2. Nystagmus is a rhythmic, biphasic, repetitive,
involuntary, to and fro oscillation of the eyes
Consist of a defoveating & a re-foveating
movement
Usually bilateral
Greek word – to nod
3. Disturbance in sensory –motor apparatus
Exaggeration of fine persistent movement of the
eyes
A defect in slow eye movement system
5. Based on onset
Congenital
Acquired
Based on direction of movement
Horizontal
Vertical
Rotatory
6. Based on pattern of movement
Jerk
- slow drift followed by fast corrective phase
-gaze evoked (ie. vestibular )
-gaze paretic (brainstem)
Pendular-
-velocity equal in both directions
-horizontal, vertical, oblique, rotatory
Mixed
-pendular in primary position, jerk on lateral gaze
9. Based on Pattern of Manifestation
Manifest
Latent
Manifest-latent
On the basis of Amplitude (how far the eyes move)
Fine
Coarse
On the basis of Frequency (how often the eyes
oscillates)
High
Moderate
low
10. Moderate frequency
Moderate amplitude
Upbeat nystagmus
Low frequency
High amplitude
Right beating nystagmus
Low frequency
Moderate amplitude
Pendular nystagmus
High frequency
Low amplitude
Left beating nystagmus
Low frequency
High amplitude
Circumrotary nystagmus
↶
11. End- gaze Optokinetic Vestibulo-ocular reflexes
Occurs in extreme gaze Induced by moving,
repetitive stimuli across
the visual field
Elicited by caloric tests-
COWS
Jerk Jerk Jerk
Fast phase being in the
direction of the gaze
Slow phase follows target
& fast phase fixates on to
next target
Slow phase controlled by
ipsilateral parito occipetal
lobe & Fast phase
controlled by contra lateral
FEF
Slow phase controlled by
vestibular Nucleus &
Fast phase controlled by
fronto mesencephalic path
way
Subside after 10- 20 sec Useful in determining
malingering & recording
V/A in non verbal child
15. Due to congenital anomaly of motor system or
congenital disorder of vision
Conjugate horizontal jerk/ pendular pattern
Visual impairment is variable
Null point present
No osscilopsia
Accentuate by distant fixation, decreased by
convergence
Absent in sleep
16. Acquired nystagmus
Spontaneously disappear by the age of 4 years
May be assymmetric and monocular
Triad of signs – Nystagmus, Head nodding,
Torticollis
Associated with glioma, empty sella syndrome.
23. CLINICAL HISTORY
Age of onset
Oscillopsia-a sense of oscillation of
environment
Vestibular abnormalities
CNS Lesion
Strabismus/ Amblyopia
Family history
Drug history
H/O previous treatment taken
24. VA recorded with and without AHP, distant and near
Binocular vision assessment
Extra-ocular motility examination
Slit-lamp examination
Fundoscopic examination
25. Physical Examination
Character of nystagmus
Character to be scanned—
Rate
Amplitude
Direction
Null point
Coexisting head turn or oscillation
26. Routine investigation
Special investigation
Electro-nystagmograph
Video Nystagmography
CT scan / MRI of brain
27. Decrease abnormal eye movements
Decrease oscillopsia
Gain maximum visual acuity
Treatment of underlying cause
28. PRISMS- to shift gaze into null point
SOFT CONTACT LENSES - help probably by
stimulating trigeminal afferent nerve
SPECTACLE- improves vision and this
suppresses latent nystagmus
30. AIM – to shift the null point from eccentric
position to straight ahead position
KESTENBAUM ANDERSON procedure-
Recession of horizontal muscles-version is
blocked, to make the null point in primary
position
FADEN procedure
32. Nystagmus is a clinical sign, not a disease itself
Usually congenital
Treatment depends upon a correct
identification of cause
Early detection and treatment of underlying
cause can cure nystagmus