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406 Theory and Practice of Squint and Orthoptics
Fig. 14.10 Symbolic recording of a case of bilateral gaze-
evoked nystagmus. Note horizontal jerk nystagmus of small
amplitude and low-frequency with fast phase in the direction
of gaze.
• Waveform is dependent on effect of fixation.
• If fixation is impaired, the slow phases consist
of exponentially decaying waveform.
• If visual fixation is possible, however, the slow
phase has a linear profile.
To hold gaze at an eccentric position, the
elastic force of the fascia and ligaments has to
be overcome. This is achieved by a tonic
contraction of the extraocular muscles. The
neural signal involved in this contraction has
been termed as ‘step’, that is generated by the
gaze-holding network, also called the neural
integrator. This network includes the vestibulocerebellum, the medial vestibular nucleus and
adjacent nucleus prepositus hypoglossi in the
medulla, and the interstitial nucleus of Cajal
(INC) in the midbrain.
Etiology. Gaze-evoked nystagmus is caused by
a deficient step, so that the eyes cannot be
maintained at an eccentric orbital position and
are pulled back toward central position by the
elastic forces of the orbital fascia. Corrective
quick phases then move the eyes back towards
the desired position in the orbit.
Additionally, lesions that produce gazeevoked nystagmus also impair visual fixation
and smooth pursuit.
Causes of gaze-evoked nystagmus include:
• Medications, including alcohol, anticonvulsants
and sedatives.
• Structural lesions that damage the gaze-
holding neural network.
• Nucleus prepositus hypoglossi/medial
vestibular nucleus region
• Interstitial nucleus of Cajal
• Rarely, cerebellar lesions.
• Familial episodic ataxia type 2 (EA-2), which
also has attack of ataxia and vertigo.
Dissociated nystagmus (ataxic nystagmus)
It is a special type of pathologic gaze-evoked
nystagmus, most commonly associated with an
internuclear ophthalmoplegia (INO). Dissociated
nystagmus includes a series of saccades
followed by post-saccadic drift that occurs,
when the patient attempts to look laterally away
from the side of the lesion. Since the saccades
initiate the oscillations, this is not a true
nystagmus. It represents an attempt by the brain
to adaptively correct hypometric saccades due
to the weak medial rectus muscle, which
because of Hering’s law of equal innervation
leads increase in the innervation to the normal,
abducting eye, thereby resulting in overshooting
saccades and post-saccadic drift of the normal
eye if the patient attempts to fixate with the
diseased eye. Thus, whenever a patient
habitually prefers to fixate with a paretic eye,
the normal eye, will show a dissociated
nystagmus while looking in the direction of
action of the paretic muscle, regardless of the
pathogenesis of the weakness.
Other causes of dissociated nystagmus are:
• Previous extraocular muscle surgery
• Myasthenia gravis
• Miller Fisher syndrome
Bruns’ nystagmus
Tumours in the cerebellopontine angle, produce
a low-frequency, large-amplitude nystagmus,
when the patient looks toward the side of the
lesion, and a high-frequency, small-amplitude
nystagmus, when the patient looks toward the
side opposite the lesion. The nystagmus that
occurs on gaze towards the side of the lesion is
gaze-evoked nystagmus caused by defective
Fig. 14.11 Symbolic recording of a case of Bruns’
nystagmus depicting a high frequency, small amplitude,
right-beating horizontal and rotary waveform.
gaze holding, whereas the nystagmus that
occurs during gaze towards the side opposite
the lesion is caused by vestibular imbalance.
This is called Bruns’ nystagmus (Fig. 14.11).
Convergence-retraction nystagmus
It is characterized by quick phases that converge
or retract the eyes on attempts to look up.
Affected patients usually have impaired or
absent upward gaze for both pursuit and
saccadic eye movements. It is a saccadic disorder
rather than nystagmus because the primary
adductive movements are asynchronous
saccades. Causes include:
• Lesions of the mesencephalon that damage the
posterior commissure, e.g. pineal tumours.
• Chiari malformation
• Epileptic seizures
Centripetal and rebound nystagmus
If a patient with gaze-evoked nystagmus
attempts to look eccentrically for a sustained
period, the nystagmus begins to decrease in
amplitude and may even reverse direction, this
is called centripetal nystagmus. If the eyes are
then returned to the central position, a shortlived nystagmus with slow drifts in the direction
of the prior eccentric gaze occurs. This is called
Nystagmus and Related Oscillations
407
rebound nystagmus. Both centripetal and
rebound nystagmus reflect an attempt by
brainstem or cerebellar mechanisms to correct
for the drift of gaze-evoked nystagmus.
Rebound nystagmus occurs in patients with:
• Cerebellar disease
• In normal subjects with typical gaze-evoked
nystagmus
• Lateral medullary infarction
• Tumour confined to the flocculus.
CLINICAL EVALUATION AND ELECTROPHYSIOLOGICAL RECORDING AND
NEUROIMAGING
A. CLINICAL EVALUATION
It is often possible to diagnose the cause of
nystagmus through careful history and
systematic examination of the patient.
History
History should include:
• Duration of nystagmus
• Whether it interferes with vision and causes
oscillopsia
• Accompanying neurological symptoms
• Whether nystagmus and other visual
symptoms are worse with viewing far or near
objects, or with patient motion, or with
different gaze angles.
• If abnormal head posture is present, whether
or not these features are evident on old
photographs.
• Family history: Inquiring about a family history
of nystagmus or other eye conditions, as some
forms of nystagmus can be hereditary.
Examination of a patient with nystagmus
General physical examination: Assessing for
signs of systemic or neurological conditions that
may be associated with nystagmus.
Comprehensive examination of the visual
system
• Visual acuity assessment with and without
posture, for both near and distance and both
binocularly and uniocularly. Binocular acuity
should be recorded before occlusion. Methods
of measuring monocular vision while
avoiding total occlusion include fogging the
408 Theory and Practice of Squint and Orthoptics
other eye with plus spheres, polarizing lenses,
central field occlusion and the red-green
duochrome slide test.
• Anterior and posture segment examination to rule
out cause of low vision. Especially look for
• Measurement of head posture. In most patients
with infantile nystagmus, the head position
corresponds roughly to the null zone.
However, an anomalous head posture may be
present in patients with INS for reasons other
than nystagmus, e.g. uncorrected astigmatism,
incomitant squint, muscular torticollis.
Nevertheless, presence of AHP in a patient
with INS has better visual prognosis than no
AHP. All the components of head posture, i.e.
face turn, chin elevation or depression and
head tilt should be noted. Face turn can be
measured using the Goniometer (Fig. 14.12)
or by simply using a scale and a protractor.
Systematic examination of each functional class
of eye movements (vestibular, optokinetic,
smooth-pursuit, saccades, vergence) and their
effect on nystagmus.
Examination of nystagmus in a systematic
manner. It is essential to have a mental checklist
during clinical examination. ABCDEF is a
suggested pneumonic for systematic examination
of nystagmus where:
A is amplitude
B is basic shape or waveform
C is conjugacy
D is direction
E is effect of gaze position and fixation, e.g.
Fig. 14.12 Goniometer: An orthopaedic instrument which
can be used to measure face turn.
• The stability of fixation (with the eyes close to
primary position) viewing near and far
targets, and at eccentric gaze angles.
• In patients with head turn or tilt, the eye
should be observed in various directions of
gaze, when the head is in that position as well
as when the head is held straight.
• During fixation, occlude each eye in turn to
check for latent nystagmus.
• The effect of removal of fixation (with
Frenzelor high-plus spherical lenses).
F is frequency.
Foveation period assessment: The foveation
period refers to the brief moments when
nystagmus movements slow down, allowing for
improved visual clarity. It can be assessed by
observing the patient's ability to fixate on a
target or by using specialized eye-tracking
technology.
Note. Details of the features of nystagmus and
method of their clinical documentation has been
described earlier (see pages 393–396).
B. ELECTROPHYSIOLOGICAL RECORDING OF
EYE MOVEMENTS
Electrophysiological recording of ocular motility
has provided a new basis for eye movement
abnormality classification, etiology and treatment. Only salient features of some of the
techniques available for ocular motility
recordings are mentioned here.
1. Electro-oculography
Electro-oculography (EOG) is based on the
measurement of resting potential of the eye
which exists between the cornea (+ve) and back
of the retina (–ve).
Technique of recording is shown in Fig. 14.13A and
B. Electrodes are placed over the orbital margin
near the medial and lateral canthi serve as active
electrodes (E1–E4 in Fig. 14.13A). A forehead
electrode serves as a ground electrode or indifferent electrodes (E5 in Fig. 14.13A).
Salient features.
• Horizontal range of measurement of 1 to 40°
with a resolution of 1°.
• Useful for horizontal and some vertical
movements.
Nystagmus and Related Oscillations
409
Fig. 14.13 Technique of recording electro-oculogram: (A) Position of electrodes; (B) Ocular movements during recording;
(C) Record of EOG.
• A bit noisy–1°.
• Best clinical all-rounder with good electrodes.
2. Electronystagmography
Electronystagmography (ENG) is an adaption
of electro-oculography (EOG). For ENG like
EOG (Fig. 14.13), a ground electrode is attached
to the forehead and three recording electrodes
are placed one each to the side, above and below
each eye which measure the eye movement.
• Caloric test is performed to assess the
vestibular system.
3. Binocular infrared reflectance oculography
(BIRO)
• Useful for horizontal and some vertical
movements.
• Has a restricted range.
• Noise–0.1°
Tests performed with ENG include:
• Oculomotor tests. ENG is used to record
nystagmus during oculomotor tests such as
saccades, pursuit and gaze testing and
optokinetics. Abnormal oculomotor test
results may indicate either systemic or central
pathology as opposed to peripheral (vestibular) pathology.
• Positional testing is performed to see the effect
of head or body movements on the eye
movements.
4. Electromagnetic scleral search
coil method
• Useful for horizontal, vertical and torsional
movements.
• Good resolution and frequency response.
• Requires mind bending mathematical analysis.
• Eye has to be anaesthetized and a thick
silicone lens is needed.
• Expensive.
410 Theory and Practice of Squint and Orthoptics
5. Videonystagmography
Videonystagmography (VNG) is a sophisticated
technique in which nystagmus is recorded with
the help of the infrared video camera which is
incorporated in the specially designed infrared
camera goggles (worm by the patient during the
recording technique (Fig. 14.14). A very sensitive head movement sensors are also incorported in it.
Tests performed with VNG. Similar to ENG,
there are three parts of VNG testing:
• Ocular and optokinetic testing
• Positional nystagmus testing and
• Caloric testing
Advantages of VNG over ENG
• Less cumbersome and less time consuming as
electrodes are not required.
• Direct observation of video images of eye
movements available.
• Simultaneous comparison of waveform can be
performed.
• Computerised record allows storage, processing
and analysis.
• Provides more information than ENG. In addition
to information about amplitude, frequency
and intensity obtained from ENG; the VNG
also provides information about slow phase
velocity and foveation window with the help
of intrinsic software.
Clinical uses of eye movement recording
Important clinical uses of eye movement
recording are as follows:
• Identifies congenital type of nystagmus on the
basis of waveform. About 40–60% cases of
nystagmus have associated squint. About 35%
of these patients have FMNS. The best method
to differentiate INS form FMNS is eye
movement recordings.
• Allows classification of acquired nystagmus
with greater certainty.
• VNG helps to evaluate the evolution of nystagmus.
Many INS waveforms begin as pendular
nystagmus. Growth and development of the
visual sensory system evoke evolution of
waveforms during early infancy from pendular
to jerk type nystagmus by development of
corrective fast phases as well as breaking
saccades in slow phases producing the so called
‘mature’ waveforms associated with better
vision.
• Measures slowness of saccades which can be
diagnostic, e.g. internuclear ophthalmoplegia.
• Allows observation of motility in darkness
(vestibular nystagmus).
• Allows temporal resolution of very fast eye
movements such as flutter, opsoclonus,
convergence nystagmus, dysmetria which are
difficult to evaluate with the naked eye.
• Trains one to interpret what is’ seen’.
• Helps in objective assessment of visual functions
of a patient with nystagmus by calculating
foveation time, foveation eye position, and eye
velocity criteria.
• Tells about the potential for visual improvement
with treatment.
• Useful in objective documentation of response to
treatment.
• Helps in null point evaluation.
Fig. 14.14 Technique of videonystagmography with infrared
goggles worn by the patient.
C. NEUROIMAGING
Neuroimaging is indicated to find out associated
CNS abnormalities especially in patients with
acquired nystagmus, periodic alternating
nystagmus, see saw nystagmus, spasmus nutans
syndrome and infantile nystagmus syndrome
with pallor disc and poor vision.
Hertle’s criteria for neurological workup in
patients with nystagmus are as follow:
I. History of:
• Onset of nystagmus after 6–9 months of age.
Nystagmus and Related Oscillations
411
• History of prematurity or LBW or develop-
mental delay.
• Abnormal pregnancy/delivery.
• Exposure to toxins/drugs.
II. Ocular features:
• Photophobia, delayed visual behaviour.
• Structural abnormalities like foveal or optic
nerve dysplasia.
• Nystagmus pattern vertical, asymmetric,
dysconjugate or associated with other ocular
motor disorders (decrease pursuit, abnormal
saccades, paretic gaze).
III. General features:
• Patient having manifest hard, soft, focal or
diffuse neurologic signs.
• Localising signs of acquired nystagmus.
D. OTHER TESTS
OCT is indicated in retinal dystrophies,
degenerations, foveal hypoplasia, schisis cavity,
retinal thinning, choroidal thinning.
Autofluorescence can be used for diagnosing
accumulation of lipofuscin in macular
dystrophies.
ERG is useful in sensory nystagmus associated
with conditions like achromatopsia, CSNB, LCA
and other atypical retinal dystrophies.
Blood tests: Blood tests may be performed to
check for metabolic or systemic conditions that
could be associated with nystagmus, such as
vitamin deficiencies, thyroid dysfunction, or
autoimmune disorders.
Genetic testing: In cases of congenital
nystagmus or when a hereditary component is
suspected, genetic testing may be recommended
to identify specific gene mutations or
abnormalities.
TREATMENT OF NYSTAGMUS
Aims of treatment
• To improve visual acuity by stabilizing the
eyes
• To shift the null zone, if any, in the primary
position, i.e. to reduce abnormal head posture.
• To correct the associated strabismus
• To decrease any oscillopsia wherever possible.
Treatment modalities
Treatment modalities for nystagmus include:
• Optical,
• Medical, and
• Surgical.
I. OPTICAL TREATMENT
1. Correction of refractive error may sometimes
significantly decrease nystagmus, especially in
patients with bilateral aphakia. Although
refraction is difficult in the presence of nystagmus
but every effort should be made to correct any
significant refractive error. Retinoscopy may be
performed in null zone, whenever it is present.
Further, contact lenses are more useful than the
spectacles (especially in high myopes), since
these move with the movement of eye and so
the visual axes always coincide with their optical
axes. In addition to optical advantage, at actile
feedback from the contact lenses have also been
reported to decrease the nystagmus.
Clear or tinted contact lenses can be prescribed.
• Accommodation may be deficient in patients with
congenital nystagmus. Dynamic retinoscopy
should be performed before dilation. If
accommodation is deficient, a bifocal
correction should be provided.
2. Treatment of amblyopia. Amblyopia if
present, should be treated with standard
treatment. Penalization with plus lenses or
atropinization is preferred over occlusion by
some workers.
3. Stimulating accommodative convergence by
over correcting minus lenses may improve
visual acuity at distance fixation by dampening
the nystagmus.
Patients chosen to have this treatment must
show evidence of good accommodative facility.
4. Partial field occlusion. An unusual method
of decreasing the intensity of congenital
nystagmus, based on partial field occlusion was
suggested by Sasso. “Porthole” glasses that had
a clear 10° central field but an occluded
periphery were prescribed. For some patients
having torticollis and nystagmus, occlusion of
some parts of peripheral field alleviated
anomalous head posture. However, the data
was inadequate for evaluating this concept
thoroughly.
412 Theory and Practice of Squint and Orthoptics
5. Prismotherapy in nystagmus may be useful
as follows:
i. Base-out prisms may stimulate fusional
convergence (especially in patients with
congenital motor nystagmus) and thus
improve the visual acuity by dampening the
nystagmus.
This results in improvement of visual acuity
both for distance and near. The prism power
is usually split between the two eyes. Both
ground in and membrane style prisms may
be used. This option is best reserved for
patients with good vision, normal fusion and
modest nystagmus.
ii. Prisms with base opposite to preferred direction
of gaze may be helpful in correcting the head
posture. Prisms minimize a head turn by
reorienting the visual axis towards primary
gaze. Often the preferred eye is held in
adduction. Equal power prisms are placed
before each eye and oriented in the same
direction so that the apex is in the direction
of preferred gaze, and the base in the
direction of head turn. For example, in a
patient with head turn to the left, the null
zone is in dextroversion and a prism base-in
before the right eye and base-out before the
left eye will be helpful in correcting the
abnormal head posture (Fig. 14.15).
Similarly, the appropriate prisms can also be
used to correct the vertical and oblique head
turns. Because of optical disadvantages, the
long-term use of prisms incorrecting the head
posture is discouraged. However, on the basis
of patient’s response to prismotherapy, the
results of surgery for head turn can be predicted.
6. Galilean arrangement of contact lenses and
glasses (optical device by Rushton and Cox) can
be used to stabilize the retinal images in patients
Fig. 14.15 Use of prism to correct head posture (for explan-
ation see text).
with acquired nystagmus and oscillopsia. This
device reduces the magnitude of image
movement by limiting image slip along the
retina. As a result the visual acuity may improve
through an increase in the foveation time. There
occurs a decrease in oscillopsia also because of
the reduced image motion. This device consists
of a high minus contact lens combined with a
high plus spectacle lens. Rigid contact lenses of
–58D or –28D are paired with spectacle lenses
of +32D or +20D irrespectively. Stabilization of
retinal image up to 90% is possible using this
system. The prismatic effect of the large plus lens
plays key role in stabilization of retinal image.
This lens images all objects at centre of rotation
of the eye, irrespective of exact direction of the
visual axis. Thus if eyeball rotates, light rays
from the object will remain focused at the same
central point within the eye. The minus contact
lens refocuses the image on retina. As the contact
lens moves with the eyes, there should be no
prismatic effect from the high power plus lens.
This has the added benefit of magnifying central
30° field. However, the peripheral field is not
stabilised, leading to ring scotoma.
Low vision aids: For individuals with severe
nystagmus that significantly impairs vision, low
vision aids such as magnifiers, telescopes, or
electronic devices can be beneficial for reading
and other visual tasks.
Supportive care: Nystagmus can be associated
with visual fatigue and reduced depth
perception. Adequate lighting, large print
materials, and screen magnification software on
electronic devices can make daily tasks more
manageable for individuals with nystagmus.
II. MEDICAL TREATMENT
The treatment of nystagmus with medications
can be challenging, and the choice of medication
depends on the underlying cause of the
nystagmus, its severity, and the potential
benefits and risks associated with the
medication. Medications are often considered in
cases of acquired nystagmus, especially when
there is an identifiable cause or when the
nystagmus is causing significant discomfort or
visual impairment. Here are some medications
Nystagmus and Related Oscillations
413
that may be used in the treatment of different
types of nystagmus:
1. Cyclopentolate used as 1% eyedrops twice a
day has been reported to reduce the amplitude,
velocity and frequency of latent nystagmus in
about 60% of patients.
2. Botulinum toxin a muscle relaxant, injected
into the retrobulbar space (dose: 10–25 U in 0.1–
1 ml) every 3–4 months has been reported to
dampen nystagmus and improve visual acuity
in patients with acquired nystagmus and
oscillopsia.
3. Baclofen, a muscle relaxant, has been
observed to suppress the acquired periodic
alternating nystagmus. The initial
recommended dose is 5 mg TDS, which in case
of no response can be increased stepwise every
3 days to a maximum of 80 mg/day.
4. Clonazepam may be useful in patients with
downbeat nystagmus and see-saw nystagmus.
Clonazepam is used in dose of (0.5–1 mg/bd).
5. Carbamazepine is useful in superior oblique
myokymia.
6. Propranolol is reported to be effective for
opsoclonus.
7. Brinzolamide (1%) eye drops used thrice a day
is noted to improve foveation by 50%, with
broadening of the null zone. Its effect may be
equivalent to systemic acetazolamide or eye
muscle surgery but intermediate between those
of soft contact lenses or convergence. 80%
Patients on the brinzolamide eyedrops may
experience improvement in the best corrected
vision corresponding to one line on the Snellen
chart. Visible reduction in nystagmus takes place
in 27% and reduced AHP in 22% patients and
nearly 30% would experience no change.
The effect comes within one week and lasts
as long as the drops are continued. There may
be additive effect of the drops when used after
the tenotomy and reattachment procedure.
Topical brinzolamide may be contraindicated in
congenital or acquired pathologies of corneal
endothelium.
8. Gabapentine (300 mg/qid) and memantine (10
mg/qid) are reported to be useful in patients
with upbeat nystagmus, acquired pendular
nystagmus and alternating periodic nystagmus.
These drugs can also be tried in patients with
congenital nystagmus.
9. Glycopyrrolate: Glycopyrrolate, an anti-
cholinergic medication, has been explored as a
treatment option for acquired nystagmus. It may
help reduce nystagmus amplitude by affecting
certain neural pathways.
10. Scopolamine: Scopolamine, an anti-
cholinergic medication often used for motion
sickness, can be applied as a transdermal patch.
It may help reduce nystagmus amplitude in
some cases.
11. Dalfampridine: Dalfampridine is a medica-
tion that can improve walking in individuals
with multiple sclerosis. It may have a positive
effect on nystagmus in some cases, although the
mechanism is not fully understood.
12. Clomipramine: Clomipramine, a tricyclic
antidepressant, has been reported to be effective
in treating some forms of acquired nystagmus,
such as PAN. It may help reduce nystagmus
intensity.
It's important to note that medication therapy
for nystagmus is often considered as an adjunct
to other treatments and may not be effective for
all individuals. Additionally, medications can
have side effects, and their use should be
carefully monitored by a healthcare provider.
III. SURGICAL TREATMENT
INDICATIONS
• To eleminate abnormal head posture by
shifting the null point to primary position.
• To decrease the intensity of nystagmus in
patients having no abnormal head posture.
• Both of the above.
• To improve visual acuity (usually by 1–3 logmar
lines), contrast sensitivity and reaction time
(improves by 0.3 seconds) by improving
foveation.
• To correct strabismus and to restor binocular fusion
and stereopsis, where ever possible.
Important points to be considered while
planning surgery for nystagmus are as follows:
1. Surgical intervention is useful in patients with
congenital motor nystagmus and nystagmus
blockage syndrome.
414 Theory and Practice of Squint and Orthoptics
2. Surgery should be performed, only if the
abnormal head posture causes a significant
cosmetic disturbance and/or visual difficulties,
i.e. when head turn-or tilts more than 15°.
3.Surgery should always be performed after the age
of 5–6 years; since spontaneous improvement
in abnormal head posture can occur in some
cases up to this age. Moreover, by this age, it is
possible to have more reliable examination
demonstrating head posture and ocular
alignment. For children with strabismus, earlier
intervention may provide the best opportunity
for bifoveal fixation to develop. With an
acquired nystagmus and torticollis, it is prudent
to wait at least a year to be certain that the
abnormal eye movements are consistent and the
head turn is stable.
GENERAL PRINCIPLES OF SURGERY
• Null point needs to be shifted in primary position.
For this, the eyes should always be moved in
the same direction as the abnormal head
posture.
• Face turn will be corrected only if the surgery
is done on the fixating eye.
• In the presence of strabismus and an abnormal
head posture due to nystagmus, the head
position can be corrected only by operating
on the fixing eye.
• Strabismus can be corrected by operating on
the fixating eye or nonfixating eye.
• Surgery for face turn is performed first
followed by surgery for the strabismus.
• Surgical therapy should be based on the greatest
amount of abnormal head position that is
measured at distance.
(A) SURGICAL TECHNIQUES FOR
ABNORMAL HEAD POSTURE
Patients with nystagmus who have null point
(other than the primary position) assume an
abnormal head posture (AHP) to dampen the
nystagmus. A significant AHP needs to be
corrected. Kestenbaum and Anderson were the
first to report on the surgical techniques for the
treatment of abnormal head posture in
congenital nystagmus.
• Kestenbaum procedure originally comprised of
recession-resection of all the four horizontal
recti
• Anderson procedure comprised of only
recessions, e.g., for right face turn recession
of right MR and left LR muscle.
• Modified Kestenbaum-Anderson procedures have
been suggested by various workers thereafter.
Different modified surgical techniques are
now recommended for the face turn without
strabismus, for face turn with strabismus and
for nystagmus blockage syndrome.
I. Surgical techniques for face turn
1. Surgical techniques for face turn
without strabismus
Modified Kestenbaum-Anderson procedure. It
consists of bilateral recess-resect operations.
Up to 30° of face turn (e.g. in a patient with head
turn to the left) the modified Kestenbaum-
Anderson procedure, as described by PARK, is
effective. It comprise lesser amount of recessions
and also lesser amount of surgery on MR
muscles as compared to LR muscles. He
suggested the ‘5, 6, 7, 8’ guidelines for a bilateral
equal surgery as below (Fig. 14.16):
• Right lateral rectus (RLR) recession 7 mm
• Right medial rectus (RMR) resection 6 mm
• Left medial rectus (LMR) recession 5 mm
• Left lateral rectus (LRL) resection 8 mm
Modified Kestenbaum-Anderson procedure, as
described by PARK, is also called ‘classic
maximum’ (Table 14.2)
Up to 45° of face turn a 40% augmentation in the
above surgery is recommended (Table 14.2).
Up to 60° of face turn a 60% augmentation in
Park’s figures are suggested Table 14.2.
2. Surgical techniques for face turn with
associated strabismus
a. Face turn with esotropia
i. Face turn ipsilateral to the fixing eye can be
corrected by recess-resect procedure on the
Fig. 14.16 Diagrammatic depiction of position of eyes in a
patient with left face turn and the suggested Kestenbaum
procedure to correct it.
Nystagmus and Related Oscillations
Table 14.2 Modified Kestenbaum-Anderson procedures for nystagmus in a patient with left face turn
Type of surgery Dosage extraocular muscle surgery
Classic maximum 40% augmentation 60% augmentation
RMR resection 6 8.4 9.6
RLR recession 7 9.8 11.2
LMR recession 5 7 8
LLR resection 8 11.2 12.8
415
horizontal recti of the fixing adducted eye. For
example, in a patient with left esotropia having
right face turn and fixating with right adducting
eye, MR recession and LR resection of the right
eye should be performed. This procedure will
correct face turn as well as an esotropia up to
30PD. The residual esotropia, if any, can be
corrected later by surgery on the other eye.
ii. Face turn ipsilateral to the deviating
esotropic eye, should be first tackled with recess-
resect procedure on the opposite fixing eye. This
procedures will correct the face turn but will
increase the esotropia in the deviating eye,
which can be later corrected surgically. For
example, in a patient with right face turn and
right esotropia, surgery for the face turn should
be first done on the left fixing eye (MR resection
and LR recession) to move it in the direction of
face turn. The resulting increased right esotropia
can be later corrected surgically by right MR
recession and LR resection.
b. Face turn with exotropia
i. Face turn ipsilateral to the fixing eye can be
corrected by recess-resect procedure on the
horizontal recti of the fixing adducted eye. This
procedure will correct the face turn but will
increase the exotropia in the deviating nonfixing
eye, which can be later corrected surgically. For
example, in a patient with right face turn and
left exotropia, surgery for the face turn should
be first done on the right fixing eye (MR
recession and LR resection) to move it in the
direction of right face turn. The resulting
increased left exotropia can be later corrected
surgically by left MR resection and LR recession.
ii. Face turn ipsilateral to the deviating
exotropic eye, should be first tackled with recess-
resect procedure on the fixing eye. This
procedure, in addition to correcting face turn,
will also correct/reduce the associated
exotropia. For example, in a patient with right
exotropia having right face turn and fixating
with left eye, surgery for the face turn should
be done on the left eye (MR resection and LR
recession) to move it in the direction of right face
turn. This procedure will correct right face turn
as well as the right exotropia. The residual
exotropia, if any, can be later corrected surgically
by right MR resection and LR recession.
II. Surgical techniques in patients having head
tip (chin elevation or depression) associated
with childhood nystagmus
Headtip occurs in patients having a null zone
with eyes in depression or elevation. The basic
principle for surgically correcting the headtip
is like that for correcting face turns, i.e. the eyes
should be moved in the direction of abnormal head
posture. Symmetrical surgery on all the four recti
(vertical Kestenbaum) may be useful.
Vertical Kestenbaum. Recommended procedures
by Park are as follows:
1. For headtip of more than 25°
• For chin elevation. Bilateral 4 mm resection
of the superior recti combined with bilateral
4 mm recession of the inferior recti.
• For chin depression. Bilateral 4 mm resection
of the inferior recti combined with bilateral
4 mm recession of the superior recti.
2. For headtip of less than 25°
The operation is limited to bilateral 4 mm
recession of the depressors or elevators without
resection of their antagonists.
However, recently most workers recommend
that the amount of surgery to be performed should
be at least 5–6 mm to obtain satisfactory results.