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54 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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figure 3–5. Graviceptive pathways from the otoliths and vertical semicircular canals mediating the vestibular reactions in the roll plane.
projections from the otoliths and the vertical semicircular canals to the
ocular motor nuclei (trochlear nucleus IV, oculomotor nucleus III, abducens nucleus
of Cajal (
nal fasciculus (ri
(
VOR) in three planes. The VOR is part of a more complex vestibular reaction that also involves vestibulospinal connections via the medial and
lateral vestibulospinal tracts for head and body posture control. Ocular
tilt reaction is depicted on the right in relation to the level of the lesion
(i.e., ipsiversive with peripheral and pontomedullary lesions and contraversive with pontomesencephalic lesions).
al. (2006) with permission from Elsevier.
VI), and the supranuclear centers of the interstitial nucleus
INC) and the rostral interstitial nucleus of the medial longitudi-
MLF), are shown. They subserve the vestibulo-ocular reflex
input as translation. The brainstem velocity storage
mechanism may also contribute by computing an internal estimate of gravity by integrating angular head
velocity signals from the SCCs.
Velocity Storage Mechanism
The velocity storage mechanism is a central phenomenon by which the raw rotational vestibular signal from
the cristae ampullaris is prolonged or perseverated in
order to improve the ability of the aVOR to transduce
The
Reproduced from Brodsky et
the low-frequency components of sustained head rotation. The result is that the time constant (the time for an
exponential function to decay to 37% of its initial value)
of the aVOR is improved from 6 to 7 s (based on the
physical properties of the cupula) to about 15 to 20 s
(based on the nystagmus response to sustained rotation). Optokinetic afternystagmus is attributed to the
vestibular velocity storage mechanism. The velocity
storage mechanism may also be important for helping
distinguish tilt from translation. The vestibular commissure connects the two vestibular nuclear complexes
3. PrACtiCAl AnAtomy And PHysiology oF tHE oCulAr motor systEm 55
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and appears to be important for velocity storage, as if it
is sectioned, velocity storage is abolished.
Clinical Correlation:
Periodic Alternating Nystagmus
Acquired periodic alternating nystagmus (PAN)
is a spontaneous horizontal jerk nystagmus present in straight-ahead gaze that reverses directions
about every two minutes. It reflects instability of
the velocity storage mechanism (Furman, Wall, &
Pang, 1990; Leigh, Robinson, & Zee, 1981). Normally, GABAergic inhibitory inputs from the cerebellar nodulus and ventral uvula help control
vestibular rotational responses. In the setting of a
nodulus or ventral uvula lesion, the velocity-storage mechanism becomes unstable, and short-term
vestibular adaptation leads to sustained horizontal nystagmus that reverses directions every two
minutes as PAN. Although in pure form PAN is
only present in darkness, it may be present during
attempted visual fixation if the adjacent flocculus
and paraflocculus are also involved (because of
the floccular role in VOR suppression).
CONTROL OF SACCADIC EYE MOVEMENTS
In order to properly execute a saccadic eye movement
to bring an image detected in the visual periphery to
the fovea (for the purpose of visual search, reading,
or to view a specific target), the brain must simultaneously carry out several complex tasks. The location of
a visual stimulus is represented on the surface of the
visual cortex, with different parts of this two-dimensional cortical map corresponding to different locations
on the retina. However, the final effectors of the ocular motor system, the ocular motor neurons (OMN),
encode the characteristics for saccades in terms of their
temporal discharge, with the size of a saccade proportional to the total number of discharge spikes. Furthermore, the OMN cause the extraocular muscles to move
the eyes with respect to the head, not to the environment. Thus, the brain must transform the visual stimulus that is two-dimensionally “place-coded” in terms of
the location of active neurons in the visual cortex into
a saccadic command to the OMN that is “temporally
coded” in terms of discharge frequency and duration,
further taking into account the three-axis nature of eye
rotation. Once the trajectory for the saccade is determined, this vector must be separated into horizontal
and vertical components to stimulate specific premotor
burst neurons for oblique saccades. To ensure accuracy,
the desired size of the saccade must take into account
overcoming the elastic inertia of the extraocular orbital
tissues, as well as whether the gaze change will consist
of combined head and eye movements or eye movements alone (Sparks, 2002).
Brainstem Control of Saccades
Two main types of neurons are important in the brainstem network for generating the premotor commands
for saccades: burst neurons and omnipause neurons
(Scudder, Kaneko, & Fuchs, 2002).
Excitatory Burst Neurons
Brainstem excitatory burst neurons ([EBN], sometimes
referred to as short or medium-lead or premotor burst
neurons) carry the immediate supranuclear premotor
saccadic command and project monosynaptically to
OMN. They begin firing 8 to 12 ms before a saccade
and fire throughout the duration of the saccade. They
are silent during fixation and slow eye movements. The
discharge characteristics of EBN are tightly correlated
with saccade properties when the head is in a fixed
position during the saccade. For example, the number
of spikes in the burst discharge is correlated with the
size of the saccade, the duration of the burst discharge
is correlated with the duration of the saccade, and the
peak frequency of the burst discharge is correlated with
the peak velocity of the saccade. These relationships
between neuronal discharge and saccade properties
may be uncoupled when the head is not fixed during
the saccade because small head movements also contribute to gaze changes and stabilization.
Excitatory burst neurons for horizontal saccades
are located in the paramedian pontine reticular formation (PPRF) in the pons just rostral to the abducens
nucleus. EBN for vertical and torsional saccades lie
in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) rostral to the oculomotor
nucleus and ventral to the periaqueductal gray in the
mesencephalic reticular formation (Bhidayasiri, Plant,
& Leigh, 2000). For horizontal saccades, premotor burst
signals project to the ipsilateral abducens nucleus,
contacting both abducens motor neurons and internuclear neurons, to generate a conjugate ipsilateral
saccade (Figure 3–6). For vertical saccades, EBN for
upward and downward saccades are intermingled in
the riMLF. Upward EBN project bilaterally to elevator
OMN, while downward EBN project only ipsilaterally
to depressor OMN. EBN discharge most vigorously for
figure 3–6. A brainstem neural network model for generating horizontal saccades. Projections with flat ending
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are inhibitory; the others are excitatory. Saccades require reciprocal innervation to the medial rectus (MR) and
lateral rectus (LR) of both eyes. The LR is driven by the ipsilateral abducens nucleus (VI n) motoneurons (AM). The
VI n also contains abducens internuclear neurons (AI) that send axons to the contralateral oculomotor nucleus
(III n), which drive the MR of the other eye. Excitatory burst neurons (EBN) provide the saccadic drive to ipsilateral
AM and AI. EBN also project to inhibitory burst neurons (IBN). IBN provide inhibition to the contralateral AM and AI.
thus, an EBN/IBN pair provides reciprocal innervation. IBN also provide inhibition to the contralateral EBN and IBN.
A consequence of this cross-coupling is that the EBN/IBN pairs form a short-latency, positive feedback loop. When
omnipause neurons (OPN) are active, they prevent this loop from oscillating. At the beginning of a saccade, OPN
cease discharge, allowing one set of EBN (1) to start firing and activate ipsilateral IBN (2). During IBN (2) firing, contralateral EBN (3) receive a hyperpolarizing input that keeps them silent. At the end of the saccade, when the IBN
(2) cease firing, the EBN (3) start to discharge because of rebound depolarization, which stimulates ipsilateral IBN
(4), which in turn, inhibit original EBN (1) that fired. Thus, the EBN/IBN pairs tend to spontaneously oscillate whenever
the OPN are inhibited and there is no specified saccadic command. Reproduced from Leigh and Zee (2006) with
permission from Oxford University Press.
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saccades that rotate the eyes in a plane parallel to that of
a pair of reciprocally acting vertical semicircular canals,
which creates a torsional component. For example, EBN
in the right riMLF discharge to extort the right eye and
intort the left eye. Therefore, ipsilateral riMLF lesions
abolish ipsilesional torsional quick phases of nystagmus
and impair downward more than upward saccades.
Clinical Correlation:
Supranuclear Saccadic Palsies
Disorders affecting excitatory burst neurons will
impair saccades (rendering them slow or absent)
but may leave smooth pursuit and the VOR intact.
Progressive conditions like spinocerebellar ataxia
type 2 may gradually affect saccades, whereas
acute saccadic palsy may occur with an infarction or demyelinating plaque in the EBN, such
as the PPRF. Conditions may preferentially affect
the pontine horizontal or midbrain vertical EBN.
Progressive supranuclear palsy affects the riMLF
early in its course, leading to slowing of vertical
saccades (Bhidayasiri et al., 2001). Pontine gliomas
may affect the PPRF and lead to loss of horizontal
saccades and quick phases, with preserved horizontal vestibular and vertical saccadic eye movements (Baloh, Furman, & Yee, 1985). Rarely after
cardiopulmonary bypass, patients can awaken with
permanent loss of all saccades and quick phases in
all directions, with other functional classes of eye
movements preserved, apparently from damage to
perineuronal nets surrounding brainstem saccadegenerating neurons (Eggers et
Inhibitory Burst Neurons
In addition to the EBN described above, inhibitory
burst neurons (IBN) are another type of premotor
burst neuron that project monosynaptically to inhibit
antagonist OMN and their extraocular muscles during
a saccade. The IBN are located caudal to the abducens
nucleus in the medullary reticular formation for horizontal eye movements and are intermingled with neurons in the interstitial nucleus of Cajal (INC) for vertical
eye movements. For horizontal eye movements, IBN
project to the contralateral abducens nucleus to inhibit
it during ipsilateral saccades, in addition to inhibiting
the contralateral EBN and IBN. IBN receive excitatory
input from the contralateral superior colliculus and
inhibitory inputs from omnipause neurons (OPN) and
contralateral IBN.
al., 2015).
Omnipause Neurons
In order to maintain stable fixation, EBN require constant
inhibition except when a saccade is called for. This inhibition is mediated by tonically discharging glycinergic
OPN located in the nucleus raphe interpositus, medial
to the abducens nerve fascicles. OPN firing ceases just
prior to saccades in any direction and resumes immediately at saccade end. Microstimulation of OPN in the
middle of a saccade will stall the saccade midflight. The
mechanism by which OPN are inhibited to allow a saccade to occur appears complicated. The initial inactivation of the OPN may result from activity in trigger-latch
long-lead burst neurons (LLBN) in the rostral pons and
midbrain, from the “fixation zone” of the superior colliculus, and from the frontal eye fields, supplementary
eye fields, and fastigial nucleus of the cerebellum.
Long-Lead Burst Neurons
LLBN exhibit activity 40 to 100 ms prior to saccade
onset. They are located throughout the midbrain and
pontine reticular formations and likely consist of several types: relay LLBN, trigger-latch LLBN, and precerebellar LLBN. Relay LLBN may form a connection
between the superior colliculus and excitatory burst
neurons, synchronizing the onset and end of saccades.
The role of trigger-latch LLBN is unclear, but they may
Clinical Correlation:
Opsoclonus and Ocular Flutter
A striking eye movement disorder occurs in
which patients make involuntary bursts of highfrequency conjugate oscillations of the eyes, each
consisting of a series of back-to-back saccades
that lack an intersaccadic interval. When confined
to the horizontal plane it is termed ocular flutter,
and when it also includes vertical and torsional
movements it is termed opsoclonus (Wong, 2007).
Patients complain of oscillopsia and vertigo.
Ataxia is a commonly accompanying feature. Diseases causing this include brainstem encephalitis
and paraneoplastic syndromes (neuroblastoma in
infants, breast or small cell lung cancer in adults).
The pathophysiological basis for opsoclonus and
flutter remains unclear. A current hypothesis
based on brainstem models suggests that alterations in the membrane properties of saccadic burst
neurons may produce instability in the burst neuron circuit and that the level of activity in OPN
may also play a role (Shaikh et al., 2008).
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function to inhibit omnipause neurons and to hold
omnipause neurons off for the duration of the saccade.
Precerebellar LLBN receive input from the superior colliculus and project to the nucleus reticularis tegmenti
pontis (NRTP) which, in turn, projects primarily to the
cerebellar saccadic areas (the oculomotor vermis and
the fastigial oculomotor region) via the middle cerebellar peduncle.
Superior Colliculus
The superior colliculus (SC) is a multilayered structure
that lies in the midbrain tectum as the upper portion
of the quadrigeminal plate. It is the primary source
of commands to the brainstem immediate premotor
structures for generating saccadic eye movements.
It receives signals from many cortical and subcortical areas and sends output, at least indirectly, to all of
the premotor areas involved with controlling eye and
head movements, including EBN, OMN, LLBN, and
the vestibular nuclei. Inputs descend to the SC from
frontal and parietal eye fields (directly and through the
basal ganglia), as well as from visual cortex containing retinotopically coded information regarding target
location. The SC contains a “motor map” where information about saccade direction and amplitude is represented as a “place code.” The location of an SC neuron,
not its discharge characteristics, determines the direction and amplitude of the saccade for which it encodes.
This map is two dimensional, and downstream modifications (possibly in the NRTP) must convert collicular
commands to three-dimensional displacement vectors
for eye and head movements.
The rostral pole of this motor map seems important
for maintaining steady fixation (suppressing saccades),
and this “fixation zone” sends tonic excitatory projections
directly to OPN. The more caudal portions are important
for target selection (size and direction of movement) and
initiation of eye and eye–head gaze shifts. Deeper layers
of the caudal SC are important for coordinated movements of the head and eyes, including projections as the
tectospinal tract. Discrete lesions of the SC are rare but
may cause increased latency and slowing of saccades,
although redundant pathways from the frontal eye
fields prevent loss of saccade generation altogether.
Cortical Control of Saccades
Lesional and stimulation experiments in animals as
well as functional neuroimaging studies in humans
show that widespread areas of the frontal and parietal
cortex are important for saccadic control. These cortical
structures are integral for attention, motivation, target
selection, and programming of eye movements. Rather
than a top-down arrangement, these regions probably
form a vast network with many reciprocal connections
(Figure 3–7). The frontal regions include the frontal eye
fields (FEFs), supplementary eye fields (SEFs), dorsolateral prefrontal cortex (DLPC), and cingulate cortex.
The primary parietal region is the parietal eye fields
(PEFs) within the posterior parietal cortex (PierrotDeseilligny, Milea, & Muri, 2004).
The FEFs dispatch contralateral voluntary and
visually guided saccades to targets. They project to
the ipsilateral SC both directly and indirectly through
the basal ganglia (caudate and substantia nigra pars
reticulata). FEFs also project directly to the contralat-
Clinical Correlation:
Cortical Saccadic Abnormalities
Frontal lobe lesions produce various saccade
abnormalities based on the location of the lesion.
Unilateral FEF lesions increase the reaction time
of saccades, impair contralateral anticipatory saccades, and impair ability to inhibit inappropriate
saccades to visual stimuli, as well as impair pursuit and optokinetic following toward the side of
the lesion (Thurtell, Tomsak, & Leigh, 2007). SEF
lesions impair memory-guided saccades after gaze
shifts and affect ability to make a remembered
sequence of saccades to an array of visible targets.
DLPC lesions produce inaccurate contralateral
memory-guided saccades and impair predictive
saccades and antisaccades.
Larger acute destructive hemispheric lesions
such as infarctions, especially right posterior
lesions, may cause ipsilateral sustained horizontal conjugate gaze deviation (where patients may
“look away from the hemiparesis,” as opposed to
gaze directed toward the hemiparesis in an acute
pontine lesion). In a hemispheric lesion, it is usually possible to drive the eyes across the midline
with head rotation or caloric stimulation. If able
to make contralateral saccades, patients with parietal lobe lesions may have contralateral inattention (with or without homonymous hemianopia),
ipsilateral gaze preference, increased latency for
visually guided saccades, and impaired smooth
pursuit ipsilaterally. Intermittent horizontal conjugate gaze deviation suggests seizures from the
contralateral hemisphere.
figure 3–7. Higher-level control of the saccadic pulse generator. shown here are the major structures that project
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to the brainstem saccade generator (premotor burst neurons in PPRF and riMLF). Also shown are projections from
cortical eye fields to superior colliculus. DLPC, dorsolateral prefrontal cortex; FEF, frontal eye fields; IML, intramedullary
lamina of thalamus; NRTP, nucleus reticularis tegmenti pontis; PEF, parietal eye field; PPC, posterior parietal cortex; SEF,
supplementary eye field; SNpr, substantia nigra pars reticulata; STN, subthalamic nucleus. −, inhibition; +, excitation.
Reproduced from Leigh and Zee (2006) with permission from Oxford University Press.
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60 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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eral NRTP and OPN of the pontine tegmentum. The
SEFs lie anterior to the supplementary motor cortex.
They are important for programming saccades as part
of a learned or complex behavior. DLPC facilitates
memory-guided saccades, antisaccades, and advanced
planning of environmental scanning using memory
of target location. PEFs receive input from secondary
visual areas and the thalamic pulvinar nucleus. Projections go to the FEF and to the SC directly. The PEFs
are important for directing visual attention in extrapersonal space and initiating visually guided reflexive
saccades. Inhibitory projections from the basal ganglia to SC inhibit extraneous reflexive saccades during
attempted fixation and facilitate volitional saccades in
the context of remembered and learned behavior.
GAZE HOLDING AND THE
NEURAL INTEGRATOR
Once a visual target is acquired, the eyes must be held
steady in an eccentric position to maintain fixation.
To counteract the orbital elastic restoring forces that
would tend to pull the eyes back to central position,
tonic contraction of the extraocular muscles is achieved
by an increase in the sustained rate of discharge of
the OMN. This gaze-holding function is achieved by
networks of neurons that mathematically integrate
saccadic velocity “pulse” signals into position “step”
commands, collectively referred to as the neural integra-
tor (Figure 3–8).
Figure 3–8. Neural integrator physiology. For saccades, a pulse of innervation is the input to the neural integrator that generates a step. If the system
is perfect, the pulse (an eye velocity command) becomes a step (eye position command), as seen in A . If the neural integrator is leaky or imperfect (B),
the eye position signal decays with time. In this case, the eye will drift toward
the midline until a corrective saccade repositions the eye on target, creating gaze-evoked nystagmus. C. The centripetal drift of the eyes that occurs
with a leaky integrator can be described by its time constant (Tc), given by
the time at which the eye has drifted 63% of the way back to the midline.
From The Neurology of Eye Movements, by R. J. Leigh and D. S. Zee, 2006, p.
246, Figure 5–4. Reprinted with permission from Oxford University Press.
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The basic scheme for the neural integrator begins
with the EBN. A pulse discharge from the EBN projects a velocity command signal to the OMN to cause
phasic contraction of the extraocular muscle and overcome viscous drag of the orbit to generate a saccadic
eye movement. Abnormalities of the pulse can result
in hypometric or slow saccades (Figure 3–9). The same
pulse signal from EBN is also sent through the neural
integrator to generate a step of innervation, that is, a
position command to the OMN that changes the tonic
contraction of the extraocular muscle appropriate to
hold the eye in the new position. If the performance
of the neural integrator is perfect, the eye will be held
perfectly on the eccentric target.
Clinical Correlation:
Gaze-Evoked Nystagmus
Gaze-evoked nystagmus reflects dysfunction of
the neural integrator. In this situation, attempts
to hold the eyes in an eccentric position lead to
the eyes exponentially drifting back toward the
center because of inability to counteract the elastic
restoring forces of the orbit. The neural integrator
is said to be “leaky” in this case. When a leaky
integrator causes centripetal drift of the eyes, corrective saccades are required to bring the eye back
to the desired eccentric position, thus producing
gaze-evoked nystagmus. The rate of centripetal
drift reflects the time constant of the neural integrator — the faster the drift, the worse the integrator. Dysfunction can occur in a wide variety
of structural and functional disorders affecting
the neural integrator or the cerebellar structures
that serve to regulate the neural integrator. In the
setting of conditions such as cerebellar degeneration or Chiari malformation (where the tonsils are
compressed), gaze-evoked nystagmus commonly
develops.
The neural substrate for gaze holding consists of
cell groups throughout the brainstem and cerebellum.
The nucleus propositus hypoglossi and adjacent medial
vestibular nucleus (NPH-MVN) in the dorsal rostral
medulla play a key role in integration of horizontal
eye movements. The NPH-MVN receives inputs from
every structure that projects to the abducens nucleus
and encodes position signals to abducens neurons and
interneurons, mainly those innervating fatigue-resistant extraocular muscle fibers capable of sustained contraction. The INC, located just caudal to the riMLF in
the mesencephalic reticular formation, is the primary
structure responsible for integration of vertical and torsional eye movements (as well as appearing important
for eye–head coordination in the roll plane). It receives
inputs from the riMLF and from the vestibular nuclei
via the MLF. The primary output from the INC decussates in the posterior commissure to project position
commands to the contralateral INC and CN III and IV
nuclei. The cerebellum, particularly the paraflocculi
(tonsils) and flocculi (collectively part of the “vestibulocerebellum”), appears critical for improving the performance of an inherently leaky neural integrator. For
example, the NPH-MVN has connections with the vestibulocerebellum that likely serve as part of a positive
feedback loop to OMN, helping to increase the gain of
the neural integrator.
smooth Pursuit
The smooth pursuit system probably evolved to keep
the fovea pointed at a stationary target ahead as we
navigate through our environment. Minimizing foveal
“slip” of a visual object of interest improves vision,
while the “optic flow” of images across the rest of our
retina as we walk provides information about the threedimensional layout of our environment and our direction of movement within it. Subsequently, this system
could be harnessed to pursue a small object moving
across a complex background (without inducing a perception of motion of self or the stationary world) as
well as assist with visual fixation (holding the image
of a stationary object on the fovea while the observer
is stationary).
Signals encoding speed and direction of retinal
image motion pass via the lateral geniculate nucleus
(LGN) to striate and extrastriate (middle temporal and
medial superior temporal [MST]) cortex and posterior parietal cortex (i.e., PEF) (Figure 3–10). The MST
seems to contain visual tracking neurons that encode
representations of object motion in world-centered
coordinates, being sensitive to retinal slip, slow eye
movements, and slow head movements. From there,
further projections to the FEF and SEF may contribute to predictive aspects of pursuit, utilizing some of
the same corticofugal pathways as the saccadic system. The nucleus of the optic tract and accessory optic
system in the midbrain pretectum receives retinal slip
information directly from the retina and may help initiate pursuit.
The main pursuit projections descend from parieto-temporo-occipital cortex to the pons, particularly
the dorsolateral pontine nuclei (DLPN) and NRTP,
encoding various visual and ocular motor signals,
figure 3–9. Disorders of the saccadic pulse and step. Innervation patterns are shown on the left, eye movements
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on the right. Dashed lines indicate the normal response. A . Normal saccade. B . Hypometric saccade: pulse amplitude (width × height) is too small but pulse and step are matched appropriately. C . Slow saccade: decreased
pulse height with normal pulse amplitude and normal pulse-step match. D. Gaze-evoked nystagmus: normal pulse,
poorly sustained step. E . Pulse-step mismatch (glissade): step is relatively smaller than pulse. F. Pulse-step mismatch
due to internuclear ophthalmoplegia (INO: the step is larger than the pulse, and so the eye drifts onward after the
initial rapid movement. Reproduced from Leigh and Zee (2006) with permission from Oxford University Press.
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figure 3–10. Smooth pursuit pathways. Shaded area represents common pathway shared by horizontal VOR
and smooth pursuit. LGN, lateral geniculate nucleus; V1, striate cortex; V2 and V3, extrastriate cortex; MT, middle
temporal visual area; MST, medial superior temporal visual area; FEFsem, pursuit subregion of the frontal eye field;
SEF, supplemental eye field; LIP, lateral intraparietal area; NOT, nucleus of the optic tract; DLPN, dorsolateral pontine
nuclei; MVN, medial vestibular nucleus; LHC, left horizontal canal; NPH, nucleus prepositus hypoglossi; MLF, medial
longitudinal fasciculus; III, oculomotor nucleus; IV, trochlear nucleus; VI, abducens nucleus; MR, medial rectus; LR,
lateral rectus. Reproduced from Wong (2008) with permission from Oxford University Press.
including eye velocity. The DLPN projects contralaterally to the cerebellar flocculus and paraflocculus via
the middle cerebellar peduncle, whereas the NRTP
projects to the dorsal vermis and then to the caudal fastigial nucleus. From these cerebellar structures, fibers
then reach the superior and medial vestibular nuclei,
which then (for horizontal pursuit) project back across
the midline to the abducens nucleus (completing a
double decussation). The paraflocculus appears important for controlling smooth pursuit and the flocculus
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