Nystagmus

NYSTAGMUS

Nystagmus

Periodic rhythmic biphasic ocular oscillation with slow

followed by fast or slow phase

Slow eye movements are responsible for its genesis and

continuation

Nystagmus

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)

Mechanism of nystagmus

Aim of occular movements

to maintain foveal centration of an object of interest

Nystagmus due to distubance of

1. Visual fixation

2. Occular movements - Neural integrator

3. vestibulo-ocular reflex

Saccades

Pulse (a velocity command)

Overcoming the resistance of the orbital tissues and the

inertia of the globe, changes the position of the eye in the

orbit

Accomplished by burst neurons

Step (a position command)

Change in tonic contraction of the orbital muscles, which,

overcoming the elasticity of the orbital tissues, keeps the

eye in the new position

Accomplished by neural integrators

Horizontal saccades

Pulse

EBNs in the PPRF

↓

ipsilateral abducens nucleus

IBNs in rostral medulla

↓

contralateral abducens nucleus

Supra nuclear control

Horizontal saccades

Step

Neural Integrator

Nucleus propositus hypoglossi (NPH) and the adjacent

MVN.

↕

vestibulocerebellum, especially the flocculus and

paraflocculus

Vertical saccades

Pulse

riMLF in the prerubral field of the ventral

diencephalomesencephalic junction

upward and downward saccades and I/L torsional saccades

lateral portion concerned with upgaze, the medial portion with

downgaze

↓

B/L elevator muscles

I/L depressor muscles

Step

Neural Integrator

Interstitial Nucleus of Cajal

lies caudal to the riMLF

↓ via the posterior commissure

C/L oculomotor and trochlear subnuclei through the PC

Vertical saccades

Neural integrator depends on retinal inputs for its

calibration

Bilateral blindness may also cause an inability to hold the

gaze steady

Pursuit system

Vestibulo ocular reflex

vestibular system perceives head movement and makes

the eyeball move in the opposite direction

VOR

Connections from the anterior and posterior SCCs also

contact

Nucleus of Cajal

Important in eye head coordination in roll and in

vertical gaze holding

riMLF

Important in generating quick phases of vestibular

nystagmus in the vertical and torsional planes

Causes of Nystagmus

Result from dysfunction of

Vestibular endorgan

Vestibular nerve

Brainstem

Cerebellum

Cerebral centers for ocular pursuit

Causes of nystagmus

Symmetric, equal activity of the vestibular systems on

each side normally maintains the eyes in straight-ahead,

primary position. Vestibular imbalance causes the eyes to

deviate toward the less active side

In an alert patient, the frontal eye fields generate a saccade

to bring the eyes back toward primary position, creating

the fast phase of vestibular nystagmus.

Symptoms

Oscillopsia (absent in congenital nystagmus)

Decreased acuity

Nausea or vomiting

Vertigo

Coexisting neurologic deficits

Oscillopsia

Illusory perception of environmental movement

Four forms

1. associated with acquired jerk nystagmus (the

environment moves in the direction opposite the slow

phase of the nystagmus)

2. associated with pendular nystagmus (perceived as a to-

and-fro movement)

3. associated with SOM (jelly-like quivering)

4. associated with bilateral labyrinthine dysfunction

(continuous environmental jumping, e.g., With the

heartbeat)

Nystagmus

physiological pathological

Vestibular disorder

gaze-holding disorder

visual stabilization and pursuit mechanisms disorder

Jerk Vs Pendular

Jerk nystagmus Pendular nystagmus

Slow phase drift with rapid corrective saccade in opposite direction

Sinusoidal oscillation with slow phase in both directions and no corrective saccades

Direction is that of fast phase Horizontal or vertical

Direction of eye movement

Direction of nystagmus determined by direction of the fast

phase

According to plane of eye movement

Horizontal (right or left beating )or vertical (up or down

beating) or rotatory (clock wise or anti clockwise)

Types of nystagmus

Intensity of nystagmus: first, second, or third.

First degree nystagmus is present only wnen the eyes are turned

in direction of nystagmus. This is the weakest form ot

nystagmus.

second degree nystagmus is present when the eyes are in the

midline, increases when the eves are turned towards the side of

the slow phase.

In third degree nystagmus, nystagmus is present in all

three eye positions

Types of nystagmus

Amplitude of the nystagmus beat

large amplitude, small amplitude or medium amplitude

depending upon the

excursion of eyeball during the nystagmus.

Clinically irrelevant

Types of nystagmus

congenital or acquired

Acquired most often by abnormalities of vestibular input.

Congenital form with afferent visual pathway

abnormalities

Types of nystagmus

Acquired VS congenital

Feature Acquired Congenital

Form Pure sinusoidal variable

Different in two eyes Frequent Rare

Direction Omnidirectional –vertical, circular, elliptical

Horizontal, uniplanar,

Rarely vertical or

torsional

OKN reversal Never Frequent

Oscillopsia Frequent Mild

Clinical classification of nystagmus

Monocular

Binocular asymmetric or dissociated

(Involve mainly one eye)

Binocular symmetric

(involve both eyes symmetrically)

Monocular and Asymmetric Binocular Eye Oscillations

Monocular visual deprivation or loss

Monocular pendular nystagmus

Internuclear ophthalmoplegia and its mimickers

Spasmus nutans and its mimickers

Partial paresis of extraocular muscles

Restrictive syndromes of extraocular muscles

Superior Oblique Myokymia

Acquired Monocular Visual Loss

small, slow vertical pendular oscillations in the primary

position of gaze

may develop years after uniocular visual loss (Heimann-

Bielschowsky phenomenon) and may improve if vision is

corrected

Acquired monocular pendularnystagmus

Multiple sclerosis

Neurosyphilis

Brainstem infarct (thalamus and upper midbrain)

INO and in pseudo-INO syndromes

nystagmus in the abducting eye contralateral to a MLF

lesion

nystagmus beating in direction of abduction

occurs in midline lesions in the dorsal part of the brain

stem affecting MLF between the abducen nucleus on one

side of the brain with the oculomotor nucleus

tumors and vascular lesions may also cause

Epileptic Monocular Horizontal Nystagmus

Focal seizures originated in the occipital lobe contralateral

to the involved eye

forme fruste of the Sturge-Weber syndrome

Monocular DBN

Acute infarction of the medial thalamus and upper

midbrain

Pontocerebellar degeneration ( due to dysfunction of the

ipsilateral brachium conjunctivum)

Triad of

1. Head nodding

2. Nystagmus

3. Abnormal head

posture

Spasmus nutans

Spasmus nutans

Onset in the first year of life

Remits spontaneously within one month to several years

(up to 8 years) of onset

Sinusoidal nystagmus intermittent, asymmetric or

unilateral

High frequency and small amplitude with a shimmering

quality

Usually horizontal but may have a vertical or torsional

component

Must consider tumor of the optic nerve, chiasm, third

ventricle, or thalamus

Superior Oblique Myokymia

Paroxysmal, rapid, smallamplitude, monocular torsional-

vertical oscillation

Caused by contraction of the superior oblique muscle

predominantly on the right side

Difficult to detect with the unaided eye and is more easily

detected with a direct ophthalmoscope

Reported with adrenoleukodystrophy, lead poisoning,

cerebellar astrocytoma, dural arteriovenous fistula, and

microvascular Compression

Respond dramatically to carbamazepine or gabapentin

Bilateral symmetric eye oscillations

Disconjugate

(eyes moving in opposite directions)

Vertical disconjugate

See-saw nystagmus

Horizontal disconjugate

Convergence-retraction nystagmus(nystagmus retractorius)

Divergence nystagmus

Repetitive divergence

Oculomasticatory myorhythmia

Conjugate

(both eyes moving in same direction)

See-saw Nystagmus

cyclic movement : while one eye rises and intorts, the

other falls and extorts; the vertical and torsional

movements are then reversed, completing the cycle

See-saw Nystagmus

Usually pendular

See-saw jerk nystagmus → brainstem lesions affecting the

mesodiencephalon or lateral medulla

Represents sinusoidal oscillations involving central otolith

connections, especially the INC

May also be partly due to an unstable visuovestibular

interaction control system

See-saw Nystagmus

Congenital see-saw nystagmus

lack the torsional component or even present with an

opposite pattern (i.e., extorsion with eye elevation and

intorsion with eye depression)

Etiologies of See-Saw Nystagmus

Parasellar masses

Brainstem and thalamic stroke

Multiple sclerosis

Trauma

Arnold-Chiari malformation

Hydrocephalus

Syringobulbia

Paraneoplastic encephalitis (with testicular cancer and anti-Ta antibodies)

Whole brain irradiation and intrathecal methotrexate

Septo-optic dysplasia, retinitis pigmentosa, and cone degeneration

Congenital see-saw nystagmus

Convergence-retraction nystagmus

repetitive adducting saccades accompanied by retraction

of the eyes into the orbit, occur spontaneously or on

attempted upgaze

elicited by Sliding an optokinetic tape downward in front

of the patient's eyes

caused by Mesencephalic lesions affecting the pretectal

region

Convergence nystagmus

In dorsal midbrain stroke and arnold-chiari malformation

Whipple's disease - ~ 1 hz (pendular vergence oscillations)

Divergence nystagmus

Occur with hindbrain abnormalities (e.G., Chiari

malformation)

Associated with DBN

Repetitive divergence

Slow divergent movement followed by a rapid return to

the primary position at regular intervals

Seen in coma from hepatic encephalopathy or related to

seizures

Oculomasticatory Myorhythmia

Acquired pendular vergence oscillations associated with

concurrent contraction of the masticatory muscles

Smooth, rhythmic eye convergence, which cycles at a

frequency of approximately 1 hz, followed by divergence

back to the primary position

Synchronous with rhythmic elevation and depression of

the mandible

May also have paralysis of vertical gaze, progressive

somnolence, and intellectual deterioration

Recognized only in whipple's disease

Binocular Symmetric

Conjugate Eye Oscillations

pendular nystagmus

Jerk nystagmussaccadic

intrusions

Pendular conjugate eye oscillations

Congenital nystagmus

Acquired pendular nystagmus

Oculopalatal myoclonus

Spasmus nutans

Visual deprivation nystagmus


At birth or in early infancy, or may emerge or enhance in

teenage or adult life, often without apparent provocation

Seldom familial and most often idiopathic

Due to metabolic derangements and structural anomalies

of the brain, including abnormalities of the eye or anterior

visual pathways

Wholly pendular or have both pendular and jerk

components


Slow phase with a velocity that increases exponentially as

the eyes move in the direction of the slow phase

Visual fixation accentuates it and active eyelid closure or

convergence attenuates it

Nystagmus decreases in an eye position (null region) that

is specific for each patient

Quick phase of the elicited nystagmus generally follows

the direction of the tape (reversed optokinetic nystagmus)

Latent nystagmus

Generally congenital

Appears when one eye is covered

Usually associated with strabismus

Marker for congenital ocular motor disturbance and does

not indicate progressive structural brain disease

Acquired Pendular Nystagmus

may be wholly horizontal, wholly vertical, or have mixed

components (circular, elliptical, or windmill pendular

nystagmus)

most often caused by multiple sclerosis, stroke, or tumor

of the brainstem or other posterior fossa structures

In multiple sclerosis → sign of cerebellar nuclear

involvement or result from optic neuropathy

lesion in the dorsal pontine tegmentum, perhaps affecting

the central tegmental tract

Acquired Pendular Nystagmus

Other causes of acquired binocular pendular nystagmus

include Pelizaeus-Merzbacher disease, mitochondrial

cytopathy, Cockayne's syndrome, neonatal

adrenoleukodystrophy (a peroxisomal disorder), and

toluene addiction

Windmill Nystagmus

seen in Blind patients

repeated oscillations in the vertical plane alternating with

repeated oscillations in the horizontal plane

Palatal myoclonus

continuous rhythmic involuntary movement of the soft

palate

association of pendular nystagmus (oculopalatal

myoclonus )

Palatal myoclonus

Damage to the dentatorubroolivary pathways (Guillain-

Mollaret triangle)

most often caused by multiple sclerosis or vascular lesions

of the brainstem

MRI often shows enlargement of the inferior olivary

nuclei

Binocular Symmetric Jerk

Nystagmus

Spontaneous

present in primary position

present predominantly on

eccentric gaze

Induced

Spontaneous symmetric conjugate jerk nystagmusthat occurs in primary position

Horizontal


Latent nystagmus

Vestibular nystagmus

PAN

Drug-induced nystagmus

Epileptic nystagmus

Torsional

Form of central vestibular nystagmus

Vertical

UBN

DBN

Vestibular Nystagmus

Predominantly a horizontal or vertical unidirectional jerk

nystagmus, often with a slight torsional component, that is

evident when the eyes are close to the central position

Does not change with the direction of gaze

More prominent when visual fixation is eliminated


Results from unilateral destruction of

Horizontal canal

Total labyrinthine

Torsional slow component causing the upper part

of the globe to rotate toward the lesioned side


Linear (constant velocity) slow phase toward the lesion

Horizontal component is diminished when the patient lies

with the intact ear down and is exacerbated with the

affected ear down

Slow-phase velocity is greater when the eyes are turned in

the direction of the quick component (Alexander's law)

Peripheral Central

Vary with head position

and movement+ +

Latency + No

Fatigue + No

Direction Fixed Changing

Effect of fixation Suppresses No

Pure vertical or torsional

nystagmusNo +

Associated symptomsSubjective

vertigo.

Neurologic signs and

symptoms of brainstem

dysfunction

Periodic Alternating Nystagmus

Eyes exhibit primary position nystagmus, which, after 60

to 120 seconds, stops for a few seconds and then starts

beating in the opposite direction


Often caused by disease processes at the craniocervical

junction

May be provoked by an attack of meniere's disease

Prominent finding in some patients with creutzfeldt-jakob

disease

Mechanism

Nodulus and uvula of the cerebellum maintain inhibitory

control over vestibular rotational responses by using the

neurotransmitter GABA and over the course of

postrotational nystagmus

following ablation of these structures, the postrotational

response is excessively prolonged

So normal vestibular repair mechanisms act to reverse the

direction of the nystagmus, which may result in PAN

Baclofen, a GABA-B agonist, may abolish PAN



Predominantly horizontal, vertical, rotatory, or, most

commonly, mixed

Most often seen with tranquilizing medications and

anticonvulsants

More often evident with eccentric gaze

Epileptic Nystagmus

Usually horizontal

Often associated with altered states of consciousness

Epileptiform activity ipsilateral or contralateral to the

direction of the slow component of the nystagmus

Seizure-induced ipsilateral linear slow phases → smooth

pursuit region in the temporo-occipital cortex

Seizure-induced contralateral quick phases → saccade-

controlling regions of the temporo-occipital or frontal

cortex

Purely Torsional Nystagmus

Rare form of central vestibular nystagmus

Difficult to detect except by the observation of the

conjunctival vessels or by noting the direction of retinal

movements on either side of the fovea

Purely Torsional Nystagmus

Seen with brainstem and posterior fossa lesions, such as

tumors, syringobulbia, syringomyelia with arnold-chiari

malformation, lateral medullary syndrome, multiple

sclerosis, trauma, vascular anomalies, post-encephalitis,

and sarcoidosis, and as part of the stiff-person syndrome

DBN

usually present in primary position, but is greatest when

the patient looks down (Alexander's law) and to one side

convergence may increase, suppress, or convert the

nystagmus to UBN

DBN

Causes

Occur with cervicomedullary junction disease, midline

medullary lesions, posterior midline cerebellar lesions, or

diffuse cerebellar disease

Most lesions responsible for DBN affect the

vestibulocerebellum (flocculus, paraflocculus, nodulus,

and uvula) and the underlying medulla

Intermittent DBN, accompanied by episodic vertical

oscillopsia, may be an early sign of arnold-chiari

malformation

Mechanisms

Deficient drive by the posterior SCCs

Interruption of downward vestibulo-ocular

reflex pathways, which synapse in the MVN

and cross in the medulla

Cerebellar, especially floccular and

uvulonodular, lesions by disinhibition of the

cerebellar effect on the VN

Damage to the nuclei propositus hypoglossi

and the medial VN (the neural integrator) in

the medulla

DBN

Etiologies of Downbeat Nystagmus

UBN

Usually worse in upgaze (Alexander's law)

Unlike DBN, it usually does not increase on lateral gaze

Convergence may increase or decrease the nystagmus, or

convert DBN to UBN

UBN

Causes

Damage to the central projections of the

anterior SCCs

Damage to the ventral tegmental

pathways

Lesions of the anterior cerebellar vermis,

perihypoglossal and inferior olivary

nuclei of the medulla, pontine

tegmentum, brachium conjunctivum,

midbrain, and brainstem diffusely

UBN

Primary position UBN increased in downward gaze

Due to impairment of the vertical position-to-velocity

neural integrator in the Nucleus Intercalatus Of Staderini

Structure in the paramedian caudal medulla located caudal

to the VN and to the most rostral of the perihypoglossal

nuclei (NPH and nucleus of roller)

UBN

Primary position UBN combined with binocular elliptical

pendular nystagmus

characteristic of Pelizaeus-Merzbacher disease

Bow-tie nystagmus

quick phases are directed obliquely upward with

horizontal components alternating to the right and left

probably a variant of UBN

Both downbeat and upbeat nystagmus are poorly suppressed

by visual fixation and may be exacerbated by simply

placing patient in head hanging position

Mechanism of spontaneous vertical nystagmus

Primary dysfunction of the SVN-VTT pathway

Hypoactive after pontine or caudal medullary lesions →UBN

Hyperactive after floccular lesions → DBN

Binocular Symmetric Jerk NystagmusPresent in Eccentric Gaze

Gaze-evoked nystagmus

Nystagmus due to brainstem/cerebellar disease

Bruns' nystagmus


Physiologic nystagmus

Rebound nystagmus

Convergence-induced nystagmus

Gaze-evoked Nystagmus

eyes fail to remain in an eccentric position of gaze but

drift to midposition

velocity of the slow component decreases exponentially as

the eyes approach midposition

more pronounced when the patient looks toward the lesion

Gaze-evoked Nystagmus

Leaky neural integrator or cerebellar (especially

vestibulocerebellar lesion )

Side effect of medications, including anticonvulsants,

sedatives, and alcohol

Adult-onset alexander's disease with the involvement of

the middle cerebellar peduncles and dentate nuclei

Familial episodic vertigo and ataxia type 2

Bruns' nystagmus

Cerebellopontine angle tumors

Combination of

Ipsilateral large-amplitude, low-frequency nystagmus that

is due to impaired gaze holding

Contralateral small-amplitude, high-frequency nystagmus

that is due to vestibular impairment

Physiologic or endpoint nystagmus

Benign low-amplitude jerk nystagmus with the fast

component directed toward the field of gaze

Usually ceases when the eyes are brought to a position

somewhat less than the extremes of gaze

Rebound nystagmus

Brainstem and/or cerebellar disease (e.g., Olivocerebellar

Atrophy, Brainstem/Cerebellar Tumor Or Stroke,

Marinesco-sjogren Syndrome, Dandy-walker Cyst,

Gerstmann-straussler-scheinker Disease, Adult-onset

Alexander's Disease, etc.)

Probably reflects an attempt by the brainstem or the

cerebellar mechanisms to correct for the centripetal drift

of gaze-evoked nystagmus

Convergence-evoked Nystagmus

Usually vertical (upbeat is more common than downbeat)

Seen most commonly with multiple sclerosis or brainstem

infarction

Converting downbeat to upbeat, upbeat to downbeat, or

pendular to upbeat

Induced Nystagmus

Optokinetic nystagmus

Rotational/caloric vestibular nystagmus

Positional nystagmus

Valsalva-induced nystagmus

Hyperventilation-induced nystagmus

OKN

follow objects in motion when head remains stationary

develops at 6 months of age

slow pursuit movements on direction of drum and then a

quick saccade to opposite side

OKN

Paradoxical reversal in congenital nystagmus

With unilateral hemispheric lesions, especially parietal or

parietal-occipital lesions show impaired OKN when the

drum is rotated toward the side of the lesion

Each eye can be tested separately to exclude monocular

blindness

Hysterical patients and malingerers who claim that they

cannot see, and of neonates and infants

Positional Nystagmus

Possibly related to degeneration of the macula of the

otolith organ or to lesions of the posterior SCC

After rapid head tilt toward the affected ear or following

head extension, when the posterior SCC is moved in the

specific plane of stimulation

Other causes of positional vertigo include trauma,

infection, labyrinthine fistula, ischemia, demyelinating

disease, arnold-chiari malformation, and, rarely, posterior

fossa tumors or vascular malformations

Caloric testing

While in supine. Elevtes the head 30°; this brings the

horizontal semicircular canals in vertical plane

Cold water instilled into the right ear causes the

endolymph in the right semicircular canal to cool and

sink.This movement is the same movement induced by a

rotation or the head to the left, inducing a horizontal

nystagmus directed to the left

Warm water in the same ear produces the opposite effect

Failure to respond to otolithic stimuli implies peripheral

vestibular disease.

Nystagmus Induced By The ValsalvaManeuver

may occur with Arnold-Chiari malformation or perilymph

fistulas

Hyperventilation Induced Nystagmus

Tumors of the eighth CN (e.G., Acoustic neuroma or

epidermoid tumors), after vestibular neuritis, or central

demyelinating lesions

Slow phase away from the side of the lesion (an excitatory

or recovery nystagmus)

Due to the effect of hyperventilation upon serum PH and

calcium concentration, which improves nerve conduction

in a marginally functional, demyelinated nerve

Head-shaking nystagmus

nystagmus induced by head oscillation

usually beats to the healthy side in unilateral peripheral

vestibulopathy

Perverted HSN

nystagmus develops in the plane other than that being

stimulated, that is, downbeat or upbeat after horizontal

head oscillation

in diffuse cerebellar degeneration, with focal caudal

cerebellar stroke, or with medullary lesions

signifies central vestibular lesion

Superior SCC Dehiscence Syndrome

Vertigo and nystagmus induced by sound (tullio

phenomenon) or changes of middle ear (hennebert sign) or

intracranial pressure

Caused by bony dehiscence of the superior SCC

vibration induced nystagmus

Bone conducted vibrations (BCV) of the head at low

frequencies ( 60-100 hz )

Activating probably only semicircular canals and not

otolithic afferent neurons

High frequencv (500 hz) BCV is a selective means of

activating otoliths

Delivered at the mastoids and at the midline of the

forehead at the hairline

Saccadic Intrusions

Interfere with macular fixation of an object of interest

Essential difference between nystagmus and saccadic

intrusions

Initial eye movement

Nystagmus → slow drift or slow phase

Saccadic intrusions → inappropriate saccadic movement

that intrudes on steady fixation

Lid Nystagmus

Rhythmic jerking movements of the upper eyelids

1. Synchronous with vertical ocular nystagmus

2. Synchronous with the fast phase of gaze-evoked

horizontal nystagmus in some patients with the lateral

medullary syndrome

3. Evoked by horizontal gaze in some patients with

midbrain tumors that injure the m-group of neurons

adjacent to the rimlf

4. During voluntary convergence (pick’s sign) in some

patients with medullary or cerebellar disease

Nystagmus Evaluation

Does the nystagmus involve both eyes?

Does the nystagmus involve both eyes symmetrically

Does the nystagmus cause the eyes to move in same or

opposite direction (conjugate or dysconjugate)

Docs the nystagmus occur spontaneously in primary

position

Does the nystagmus onlv occur when gaze is directed to

an eccentric gaze position

Low amplitude nystagmus mav be detected during

ophthalmoscopy; note that the direction of horizontal or

vertical nystagmus is inverted when viewed through the

ophthalmoscope.

Electronvstagmogram ENG for identifying nystagmus not

present with eyes open

Dix-Hallpike or Barany maneuver for assessing positional

nystagmus

Nystagmus Evaluation

Treatment of nystagmus

Pendular nystagmus

central (brainstem or cerebellum

Jerk nystagmus

either central or peripheral.

NYSTAGMUS SYNDROME and LOCALIZATION

Jerk nystagmus

Linear (constant velocity) slow phase

Peripheral vestibular dysfunction

Slow phase has a decreasing velocity exponential

Brainstem neural integrator

Increasing velocity exponential slow phase in the horizontal plane

Central in origin and is the usual form of congenital nystagmus



Downbeat nystagmus

Bilateral cervicomedullary junction (flocculus)

Floor of the fourth ventricle

Periodic alternating nystagmus

Cervicomedullary junction (nodulus)

Upbeat nystagmus

Bilateral pontomesencephalic junction

Bilateral pontomedullary junction

Cerebellar vermis


Pendular nystagmus

Paramedian pons

Deep cerebellar (fastigial) nuclei

Seesaw nystagmus (SSN)

Mesodiencephalic junction, chiasm, disorders that disrupt

central vision

Rebound nystagmus

Cerebellum


Brun’s nystagmus

Cerebellopontine angle

AICA territory stroke

Torsional nystagmus, jerk

Central vestibular system

Torsional nystagmus, pendular

Medulla

Thank you

The oscillations may be sinusoidal and of approximately

equal amplitude and velocity (pendular nystagmus) or,

more commonly, with a slow initiating phase and a fast

corrective phase (jerk nystagmus)

horizontal nystagmus usually (but not always) of

vestibular origin

Vertical nystagmus is usually of CNS origin

Direction -changing or direction-fixed

change in direction of nystagmus. be it when the eyes are

in a specific position or when the position of the eye is

changed indicates a lesion in the central nervous svstem.

• nystagmus due to vestibular lesion never changes

direction irrespective of whether the eyes are in a fixed

position or changed

Manner of occurrence

Effect of optic fixation on the nystagmus

Due to peripheral vestibular pathology decreases

Due to central vestibular pathology increases when eyes

open and decreases when closed

Although nystagmus described by direction of quick

phase, it is the slow phase that reflects underlying disorder

differentiated from saccadic intrusions and oscillations

rapid movements which take the eye away from the target

Nystagmus mav be unilateral or bilateral, but when

unilateral its rather asymmetrical rather than truly

unilateral

Localizing acquired central nystagmus: Jerk

Downbeat nystagmus

Upbeat nystagmus

Periodic alternating nystagmus

Rebound nystagmus

Bruns'nystagmus

Localizing acquired central nystagmus: pendular

Occular bobbing

intermittent often conjugate fast downward movement of

the eyes followed after a brief tonic interval by slower

return to primary position.

associated with intrinsic pontine pathology, particularly

heamorrhage tumours or infarction

in association with paralysis of spontaneous and reflex

horizontal eve movements

occular flutter

intermittent bursts of conjugate horizontal saccades

without an intersaccadic interval.

Impaired control by cerebellar fastigial nucleus especially

of horizontal saccadic system

opsoclonus

rare disorder of saccadic system

involuntary arrhythmic, chaotic, multidirectional saccades

without intersaccadic intervals

fixation continuously interrupted by multivectorial, back

to back saccades

at times seen only with ophthalmoscope

harbinger of an occult malignancy, though manv cases are

postinfectious, toxic-metabolic or idiopathic

usually neural crest tumors in children and lung, breast or

gynaecological cancer in adults

dysfunction of glycinergic omnipause neurons in nucleus

raphe interpositus

disinhibition of occulomotor region of fastigial nucleus

(FOR) in the cerebellum can generate opsoclonus

opsoclonus

Occulocephalic reflex

from first week of life

essentially represents a vestibulo-ocular reflex

Gaze-provoked nystagmus

The commonest form of nystagmus

eyes moved into eccentric gaze, especially in lateral and

up gaze

end point nystagmus

usuallv unsustained, . of low frequency and amplitude,

and not accompanied by other ocular motor abnormalities

Pathological gaze evoked nystagmus

sign of extraocular muscle weakness;, for example, in

patients with myasthenia gravis ("fatigue nystagmus").

result of central disorders that involve the gaze holding

neural network, which includes the nucleus prepositus

hvpoglossi and medial vestibular nucleus for horizontal

gaze, the interstitial nucleus of Cajal for vertical gaze, and

the vestibulocerebellum, which optimises gaze holding

Afferents to vestibular nuclei

• Semicircular canals → Superior and medial subnuclei

• Otolith organs → Lateral and inferior subnuclei

• Cerebellovestibular fibers through the inferior cerebellar

peduncle, primarily from the flocculonodular lobe

• Spinal cord

• Reticular formation

Ocular Connections

Vestibular

Nuclei

Mainly from superior and medial

nuclei

Superior nucleus projects to I/L

MLF; other nuclei to C/L MLF

CNs III, IV, and VI Nuclei

CN XI and upper

cervical nerves nuclei

Regulating movements of the eyes, head, and neck in response to

stimulation of the semicircular canals

MLF

Horizontal

semicircular canal

Anterior (superior) and

posterior canals

Abducens Nuclei &

Oculomotor Complex Oculomotor &

Trochlear Nuclei

Medial Longitudinal Fasciculus

Ocular Connections

Nystagmus

Health & Medicine

Transcript of Nystagmus