Nystagmus ppt PowerPoint Presentation

					      NYSTAGMUS
    AETIOPATHOGENESIS
TYPES AND CLINICAL FEATURES




    SPEAKER : KUMAR SAURABH
HISTORICAL OVERVIEW




   Nystazho{Greek} Wobbly head movements
                    of a sleepy or inebriated
                    individual.
DEFINITIONS

Nystagmus : Involuntary,biphasic,rhythmic ocular
                oscillation which can be either physiological or
                pathological.



Pursuit       : Slow and smooth movements of the eyes to follow a
                moving target in the environment.




Saccade       : Rapid jerky movement of the eyes to bring back the
                image of the target on to the fovea.
CLASSIFICATION
AETIOLOGICAL CLASSIFICATION

                           Nystagmus


 Physiological                                     Pathological

                              Congenital                          Acquired
 End gaze

                                                                  Toxic
                             Infantile manifest
 Optokinetic

                                                                  Neurological
                             Infantile Latent
 Vestibulo-ocular reflex

                                                                  Visual loss
                             Infantile Manifest-latent

                                                                  Functional
BASED ON MANIFESTATION
                                Manifest

                                Latent

                                Manifest-latent


BASED ON PATTERN OF MOVEMENT
                                Jerk

                                Pendular


BASED ON DIRECTION OF MOVEMENT
                             Horizontal

                             Vertical

                             Rotary
PATHOGENESIS OF NYSTAGMUS
SIX LEVELS OF OCULAR MOTOR SYSTEM   1.
                                    UPPER MOTOR NEURON
                                       (Cerebral cortex)
  4.
       CEREBELLUM

                                    2.
                                     PRE-MOTOR NEURONS
                                         (Brain stem)




                                    3.
                                    LOWER MOTOR NEURON
                                      (Ocular motor neuron,
                                     Neuromascular junction)

  5.
  VESTIBULAR NUCLEUS

                                    6.
                                    EXTRAOCULAR MUSCLES
Upper Motor Neuron   Nystagmus
Lesion               Gaze palsy
(Supranuclear)
                     Involuntary eye movements




Lower Motor
Neuron               Paralytic strabismus
(Infranuclear)
CORTICAL CENTRES FOR MOTOR CONTROL


                         PURSUIT SACCADE

                Occipital motor area Frontal eye field (FEF)


                                         Supplementary eye field (SEF)
            Middle temporal area (MT)


   Middle superior temporal area (MST)   Dorsolateral prefrontal cortex (DLPFC)


                                         Posterior eye field (PEF)
BRAINSTEM CENTRES FOR MOTOR CONTROL
(Saccade+Pursuit)


HORIZONTAL GAZE CENTRE   VERTICAL GAZE CENTRE




   PARAMEDIAN PONTINE      ROSTRAL INTERSTITIAL
   RETICULAR FORMATION     NUCLEUS OF
         (PPRF)            MEDIAL LONGITUDINAL
                           FASCICULUS (riMLF)
CLINICAL FEATURES
  GENERAL SYMPTOMS :    To-and-fro Movement of Eyes.
                        Reduced Visual Acuity.
                        Blurred or Unstable Vision.
                        Oscillopsia : At >8 years of age.



      GENERAL SIGNS :   Repetitive movements of eyes.


                        • Binocular or monocular
                        • Direction
                        • Waveform
                        • Effect of gaze
                        • Conjugate or dysconjugate
                        • Any change with change in posture.
                        • Periodicity
                        • Any associated movement.
  JERK NYSTAGMUS

• Slow defoveating drift
• Fast refoveating saccade
• Direction – Fast component
• Horizontal,vertical or rotatory
• Gaze evoked : Vestibular
• Gaze paretic : Brain stem damage
 PENDULAR NYSTAGMUS


•Sinusoidal,nonsaccadic
•Slow and equal velocities
•Congenital or acquired
•Horizontal,vertical,elliptical,torsional
•Involvement of pontine tegmentum mainly
•Special types :--
CONVERGENT-DIVERGENT    NYSTAGMUS


                Dysconjugate
                Horizontal in opposite direction
                Demyelinating disease

CYCLOVERGENT   NYSTAGMUS


                Dysconjugate
                Torsional
                Upper poles move in opposite direction.
PHYSIOLOGICAL NYSTAGMUS




         END POINT NYSTAGMUS


         Jerk nystagmus


         On looking extreme lateral or upwards


         Angle of gaze > 45 degrees
 VESTIBULAR NYSTAGMUS

        Jerk nystagmus

         Altered inputs from vestibular nuclei to PPRF

         Demonstrated by Caloric Test
                    Cold water – Opposite direction
                    Warm water – Same direction
                    Cold water in both ears – Upwards
                    Warm water in both ears -- Downwards
 OPTOKINETIC NYSTAGMUS

               Jerk nystagmus


               Induced by moving a full visual field stimulus


               Slow phase (Pursuit): Eye follows the target


               Fast phase (Saccade): Eye fixates on the next target


               Used for– Detecting malingerers
                         Testing visual acuity in young
PATHOLOGICAL NYSTAGMUS



          UPBEAT NYSTAGMUS

      Jerk nystagmus with fast phase upwards.

      Defect : Anterior semicircular canal projections.

      Lesion:Pontomedullary or pontomesencephalic
      junctions.

      Amplitude increases on upgaze and supine posture.

      Causes : Wernicke’s encephalopathy,
              Organophosphates and anticonvulsants,
              Lithium,Nicotine,Thallium.
       DOWNBEAT NYSTAGMUS
Jerk nystagmus with fast phase downwards.
Defect : Posterior semicircular canal projections.
Lesion : Commissural fibers between vestibular nuclei.
         Flocculus at the craniocervical junction.


Amplitude increases with lateral and downward gaze { Daroff's sign }
May be visible only with change of posture viz. head hanging.


Causes: Chiary malformation Type I,
         Foramen magnum tumors,
        Alcoholism,
        Amiodarone,toluene,anticonvulsants
         Magnesium depletion,
         Vitamin B12 deficiency.
 SEESAW NYSTAGMUS (SSN)

   Pendular nystagmus.
   One eye rises and intorts;other eye falls and extorts.
   Lesion : Midbrain-thalamic junction.


   Faster and smaller on upgaze;
   Slower and larger on down gaze.
   Ceases in darkness.


   Acquired SSN: Suprasellar tumors,
                  Leigh’s syndrome,
                  Jobert’s syndrome
   Congenital SSN : Achiasmia.
 GAZE EVOKED NYSTAGMUS

  Jerk nystagmus.

  Absent in primary gaze.
  Appears on eccentric gaze.

  Fast phase in the direction of gaze.

  3-8 beats/second ,coarse.

  Defect in neural integrator.

  Causes : Old age, Alcohol intoxication,
           Cerebellar or brain stem disease,
           Barbiturates.
 GAZE PARETIC NYSTAGMUS

            Jerk nystagmus.
            Most common nystagmus.

            Absent in primary position.
            Appears on eccentric gaze.

            Fast phase in the direction of gaze.

            1-2 beats/second, symmetrical or asymmetrical.

            Causes : Brain stem damage at pontine level.
 PERIODIC ALTERNATING NYSTAGMUS

  Horizontal jerk nystagmus.

  Present in primary position.

  Crescendo-decrescendo fashion.
  During transition nystagmus stops or beats vertically.

  90 + 90 = 180 seconds or 3 minutes (approximately).

  May be congenital or acquired.

  Lesion : Damage to the craniocervical junction.
 REBOUND NYSTAGMUS


 Horizontal gaze evoked nystagmus.

 Nystagmus beats transiently in opposite
 direction after return to primary position.
 ( 3 – 25 seconds ).
 BRUN’S NYSTAGMUS
        Jerk nystagmus.
        Bilateral, asymmetrical.
        On the side of lesion :Large amplitude,low frequency oscillations.
        On the opposite side :Small amplitude,high frequency oscillations.
        Cause : Large cerebello-pontine angle tumor.




 EPISODIC NYSTAGMUS
        Paroxysmal episodes of ataxia, vertigo and nystagmus.

        Lasting up to 24 hours.

        Causes :Inborn errors of metabolism
                Basilar migraine
                Multiple sclerosis
 ICTAL NYSTAGMUS

          Occurs during refractory seizures.

          Mostly horizontal ; may be vertical.

          Generally directed opposite to the site of epileptogenic focus.




 LID NYSTAGMUS
          Rhythmic jerky movements of the upper eye lid.

          Conditions when lid nystagmus occurs:

               Synchronous with vertical nystagmus

               Synchronous with fast phase of gaze evoked nystagmus.

               Midbrain tumors.

               During voluntary convergence in cerebellar disease
CONGENITAL NYSTAGMUS

    Pendular or jerk type.
    Pendular nystagmus often becomes jerk on lateral gaze.


    Mostly horizontal,rarely vertical.
    Increased amplitude on vertical tracking and distant fixation.
    Decreased amplitude on convergence.
    Increased amplitude when one eye is covered (Latent superimposition).
    May be minimal at a particular point of gaze (Null zone).
    Reversal of optokinetic response is characteristic.
FEATURES OF CONGENITAL NYSTAGMUS


          Present at birth but may be detected later.

          Good vision unless there is an afferent defect.

          No oscillopsia.

          Head titubation may be seen.

          Causes :Autosomal recessive or X linked.
                  Achiasmia,
                  Achromatopsia,
                  Albinism,
                  Aniridia,
                  Congenital cataract
                  Retinopathy of prematurity,
                  Optic nerve hypoplasia.
    MANIFEST NYSTAGMUS
  Nystagmus present with binocular vision.


       LATENT NYSTAGMUS
No nystagmus with binocular vision.

Nystagmus with monocular fixation with other eye covered.

Slow phase is directed towards covered eye.

Amplitude increases with abduction of fixating eye.


   MANIFEST LATENT NYSTAGMUS
 Nystagmus present with binocular vision.


 Amplitude increases when one eye is covered.
 SPASMUS NUTANS
                Transient pendular nystagmus.

                High frequency, low amplitude.

                Horizontal, vertical or torsional.

                Dysconjugate and asymmetrical.

                May be monocular.

   Spasmus Nutans Triad : Nystagmus, Torticollis, Titubation.

                Onset : 6 – 12 months

               Duration : Up to 2 years; maximum 5 years of age.

               Causes : Glioma of anterior visual pathway
                        Empty sella syndrome
                        Porencephalic cyst.
NYSTAGMOID MOVEMENTS



               OCULAR FLUTTER

     Horizontal and conjugate movements.
     Intermittent bursts of back-to-back saccades.
     Triggered by change of posture.
     Aggravated by attempt at fixation.




     Defect : Loss of pause cell inhibition of burst neurons at PPRF.
 OPSOCLONUS



         Multivector saccadic eye movements.

         Spontaneous, chaotic but conjugate movements.

         Aggravated by attempt at fixation.

         May be associated with myoclonic jerks of limbs
         and cerebellar ataxia.
         { Dancing feet-dancing eye syndrome }

         Cause :Viral encephalitis,
               Multiple carboxylase deficiency,
               Hyperosmolar coma,
               Multiple sclerosis,
               Neuroblastoma.
 CONVERGENT RETRACTION NYSTAGMUS

         Dysmetric horizontal eye movement upon
         attempted upward saccade.

         Rapid convergence with retraction of both globes.
         Followed by slow divergent movement.

         Cause : Co-contraction of extraocular muscles.

         Seen in : Dorsal midbrain ( Perinaud’s ) syndrome.
 OCULAR BOBBING


        Rapid downward movement of both eyes.

        Followed by slow drift back to primary position.

        Seen in : Comatose patients.
 OCULAR MYOCLONUS


        Vertical pendular oscillations.

        Frequency : 160 Hz.

        Associated with similar oscillations of soft palate.
                        { Oculopalatal syndrome }


        Cause : Infarction at the pons.
 VOLUNTARY NYSTAGMUS


         Ocular flutter under voluntary control.

         Usually horizontal.

         May be vertical, torsional or cycloid.

         Patient converges to initiate the ‘nystagmus’.

         Can be sustained up to 30 seconds.

         Familial inheritance.

				
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