute UBN, however, may be the early sign of an
impending basilar artery thrombosis because the
vestibular brain stem structures are affected bilater-
ally; it therefore requires further diagnostics. What
determines the direction of a tone imbalance in the
pitch plane? Different neural transmitters mediate
the up and down tone in the pitch plane. This is com-
patible with clinical experience that the causative le-
sions themselves occur in separate locations (Fig. 1).
Moreover, it explains, on the one hand, why certain
toxic effects of antiepileptics or nicotine-induced
nystagmus are directionally specific.53 On the other
hand, transitions from UBN to DBN or DBN to
UBN with head tilt, convergence, or simply during
the course of the disease17,54 reflect the intricate net-
work that maintains directional balance in the pitch
plane.
DBN is frequently persistent and often the result
of a bilateral lesion or dysfunction of the floccu-
lus or the paraflocculus.55 This is mainly due to
atrophy of the cerebellum, but also seldom caused
by intoxication due to anticonvulsant drugs. DBN
is only rarely induced by a lesion on the floor of
the fourth ventricle.17 Accordingly, idiopathic cases
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Dieterich & Brandt
Figure 4. Hypothetical explanation of how the vestibulo-
ocular reflex (VOR) in the pitch plane can be mediated by the
same graviceptive pathways as the VOR in roll: a schematic
representation of crossed excitatory anterior semicircular canal
pathways (AC), which convey a mixed vertical and torsional
ocular motor impulse to both eyes (both eyes upward). A bilat-
eral lesion causes a transition of the plane of action from roll
to pitch, because torsional components cancel each other and
the loss of upward impulse leads to a downward deviation of
the eyes. Downward deviation with upward refixation saccades
manifest as upbeat nystagmus. Upbeat nystagmus typically in-
dicates bilateral brain stem lesions, which affect, for example,
the MLF.
occur most often (38%), degenerative disorders of
the cerebellum in 20% of cases, vascular lesions in
9%, malformations in 7%; the less frequent causes
like toxic drug damage, lesions in MS, paraneoplas-
tic syndromes, vestibular migraine, vitamin B12 de-
ficiency, and traumatic and hypoxic injuries occur
with decreasing frequency.51 It can, however, also
be caused by a paramedian lesion of the medulla
oblongata, for example, in MS, hemorrhage, infarc-
tion, or tumor.
UBN is rarer than DBN. Pathoanatomical find-
ings indicate that most acute lesions occur in the
paramedian medulla oblongata, in neurons of the
paramedian tract, close to the caudal part of the per-
ihypoglossal nucleus, which is responsible for ver-
tical gaze holding.50,56 However, lesions have also
been reported to occur in a paramedian location
in the tegmentum of the pontomesencephalic junc-
tion, the brachium conjunctivum, and probably in
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The bilateral central vestibular system
the anterior vermis.17,56 Finally, there are indica-
tions that a lateral lesion in the caudal pons, which
includes the superior vestibular nucleus and its con-
nection to the central ventral tegmental tract, can
lead to a UBN.57
The vestibular thalamus: gatekeeper for
projections of vestibular information
to cortical structures
The thalamus relays vestibular information to the
bilateral network of different multisensory cortex
areas. Tracer and electrophysiological animal stud-
ies have revealed more than 10 regions within the
thalamus that have been attributed to vestibular
processing.58 These regions belong to the ventro-
lateral and posterolateral as well as the paramedian
thalamus. The involvement of the posterolateral tha-
lamus was first determined by vestibular stimulation
in animal experiments of different species.26,59–63
The ventrolateral parts of the thalamus receive
signals from the superior and medial vestibular
nucleus,63 the contralateral cerebellum via the supe-
rior cerebellar peduncle, and the ipsilateral globus
pallidus.64 Electrical stimulation of the human ven-
trolateral thalamus (Vim) elicited a sensation of
rotation or spinning of the body and head, either
counterclockwise (more often) or clockwise.65–67
Thalamic lesions can cause ipsi- or
contralesional tilts of visual verticality
These effects are in line with findings in patients with
acute unilateral posterolateral thalamic infarctions
who presented with tilts of perceived verticality ei-
ther to the ipsilateral or contralateral side but not
with eye–head tilts (i.e., no skew deviation or ocular
tilt reaction).41,68,69 Only unilateral vestibular thala-
mus and cortex lesions manifest with both ipsilateral
and contralateral tilts of the subjective visual verti-
cal (SVV), in contrast to lesions of the vestibular
brain stem structures.35,36,41 Lesion sites of ipsi- and
contralateral tilts largely overlap.41 This may be due
to the special structural feature that provides these
thalamic regions with several contralateral and ipsi-
lateral pathways,19 which may mediate directionally
opposite spatial percepts in the roll plane.
Zwergal et al.70 first reported that unilateral in-
farctions of the pontomesencephalic medial lemnis-
cus cause isolated ipsilateral rather than contralat-
eral deviations of perceived verticality. This pathway,
called the ipsilateral vestibulothalamic tract, was
15
The bilateral central vestibular system
then retrospectively identified by reanalyzing the
data from an earlier tracer study in monkeys.26,70,71
This tract most likely corresponds to a three-
neuronal rapid pathway extending from the vestibu-
lar end organ to the vestibular cortex. One is tempted
to speculate that this rapid pathway in nonhuman
and human primates could serve for perception of
self-motion rather than ocular motor and postu-
ral control. It might provide a suitable vestibular
signal in situations with large-field optic-flow stim-
ulation, thus allowing a decision as to whether the
visual stimulus is the consequence of self-motion
or simply indicates real motion of the surround.
Functionally, this is quite important, since postural
adjustment to large-field visual-motion stimulation
is only required in cases of self-motion. In our early
experiments on posterolateral thalamic infarctions,
about 69% of the patients presented with tilts of
verticality; these were ipsilateral in 44% and con-
tralateral in 25%.41 At that time, it was technically
not possible to separate small critical regions with
routine imaging techniques. More recently, an anal-
ysis applying voxel-based lesion behavior–mapping
techniques in patients with thalamic infarctions and
SVV tilts has presented the first evidence that two
distinct anatomical sites are affected in the direc-
tional processing of graviceptive signals at the thala-
mic level:72,73 contraversive SVV tilts were associated
with dorsolateral and dorsomedial subnuclei lesions
(VPLp, VPLv, CL, nucleus parafascicularis thalami,
CM, parts of the VPM, Po, and CL), whereas re-
gions associated with ipsiversive SVV tilts were lo-
cated lower and more medial (nucleus endymalis
thalami, the lower part of the nucleus parafascicu-
laris, and the nucleus ruber tegmenti bordering the
brachium conjunctivum).72
Thalamic astasia: a vestibular disorder?
Thalamic lesions may induce a specific disorder
of posture and gait called thalamic astasia, a term
first used by Masdeu and Gorelick74 for unilateral
lesions that primarily involved the superopostero-
lateral portion of the thalamus. This disorder man-
ifested in subjects’ inability to stand, although they
had no motor weakness or marked sensory loss.
We believe that the clinical characteristics of tha-
lamic astasia, however, fulfill the criteria of a tran-
sient central vestibular tone imbalance in the roll
plane. The imbalance of posture and gait evident as
deviations and falls to one side occur without
16 Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
Dieterich & Brandt
associated sensory or motor deficits.41 This view
is supported by the fact that the lesion site is in the
posterolateral thalamus.
Interestingly, thalamic astasia with associated
contralesional SVV tilts was also reported in a
patient with a small circumscribed paramedian
infarction.75 The involvement of the paramedian
thalamus as a vestibular relay station is less es-
tablished in clinical studies.41,75 These data are in
line with a recent study on vestibular fiber track-
ing by DTI of the VN to the cortex. Five separate
and distinct vestibular brain stem pathways were
identified:19 the two contralateral projections travel
through the posterolateral thalamus, while one ip-
silateral projection runs through the posterolateral
and one through the paramedian thalamic subnu-
clei to the PIVC. The third ipsilateral projection
bypasses the thalamus.
Detailed clinical studies that identify and differ-
entiate disorders on the basis of lesions of the vari-
ous vestibular thalamic and extrathalamic pathways
are lacking. These pathways are probably an integral
part of a sensorimotor network connecting the cor-
tex, basal ganglia, and cerebellum. The hierarchic
network mediates voluntary postural balance and
locomotion in a top-down fashion together with
largely automated locomotor pattern generators of
the brain stem, cerebellum, and spinal cord.76,77
The particular functional role of the vestibular sys-
tem within the basal ganglia–thalamocortical loop
for controlling body movements as described by
Alexander et al.78 remains unclear. Cortical shap-
ing of postural control is assumed to occur via a
cerebellar–cortical loop for the adaptation of pos-
tural responses based on prior experience and via a
basal ganglia–cortical loop for the preselection and
optimization of postural response patterns based on
the situational context.79
An extrathalamic vestibular projection to
the insular cortex
The above-mentioned third ipsilateral projection
bypasses the thalamus to directly contact the infe-
rior part of the insular cortex. This direct projection
to the inferior part of the insula was first demon-
strated in an H2 O15 –positron emission tomography
(PET) study during caloric irrigation of patients
with acute unilateral thalamic infarctions:68 caloric
stimulation did not activate any of the vestibular
cortex areas except the most inferior part of the
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Dieterich & Brandt
insula. The DTI study by Kirsch et al.19 provides
evidence that this activation in the inferior insula is
due to a direct projection from ascending vestibular
input rather than excitatory corticocortical inter-
action, which is known to occur in the visual sys-
tem for the motion-sensitive areas MT/V5.80,81 The
existence of such a direct projection is supported
by earlier electrophysiological and tracer studies in
the cat:82,83 the tracer labeled not only neurons in
the ventral posterolateral thalamic nucleus but also
those directly adjacent and outside the thalamus.
In both locations, short-latency, large-amplitude
evoked potentials from vestibular nerve stimula-
tion and antidromic field potentials from cortical
stimulation of vestibular areas were recorded.82 This
indicates that these neurons relay vestibular activ-
ity directly to vestibular cortex areas with a short
latency, probably via an ipsilateral ascending disy-
naptic pathway. Thus, posterolateral as well as para-
median thalamic subnuclei appear to relay vestibu-
lar information to cortical and subcortical areas.
Moreover, a rapid direct pathway to the inferior in-
sula seems to bypass these thalamic subnuclei.
Vestibular cortex
The bilateral structure of the vestibular cortex
raises a number of questions about its functional
meaning:
r Why do we have multiple multisensory cortex
areas?
r How do the vestibular and visual systems in-
teract for motion perception and spatial ori-
entation, especially in situations of a sensory
mismatch?
r How is the bihemispheric cortical representa-
tion for vestibular processing used to produce
a single global vestibular percept?
r Why is there a hemispheric dominance in the
vestibular cortex that is dependent on handed-
ness?
r What does this dominance mean for normal
function and disorders?
The parietotemporal network of multiple
multisensory vestibular cortex areas
In the past decade, brain activation studies with
PET and fMRI have disclosed the central con-
nectivity of the peripheral and central vestibular
structures in humans. Using caloric irrigation of the
Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
C 2015 New York Academy of Sciences.
The bilateral central vestibular system
horizontal semicircular canals, galvanic stimulation
of the entire vestibular nerve, or otolith stimula-
tion by means of vestibular evoked myogenic poten-
tials, researchers have demonstrated the existence of
a network of several separate and distinct cortical
areas in humans. These areas correspond to those
identified earlier by tracer and electrophysiological
studies in animals. The most robust of these cortical
structures include the posterior insula and retroin-
sular cortex with the parietoinsular vestibular cor-
tex (PIVC).14,20,84–93 Also a part of this ensemble
are those additional areas like the superior tempo-
ral gyrus (STG), the inferior parietal lobule (IPL),
the precuneus, the anterior cingulum, the anterior
insula, and the hippocampus, all of which belong to
the multisensory (vestibular) cortical network.
The PIVC, a multisensory vestibular cortex area in
monkeys with close connections to the other areas,
is considered a core region within this network.5–7
In parallel, the importance of this area in the
posterior insula for vestibular processing is also
evident in humans, as recently demonstrated by
data on activation likelihood estimation in meta-
analyses of vestibular activation in the operculoinsu-
lar complex.16,93 This network is found primarily in
the temporoinsular and temporoparietal cortex and
has been delineated in both human hemispheres,
but the right hemisphere in right handers shows a
dominance.14,16
Why multiple multisensory vestibular
cortex areas?
Not all neurons within the network seem to re-
ceive and process the same information from the
vestibular, visual, or somatosensory end organs.
We know from earlier animal studies, for exam-
ple, that the neurons of area 2v at the anterior
part of the intraparietal sulcus94 and area 3a in the
central sulcus95,96 respond not only to vestibular
but also to somatosensory and optokinetic stim-
uli. Neurons in and around the lateral sulcus (the
PIVC) of both Java and squirrel monkeys responded
to vestibular semicircular canal stimulation, and
many cells showed convergent somatosensory and
optokinetic responses.5–7 The first identification of
PIVC neurons in rhesus macaque monkeys located
them in the retroinsular (Ri) and adjacent sec-
ondary somatosensory (S2) cortices; more recently,
the responses were quantified to a set of stimuli
including 3-D rotations, 3-D translations, and 3-D
17
The bilateral central vestibular system
optic flow.8 These neurons responded to both trans-
lational and rotational vestibular stimuli, but not to
visual optic flow stimulation, thus they were driven
by semicircular and otolith signals.8 Robust optic
flow and vestibular tuning, however, were found in
an area strongly interconnected with the PIVC at
the posterior end of the sylvian fissure, in the visual
posterior sylvian area (VPS) of macaque monkeys,
which receives projections from a visual area, the
dorsal medial superior temporal area (MSTd).9 Op-
tic flow responses in the VPS were weaker than those
in the MSTd, whereas vestibular responses were
stronger in the VPS than in the MSTd. When vi-
sual and vestibular stimuli were presented together,
vestibular signals dominated the VPS responses, in
contrast to responses to the MSTd, where optic-
flow tuning typically dominated.9 These data, as
well as a comparison of vestibular spatiotemporal
tuning in macaque cortical areas PIVC, VIP, and
MSTd, suggest a hierarchy in the cortical processing
of vestibular information, with PIVC most prox-
imal to the vestibular periphery and MSTd most
distal.97 A meta-analysis and conjunction analy-
sis of functional imaging studies in humans using
caloric, galvanic, or auditory vestibular stimula-
tion revealed that the only area of convergence be-
tween all methods of stimulation is the retroinsular
cortex.93
Thus, the animal data suggest that different ar-
eas of the widespread cortical network receive in-
formation from several sensory systems; however,
the distribution of this information varies depend-
ing on the prevailing local modality. In humans,
the evidence for a topological separation and spe-
cialization of vestibular and ocular motor subfunc-
tions is based on the findings of different imaging
studies in healthy subjects and patients with acute
vestibular lesions. Correlation analyses in patients
with vestibular neuritis have shown that some of
the vestibular cortex areas such as the STG, IPL, and
precuneus seem to be involved in special aspects of
vestibular function or dysfunction.98 For example,
the slow phase velocity of the spontaneous nystag-
mus occurring during the acute stage of vestibular
neuritis correlated positively with the increase in re-
gional glucose metabolism (rCGM) in the area of
the STG bilaterally (BA 22), as well as in an ocular
motor area in the right inferior medial frontal gyrus
(BA 9/44) of the frontal eye field (FEF).99 Further-
more, a quantitative index of vestibular failure (mea-
18 Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
Dieterich & Brandt
sured as the caloric asymmetry between the affected
and unaffected ears) also correlated positively with
an area in the left IPL (BA 40) known to represent
a multisensory (vestibular) cortex area that is also
involved in the modulation of gain and time con-
stants of the VOR.100 The data of patients with left-
sided and right-sided vestibular neuritis provided
evidence that the latency occurring before perfor-
mance of the first PET after onset of labyrinthine
failure correlated positively with the increase in
rCGM in the visual cortex and negatively in the FEF
and the IPL. This means that the sooner the PET
is performed after disease onset (i.e., the stronger
the spontaneous nystagmus), the more activity is
seen in the FEF and the IPL, in other words, specific
areas of the vestibular and ocular motor network.
Finally, the signs of a vestibular graviceptive deficit
(deviations of the SVV) correlated positively with
the rCGM for the posterior insula and retroinsular
region bilaterally, more in the right hemisphere than
in the left hemisphere, as well as for the medial tem-
poral gyrus bilaterally. These studies, together with
the imaging data on healthy subjects during galvanic
vestibular101 or visual-motion stimulation, which
induced circular vection,102 allow us to attribute cer-
tain aspects of the applied stimulus, such as inten-
sity, frequency, or duration, to particular parts of the
network.
Thus, there is first evidence that vestibular sub-
functions are mediated in separate and distinct parts
of the multisensory cortical network of vestibu-
lar and ocular motor areas. Recently, a functional
separation was proposed in a review by Ventre-
Dominey,103 who distinguished between two sep-
arate cortical vestibular subsystems: (1) a velocity
pathway including MST and direct descending tracts
to the VN, which receives visual and vestibular ve-
locity signals and is involved in heading perception
and rapid top–down regulation of eye–head coor-
dination; and (2) an inertial processing pathway in-
volving the parietal cortex in connection with the
subcortical VN complex responsible for velocity
storage integration.103 The latter was interpreted to
be a perisylvian network active in higher-order cor-
tical processes related to spatial references.
In humans, the cortical localization of vestibu-
lar subfunctions was established in middle cere-
bral artery infarctions affecting the posterior insula
and causing ipsilateral or contralateral SVV tilts.104
Use of voxel-based lesion-behavior mapping in MRI
C 2015 New York Academy of Sciences.
Dieterich & Brandt
determined the location more precisely. The lesions
of the posterior insular cortex (long insular gyrus
IV) were associated with a dysfunction of the per-
ception of verticality (SVV tilt). Moreover, these
patients showed a positive correlation between the
severity of SVV tilts and thermal pain perception
contralateral to the stroke.105,106
Reciprocal inhibitory interaction between
the vestibular, the visual, and the
somatosensory systems
When the neurons within the temporoparietal
vestibular network are activated in both hemi-
spheres, a downregulation (deactivation) occurs
within the visual and somatosensory cortex
bilaterally.88,107 Since opposite activation–
deactivation patterns were found during visually
induced self-motion perception (e.g., activations
of occipital and parietal visual areas co-occurring
with deactivations of the multisensory vestibular
cortex (e.g., the PIVC)),81,108,109 it was assumed that
a reciprocal inhibitory cortical interaction takes
place between the two sensory systems, the visual
and the vestibular systems.108 This interaction
provides a powerful means for shifting the sensorial
weight from the less to the more reliable modality
in order to resolve potential perceptual conflicts
in situations with mismatched sensory inputs. A
reciprocal inhibitory interaction between sensory
systems is a fundamental perceptual mechanism
of the cortex.110 Such interactions were also
seen between other sensory modalities (e.g., the
somatosensory and nociceptive, the nociceptive
and the vestibular, the tactile sensory and visual,
and the visual and auditory systems).88,111–114 The
clinical relevance of a reciprocal visual–vestibular
interaction is best demonstrated by PET studies in
patients with unilateral vestibular neuritis causing
severe rotatory vertigo and spontaneous nystagmus
in the acute phase.98,99 On the one hand, the
beneficial effect of downregulation of the visual
cortex can be explained by psychophysical experi-
ments, which demonstrated that the amplitude of
oscillopsia in patients with acquired nystagmus is
always significantly smaller than the net retinal slip
owing to the involuntary eye movement.115,116 In
addition, perception of object motion is reduced
in these patients with acquired nystagmus,116
as well as in patients with a deficient VOR due
Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
C 2015 New York Academy of Sciences.
The bilateral central vestibular system
to bilateral vestibular failure.117,118 Interestingly,
the latter patients showed an enhanced activity
in the visual cortex bilaterally, including the
motion-sensitive area MT/V5,119 whereas patients
with unilateral vestibular failure showed dimin-
ished activations of the visual motion-processing
areas.120
On the other hand, the deactivation of the vi-
sual cortex can depend not only on eye movements
(retinal slip due to vestibular nystagmus or defec-
tive VOR) but also solely on the vestibular input.
The deactivation of the visual cortex appears to
be more dependent on the vestibular input, since
galvanic stimulation of the vestibular nerve dur-
ing functional MRI also induced significant bilat-
eral signal decreases of the visual cortex,88 although
no vestibular nystagmus was elicited. The only eye
movement was a mild tonic ocular torsion without
oscillopsia.
The rare paroxysmal syndrome of room-tilt illu-
sion may serve as a clinical example of a recipro-
cal inhibitory interaction between the visual and
vestibular systems. Transient upside-down inver-
sion of vision has been repeatedly described in pa-
tients with unilateral peripheral and central vestibu-
lar lesions.121 Transient upside-down vision or 90°
tilts are obviously vestibular signs that indicate a
misperception of verticality. Spatial orientation of
verticality is based on the interactions between the
visual and vestibular systems. Both senses provide
us with cues about vertical orientation in 3-D co-
ordinates. The visual and vestibular cortices have
to match vestibular spatial coordinates in three di-
mensions with the orientation of the visual scene
to determine the unique egocentric perception of
right and left, up and down, and fore and aft.
It is not possible to perceive two different verti-
cals, a visual and a vestibular one, at the same
time. Therefore, room-tilt illusions are transient
mismatches of the visual and vestibular 3-D map
coordinates.11 They are the erroneous result of an at-
tempted cortical match.2 Thus, the transient course
of room-tilt illusion may reflect the perceptual con-
sequence of a shift of the sensorial weight from
the misleading vestibular to the more reliable visual
sense.
While having to resolve intersensory mismatches
between the visual and vestibular systems, the
brain also has to resolve potential intrasensory mis-
matches between the two hemispheres.
19
The bilateral central vestibular system
Why bihemispheric representation of the
network but only one global percept?
All sensory modalities are represented in both hemi-
spheres. This makes possible the simultaneous eval-
uation of different external and internal stimuli. The
vestibular sense is special in that simultaneous bi-
lateral activation, even competing inputs, have to
be integrated into a global percept of body orien-
tation and self-motion. There is evidence that the
corpus callosum is essential for the integration of
perception and action within a subcorticocortical
network, thus leading to a unified experience of the
way we perceive the visual world and prepare our
actions.12 Patients with callosal degradation, with
and without disconnection of the two hemispheres,
exhibit a dissociation of callosal functions. While
anterior callosal regions are associated with inter-
hemispheric inhibition in situations of semantic and
visuospatial competition, posterior callosal areas are
associated with interhemispheric facilitation from
redundant information at visuomotor and cogni-
tive levels.12 Animal experiments in rodents sug-
gest that the claustrum plays a particular role in the
interhemispheric transfer of sensorimotor informa-
tion: subregions within the claustrum are critical for
the coordination of the cortical areas regulating the
acquisition of modality-specific sensory informa-
tion during exploration and other behaviors need-
ing sensory attention.13 These authors hypothesized
that the claustrum has circuit connections similar
to those of the visual system, allowing explorative
eye movements and attention to perceive a broad
spatial region. In their view, the claustrum facili-
tates interhemispheric corticocortical transmission
so that multiple sensorimotor cortical regions can
work together to produce a stable global percept out
of the continuously changing sensory information
provided by sensors on both sides of the head.12,13
As regards vestibular dysfunction in cases of uni-
lateral vestibular cortex lesions, it is unclear why
these patients do not usually exhibit vertigo or di-
rectional falls.48,122 Only single cases have been de-
scribed; patients with strokes within the middle
cerebral artery territory involving the vestibular cor-
tex presented with transient nonepileptic rotational
vertigo, ipsi- or contraversive nystagmus, and pos-
tural imbalance, which gradually resolved within
days.123–126 The only regular finding of transient
vestibular dysfunction in unilateral vestibular cortex
20 Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
Dieterich & Brandt
lesions is a tilt of the perceived verticality when tested
in a visual environment without additional cues of
true verticality.104,105,123,126 The correct global per-
cept might be maintained by increasing the sen-
sorial weight of the vestibular cortex of the unaf-
fected hemisphere, on analogy to visual–vestibular
sensory mismatches in transient room-tilt illusions.
This was achieved by inhibitory transcallosal con-
nections between the vestibular system,19,127 and has
also been shown for the visual system.81
Most of the single cases of unilateral vestibular
cortex lesions that manifested with transient ro-
tatory vertigo affected the posterior insular cortex
more often in the right than the left hemisphere.
This can be explained by the dominance of the
right hemisphere in the majority of the population
(right handers). It is more difficult for the non-
dominant hemisphere to overcome the misleading
cortical vestibular tone imbalance.
Dominance of the nondominant
hemisphere
The vestibular sense is characterized by a hemi-
spheric dominance that is located in the right
hemisphere in right handers and in the left hemi-
sphere in left handers. This has been determined
with caloric irrigation in PET14 as well as gal-
vanic stimulation91 and auditory-evoked vestibu-
lar otolith stimulation15,92 in fMRI (Fig. 5). The
dominance of the right hemispheric opercular area
OP2 in right handers has been confirmed in a
meta-analytical definition and functional connec-
tivity of the human vestibular cortex.16 The loca-
tion of handedness and vestibular dominance in
opposite hemispheres is an evolutionary product.
It might conceivably indicate that the vestibular
system and its hemispheric dominance, which oc-
curs earlier during ontogeny, determine right or left
handedness.128
In patients with acute vestibular neuritis, the
vestibular dominance of the right hemisphere may
be responsible for the faster recovery of perceptual
tilts (SVV tilts) after left-sided as compared to right-
sided lesions, as well as for the faster recovery in
left handers as compared to right handers.129 These
findings can be interpreted as both the dominance
of the ipsilateral pathways from the right labyrinth
and the central dominance of the right hemisphere
in right handers.
C 2015 New York Academy of Sciences.
Dieterich & Brandt
Figure 5. Activation pattern in imaging studies with PET
during caloric vestibular stimulation (A, B) and with fMRI
during acoustic-evoked vestibular otolith stimulation (by cer-
vical vestibular evoked myogenic potentials, cVEMPs (depicted
here: cVEMP stimulation minus acoustic stimulation)) (C, D)
in healthy right handers (A, C) and left handers (B, D). Note that
the activation in areas of the insular and retroinsular cortex, the
superior temporal gyrus, and inferior parietal lobule is more
pronounced in the right hemisphere in right handers and in the
left hemisphere in left handers for both types of stimulation and
imaging methods. Modified from Refs. 14, 15, and 92.
Dominance seems to also be a key to under-
standing the cortical mechanisms of disorders of
higher (cognitive) vestibular function,2 for example,
in spatial hemineglect130 and pusher syndrome.131
These clinical disorders occur with acute unilat-
eral hemispheric or thalamic lesions, mostly infarc-
tions. The dominance is reflected in, for example,
the frequency of pushing behavior, which is signif-
icantly higher in patients with strokes of the right
hemisphere than in strokes of the left hemisphere
Ann. N.Y. Acad. Sci. 1343 (2015) 10–26 
C 2015 New York Academy of Sciences.
The bilateral central vestibular system
and is associated with a slower recovery during
rehabilitation.132 Both conditions are not merely
vestibular disorders. They reflect dysfunction of spa-
tial orientation, attention, and postural control—all
of which are based on multisensory integration (vi-
suovestibular, somatosensory). However, both syn-
dromes have features that can best be explained by
the dominance of the vestibular system (e.g., that
of the right hemisphere in right handers). Spatial
neglect is a disorder caused by a disrupted aware-
ness of visual stimuli in an egocentric hemifield that
is contralateral to an acute temporoparietal lesion
of the right hemisphere.130 Less frequently, tran-
sient neglect may also occur after acute right or left
lesions of the frontal premotor cortex.133 A less se-
vere disorder of spatial attention occurs in visual
extinction. During rehabilitation, the amelioration
of neglect before complete recovery often involves
a transition to extinction.134 The critical cortical le-
sion sites that cause a neglect include several areas
within the temporoparietoinsular region, which are
known to belong to the multisensory vestibular cor-
tical network around the core region PIVC.135,136
Computational modeling has to take into account
the double organization of the spatial attention
and multisensory orientation center in each hemi-
sphere as well as the dominance of the right
hemisphere.127,137
The pusher syndrome is underrecognized by neu-
rologists during acute stroke management but well
known to physical therapists.138 It is characterized
by a disturbance of perceived body orientation that
manifests as actively pushing away the body to the
contralesional side using the nonparetic arm or
leg.139–141 Several lesion sites have been described
as the responsive structures (e.g., the thalamus and
the posterior part of the insula131,139 ), all of which
also belong to the multisensory cortical vestibular
network.
Another example of a higher vestibular disorder
that manifests with deficits of orientation and spatial
memory is caused by peripheral bilateral vestibular
failure.142,143 An intact vestibular function is im-
portant for spatial orientation, spatial memory, and
navigation, as shown in rodents.1,144 Spatial naviga-
tion requires a continuous representation of the lo-
cation and motion of the individual within a 3-D en-
vironment whose coordinates are provided mainly
by vestibular and visual cues.142 Use of the mental
rotation test and a virtual pond maze in older adults
21
The bilateral central vestibular system
has demonstrated a significant relationship between
vestibular and topographical memory measures.143
Acknowledgments
We thank J. Benson for copy editing the manuscript.
The work was supported by the German Federal
Ministry of Education and Research (Grant No. 01
EO 0901), the Hertie Foundation, and the German
Foundation for Neurology (DSN).
Conflicts of interest
The authors declare no conflicts of interest.
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