Nystagmus

Nystagmus
It is a rhythmic to and fro involuntary oscillation of the eye which

may be physiological or pathological
Causes of Nystagmus
Saccades is s high a high velocity movement with a speed ranging
from approximately 400-700 of arc/sec during saccades visual
perception is suspended therefore individual is not conscious of the
rapid movement
The saccades may not result in the eye arriving a desired position. It
undershoots or overshoots if error is small than final gauze position
is reached by microsccades
Theories Of Nystagmus:
1.) Pulse Step Theory:
2.) Neural Integrator
Manifest Congenital Nystagmus (MCN):

The Common Cause of MCN are:
1. Congenital Cataract
2. Congenital Glaucoma
3. Anirida
4. Down’s Syndrome
5. High Myopia
6. Oculocutaneous Albinism
MNC is infrequently observed at birth its onset being usually at the
first 3rd of 4th month of life better term Infantile Nystagmus and may
or may not settle by the age of 5 years
Types Of Congenital Nystagmus:

A.) Sensory Defect Nystagmus:
Primary cause is the inadequate formation of the image on the
fovea. This causes a disturbance of feedback from the fovea
that interferes with the occulomotor control of fixation
mechanism. It is always bilateral and often perpendicular in type
however perpendicular acquires the jerk type character in
extreme positions. Pure perpendicular is very rare and this
afferent pathway is normal
B.) Motor Defect Nystagmus:
In this the primary defect is in the efferent mechanism possible
involving centre or pathway of conjugate occulomotor control.
No ocular abnormality is found the amplitude and frequency
may decrease or disappear in one position of gauze and the VA
may improve. This may cause the patient to assume anomalous
head posture to improve its VA.
Examination of Nystagmus:
A.) History
1.) Concerning Birth
2.) Visual development
3.) Neurological Abnormalities – Dizziness, pain, numbness,
poor balance
4.) Family History
5.) Birth trauma and Brain Damage
6.) Prematurely
7.) Cerebral palsy
8.) H/O oscillopsia
B.) Ophthalmic Examination:

1.) Visual Acuity
2.) Pupils
3.) Motor Alignment: check for presence of ant strabismus,
abnormal head tilt.
4.) Slit Lamp Examination
5.) Opthalmoscopy: Look for optic nerve Hypoplasia, Coloboma
Evaluation of Nystagmus – 3 distances
1.) 4 – 6 meter
2.) Near fixation
3.) At Preferred Reading Distance
1.) Type:
A.) Jerk
It is a fast and a slow phase through the abnormality is the slow
phase, the Nystagmus is described according to the fast phase.
There may be foveation when eye movements are relatively slower
for a short duration as the target cross the fovea and then again the
velocity increases. The foveation is sufficient (60m/s) VA may not be
impaired
B.) Pendular:
The to and fro eye movement approximately of the equal velocity in
each direction. A Pendular wave from can be sinusoidal i.e. smooth
transition to opposite direction or triangular i.e. and abrupt direction
shift
2.) Direction: it is described with the reference to the horizontal(X),

vertical(Y), and rotary(Z).
3.) Amplitude: is estimated using a mm ruler or a reticule patients

fixation at a 6m target peak to peak movement
1mm movement at the plane of the cornea = 22 prism
(12° visual angle)
4.) Frequency: Hertz (1cycle/sec) i.e. waveform completes one full

rotation in 1 sec
Frequency > 2hz is Fast and Frequency <1hz is Slow
Examined on SL with low magnification
5.) Intensity: Intensity = Amplitude x Frequency
Alexander’s law: it states that the amplitude of the jerk Nystagmus

is usually large dependent upon gaze in direction of fast component
based on these there are 3 degrees of Nystagmus :
Grade I: Present only in right Gaze
Grade II: Right Gaze Primary Position
Grade III: Even on Left Gaze
Neutral Zone: Point where Nystagmus fast component changes

direction
Null Zone: or point where the Nystagmus is no longer elicited
Nystagmus is described on the basis of:
1.) Type : Jerk, Pendular, Mixed
2.) Amplitude : Small (<2), Moderate (2 – 9), Large (<10)
3.) Direction: Horizontal, vertical, torsional, mixed
4.) Frequency: Slow ( >0.5Hz), Moderate (0.5 – 2 Hz), Fast
( <2Hz)
5.) Conjugacy: Eye moves in same direction or no
6.) Constancy: always present, Intermittent or Periodic
7.) Symmetry: Symmetrical, Asymmetrical or monocular.
8.) Field of gaze: Null point in some field of gaze of change in
Nystagmus with convergence.
9.) Latency: Increases or changes with occulution of one eye
Presentation of Nystagmus:
 : Fast Phase
 : Perpendicular
< : Higher frequency
<==: Higher Amplitude
(/ = Torsional
Clinical Characteristics of Congenital Nystagmus:

1.) Always BILATERAL and CONGUGATE in direction and
frequency
2.) UNI planar : Horizontal in up-down gaze namely vertical or
horizontal
3.) Similar AMPLITUDE in BE
4.) Waveforms: Jerk, Pendular, Mixed.
5.) Dampened with convergence
6.) Accentuation by fixation
7.) Null Zone often Present
8.) Associated head nodding present but does not offer
significant visual gain.
9.) Disappears during Sleep
10.) No oscillopsia
11.) Inversion of OKN i.e. direction of fast component is same as
that of drum
12.) Nystagmus blockage Syndrome
Compensatory Mechanisms:
This may be in the form of face turn to right or left, chin up or down
or head tilt. Patients adopt this posture to improve the VA. Patients
tend to make the use of the minimum amplitude zone (MAZ) or
minimum intensity zone (MIZ). Other factors that influence the head
posture are velocity distribution of slow phase, nystagmsus best
direction.
Although oscillopsia is not so common consequence of CN, some
patients complain of the same which generally coincide with the high
intensity oscillation. The preference for a particular head posture
may be the need to minimize the head posture.
Over convergence may be called as nystagmus blockage syndrome
defined as esotropia with an onset in infancy often preceded by
nystagmus or pseudo abdusence palsy or straightening of eye under
anesthesia
Latent or MLN:
LM is evoked on occluding one eye and decrease or absent with BE
open. The difference in quality of retinal image of two eyes is trigger
latent phase of nystagmus.
There are various theories for the cause of LN unstable equilibrium
of occulomotor co-ordination possibly caused by maldevelopment of
monocular and binocular reflexes.
Amplitude of LN decreases in adduction and increases in abduction,
fast phase being towards the side of fixating eye.
MLN is a latent nystagmus. Manifest by blindness is of one eye by
strabismic suppression
Sr. Manifest Latent(LN) or Manifest
No Latent(MLN)
.
1. Biohasic Mostly Mostly Jerky or Mixed
2. Do not increase on Increases on abduction
abduction
3. No change on unilateral Accentuated on unilateral
occulution occulution
4. Direction dependent on Fast phase followed fixating
fixing eye eye
5. In frequency associated with Nearly always associated with
infantile esotropia infantile esotropia
6. Binocular VA = Monocular Binocular VA better than
VA monocular
7. Wave form increasing Decreasing velocity slow phase
velocity slow phase
Treatment:
The treatment of any nystagmus aimed at stabilizing the eye to
improve VA to decrease oscillopsia or in order to to correct
compensatory head posture
Medical:
Various drugs like Phenoobarital, Baclofen, tranquillizer have been
tried in congenital nystagmus to improve VA, but because of their
side-effects prolonged treatment with these medications are not
successful
Glasses and Contact Lenses:

Important to correct the refractive error dramatic decrease in
nystagmus has been noted once patients refractive error has been
corrected.
CL are also used especially soft CL and in high Myopes as they move
synchronously with the eye and hence has an optical advantage
besides this, optical advantages there is suppose to be some kind of
tactile feedback from CL that decrease nystagmus.
Minus lenses:
Overcorrection with minus lenses stimulates accommodative
convergence and may improve the VA.
Prisms:
They are used to improve the VA and to eliminate the anomalous
head posture.
Base Out prisms are prescribed to stimulate fusional convergence
and hence dampening the nystagmus and hence improving the VA
Normal BV is a pre-requisite for the use of Prisms BO. Since fusional
convergence result of temporal disparity and this cannot be
expected with patients with nystagmus
Pre-operative evaluation or non-surgerical therapy of a patient with
head turns resulting form nystagmus. Here the prisms are inserted
with their prisms’ apex pointing towards the direction of the eye.
Combination of vertical and horizontal prisms in oblique position
Thus the result of surgery for the head turn can be predicted well
with prism and residual head turn can also be managed after surgery
with prisms.
Though the main drawback is large amount of prism power is
required to correct even 20° of face turn.
Surgery therefore is a better option
Surgerical Treatment:
1. To eliminate the CHP
2. To decrease the nystagmus , amplitude
3. For Both
4 .Surgery names:
1. Kestenbaurn : face turn to left by recessing the Right Lateral
Rectus
2. Botulium Toxin: for Congenital nystagmus
3. Enhanced Anderson :Yoke Muscles
4. Chin elevation or Depression Surgery
5. Head tilt surgery
6. Spielmann: slanning the insertion of the 4 rectii
Physiologic nystagmus → Fixation reflex

Horizontal gaze
Abducens nucleus → PPRF → MLF → Oculomotor nucleus → Medial
rectus muscle
Vertical gaze
Rostral interstitial nucleus → Oculomotor nucleus, Trochlear nucleus
→ Muscles of orbit

Nystagmus

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Nystagmus

It is a rhythmic to and fro involuntary oscillation of the eye which

Manifest Congenital Nystagmus (MCN):

Types Of Congenital Nystagmus:

B.) Ophthalmic Examination:

2.) Direction: it is described with the reference to the horizontal(X),

3.) Amplitude: is estimated using a mm ruler or a reticule patients

4.) Frequency: Hertz (1cycle/sec) i.e. waveform completes one full

Alexander’s law: it states that the amplitude of the jerk Nystagmus

Neutral Zone: Point where Nystagmus fast component changes

Clinical Characteristics of Congenital Nystagmus:

Glasses and Contact Lenses:

Physiologic nystagmus → Fixation reflex

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