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Dr. Ashraful Huq (Ridoy)
FCPS
+8801811999070
dr.ashraf.ridoy@gmail.com
Eye Specialist & Surgeon
Bangladesh Eye Hospital Ltd.
 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
 Disturbance in sensory –motor apparatus
 Exaggeration of fine persistent movement of the
eyes
 A defect in slow eye movement system
 Physiological
• End- gaze
• Optokinetic
• Vestibulo-ocular reflexes
 Pathological
• Motor imbalance nystagmus
• Sensory deprivation nystagmus
 Based on onset
 Congenital
 Acquired
 Based on direction of movement
 Horizontal
 Vertical
 Rotatory
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
Courtesy : Neuro-Ophthalmology Dept., NIO&H
 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
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
↶
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
Congenital
 Infantile manifest
 Idiopathic
 Albinism
 Aniridia
 Bilateral congenital
cataract
 Bilateral optic nerve
hypoplasia
 Infantile latent
 Infantile manifest-
latent
Acquired

Secondary to visual
loss

Toxic or metabolic
(alcohol, barbiturates,
phenytoin, salicylates)

Neurological
disorders
( tumour, trauma, MS,
stroke)

Non-physiological,
non-organic i.e.
functional
 Congenital
 Spasmus nutans
 Latent
 Sensory deprivation nystagmus
 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
 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.
 Congenital
 Upbeat
 Down beat
 See-saw
 Convergence retraction
 Periodic alternating
 Ataxic
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
 VA recorded with and without AHP, distant and near
 Binocular vision assessment
 Extra-ocular motility examination
 Slit-lamp examination
 Fundoscopic examination
Physical Examination
 Character of nystagmus
 Character to be scanned—
 Rate
 Amplitude
 Direction
 Null point
 Coexisting head turn or oscillation
 Routine investigation
 Special investigation
 Electro-nystagmograph
 Video Nystagmography
 CT scan / MRI of brain
 Decrease abnormal eye movements
 Decrease oscillopsia
 Gain maximum visual acuity
 Treatment of underlying cause
 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
 Gabapentin
 Memantine
 4-aminopyridine
 3,4-diaminopyridine
 Baclofen
 Clonazepam
 Valproate
 Trihexyphenidyl
 Benztropine
 Scopolamine
 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
 Botulinum toxin
 Acupuncture
 Biofeedback
 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
Nystigmus

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Nystigmus

  • 1. Dr. Ashraful Huq (Ridoy) FCPS +8801811999070 dr.ashraf.ridoy@gmail.com Eye Specialist & Surgeon Bangladesh Eye Hospital Ltd.
  • 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
  • 4.  Physiological • End- gaze • Optokinetic • Vestibulo-ocular reflexes  Pathological • Motor imbalance nystagmus • Sensory deprivation nystagmus
  • 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
  • 8.
  • 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
  • 12.
  • 13. Congenital  Infantile manifest  Idiopathic  Albinism  Aniridia  Bilateral congenital cataract  Bilateral optic nerve hypoplasia  Infantile latent  Infantile manifest- latent Acquired  Secondary to visual loss  Toxic or metabolic (alcohol, barbiturates, phenytoin, salicylates)  Neurological disorders ( tumour, trauma, MS, stroke)  Non-physiological, non-organic i.e. functional
  • 14.  Congenital  Spasmus nutans  Latent  Sensory deprivation nystagmus
  • 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.
  • 17.
  • 18.  Congenital  Upbeat  Down beat  See-saw  Convergence retraction  Periodic alternating  Ataxic
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  • 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
  • 29.  Gabapentin  Memantine  4-aminopyridine  3,4-diaminopyridine  Baclofen  Clonazepam  Valproate  Trihexyphenidyl  Benztropine  Scopolamine
  • 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
  • 31.  Botulinum toxin  Acupuncture  Biofeedback
  • 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