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Eye Movement Abnormalities

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Eye movement

abnormalities
Introduction
• The eyes move in the service of vision, bringing
objects of regard into the field of vision and following
them if they move.

• Eye movements are divided into


– Ductions - movements of one eye
– Versions - binocular conjugate movements
– Vergences-binocular dysconjugate movements
Eye movement control systems
• Normally function harmoniously to secure and
maintain vision
• They include
– Saccade
– Pursuit
– Vergence
– Fixation
– Optokinetic and vestibulo-ocular reflex
Disordered Ocular Motility
Abnormal eye movements

central (internuclear and peripheral


supranuclear). (infranuclear and nuclear)

cranial nerve nuclei, fascicles,


supranuclear internuclear or peripheral trunks or
extraocular muscles

optomotor pathways connecting and coordinating


control centers the activity of the ocular motor nuclei,
primarily the MLF.
Eg: PSP, Neimann pick
disease,
Peripheral disorders of ocular motility

Orbital Disease Muscle Disease:


– Masses within the orbit Due to weakness or
– Trauma to the orbit restriction of movement of
– Eye muscles injury muscle
•Thyroid eye disease
during ophthalmic deposition of
surgery mucopolysaccharide and
– Orbital pseudo-tumor lymphocytic infiltration in eye
muscles
– Lymphoma •Restrictive myopathy
rhabdomyosarcoma. confused with weakness of the
antagonist
Peripheral disorders of ocular motility

• Forced ductions - pushing or pulling on the


anesthetized globe in order to passively move it
through the impaired range.
• Restrictive myopathy or an entrapped muscle :
– Mechanically limited eye excursions
– Exist for passive as well as active movements.
• An eye affected by ocular muscle weakness, MG,
or an ocular motor nerve palsy moves freely and
easily through a full range
Peripheral disorders of ocular motility
Peripheral disorders of ocular motility

• CPEO
– progressive ptosis and
– symmetric eye muscle
weakness,
• marked ptosis and immobile.
– not typically have diplopia
– Reflex eye movements and
Bell’s phenomenon is absent.
• Kearns-Sayre syndrome,
MELAS, MERRF, MNGIE
Peripheral disorders of ocular motility

• NMJ disorders like MG


– With ptosis or diplopia, or both. then later
develop generalized MG
– Hallmark: fatigable and fluctuating weakness
• Ptosis worse with prolonged upgaze.
• Develop diplopia with sustained eccentric gaze
• Fluctuating ptosis and diplopia, and worsening
symptoms toward the end of the day
• usually asymmetric and may vary from minute to
minute
Peripheral disorders of ocular motility:
Third cranial nerve
• Severe ptosis of the upper lid,
• The eye rests in a down and out
position
– due to preservation of the lateral rectus and
superior oblique functions.
• Impairment of medial,upward,
and downward gaze; and loss of
accommodation,with a dilated
pupil that does not react to light,
directly or consensually, or to near
• Images are often oblique because
of the combination of weak
muscles.
Peripheral disorders of ocular motility:
Isolated Third cranial nerve palsy
• Posterior communicating artery or basilar artery aneurysm.
– typically acute, painful, and involve the pupil

• Ischemic third nerve palsies:


– microvasculopathy related to diabetes and hypertension, but
they can be a feature of vasculitis, particularly giant cell arteritis.
– Patients with ischemic palsies are typically older than those with
aneurysms.
– Microvascular third nerve palsies are of sudden onset, painful,
may spare the pupil, begin to resolve by about 2 months, and do
not result in aberrant regeneration.
Peripheral disorders of ocular motility:
Fourth cranial nerve
• c/o blurry vision more than diplopia when
looking down—as when reading a book or
descending stairs.
• The diplopia is vertical or diagonal and
maximal in downgaze
• O/E: extorsion and impairment of depression
of the adducted eye
Peripheral disorders of ocular motility:
Sixth cranial nerve
• complete CN VI palsy,
• Esotropia in primary
position
• Eye cannot be abducted
and rests in a position
of adduction
Central disorders of ocular motility:
Internuclear ophthalmoplegia
• Lesions of MLF –INO
• C/L MR receives no signal to
contract when PPRF and 6th
CN nucleus acts to initiate
lateral gaze
• Right INO- Right MR plasy
• INO is commonly associated
with gaze evoked vertical
nystagmus
• Anterior INO – impaired
convergence
• Posterior INO – preserved
convergence
Central disorders of ocular motility:
Internuclear ophthalmoplegia: causes
• MS- Bilateral, young
• Stroke Unilateral, older
• Pseudo INO – INO mimics
– MG
– Wernick’s encephalopathy
– TED

One and half syndrome: PPRF + MLF (crossing from the c/l side)
Gaze palsy + INO
Right Pons lesion : right gaze palsy + right INO
(only left abduction is preserved)
Eye movement control systems
• Frontal eye field moves the eyes to contralateral
conjugate horizontal gaze
– Eyes looks straight – balance from b/l FEFs
– Frontal lobe seizures activity
• pushes the eye to opposite side
• Jerky eye movements/subtle twitches elsewhere
– Frontal lobe destructive lesion
• gaze away from the hemiparesis ,Large amplitude, pronounced,
clinically obvious, resolve in few days
• Pontine destructive lesion
– gaze towards the hemiparesis, Subtle, easily missed, persists longer
Saccades
• 1. Saccade initiation:
– Delayed initiation of saccades (prolonged latency) : oculomotor apraxia,
neurodegenerative disorders such as Huntington’s disease.
• often employ head thrusts or eye blinks to generate saccades, (sole clinical sign indicating a
mild defect in saccadic initiation).

• 2. Range of motion and conjugacy of saccades:


– Is there limitation in the range of motion?
– Do they move together at the same rate?
– If there is limited range of motion, the next step is to see if such limitations are
present with smooth pursuit and vestibular ocular reflexes (Doll’s eye maneuvers).
– supranuclear brainstem saccadic gaze palsy with impaired range of motion (eg:
PSP): prominent deficit with saccade testing that is improved with smooth pursuit
testing and completely overcome with vestibular ocular reflexes.
Saccades
3. Speed of saccades:
– Do the eyes move slowly during the trajectory from the initial position to the
target position?
– clinical pearl: one should not be able to follow with one’s own eye the full
trajectory of a voluntary saccade, due to the very fast speed of normal
saccades.
– examine vertical and horizontal saccades independently, as different
disorders selectively affect horizontal vs. vertical saccades.

4. Accuracy of saccades:
– Do the eyes move accurately to the new target?
– Are saccades hypermetric or hypometric?
– Is there correction of the saccade to target, and is this correction accurate?
Saccades
5. Saccadic intrusions or oscillations:
• occur when patients are fixating in the eye primary position, or they may
be superimposed during smooth pursuit.
• The main distinguishing features are their size, whether they move away
from and back to midline or oscillate about the midline, their trajectory,
and whether there is an intersaccadic interval between movements.
– Square wave jerks: small saccade away from and back to midline with an intersaccadic
interval b/w movements. When square wave jerks occur nearly continuously, they are
called square wave oscillations.
– Macrosaccadic oscillations: back-to-back saccades with an intersaccadic interval b/w
movements that oscillate in a crescendo-decrescendo pattern about the midline.
– Ocular flutter: back-to-back saccades without an intersaccadic interval that oscillate
about the midline in the horizontal direction only.
– Opsoclonus: similar to ocular flutter but occurs in all planes (horizontal, vertical, torsional).
Ocular motor abn in movement disorders
Ocular motor abn in movement disorders
Nystagmus
• Involuntary biphasic rhythmic ocular oscillation
• Initiated by a slow eye movement that drives the eye
off target, followed by
– Fast movement that is corrective (jerk nystagmus) or
– Another slow eye movement in the opposite direction
(pendular nystagmus)
• Nystagmus due to distubance of
1. Visual fixation
2. Occular movements -
3. vestibular diseases

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Classification of Nystagmus
• Based on etiology • Based on etiology
 Congenital Physiological
 Acquired Pathological

• Based on the type • Based on the synchronicity


 Pendular nystagmus
Conjugate nystagmus
 Jerk nystagmus
Dysconjugate nystagmus

• Based on the direction


 Horizontal
 Vertical
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Acquired and Congenital nystagmus

Acquired Congenital
nystagmus : nystagmus :
• Purely sinusoidal, • Variable in form,
• Frequently different • similar in both
in both eyes, eyes,
• Omnidirectional • usually horizontal
• Can present as and uniplanar
oscillopsia • Oscillopsia: mild
and less common.

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Physiological and pathological
nystagmus

Physiological nystagmus: Pathological nystagmus :


• Present at extremes of • Present at gazes within 30
gazes, degrees from primary
• ill sustained, position,
• symmetric. • sustained and
• usually asymmetric.

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Gaze evoked Nystagmus
• Inability to hold eccentric gaze
• Eyes drift back toward midline due to the elastic mechanical
properties of the eye muscles within the orbit (corrective
saccade)
• Slow phase is always toward primary position
• Causes:
– Toxic etiologies - ethanol ,medications -anticonvulsants, sedatives, and
hypnotics
– Structural - ipsilateral lesion of the brainstem or cerebellum, typically
structural in origin
– Peripheral or end organ disease myopathy or neuromuscular junction
dysfunction

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Vestibular Nystagmus
• Common nystagmus pattern
• Spontaneous , evident in primary position or in gaze
toward the fast phase
• Horizontal/Vertical or torsional pattern
• Slow phase towards the diseased side and fast phase in the
opposite side
• Suppressed by visual fixation (Frensel glasses)
• Fatiguability, adaptability
• Oscillopsia
• Always in one direction
• Latency
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Central vs peripheral vestibular nystagmus

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Seesaw nystagmus

• Half cycles in which one eye elevates and


intorts while the other depresses and extorts
• The cause of seesaw nystagmus varies
depending on the waveform of the nystagmus.
• Pendular waveform seesaw nystagmus
• Lesions the optic chiasm (eg, parasellar
tumors, chiasmal trauma
Localization of nystagmus

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Other abnormal ocular movements

Pons
Cerebellar outflow tracts

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