Neuronal Control of Eye Movements - part 10 ppt

Treatment of Oculomotor Disorders 179
Treatment
In the daily practice it is useful to administer vestibular sedatives such as
dimenhydrinate during acute self-limiting attacks [11, 15, 18]. One popular
prophylactic treatment regimen tries to reduce the endolymph by low-salt diet
or diuretics; another option is to administer betahistine (8–16 mg/day). Higher
dosages (up to 3 ϫ 48 mg) seem to be more effective than lower ones [15],
although the efficacy of betahistine has not been proven [18]. No randomized
studies on these treatment options have yet been conducted. A retrospective sur-
vey of the outcome of 22 patients revealed that intratympanic steroid perfusion
was only of short-term benefit [19]. A systematic review of published uncon-
trolled studies found that gentamicin reduced vestibular function in the treated
ear and achieved overall vertigo control (complete or substantial control) in
89% of the patients (range 73–100%); hearing worsened in 26% (0–90%) [20].
A meta-analysis examined the application of gentamicin, which poses the low-
est risk of hearing loss [21]. The titration technique with daily or weekly doses
until onset of vestibular symptoms, change in vertigo, or hearing loss showed
the best rate of vertigo control. Complete ablation of the vestibular function is
not typically required for such control [21], as this is also not achieved for a
long time with gentamicin instillation [22].
Superior Canal Dehiscence Syndrome
Clinical Aspects
Patients with a so-called superior canal dehiscence syndrome [23, 24]
complain of vertigo and oscillopsia, which are induced by intense sound stim-
uli, a Valsalva maneuver, or in some cases even the heart beat, when nystagmus
beats synchronously with the pulse in the plane of the involved vestibular canal
[25]. The accompanying jerk nystagmus has vertical and torsional components
[23, 24].
Etiology
The superior canal dehiscence syndrome is a special form of inner-ear peri-
lymph fistula [23]. High-resolution computed tomography has shown that the

cause is a missing bone coverage between the superior canal and the middle cranial
fossa. This results in increased pressure on the superior canal when the intracranial
pressure increases. In some patients, the dehiscence may be bilateral [23].
Treatment
Surgical plugging of the canal or resurfacing of the dehiscence can prevent
the pressure-induced oscillopsia [23]. Aftereffects are not long lasting.
Straube 180
Vestibular Paroxysmia
Clinical Aspects
If patients complain of short, repeated, paroxysmal attacks of vertigo last-
ing for seconds to minutes, which can sometimes be provoked by particular
head positions, a vestibular paroxysmia is suspected. Spontaneous nystagmus is
observed during the attack [26]. Other possible symptoms include unilateral
tinnitus, hyperacusis, or facial contractions. Clinical examination in the attack-
free intervals may in some patients reveal slight signs of permanent vestibular
deficit, hypoacusis, or facial paresis on the affected side [26, 27].
Etiology
High-resolution MR imaging may show the compression of the 8th nerve
by an artery (most often AICA) or more rarely by a vein in the region of the root
entry zone of the vestibular nerve. However, such a result does not prove the
diagnosis of paroxysmia, since such contacts can also be found in healthy sub-
jects. The proposed mechanism is similar to that of nerve-blood vessel contact
in trigeminal neuralgia.
Treatment
As in other neurovascular compression syndromes, an anticonvulsant (carba-
mazepine, slow-release formulation, 2 ϫ 200 to 2 ϫ 800 mg p.o. daily; phenytoin
1 ϫ 250 to 1 ϫ 400 mg p.o. daily; lamotrigine 100–400 mg p.o. daily) should be
given initially [26, 27]. All drugs should be first administered in the lowest recom-
mended dose and only gradually increased in order to prevent side effects. In gen-
eral, a positive response to antiepileptic drugs can be achieved with low dosages

and after a few days. If the symptoms do not resolve, a surgical approach may be
considered [28]. There are no satisfactory follow-up studies on any of these treat-
ment options, and the diagnostic criteria have not yet been fully established.
Downbeat Nystagmus
Clinical Aspects
Downbeat nystagmus is a central nystagmus that occurs during fixation and
increases on downward gaze, especially on lateral gaze [6, 29, 30]. The head
position relative to the earth’s vertical may play a role in some patients [31].
Convergence may suppress or enhance the nystagmus or even change its nystag-
mus toward an upbeat nystagmus in certain patients. Most patients also have
vestibulocerebellar ataxia. Lesions that cause downbeat nystagmus occur in the
vestibular cerebellum bilaterally and rarely in the underlying medulla [6].
Treatment of Oculomotor Disorders 181
Etiology
The main pathophysiological mechanism of downbeat nystagmus is a cen-
tral imbalance of the vertical VOR [28] in combination with an abnormality of
the vertical-torsional gaze-holding mechanism – the ‘neural integrator for eye
movements’ [32]. The neural integrator is a network consisting of the medial
vestibular complex and its connection to the cerebellum. The most common
cause of downbeat nystagmus is cerebellar degeneration (hereditary, sporadic, or
paraneoplastic). Recently, a report was published on a patient with glutamic-acid
decarboxylase antibodies and a downbeat nystagmus in addition to signs of a
stiff person syndrome [33]. Other important causes are Arnold-Chiari malforma-
tion and drug intoxication (especially anticonvulsants and lithium). In everyday
practice, cerebellar atrophy, Arnold-Chiari malformation, various cerebellar
lesions (multiple sclerosis, vascular, tumors), and idiopathic causes account for
approximately one fourth each of cases of downbeat nystagmus [30, 34].
Treatment
Since a loss of inhibitory cerebellar influence on the vestibular nuclei is one
of the main pathophysiological mechanisms of downbeat nystagmus, it seems

expedient to investigate substances that may help re-establish such cerebellar
influence on the brainstem. The vestibulocerebellar efferences to the vestibular
nuclei are gabaergic; thus, most drugs investigated were GABA-A agonists. The
GABA-A agonist clonazepam (2 ϫ 1 mg daily) was recently reported to have a
positive effect on so-called idiopathic downbeat nystagmus (e.g. no pathological
findings on MRI) [35]. This supports older observations that clonazepam (0.5mg
p.o. three times daily) and the GABA-B agonist baclofen (10mg p.o. three times
daily) [36, 37] reduce the velocity in downbeat nystagmus. Gabapentin (an alpha-
2-delta calcium channel antagonist) [38] might also have weak positive effects
and reduces in some patients downbeat nystagmus. A placebo-controlled, double-
blind study with a crossover design investigated the effect of the potassium chan-
nel blocker 3,4-diaminopyridine in 17 patients with downbeat nystagmus [39].
Potassium channel blockers can increase the spontaneous firing rate of the cere-
bellar Purkinje cells and therefore the inhibitory effect on the vestibular nuclei.
On average, the potassium channel blocker reduced the slow-phase velocity of the
nystagmus by more than 50% [39]. The same group reported a similar effect of 4-
aminopyridine (10 mg orally) in a single patient [40]. This substance penetrates
the blood-brain barrier better than 3,4-diaminopyridine and may therefore be
more effective. The potassium channel blockers also seem to have a specific
influence on the gravity-dependent component of the vertical velocity bias of
downbeat nystagmus [41]. This might explain why patients who do not show such
a vertical velocity bias and have more offset in the null position (e.g. the position
at which the nystagmus velocity is minimal) do not seem to benefit in the same
Straube 182
way from the treatment. The patients in whom the influence of the gravity-depen-
dent component is more pronounced also seem to benefit more from a supine
head position [41]. In isolated patients with a craniocervical anomaly, a surgical
decompression involving the removal of part of the occipital bone in the region of
the foramen magnum was beneficial [42, 43].
As a practical rule, treatment should be started by trying clonazepam. If

this option does not improve the nystagmus satisfactorily, 4-aminopyridine
(10 mg three times daily) should be tried.
Upbeat Nystagmus
Clinical Aspects
Upbeat nystagmus occurs when the eyes are close to the central position
and usually increases during upgaze [44]. The nystagmus usually disrupts verti-
cal smooth pursuit. In some patients, the upbeat nystagmus changes to down-
beat nystagmus during convergence. An upbeat nystagmus has in general a
better prognosis than a downbeat nystagmus and is often only a temporary
problem [11].
Etiology
A central vestibular imbalance is involved in upbeat nystagmus as in
downbeat nystagmus. The most frequently seen lesions are medullary lesions
[44]. Probable causes of upbeat nystagmus are lesions in the ascending path-
ways from the anterior canals (and/or the otoliths) at the pontomesencephalic or
pontomedullary junction, near the perihypoglossal nuclei [44, 45]. The main
causes are multiple sclerosis, tumors of the brainstem, Wernicke’s encephalopa-
thy, intoxication (e.g. nicotine), and seldom cerebellar degeneration.
Treatment
Treatment with baclofen (5–10 mg p.o. three times daily) caused an
improvement in several patients [37]. Probably 4-aminopyridine will also
improve the upbeat nystagmus in some patients [46].
Seesaw Nystagmus
Clinical Aspects
Seesaw nystagmus is a rare pendular or jerk oscillation around the line of gaze.
A half-cycle consists of elevation and intorsion of one eye with synchronous
Treatment of Oculomotor Disorders 183
depression and extorsion of the other eye [6, 47]. During the next half-cycle,
there is a reversal of the vertical and torsional movements. The frequency is
lower in the pendular (2–4 Hz) than in the jerk variety.

Etiology
Jerk hemi-seesaw nystagmus has been attributed to unilateral mesodien-
cephalic lesions [48], which affect the interstitial nucleus of Cajal and its
vestibular afferents from the vertical semicircular canals [49]. The pendular
form is associated with lesions that affect the optic chiasm; it can be congenital.
Loss of crossed visual input seems to be the crucial element in the pathophysi-
ology of pendular seesaw nystagmus [50].
Therapeutic Recommendations
Alcohol was reported to have a beneficial effect (1.2 g/kg body weight) in
2 patients [51, 52], as does clonazepam [1]. More recently, Averbuch-Heller
reported on 3 patients with a seesaw component to their pendular nystagmus,
who improved with gabapentin [53].
Periodic Alternating Nystagmus
Clinical Aspects
Periodic alternating nystagmus is a spontaneous horizontal beating nystag-
mus which periodically changes direction after 100–240 s [6]. Consequently,
the patients complain of increasing/decreasing oscillopsia. When the nystag-
mus amplitude gradually decreases, the nystagmus reverses its direction, and
then the amplitude increases again. Periodic alternating nystagmus also disrupts
visual fixation. During the nystagmus, patients often complain of increasing/
decreasing oscillopsia [11].
Etiology
Animal and human experiments show that the disinhibition of the GABA-
ergic velocity-storage mechanism, which is mediated by the vestibular nuclei,
is responsible for the nystagmus [54, 55]. Patients with periodic alternating
nystagmus commonly have vestibulocerebellar lesions or, very rarely, intoxi-
cations [56, 57]. The underlying etiologies are craniocervical anomalies,
multiple sclerosis, cerebellar degenerations or tumors, anticonvulsant therapy,
and bilateral visual loss. Recently, autoantibodies directed against glutamic
acid decarboxylase were described in a patient with progressive cerebellar

ataxia and periodic alternating nystagmus, suggesting an autoimmune mecha-
nism [58].
Straube 184
Therapeutic Recommendations
In general, periodic alternating nystagmus does not improve sponta-
neously. Several case reports describe a positive effect of baclofen, a GABA-B
agonist, in a dose of 5–10 mg p.o. three times daily [1, 57, 59, 60].
Other Supranuclear Oculomotor Disorders
Acquired Pendular Nystagmus
Clinical Aspects
Acquired pendular nystagmus is a visually distressing form of nystagmus,
in which oscillopsia and impaired vision are common. Acquired pendular nys-
tagmus is a quasi-sinusoidal oscillation that may have a predominantly horizon-
tal, vertical, or mixed trajectory (i.e. circular, elliptical, or diagonal); it can be
either predominantly monocular or predominantly binocular [6, 61, 62]. The
frequency of this type of nystagmus is 2–7 Hz [63]. It is often associated with
head titubation (a kind of head tremor with small amplitude and not synchro-
nized with the nystagmus), trunk and limb ataxia, or visual impairment. The
amplitude is small and can often be only seen with an ophthalmoscope.
Etiology
Acquired pendular nystagmus occurs with several myelin disorders (e.g. mul-
tiple sclerosis, toluene abuse, Pelizaeus-Merzbacher disease). It is also a component
of the syndrome of oculopalatal tremor (myoclonus) and is observed in Whipple’s
disease [6, 62]. Common etiologies in adults are multiple sclerosis and brainstem
stroke [62, 64]. On the basis of observations that the nystagmus is often dissociated
and that eye movements other than optokinetic nystagmus and voluntary saccades
are also disturbed, it has been suggested that a lesion in the brainstem near the ocu-
lomotor nuclei is the cause [61]. Alternative candidates such as an inhibition of the
inferior olive due to lesions of the ‘Mollaret triangle’ or an instability of the gaze-
holding network (neural integrator) have also been proposed [64].

Treatment
The first reported treatment option was anticholinergic treatment with tri-
hexyphenidyl (20–40 mg p.o. daily) [65, 66]; however, Leigh et al. [67] reported
in a double-blind study that only 1 of 6 patients improved during this oral treat-
ment. Starck et al. [68] reported that nystagmus improved with memantine, a glu-
tamate antagonist, in all 9 tested patients (15–60 mg p.o. daily). Gabapentin, an
alpha-2-delta calcium channel antagonist, substantially improved the nystagmus
(and visual acuity) in 10 of 15 patients (3 ϫ 300–400 mg daily) [53]. Gabapentin
Treatment of Oculomotor Disorders 185
was superior to vigabatrin in a small series of patients [69]; others have also
reported an improvement due to gabapentin [70, 71]. Cannabis, which acts as a
retrograde presynaptic inhibitory transmitter and in this way is similar to
gabapentin, which also acts presynaptically, was recently reported to be equally
effective [72, 73]. A bilateral retrobulbar botulinum toxin injection was success-
fully used in some patients to induce a complete external ophthalmoplegia,
thereby diminishing the acquired pendular nystagmus [74, 75]; however, it proved
unsatisfactory in other patients [76].
Opsoclonus and Ocular Flutter
Clinical Aspects
Opsoclonus consists of repetitive bursts of conjugate saccadic oscillations,
which have horizontal, vertical, and torsional components. During each burst of
these high-frequency oscillations, the movement is continuous, without any
intersaccadic interval. These oscillations are often triggered by eye closure, con-
vergence, pursuit, and saccades; amplitudes range up to 2–15Њ [6]. The same pat-
tern is restricted in ocular flutter to the horizontal plane. The ocular symptoms
are often accompanied by cerebellar signs, such as gait and limb myoclonus (the
‘dancing feet, dancing eyes syndrome’). Most of the patients complain of very
disturbing oscillopsias during these saccadic oscillations [6, 77].
Etiology
A functional disturbance of active saccadic suppression by the pontine

omnipause neurons is the most probable pathophysiological mechanism. Since
histological abnormalities of these neurons have not been shown [78], a func-
tional lesion of the glutaminergic cerebellar projections from the fastigial
nuclei to the omnipause cells is the likely cause of their disinhibition.
Opsoclonus can be observed in benign cerebellar encephalitis (postviral, e.g.
Coxsackie B37; postvaccinal) or as a paraneoplastic symptom (infants, neuro-
blastoma; adults, carcinoma of the lung, breast, ovary, or uterus) [77].
Treatment
In addition to therapy for any underlying process such as tumor or
encephalitis, treatment with immunoglobulins or prednisolone may occasion-
ally be effective [79]. Four of 5 patients with square-wave oscillations, probably
a related fixation disturbance, showed an improvement on therapy with valproic
acid [80]. In single cases, an improvement has been observed during treatment
with propranolol (40–80 mg p.o. three times daily), nitrazepam (15–30mg p.o.
daily), and clonazepam (0.5–2.0 mg p.o. three times daily) [1, 77, 81].
Straube 186
Infranuclear Oculomotor Disorders
Superior Oblique Myokymia
Clinical Aspects
Superior oblique myokymia is characterized by paroxysmal monocular
high-frequency oscillations [6, 82, 83]. These oscillations are mainly torsional
in the primary gaze position and in abduction, but when the eyes are in adduc-
tion the oscillations have a vertical component [83]. The patients usually com-
plain of oscillopsia during these paroxysmal attacks.
Etiology
The pathophysiology of this condition is not totally clear, but vascular com-
pression of the 4th nerve [84, 85] may be responsible. The same mechanism is
suspected in vestibular paroxysmia. Alternative causes may include spontaneous
discharges in the 4th nerve nucleus or of the superior oblique muscle.
Treatment

Like trigeminal neuralgia (another putative neurovascular compression
disorder), superior oblique myokymia frequently remits spontaneously for peri-
ods of a few months to years. If it does not, a number of drugs have been
reported to be beneficial, including the anticonvulsants carbamazepine [82] and
gabapentin [86, 87]. In chronic cases that did not improve with anticonvulsants,
tenotomy of the superior oblique muscle has been performed, but usually it
necessitates inferior oblique surgery as well. Surgical decompression of the 4th
nerve has also been reported to help, but this treatment should be reserved for
the most vexing cases, as it may result in superior oblique palsy [88, 89] and
bears a risk of suboccipital craniotomy. Treatment should always be started with
one of the anticonvulsants.
Benign Paroxysmal Positional Vertigo
Clinical Aspects
One of the most frequent types of vertigo as well as oculomotor syndromes
is benign paroxysmal positional vertigo (BPPV) [11, 90]. BPPV occurs when
particles in one of the semicircular canals move freely when the head is turned
in the plane of the affected canal. Theoretically, all three canals can be affected,
but in practice the posterior vertical canal (p-BPPV) is affected most often [11,
90]. The positioning of the head towards the affected canal plane induces a rota-
tory nystagmus that beats to the undermost ear with a crescendo-decrescendo
Treatment of Oculomotor Disorders 187
time course. Horizontal BPPV (h-BPPV) is characterized by a nonfatiguable
bilateral horizontal beating nystagmus that occurs while the patient lies supine
and turns his/her head to the side of the affected canal [11, 91].
h-BPPV was reported to occur in about 12% of a series of 300 patients [91].
BPPV of the anterior vertical canal probably occurs much more seldom
than that of the posterior or horizontal canal. The associated nystagmus charac-
teristically has less of a torsional component than in p-BPPV [92].
Etiology
BPPV is caused by the displacement of calcium-rich particles from the

utricle into one of the canals [11, 90]. These particles change the function of the
canal, which normally only detects angular acceleration. If the head is posi-
tioned in the plane of the affected canal, the particles move within the semicir-
cular canal according to the gravitational force, causing an endolymph flow that
is followed by a displacement of the cupula of the canal. Predisposing condi-
tions are older age, head trauma, labyrinthitis, Menière’s disease, migraine, or
longer periods of immobilization.
A differential diagnosis of positional vertigo is migrainous vertigo; it may
mimic BPPV. Several groups recently reported an association of migraine and
vertigo. A study published this year classified 10 patients of 362 consecutive
patients who had positional vertigo as well as migrainous. Diagnostic factors
that distinguish the migrainous form from idiopathic positional vertigo are
short duration of the attacks, frequent recurrences, early manifestation in life,
other migrainous symptoms like photo-/phonophobia and headache during the
vertigo episodes, and atypical nystagmus [93]. Central positional vertigo due to
lesions of the vestibular cerebellum can mimic peripheral positional vertigo
sometimes, but normally the nystagmus is less pronounced and does not show
habituation [94].
Treatment
Treatment consists of so-called liberatory maneuvers. The rationale is to
redirect the particles out of the affected canal. There are two repositioning treat-
ments for p-BPPV: Epley’s and Semont’s maneuvers. Both require active move-
ments by the patients; this may be difficult for older patients. Another possibly
effective therapeutic procedure is the so-called prolonged forced position. It
requires the patient to maintain a position in which the affected ear remains
uppermost for several hours. This is thought to allow the floating particles to
slip out of the canal into labyrinthine recesses, where they no longer have any
impact on the cupula [95].
The question as to which liberatory maneuver is superior for benign
positional paroxysmal vertigo of the posterior canal was recently addressed in

Straube 188
several published studies and meta-analyses. Updating the Cochrane database,
Hilton and Pinder [96] reanalyzed randomized trials of adult patients with
p-BPPV to determine the extent of improvement of the vertigo after the Epley
maneuver, no treatment, or other repositioning maneuvers. Using only 3 of 15
trials for the final analysis, the authors concluded that there is some evidence
that the Epley maneuver is a safe and effective treatment option, but the avail-
able data were insufficient to compare the Epley maneuver with other reposi-
tioning maneuvers [96]. Another study on the best liberatory maneuver
compared the self-applied Semont maneuver with the self-applied Epley proce-
dure. Patients who performed the Epley maneuver had a significantly higher
success rate than the group using the Semont maneuver (95 vs. 58%). Thus, the
Epley procedure, as a home-based self-applied liberatory maneuver, seems to
be the better choice [97].
For h-BPPV, the maneuver involves a 360Њ horizontal head and body (‘bar-
becue’) rotation (e.g. rotation about the longitudinal body axis in a supine
position) [91].
A small group of patients who were followed for 60 months had a recur-
rence rate of 26% for posterior canal and 50% for horizontal canal BPPV [98].
Patients with trauma or labyrinthitis had lower initial success rates of the repo-
sitioning maneuver, whereas patients with endolymphatic hydrops were pre-
dicted to have higher recurrence rates [99, 100].
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A. Straube
Department of Neurology, Klinikum Grosshadern
Marchioninistrasse 15

DE–81377 Munich (Germany)
Tel. ϩ49 89 7095 3900, Fax ϩ49 89 7095 3677, E-Mail
193
Alcohol, seesaw nystagmus management
183
4-Aminopyridine
downbeat nystagmus management 181,
182
upbeat nystagmus management 182
Baclofen
periodic alternating nystagmus
management 184
upbeat nystagmus management 182
Basal ganglia, saccadic eye movement
control 62
Benign paroxysmal positional vertigo
(BPPV)
clinical features 186, 187
etiology 187
treatment 187, 188
Betahistine, Ménière’s disease management
179
Binocular adaptation
Listing’s plane 98
phoria adaptation 97, 98
saccade adaptation 98, 99
Blinking
clinical applications 125
eye movements and effects
blink-associated 114

blink effects 115
disconjugate eye movements 101, 117,
118
saccade-vergence interactions 118,
119
saccadic eye movement 115–117
smooth pursuit eye movements 119, 120
frequency disorders 120, 122
visual consequences 114
Botulinum toxin, acquired pendular
nystagmus management 185
Brainstem saccadic generator
excitatory burst neurons 55, 56
inhibitory burst neurons 56, 57
midbrain reticular formation 55
omnipause neurons 57
paramedian pontine reticular formation 55
tonic neurons 57–60
Caloric testing, vestibulo-ocular reflex
function 45, 46
Carbamazepine
superior oblique myokymia management
186
vestibular paroxysmia management 180
Central caudal nucleus (CCN), eyelid
control 111
Cerebellum
central processing of vestibular signals
39, 40
saccadic eye movement control 66–70

smooth pursuit eye movement role
80–82
Click-evoked myogenic potential, vestibular
function testing 48, 49
Clonazepam
downbeat nystagmus management 181,
182
opsoclonus management 185
seesaw nystagmus management 183
Subject Index
Subject Index 194
Craniosynostosis, strabismus 149
Cyclovergence 92
Dimenhydrimnate
Ménière’s disease management 179
vestibular neuritis management 178
Disconjugate eye movements
binocular adaptation
Listing’s plane 98
phoria adaptation 97, 98
saccade adaptation 98, 99
blinking 101, 117, 118
cyclovergence 92
Hering’s law and asymmetric vergence
movements 95, 96
horizontal vergence movements 91
Listing’s law during convergence 93–95
overview 90, 91
pathology 101, 102
saccade-associated vergence movements

96, 97
vertical vergence movements 92
vestibular stimulation 99–101
Double Purkinje image (DPI) eye tracker,
historical perspective 17
Downbeat nystagmus, see Nystagmus
Electro-oculogram (EOG)
comparison with other eye movement
recording techniques 31, 32
historical perspective 17
infrared reflection device comparison 20,
21
noise and resolution 20
principles 19, 20
single-eye measurement 21
vestibulo-ocular reflex function 45
Epley maneuver, benign paroxysmal
positional vertigo management 187, 188
Extraocular muscles, see Eye muscles
Eye-head movement, ocular motor system
modeling 170
Eyelid, see also Blinking
disorders
blink frequency 120–122
eyelid-eye coordination 124
tonic eyelid position 122, 123
neural control
levator palpebrae muscle innervation
111
lid-eye coordination 111–113

supranuclear disorders 110
Eye movement recordings
comparison of techniques 31, 32
double Purkinje image eye tracker 17
electro-oculogram
infrared reflection device comparison
20, 21
noise and resolution 20
overview 17
principles 19, 20
single-eye measurement 21
historical perspective 16–18
infrared reflection device
calibration 23, 24
overview 17
principles 22, 23
magnetic search coil
accuracy 26
disadvantages 26, 27
error sources 25, 26
noise 26
overview 18
principles 24, 25
video-oculography
calibration 28, 29
noise 30
ocular torsion measurements 30
overview 18, 19
principles 27, 28
Eye muscles

fibers 2–4, 8–11
innervation
central pathways 7
motoneurons 7, 8
premotor circuits 8–10
Listing’s law 139, 140, 143–146, 152
magnetic resonance imaging 134, 138,
139, 142, 145, 149
morphology 2, 133, 134
ocular counterrolling 145
proprioception 10, 11
pulleys
animal studies 142, 143
Subject Index 195
functional anatomy 137–139
kinematics 139–142, 152
neural control 146–148
structure 134–137
surgery
pulley heterotopy 150
pulley hindrance 151
pulley instability 150, 151
sensory receptors
Golgi tendon organs 6
palisade endings 5, 6
spindles 4, 5
skeletal muscle comparison 2
strabismus 148–150
types 133
Eye plant, ocular motor system model 159,

160
Frontal eye field (FEF)
eyelid control 112, 113
smooth pursuit eye movement role 80, 169
Gabapentin
acquired pendular nystagmus
management 184, 185
downbeat nystagmus management 181
seesaw nystagmus management 183
superior oblique myokymia management
186
Golgi tendon organs, eye muscles 6
Hering’s law, asymmetric vergence
movements 95, 96
Infrared reflection device (IRD)
calibration 23, 24
comparison with other eye movement
recording techniques 31, 32
historical perspective 17
principles 22, 23
Lamotrigine, vestibular paroxysmia
management 180
Levator palpebrae muscle, see Eyelid
Listing’s law
Convergence 93–95
mechanical basis 143–146
ocular motor system modeling 162
pulley kinematics 139, 140, 152
violation during vestibulo-ocular reflex
143, 144

Magnetic resonance imaging (MRI), eye
muscles 134, 138, 139, 142, 145, 149
Magnetic search coil
accuracy 26
comparison with other eye movement
recording techniques 31, 32
disadvantages 26, 27
error sources 25, 26
historical perspective 18
noise 26
principles 24, 25
Medulla, smooth pursuit eye movement
pathology 84
Ménière’s disease
clinical features 178
etiology 178, 179
treatment 179
Methylprednisolone, vestibular neuritis
management 178
Neural velocity-to-position integrator,
ocular motor system model 160–162
Nitrazepam, opsoclonus management
185
Nucleus reticularis tegmenti pontis (NRTP),
saccadic eye movement control 62, 64,
65, 66
Nystagmus, see also Optokinetic nystagmus
acquired pendular nystagmus
clinical features 184
etiology 184

treatment 184, 185
bedside clinical evaluation
dynamic disturbances 42, 43
positional testing 43, 44
static imbalance 41, 42
Valsalva- and hyperventilation-induced
nystagmus 44, 45
downbeat nystagmus
clinical features 180
etiology 181
treatment 181, 182
Subject Index 196
pathology 177
periodic alternating nystagmus
clinical features 183
etiology 183
treatment 184
seesaw nystagmus
clinical features 182, 183
etiology 183
treatment 183
upbeat nystagmus
clinical features 182
etiology 182
treatment 182
vestibulo-ocular reflex pathology
40, 41
Ocular flutter
clinical features 185
etiology 185

treatment 185
Ocular following response (OFR)
anatomy and physiology 78, 81
features 78
Ocular motor nerve, eye muscle sensory
afferents 7
Oculomotor nucleus, motoneurons 7
Opsoclonus
clinical features 185
etiology 185
treatment 185
Optokinetic nystagmus (OKN)
anatomy and physiology 81
components 77, 78
definition 77
pathology 84
velocities 78
vertical versus horizontal 78
Otoliths, function testing 48
Palisade endings, eye muscles 5, 6
Paramedian pontine reticular formation, see
Brainstem saccadic generator
Parkinson’s disease (PD), eyelid disorders
121, 123, 124
Periodic alternating nystagmus, see
Nystagmus
Phenytoin, vestibular paroxysmia
management 180
Pontine nuclei, saccadic eye movement
control 62, 64, 65

Propranolol, opsoclonus management
185
Pulleys, see Eye muscles
Robinson, D.A., ocular motor system
models 158–160
Rotational testing, vestibulo-ocular reflex
function 45, 46
Saccadic eye movement
antisaccades 53
binocular saccade adaptation 98
blinking
effects 115–117
vergence interactions 118, 119
features 53
latency 53
memory-guided saccades 53
neurocircuitry
basal ganglia 62
brainstem saccadic generator
excitatory burst neurons 55, 56
inhibitory burst neurons 56, 57
midbrain reticular formation 55
omnipause neurons 57
paramedian pontine reticular
formation 55
tonic neurons 57–60
cerebellum 66–70
monkey studies 146, 147
nucleus reticularis tegmenti ponti 62,
64–66

overview 53–55
pontine nuclei 62, 64, 65
superior colliculus 60–62
ocular motor system modeling
162, 163
orienting cascade 53
resting saccades 52
spontaneous saccades 53
target-directed saccades 53
vergence movements 96, 97
Search coil, see Magnetic search coil
Nystagmus (continued)
Subject Index 197
Seesaw nystagmus, see Nystagmus
Semicircular canal (SCC)
vestibular testing 47, 48
vestibulo-ocular reflex 36
Smooth pursuit eye movements (SPEM)
anatomy and physiology 79–81
blinking effects 119, 120
features 76
latency 76
ocular motor system modeling
168, 169
pathology
cerebellum 82, 84
cortex 82
medulla 84
pontine structures 82
testing 77

Spindles, eye muscles 4, 5
Strabismus
craniosynostosis 149
muscle weakness 148
superior oblique palsy 148, 149
Subjective visual vertical (SVV), otolith
function testing 48
Superior canal dehiscence syndrome
clinical features 179
etiology 179
treatment 179
Superior colliculus
eyelid control 112, 113
saccadic eye movement control 60–62
Superior oblique myokymia
clinical features 186
etiology 186
treatment 186
Supplementary eye field (SEF), smooth
pursuit eye movement role 80
Trigeminal nerve, eye muscle sensory
afferents 7
Trihexyphenidyl, acquired pendular
nystagmus management 184
Upbeat nystagmus, see Nystagmus
Valacyclovir, vestibular neuritis
management 178
Valproic acid, opsoclonus management 185
Vergence eye movements, see Disconjugate
eye movements

Vertigo
benign paroxysmal positional vertigo, see
Benign paroxysmal positional
vertigo
vestibulo-ocular reflex pathology
40, 41
Vestibular neuritis
clinical features 177
etiology 177, 178
treatment 178
Vestibular nuclear complex, central
processing of vestibular signals 39, 40
Vestibular paroxysmia
clinical features 180
etiology 180
treatment 180
Vestibulo-ocular reflex (VOR)
angular reflex 35, 36, 183
bedside clinical evaluation
dynamic disturbances 42, 43
positional testing 43, 44
static imbalance 41, 42
Valsalva- and hyperventilation-induced
nystagmus 44, 45
click-evoked myogenic potential testing
48, 49
components
central processing of vestibular signals
37, 39, 40
motor output 40

overview 36
peripheral sensory apparatus 36, 37
function 35, 77
laboratory testing
caloric testing 45, 46
electro-oculography 45
rotational testing 45, 46
linear reflex 36
ocular motor system modeling
adaptation 164, 165
angular reflex three-dimensional
model 165, 166
overview 163–165
otolith function testing 48
Subject Index 198
pathology 40, 41, 177
semicircular canal function testing 47,
48
Video-oculography (VOG)
calibration 28, 29
comparison with other eye movement
recording techniques 31, 32
historical perspective 18, 19
noise 30
ocular torsion measurements 30
principles 27, 28
Vestibulo-ocular reflex (continued)