This document provides an overview of eye movements and disorders of eye movements. It begins with an agenda that covers topics like cranial nerves controlling eye movements, extraocular muscles, examining ocular motility, ophthalmoplegia, diplopia, gaze pathways, and types of nystagmus and non-nystagmus eye oscillations. It then defines different types of eye movements including fast and slow movements. The document discusses various physiological and pathological causes of nystagmus and other eye oscillations. It provides details on infantile, acquired, vestibular, downbeat, upbeat and other types of nystagmus. The document concludes with examining techniques for gaze, saccades, pursuit, convergence and other
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Amr Hassan's Guide to Eye Movements and Nystagmus
1. Amr Hassan, MD, FEBN
Professor of Neurology - Cairo University
Nystagmus
2. AGENDA
⢠3rd,4th, 6th nerves
⢠Extraocular muscles
⢠How to examine for ocular motility
⢠Ophthalmoplegia
⢠Diplopia and related disorders
⢠Gaze pathway
⢠How to examine for gaze
⢠Gaze palsy
⢠Types of eye movements
⢠How to examine for EM
⢠Nystagmus and non nystagmus ocular oscillation
3. AGENDA
⢠3rd,4th, 6th nerves
⢠Extraocular muscles
⢠How to examine for ocular motility
⢠Ophthalmoplegia
⢠Diplopia and related disorders
⢠Gaze pathway
⢠How to examine for gaze
⢠Gaze palsy
⢠Types of eye movements
⢠How to examine for EM
⢠Nystagmus and non nystagmus ocular oscillation
4. Eye movements
Centres controlling the nuclei â Supranuclear
Pathways connecting the nuclei â Internuclear
Nerves supplying the EOM - Infranuclear
16. ⢠Nystagmus is a repetitive, involuntary, to-and-fro
oscillation of the eyes, which may be physiological or
pathological.
⢠Ocular movements that bring about fixation on an
object of interest are called foveating and those that
move the fovea away from the object are defoveating.
Nystagmus: Definition
17. ⢠In pathological nystagmus, each cycle of movement is
usually initiated by :
â an involuntary, defoveating drift of the eye away
from the object of interest
â followed by a returning refixation saccadic
movement.
Nystagmus: Definition
19. âThe plane of nystagmus may be horizontal, vertical,
torsional or non-specific.
âThe amplitude of nystagmus refers to how far the eyes
move (fine or coarse)
âThe frequency refers to how rapidly the eyes oscillate
(high, moderate or low).
Nystagmus: Metrics
21. âJerk nystagmus
⢠Saccadic with a slow defoveating âdriftâ movement
and a fast corrective refoveating saccadic movement.
⢠The direction of nystagmus is described in terms of
the direction of the fast component.
Nystagmus: Morphology
22. âPendular nystagmus
⢠Non-saccadic in that both the foveating and
defoveating movements are slow.
(i.e. the velocity of nystagmus is equal in both
directions).
Nystagmus: Morphology
29. End-point nystagmus
⢠Fine jerk nystagmus of moderate frequency found when
the eyes are in extreme positions of gaze.
⢠Fast phase is in the direction of gaze.
Physiological Nystagmus: EPN
30. ⢠OKN is a jerk nystagmus induced by moving repetitive
targets across the visual field.
⢠The slow phase is a pursuit movement in which the eyes
follow the target; the fast phase is a saccadic movement
in the opposite direction as the eyes fixate on the next
target.
⢠OKN is useful for detecting malingerers who feign
blindness and for testing visual acuity in the very young.
Physiological Nystagmus: OKN
32. ⢠Turning the drum to the right elicits an
ipsilateral pursuit movement to the right and a
contralateral saccade to the left.
Physiological Nystagmus: OKN
33. ⢠Jerk nystagmus caused by altered input from
the vestibular nuclei to the horizontal gaze
centres
Physiological Nystagmus: VOR
35. ⢠When cold water is poured into both ears
simultaneously, a jerk nystagmus with the fast
phase upwards develops.
⢠Warm water in both ears elicits nystagmus
with the fast phase downwards
âŤŘŻŘ§ŮŮ⏠âŤŘŻŘ§ŮŮâŹ
Physiological Nystagmus: VOR
43. ⢠Presentation of this rare condition is between 3
and 18 months.
⢠Idiopathic which spontaneously resolves by age 3
years.
⢠Glioma of anterior visual pathway, empty sella
syndrome and porencephalic cyst.
Spasmas nutans
44. ⢠Unilateral or bilateral small-amplitude high-
frequency horizontal nystagmus associated with
head nodding.
⢠It is frequently asymmetrical with increased
amplitude in abduction.
⢠Vertical and torsional components may be
present.
Spasmas nutans
47. ⢠Latent nystagmus is associated with infantile
esotropia
⢠With both eyes open there is no nystagmus.
Horizontal nystagmus becomes apparent on
covering one eye or reducing the amount of light
reaching the eye.
⢠Fast phase is in the direction of the uncovered
fixating eye.
Latent nystagmus
48. ⢠Occasionally, an element of latency may be
superimposed on a manifest nystagmus so that
when one eye is covered the amplitude of
nystagmus increases.
Manifest-latent nystagmus
55. ⢠Vertical nystagmus with the fast phase beating downwards,
which is more easily elicited in lateral gaze and downgaze.
⢠Causes
⢠Lesions of the craniocervical junction at the foramen
magnum such as ArnoldâChiari malformation and
syringobulbia.
⢠Drugs such as lithium, phenytoin, carbamazepine and
barbiturates.
⢠Wernicke encephalopathy, demyelination and
hydrocephalus.
Downbeat nystagmus
57. ⢠Vertical nystagmus with the fast phase beating
upwards
⢠Causes include posterior fossa lesions, drugs
and Wernicke encephalopathy.
Upbeat Nystagmus
63. Periodic alternating nystagmus
⢠Conjugate horizontal jerk nystagmus that periodically reverses
its direction.
⢠Each cycle may be divided into active and quiescent phases as
follows:
â During the active phase, the amplitude, frequency and slow-
phase velocity of nystagmus first progressively increase then
decrease.
â This is followed by a short, quiet interlude, lasting 4â20 sec,
during which time the eyes are steady and show low-intensity,
often pendular movements.
â A similar sequence in the opposite direction occurs thereafter,
the whole cycle lasting between 1 and 3 minutes.
64. Periodic alternating nystagmus
Causes include
⢠Isolated congenital
⢠Cerebellar disease
⢠Ataxia telangiectasia (louisâbar syndrome)
⢠Drugs such as phenytoin.
66. ⢠It is the result of co-contraction of the
extraocular muscles, particularly the medial
recti followed by a slow divergent movement.
⢠Associated retraction of the globe into the
orbit.
⢠Causes include lesions of the pretectal area
such as pinealoma and vascular accidents
(Parinaud dorsal midbrain syndrome).
Convergence-retraction nystagmus
68. ⢠Coarse cerebellar horizontal jerk nystagmus in
one eye and fine high frequency vestibular
nystagmus in the other.
⢠CPA tumours such as acoustic neuroma. The
lesion is ipsilateral to the side with coarse
cerebellar nystagmus.
Bruns nystagmus
70. ⢠Voluntary nystagmus is not true nystagmus
but ocular flutter under voluntary control.
⢠It consists of a series of fast (saccadic) back-to-
back eye movements, without any interval or
slow phase.
⢠The oscillations usually are horizontal but may
be vertical, torsional, or (rarely) cycloidâa
phenomenon reported as âvolitional
opsoclonusâ or multiplanar flutter.
Voluntary nystagmus
71. ⢠The ability to induce flutter voluntarily tends
to be familial.
⢠Usually, persons with this ability must
converge their eyes to initiate the oscillation
but are unable to sustain it for longer than 30
seconds.
Voluntary nystagmus
77. ⢠Opsoclonus is a spontaneous, chaotic,
multivector saccadic eye movement disorder
in which the abnormal movements are
virtually always conjugate.
⢠Opsoclonus is aggravated by attempts at
fixation
⢠It may be associated with myoclonic jerks of
the limbs and cerebellar ataxia (dancing eyesâ
dancing feet syndrome).
Opsoclonus
78. ⢠Dysfunction of the pause cells in the pons due
to cerebellar or brainstem disease is the
cause.
⢠The most common causes are: toxic,
metabolic, and paraneoplastic disorders.
Opsoclonus
80. ⢠Ocular flutter consists of horizontal conjugate
back-to back saccades that occur
spontaneously in intermittent bursts.
⢠It is aggravated by attempts at fixation.
⢠Occasionally it is triggered by a change in
posture.
Ocular Flutter
81. ⢠It results from loss of pause cell inhibition of
the burst neurons in the paramedian pontine
reticular formation (PPRF), caused by injury
either to the PPRF or to the cerebellar
neurons that influence the pause cells, or
both.
⢠It occurs with brainstem or cerebellar disease
Ocular Flutter
83. ⢠Ocular bobbing is a rapid downward
movement of both eyes followed by a slow
drift back to primary position.
⢠The oscillation recurs between 2 and 15 times
per minute
⢠It is found in patients (usually comatose) with
severe central pontine destruction and
horizontal gaze palsies
Ocular Bobbing
85. ⢠Square-wave jerks (SWJs) are spontaneous,
small amplitude, paired saccades with an
intersaccadic latency of 150 to 200 msec that
briefly interrupt fixation.
⢠They may occur physiologically in normal
subjects (particularly in darkness) without
fixation. They are more common in the elderly.
⢠SWJs are prominent in PSP, multiple system
atrophy (MSA), and cerebellar disease.
Square-Wave Jerks
86. AGENDA
⢠3rd,4th, 6th nerves
⢠Extraocular muscles
⢠How to examine for ocular motility
⢠Ophthalmoplegia
⢠Diplopia and related disorders
⢠Gaze pathway
⢠How to examine for gaze
⢠Gaze palsy
⢠Types of eye movements
⢠How to examine for EM
⢠Nystagmus and non nystagmus ocular oscillation
87.
88. Eye movements
Centres controlling the nuclei â Supranuclear
Pathways connecting the nuclei â Internuclear
Nerves supplying the EOM - Infranuclear
89. Eye movements
Centres controlling the nuclei â Supranuclear
Pathways connecting the nuclei â Internuclear
Nerves supplying the EOM - Infranuclear
101. ⢠Turning the drum to the right elicits an
ipsilateral pursuit movement to the right and a
contralateral saccade to the left.
Physiological Nystagmus: OKN
105. (3) Primary congenital nystagmus:
â Inheritance is XLR or AD, and rarely AR.
â Presentation is about 2â3 months after birth and persists throughout life.
Adults with congenital forms of nystagmus do not notice oscillopsia
â Signs
⢠In the primary position there is low-amplitude pendular nystagmus that converts
to jerk nystagmus on side gaze.
⢠In upgaze and downgaze the nystagmus remains in the horizontal plane.
⢠The nystagmus may be dampened by convergence and is not present during
sleep.
⢠There is usually a null point (a position of gaze) in which nystagmus is minimal.
⢠In order to move the eyes into the null point, an abnormal head posture may be
adopted.
Types of nystagmus
106. (3) Ocular Microflutter
â Ocular microflutter, previously called microsaccadic ocular
flutter (a redundant term), is a rare symptomatic ocular
oscillation requiring magnification for detection
â It may be a form of opsoclonus but in some patients is a
variant of voluntary nystagmus.
â Patients complain of episodes of âshimmeringâ vision. It is
reported with cerebellar degeneration and MS.
â When it is persistent, patients should be evaluated for occult
neoplasms.
â Microflutter may respond to propranolol or verapamil.
Non Nystagmus ocular oscillation
107. (5) Ocular Dysmetria
âOcular dysmetria occurs with refixation saccades that
overshoot the target and often oscillate with an
intersaccadic latency of approximately 200 milliseconds
before coming to rest
âIt results from dysfunction of dorsal vermis and fastigial
nuclei in the cerebellum.
Non Nystagmus ocular oscillation
108. (7) Ocular Myoclonus (Oculopalatal Tremor)
â Ocular myoclonus is a vertical pendular oscillation with a frequency of
approximately 160 Hz, usually associated with similar oscillations of the
soft palate (palatal tremor) and sometimes other muscles of branchial
origin.
â The palatal tremor, referred to as the oculopalatal syndrome, occurs after
brainstem infarction, particularly of the pons, involving the central
tegmental tract
â The association of a facial nerve palsy and the one-and-a-half syndrome
may predict the development of oculopalatal myoclonus, probably
because of the proximity of the central tegmental tract to the facial nerve.
â Also, oculopalatal myoclonus can occur spontaneously in association with
progressive ataxia, a fourth ventricular tumor, or hydrocephalus following
subarachnoid hemorrhage
Non Nystagmus ocular oscillation
109. (8) Superior Oblique Myokymia
â Superior oblique myokymia is a paroxysmal, rapid, small
amplitude, monocular torsional-vertical oscillation caused by
contraction of the superior oblique muscle, predominantly on
the right side.
â Patients may complain of monocular blurring, torsional or
vertical oscillopsia, torsional or vertical diplopia, or twitching
of the eye.
â It is caused by injury or compression to 4th nerve
Non Nystagmus ocular oscillation
110. (3) Wrong-Way Eyes:
⢠Conjugate eye deviation to the âwrongâ sideâthat is, away from the lesion
and toward the hemiplegia (contraversive gaze deviation)âmay occur with
supratentorial lesions, particularly thalamic hemorrhage and (rarely) large
perisylvian or lobar hemorrhage.
⢠The mechanism is unclear, but possibilities include the following:
1. 1. An irritative or seizure focus causing âcontraversive ocular deviationâ is
unlikely, because neither clinical nor electrical seizure activity has been
reported in these patients.
2. 2. Because eye movements are represented bilaterally in each frontal lobe, it
is conceivable that the center for ipsilateral gaze alone may be damaged,
resulting in contraversive ocular deviation.
3. 3. An irritative lesion of the intralaminar thalamic neurons, which discharge
for contralateral saccades, could theoretically cause contraversive ocular
deviation.
4. 4. Damage to the contralateral inhibitory center could also be responsible.
Selected disorders of horizontal gaze
111. (4) Ping-Pong Gaze:
âPing-pong gaze is a slow conjugate horizontal
rhythmic oscillation that cycles every 4 to 8
seconds.
âIt occurs in comatose patients as a result of
bilateral cerebral or upper brainstem lesions or
metabolic dysfunction
Selected disorders of horizontal gaze