Phys Optics Nystagmus

1. Describe its relevant characteristics
2. Classify the condition
3. Identify possible causes and
associations
4. Determine and implement
appropriate management

A series of rhythmic involuntary movements of the eyes as a result of some disorder of the visual apparatus or some neurological or labrynthine disease.

The mechanisms that keep fixation stable.

The neural integrator (a neural network).

1. Pursuit
2. Optokinetic
3. Vestibular

Any lesion involving the paired nuclei of the neurologic systems involved in maintaining steady gaze.

1. Infantile
2. Acquired

genetic
traumatic
toxic
metabolic error
developmental
visual deprivation
voluntary
physiologic

Immediate Dx
Early management

Reduces long term consequences

All forms of nystagmus either present
1. At birth or
2. Noted in early infancy at the time of development of visual fixation

Throughout life.

The first few days or weeks.

No.

Establishment of accurate visual prognosis early on.

Many afferent and efferent visual disorders.

Its etioloy

The nystagmus was secondary to poor vision.

When it is known that the nystagmus wasn't there in early infancy and did develop as a consequence of poor vision.

The probable site of the lesion.

No

-Sensory (visual pathway) defect

-Primary motor abnormality

Heterogeneity

1. Autosomal dominant
2. Autosomal recessive
3. X-linked dominant
4. X-linked recessive

X-linked recessive is most common.

6p12

Variable expressivity

That expression can be modified by environmental influences.

When the nystagmus is associated with a disease or syndrome

With isolated nystagmus due to heterogeneity.

Onset
Associations
Variability
Symptoms
Ocular and General Health Hx
Family Hx!

Infection
Fevers
Meds
Trauma

Frequency
Amplitude
Gaze
Time characteristics

Developmental and Neurological
-Dizziness/nausea
-HA
-Local pain, numbness, tingling,
weakness
-seizures
-tinnitus (preipheral vestibular)
-gait irregularities

3 generations

Albinism
Achromatoplasia
Leber's

1. Global positioning
2. Type of nystagmus
3. Direction
4. Amplitude
5. Frequency
6. Constancy
7. Conjugacy
8. Symmetry
9. Latency
10. Field of Gaze Changes

Posture, head position, asymmetry

1. Pendular
2. Jerk
-long foveation
-short foveation
3. Mixed

X,Y,Z

fast phase of jerk

Less than 2 degrees

2-10 degrees

Greater than 10 degrees

Less than 0.5 Hz

Greater than 2 Hz

constant, intermittent, periodic

Conjugate
Disjunctive

symmetrical
asymmetrical
monocular

The nystagmus changes with occlusion of either eye.

Null point
Dampening
Or increase in a field of gaze or convergence

1. Physiologic
2. Congenital
3. Vestibular
4. Rare type

Before 6 months

Variable.

Any

Bilateral and horizontal (uniplanar)

In the same direction as the gaze.

Nystagmus increases when gaze coincides with direction of fast phase?

Compensatory head movement, though it doesn't usually compensate.

Because the head shaking can be equal in amplitude and opposite in direction to the waveform.

SLOFUN+

Symptoms - none

Latency - positive, beats AWAY from the occluder

OKN - double fast, inversion, Cogan's I&II

Fixation- worse when forced

Upgaze- stays horizontal

Null Point - Right, Left, Convergence

The nystagmus is gone with lid closure and sleep

40%
60%

High refractive error
ON hypoplasia or atrophy
Cataracts
Glaucoma
Albinism
Leber's Amarosis
Achromatoplasia
Pupil abnormalities (aniridia)
Retinal abnormalities (with ERG)

50%

Esotropia

1. Cause by same mechanism as
nystagmus
2. Compensates for nystagmus

1. astigmatism
2. accommodative dysfunctions

1. Pendular nystagmus (X,Y, or Z,
fast, small amplitude)
2. Head nodding (noncompensatory
and intermittent)
3. Abnormal head position

Tends to be asymmetric

4-18 months

12-24 months

Rule out pathology with CT scan
Monitor

As infantile jerk nystagmus

DAMPENS on convergence causing esotropia to reduce the nystagmus and improve visual acuity.

Infancy with the congenital nystagmus preceding the esotropia.

The adducted eye fixates

Head turned toward the adducted eye.

The eye would stay adducted when the other eye is occluded.

Forced primary gaze
Abduction

Spectacles with BO prism (possibly -1.00 D too)
Refer for surgery (but is very complicated)

Brainstem or cereballar etiology

Upbeat with upgaze and downbeat with downgaze

The side that has the lesion or disease.

Any (X,Y,Z)

Peripheral

Chiasmal glioma

Neurologist or neuro-ophthalmologist

Because determining etiology is very difficult.

1. Refer for Tx of underlying pathology
2. Therapy to dampen oscillations
3. Functional and cosmetic
improvement

Dx: Careful
Management: Aggressive

Monitoring without treatment.

1. Correct refractive error
2. Prisms to improve fusion, induce
convergence, and/or reduce head
turn
3. Vision therapy to improve fusion
capability and enhance stability
of fixation.
4. Surgery to reduce head turn or
increase foveation time.
5. Medication in some cases
dampens nystagmus or reduces
symptoms.

Improve VAs
AND
Help dampen and stabilize the nystagmus. (primate models)

RGPs

To achieve better control of nystagmus by correcting undetected corneal astigmatism AND by providing tactile feedback through lid interactions with the RGP.

Increase clarity
Reduce accommodative demand for children with distance Rx.

To place eyes in the null area and reduce head turn.

Left head turn

Base in over the left eye and equal base out over the right eye.

2 prism diopters

cosmesis
Fresnel prisms can be used for larger prism power, but cosmesis still isn't good and it reduces VAs.

Frames with small eye sizes.

greater than 15 degrees.

Base out prism

It stimulates convergence which can dampen the nystagmus and improve VA.

Induced Asthenopia

1. Orthoptic Vision Therapy
2. Visual Biofeedback
3. Auditory Biofeedback
4. Intermittent Photic Stimulation
5. Vertical Line Counting

Step 1: antisuppression and sensory fusion therapy
Step 2: enhancement of motor fusion in a natural environement

The goal: decrease the intensity of nystagmus as binocular vision is enhanced.

Used to help move the null area toward primary gaze.

Afterimage flash generated foveally is used to give biofeedback when the patient tries to stabilize their eyes on a target of progressively smaller size.

Uses IR eye movement monitors to convert the signal to an audible tone so the patient can hear the nystagmus and attempt to control it.

The old eyetrac

Rapid, but difficult to sustain.

Intermittent Photic Stimulation

6-8 months

About 6 weeks after initial strong improvement.

The patient counts the number of lines on a sheet of paper at 40 cm, and as the patient improves the lines are moved closer together or the sheet further away.

Good results

Inexpensive and easy

1. Pharmacological
2. Surgical

To compensate for faulty function of neural integrator (GABA/glycinergic)

To relieve oscillopsia

Acquired

Baclofen

Clonazepam

Gabapentin
Memantine

Scopolamine

Keep dosage down so side effects are minimal.

Reduce head turn in order to move the null area to primary position and improve VA.

greater than 15 degrees

Age 5

Anderson-Kestenbaum procedure

Mixed - confounded by stabismus

Surgery to recess, and detach all EOMS to limit movement of the globe.

Not in US, a little better in Europe

Four muscle tenotomy

Cutting and reattaching the EOMs changes the afferent-efferent feedback loop.

Measured in increased foveation time.