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update of Nystagmus 14 11-2012


update of Nystagmus

update of Nystagmus

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  • physiological( includes optokinetic , caloric test , rotation acceleration produce nystagmus in the plane of rotation with slow phase in the same and fast in the opposite direction


  • 2. Highest level of visual acuity • 3 mechanisms are involved in maintaining foveal centration of an object of interest: 1- Fixation, 2- Vestibulo-ocular reflex, 3- Neural integrator. Aymanneuro: omar3SARAm
  • 3. 1- Fixation • Fixation in the primary position involves the visual system's ability to detect drift of a foveating image and signal an appropriate corrective eye movement to refoveate the image of regard. The vestibular system is intimately and complexly involved with the oculomotor system
  • 4. 2-Vestibulo-ocular reflex • a complex system of neural interconnections that maintains foveation of an object during changes in head position. The proprioceptors of the vestibular system are the semicircular canals of the inner ear. Three semicircular canals are present on each side, anterior, posterior, and horizontal. The semicircular canals respond to changes in angular acceleration due to head rotation
  • 5. 3- Neural integrator • A gaze-holding network called the neural integrator generates the signal. The cerebellum, ascending vestibular pathways, and oculomotor nuclei are important components of the neural integrator • maintain a constant innervation of extra-ocular eye muscles to avoid backward drift of the eyes. • deficit in the neural integrator can result in gazeevoked nystagmus and oscillopsia in the eccentric eye position.
  • 6. Movement of eye ball • The movement are tested uniocular (duction) as well as binocularly (versions) in all the 9 diagnostic positions of gaze. • Uniocular – Adduction, abduction, depression, elevation, de pression and elevation in adduction and abduction
  • 7. Terminology • Duction: describes movement of one eye – Abduction – Adduction – Supraduction or elevation – Infraduction or depression – Incycloduction or intorsion – Excycloduction or extorsion
  • 8. Terminology • Version: describes movement of two eyes in the same direction(conjugate). – Dextroversion – Levoversion – Supraversion – Infraversion
  • 9. Terminology • Vergence: describes movement of two eyes in opposite directions – Convergence – Divergence
  • 10. Functions of Extra ocular Muscles • • • • • Superior rectus – moves eye up Inferior rectus – moves eye down left Medial rectus – moves eye in (a-d-duction) Lateral rectus – moves eye out (a-b-duction) IO– moves eye up when it is in an adducted position; also extorts the eye. • SO– moves eye down when it is adducted; also intorts the eye.
  • 11. Broad H Test
  • 12. Muscles and Their Fields of Action
  • 13. Broad H Test • Look for lags or overshoots at various diagnostic positions of gaze • Look for smooth and accurate pursuit movements • Look for any gaze restrictions or overactions of muscle in the 9 positions • Look for comitancy ( deviation of the visual axes remains constant in all fields of gaze, there is comitancy)
  • 14. Saccade Test • Test set-up is the same as for the broad H test • Direct patient to look quickly from positions 8 to 2, and then back to 8 • Repeat rapid shifts of gaze from positions 6 to 5, and then back to 6 • Look for accuracy of movement (i.e., overshoots and undershoots), speed of initiation ,latency and velosity.
  • 15. SYSTEMS THAT CONTROL EYE MOVEMENT Pursuit system  OKN system Saccadic system Vergence system Vestibular  Each of these systems are controlled by different anatomical pathways.
  • 16. Control of Gaze 1) Gaze Stabilisation system. 2) Gaze alignment system.
  • 17. Gaze Stabilisation System Compensates for self-motion stabilising visual world on the retina to achieve highest vision -Vestibulo-ocular system -Optokinetic System (fixation) - Neural integrator.
  • 18. Gaze Stabilisation System • Main mechanisms of maintaining steady gaze: 1) fixation (Optokinetic System) (vol): >6months a) prevent retinal image drift Moving b) suppress unwanted saccades object 2) Vestibulo-ocular reflex (VOR): is a reflex eye movement (pursuit) that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field.
  • 19. Gaze Alignment System Keeps object of interest within the visual world centred on fovea: -Saccades -Smooth pursuit
  • 20. Object Tracking Movements • Saccade : (voluntary) fast, step-like eye movement (up to 1000 deg/sec) that places image of the target on the fovea – Reading -Looking from point A to B – alternate fixation bet different objects – How to elicit? 1-Voluntary (internally triggered) 2 -Reflexive (externally trig by visual or auditory stimuli) 3- Spontaneous (searching, REM of sleep) 4-Fast phases of nystag (physiologl or patholog).
  • 21. Pursuit system • Pursuit : (reflex) slow, smooth-following movement (up to 30 deg/sec) that maintains image of the moving target on the fovea. The generation of PE movement consists of 3 essential elements: • A sensory component driven by an image moving across the fovea. • A motor component generated near the parieto– occipito–temporal junction that projects to the ipsilateral PPRF. • An attentional–spatial comp for concentration on selected targets, orientation in space.
  • 22. Centers of Conjugate eye movement • Saccades =contralateral frontal pre-motor area • Pursuit= ipsilateral occipito-parietal area • Vestibular reflexes= vestibular nuclei in the Pons: pathways contain relatively few synapses (23) → very fast response (<6 ms) • 3 primary reflexes: – vestibulo-ocular (VOR) -vestibulocerebellar – Vestibulospinal
  • 23. SUPRANUCLEAR GAZE CONTROL • Signals which control ocular movement are initiated in • • • • • the cerebral hemispheres. They are then transmitted to the gaze centres and oculomotor nuclei in the midbrain and pons and leave the brain in the 3rd, 4th and 6th cranial nerves Supranuclear neuronal pathways: conduct impulses from cerebral hemispheres to gaze centres Internuclear pathways: conduct impulses from gaze centres to ocular motor nucleii Infranuclear pathways: 3rd, 4th and 6th cranial nerves There are three forms of conjugate eye movement
  • 24. • These impulses are transmitted to the gaze centres, • • • • which mediate the conjugate eye movement. Horizontal and vertical gaze control are quite separate. The horizontal gaze centre is in the pons at the level of the 6th nerve nucleus. Horizontal movement to the left is controlled by the left horizontal gaze centre and vice-versa for the right. The vertical gaze centre is in the midbrain but not much is known about vertical gaze control.
  • 25. Lesions • Unilateral lesions of the PPRF produce characteristic findings Loss of horizontal saccades directed towards the side of the lesion. • Contralateral gaze deviation (acute lesions, such as early stroke) • Gaze-evoked lateral nystagmus on looking to the direction of previous gaze palsy (recovery). • Bilateral lesions produce horizontal gaze palsy and slowing of vertical saccades.
  • 26. Vergence System Enables eyes to move disconjugately in the H plane and allows binocular fixation of an object that moves toward (converg) or away (diverg) from the subject. The main stimuli for Verg are retinal blur (unfocused object) and diplopia (fusional disparity); converg is associated with accommod and miosis (the near triad). The pathways that generate Verg are not known precisely, but the occipital lobe, MB, and cerebellum play significant roles.
  • 27. Gaze Palsies • An inability to make a conjugate ocular movement in one direction. • This does not cause diplopia since the visual axes remain parallel. • By investigating each reflex and conjugate movement in turn, it is possible to establish where a lesion exist.
  • 28. Horizontal Gaze Palsies • • • • Unilateral horizontal GP. Bilateral HGP. INO. One and half syndrome.
  • 29. INO Think: Elderly-small vessel disease Young Adult-MS Child-Pontine Glioma
  • 30. One and a half syndrome • Complete HGP in one direction and an INO in the other". • limitation of horizontal eye movement to abduction of one eye (e.g. right eye ) with no horizontal movement of the other eye (e.g. left eye). • Nystagmus is also present when the eye on the opposite side of the lesion is abducted. • Convergence is classically spared as Cranial Nerve III (oculomotor nerve) and its nucleus is spared bilaterally.
  • 31. The syndrome usually results from single unilateral lesion of the PPRF and the ipsilat MLF. An alternative anatomical cause is a lesion of the abducens nucleus (VI) on one side, with interruption of the ipsilateral MLF after it has crossed the midline from its site of in the contralateral oculomotorius (III) nucleus (resulting in a failure of adduction of the ipsilat eye).
  • 32. One and a half syndrome Fast Rt Lt
  • 33. Vertical Gaze Palsies • Dorsal midbrain (parinaud s) syndrome (Convergence-retraction Nystagmus). • Skew deviation. • Vertical one and half syndrome • Ocular tilt reaction (OTR).
  • 34. parinaud’s Convergenceretraction Nystagmus • Loss of upword gaze involving all types of ocular movement. • Upon attempt to upword saccade there is converg with retraction of the globe followed by diverg. movement • Not a true nystagmus: co-contraction of horizontal recti on attempted upgaze • Loss light reflex • Commonly associated with dorsal midbrain syndrome • Localizes to pretectal area, posterior commissure. • Pineal cyst or tumor, demyelination, stroke.
  • 35. Skew deviation  Skew deviation, is a relatively common supranuclear vertical divergence of the eyes that is associated with lesions in the posterior fossa, particularly those involving the brainstem tegmentum from the diencephalon to the medulla oblongata  With INO higher in the side of lesion.
  • 36. Definitions • Nystagmus: involuntary rhythmic oscillation of the eyes that is initiated by a slow phase. The oscillations may be sinusoidal and of approximately equal amplitude and velocity (pendular N) or, more commonly, with a slow initiating phase and a fast corrective phase (jerk N) or mixed. • N is common with a prevalence of around 0.1%. Examined by fixation of the to 30 degree from gaze center.
  • 37. Definitions • Saccadic oscillation: burst of saccades which may be intermittent or continuous disrupting fixation ( intersaccadic interval and back to back saccades). • Oscillopsia: visual disturbance in which objects in the visual field appear to oscillate. • Previously Nystagmus considered untreatable, in recent years several pharmaceutical drugs have been identified for treatment of Nystagmus.
  • 38. Clinical features •Symptoms : TO and Fro movement of the eye , reduced visual acuity, blurred vision , oscillopsia ( > 8 years). • Signs: Repetitive movement of the eye Binocular or monocular Direction Wave form Effect of gaze Associated movement, Any change with change posture, Periodicty.
  • 39. Common Effects • Nystagmus affects people in different ways. The most significant effect is the reduced visual acuity -Factors such as stress, tiredness, and nervousness can cause changes in ability to focus. -Distance visual acuity is poorer than near vision. -Balance may be affected due to poor depth perception or due to vestibular problems. -Head nodding is common (corrective). Also, child will often tilt his/her head to temporarily improve vision.
  • 40. Clinical Assessment • Ask patient to fix and follow on your finger (about 30 cm away) • Move slowly to Broad H Test waiting 5 seconds at each position • Do not move more than 30 degrees from midline • Nystagmus must be sustained for more than a few beats to be significant.
  • 41. Broad H Test
  • 42. Grading System (e.g. for right beating nystagmus) • Grade 1 = present in right gaze only • Grade 2 = present in right gaze and primary position • Grade 3 = present even in left gaze
  • 43. Classification of Nystagmus 1) Pendular Vs Jerky 2) Physiological Vs Pathological 3) Congenital Vs Acquired 4) Peripheral Vs Central 5) Spontaneous Vs Gaze-evoked
  • 44. NYSTAGMUS Rapid oscillatory movement of the eye balls Pendular • (cong or acq. central) -thought to be a result of a delay in messages to the brainstem -characterized by eye movements that are equally paced in each direction Jerky • (phys or path) -characterized by an FEM in one direction and a slower movement in the opposite direction -thought to result from extra input to the oculomotor system from the brainstem.
  • 45. General Types • Physiological:- A normal response that is induced because of excessive demand or imbalance in the vestibular or ocular motor system. • Pathological:- An abnormal response that occurs spontaneously or appears in an individual looking at a stationary object. -Congenital (early infancy-6 months) -Acquired (after 6 months).
  • 46. Physiological Nystagmus • Not due to a disease process. • Has no benefit, except as a diagnostic tool. • Types 1-Postrotational nystagmus. 2-End point nystagmus (extreme gaze). 3- Induced caloric testing (vestibulo-ocular reflex). 4-Optokinetic nystagmus. 5- Voluntary nystagmus.
  • 47. 1- Postrotatory nystagmus • If one spins in a chair continuously and stops suddenly, the fast phase of nystagmus is in the opposite direction of rotation, known as the "postrotatory nystagmus," while slow phase is in the direction of rotation.
  • 48. 2- Gaze-evoked nystagmus • GEN: healthy subject ; called end-point N (lower intensity and, more importantly, no other ocular motor abnormalities). • Gaze paretic nystagmus (pathological).
  • 49. 3-Caloric response= vestibular function • Caloric testing is dependent on endolymph convection currents. • Supine position head elevated 30 d 1st 30 Celsius water 5ml later 44 C in EM. • Normal response (after 20 sec)  Warm water in the right ear produces a rightbeating nystagmus  Cold water in the right ear produces a left-beating nystagmus
  • 50. Significance of caloric test • 1) Absent reactive eye movement suggests vestibular weakness of the HSC of the side being stimulated (canal paresis) (peripheral lesion) . 2) In comatose patients with cerebral damage, the fast phase of nystagmus will be absent as this is controlled by the cerebrum. As a result, using cold water irrigation will result in deviation of the eyes toward the ear being irrigated. If both phases are absent, this suggests the patient's brainstem reflexes are also damaged and carries a very poor prognosis.
  • 51. 4-Optokinetic nystagmus • OKN occurs normally in response to a rotation movement. The OKR allows the eye to follow objects in motion when the head remains stationary (e.g., observing telephone poles on the side of the road as one travels them in a car). The reflex develops at about 6 months of age. • How to elicit? OK drum. • Crude assessment of the visual system, particularly in infants. When factitious blindness or malingering is suspected, check for OKN to determine whether there is an intact visual pathway.
  • 52. 5-Voluntary nystagmus Horizontal Not true nystagmus but saccadic osscillation. Pt converge to initiates nystagmus, maintained up to 30 sec, ?? familial Biphasic FAST ONLY Back to back saccades No interval.
  • 53. Congenital • ‘Early vs onset N’-can be inherited (AD). • pendular, all positions • Defect in the eye or the visual pathway from the eye to the brain (sensory nyst). It can be a side effect of vision loss from eye diseases such as albinism, cataract, and glaucoma. • People are not likely to suffer from ‘oscillopsia’- constant moving image b/c the brain can adapt. (unaware of it) Acquired • ‘Late onset nystagmus’ • Can be acquired due to neurological dysfunction such a stroke, MS, or a head injury. • People are likely to suffer from ‘oscillopsia,’ which can cause a vertigo effect. • Medications such as Dilantin and Phenobarbital given to prevent seizures may cause nystagmus.
  • 54. CHILDHOOD NYSTAGMUS Congenital nystagmus • usually recognized in first few months of life – life long • May have good vision idiopathic ( motor, efferent, • • • • • • oculomotor abnormality) or poor vision (sensory, afferent) Failure of early sensorimotor integration Most often occurs in isolation (motor), but may be associated with albinism or optic atrophy Uniplanar, horizontal irrespective of gaze position, esotropia Dampened by convergence and darkness, in sleep increase by fixation , anxiety. Gabapantin 300mg qid, Memantine 10 mg qid
  • 55. idiopathic I N Null zone, in which nystag is minimal & VA maximaum. Uncertain; ?? afferent visual system anomalies; hereditary X linked (e.g., FRMD7 mutations). Gabapentin (300 mg qid) memantine (10 mg qid). Monocular nystagmus of childhood • Usually monocular, vertical, low amplitude oscillation • Eye with nystagmus may have afferent visual (sensory) dysfunction • Requires neuroimaging (chiasmal glioma).
  • 56. Latent nystagmus • Usually appears within first few months of life. • Horizontal jerk nystagmus appearing only under monocular viewing conditions. • Absent in binocular viewing. • Fast phase beats away from occluded eye • Strong association with esotropia • If there is ambylopia it present on binocular viewing Manifest latent nystagmus.
  • 57. Spasmus Nutans • Triad of nystagmus, head nodding and Torticollis • • • • (abnormal head posture, not corrective). Onset 3-15 months with disappear by 3 or 4 years. it may be present to age 5-6 years. The nystagmus typically consists of smallamplitude, high frequency oscillations and usually is bilateral, but it can be mono-cular, asymmetric, and variable in different positions of gaze. 2% Glioma of the anterior visual pathway. (Requires neuroimaging).
  • 59. ACQUIRED NYSTAGMUS • Occurs in many CNS disorders, especially those involving the cerebellum, brainstem and vestibular mechanism. • More common in adults – labyrithitis, – central vestibular disease/tumour, – cerebellar damage – BS diseases
  • 60. 1-VESTIBULAR NYSTAGMUS PERIPHERAL • • • • Severe vertigo (closing eye) Days to weeks duration Hearing loss, tinnitus Dampened with visual fixation • horizontal with torsion • unidirectional with the fast phase opposite the lesion • Very rarely purely vert or tor • Commonly peripheral vestibular organ dysfunction: labyrynthitis, meniere’s CENTRAL • None or mild vertigo. • Often chronic • visual fixation has no effect • May be purely vertical or torsion • the direction of the fast phase is directed toward the side of gaze (eg, left-beating in left gaze, rightbeating in right gaze, up-beating in upgaze). • Downbeat, upbeat, torsional • Etiologies commonly vasc, demyelination, pharmacologic, toxic
  • 61. 2- Gaze-paretic nystagmus • Gaze-paretic N: is most common form of N., • • • • • • recovering from a gaze palsy. Fast phase to direction of gaze. Usually symmetrical. Defect in NI Drug (anticonvulsant and tranquilizers) Alcohol. Asymmetrical dt structural BS or cerebellar.
  • 62. 3-Acquired pendular nystagmus – Mainly horizontal, vertical, torsional, or any combination (usually one predominates). – Oscillopsia ++ – asymmetric or even monocular. – asymmetric brainstem disease (MS, oculopalatal myoclonus). – Gabapantin 300mg qid, Memantine 10 mg qid – Congental due diminution vision ( searching).
  • 63. 4- Oculopalatal myoclonus • APN (Vertical) (1-4 Hz) associated with rhythmic upward movement of palate even during Sleep, possibly including face, neck, upper arm and diaphragm. • Caudal brainstem pathology: red nucleus, inferior olive, and dentate nuc Occurs 2-49 months after specific brainstem injury from stroke, trauma, neoplasm, brainstem angioma, MS, syringobulbia , encephalitis, degenerating conditions. • Oculomasticatory myorhythmia: convergence induced slow 1 HZ V pendular nyst. synchronous jaw contraction.(somnolence, altered mentation, mild uveitis, retinopathy) whipple s disease, MS, IS BS.
  • 64. 5- Periodic alternating nystagmus • Horizontal jerky N • Present in primary position • Cresendodecresendo fashion • Duration of cycles from 30 seconds to 3 minutes • Craniocervical j,BS, cerebellar tumour. • MS, drugs, ethanol, paraneoplastic syndromes • Baclofen (5-10 mg) (GABAergic) effective • ?? Memantine (antiglutamate).
  • 65. 6- Upbeat nystagmus • Present in PP or upword gaze. • Large amplitude N that increases in intensity with upward gaze. • Classically localizes to a lesion of ant cerebellar vermis and pontomedullary junction. • More generally implicates posterior fossa disease stroke, cerebellar deg, demyelination,tumours and Wernicke’s encephalopathy Baclofen (5–10 mg tid) 4-aminopyridine (5–10 mg tid)
  • 66. 7-Downbeat nystagmus • Vertical, upward slow drift of eyes. • Secondary downward corrective fast phase. • Present in PP or maximal intensity when the eyes are deviated laterally and slightly inferiorly, supine posture change to upbeats n. • Localizes to cervico-medullary junction. • Arnold-Chiari malformation 1.  Ttt with 4-Aminopyridine (Neurelan in USA) (5– 10 mg tid), 3,4-diaminopyridine (10–20 mg tid), baclofen (5 mg tid) clonazepam (0.5 mg tid).
  • 67. 8- Torsional nystagmus • Rotary movement of the globe about its AP axis accentuated on lateral gaze. • associated with other types of nystagmus APN . • lesions of the anterior and posterior SC on the same side (eg, lateral medullary syndrome). TN with the fast phase directed away from the side of the lesion. • accentuated by otolithic stimulation by placing the patient on their side with the intact side down (eg, if the lesion is on the left, the nystagmus is accentuated when the patient is placed on his right side).
  • 68. 9- Horizontal nystagmus • HN is a well-recognized finding in patients with a unilateral disease of the cerebellar hemispheres, especially with large, posterior lesions. It often is of low amplitude. Such patients show a constant velocity drift of the eyes toward the intact hemisphere with fast saccade directed toward the side of the lesion.
  • 69. 10- Bruns Nystagmus •Jerky , bilateral N •Slow, large amplitude nystagmus (gaze paretic N) when looking towards the side of the lesion (Lt). •Rapid, small amplitude nystagmus (vestibular N) when looking away from the side of the lesion. •Small vestibular schwannoma (11% <3.5 cm) •Large cerebello-pontine tumour >3.5 cm (CPA) 67%. •??AICA stroke
  • 70. 11- Ataxic Nystagmus • Abducting nystagmus of INO • Abducting nystagmus of INO is, as the name implies, nystagmus in the abducting eye contralateral to a medial longitudinal fasciculus (MLF) lesion • Fast away from side of lesion.
  • 71. One and a half syndrome Fast Rt Lt
  • 72. 12- Rebound Nystagmus • Horizontal • Gaze evoked • Beats transiently in opposite direction after return to primary position • 3-25 sec • cerebellar
  • 73. 13-See-saw nystagmus • Vertical (MB) N (pendular) • Upward moving eye intorts followed by downward and extorts other eye that alternates. • Chiasmal lesions , suggesting loss of the crossed visual inputs from the decussating fibers of the optic nerve or lesions in the midbrain-thalamic. • Bitemporal hemianopia. • Acquired SSN: suprasellar lesion or leigh disease. • Congential SSN (REVERSE): achiasma.
  • 74. 14-Searching Nystagmus Pendular common with congenital severe visual impairment, MS.
  • 75. 15- Episodic Nystagmus • Paroxysmal attacks of Ataxia, Vertigo, N. • Lasting 24 h. • Inborn error of metabolism. • Basilar migraine. • MS.
  • 76. 16- Ictal Nystagmus • • • • • • Occurs during refractory seizures. Horizontal. ?? Vertical (comatosed). ?? monocular. Fast phase opposite to epileptic focus. Adversive fits Pupillary dilation even oscillation may occur synchronous. • Periodic gaze deviation associated with periodic head rotation may be clue for seizure.
  • 77. 17- Lid Nystagmus • Rhythmic jerky movement of the upper eyelid. • 1st Synchronous with V N (Midbrain tumour) most common. • 2nd Synchronous with fast phase of HGEN ( lateral medullary syndrome). • 3rd type with voluntary convergence evoked nyst.
  • 78. Saccadic oscillation • Saccadic oscillation: burst of saccades which may be intermittent or continuous disrupting fixation ( intersaccadic interval and back to back saccades). • Nystagmus: involuntary rhythmic oscillation of the eyes that is initiated by a slow phase. The oscillations may pendular N or, more commonly, with a slow initiating phase and a fast corrective phase (jerk N) or mixed.
  • 79. Saccadic disorders 1-Square-wave saccadic jerks • (SWJ), the most common saccadic oscillation, consist of small saccades that take the eyes away from a fixation target, followed by a saccade in the opposite direction to bring the eyes back to the target, with an intersaccadic interval of 200 ms . • micro healthy individuals, • Macro in MS&OPCA and PD, PSP. . ?? cerebellar. NOT in dark • SWJ rarely degrade vision.
  • 80. 2- Oculomotor apraxia • failure to initiate saccades on command (congental or acquired (BS). • more correctly, congenital saccadic palsy, is more common in boys than in girls. Children > 4 m often 'thrust' their head from side to side to change the direction they are looking. 'Head Thrusts' are a typical movement that helps a child overcome their difficulty in moving their eyes quickly. Children may also blink to start a fast eye movement.
  • 81. OMA • MRI normal or may reveal poor development of • • • • regions of the brain, in particular the corpus callosum, cerebellum, and/or fourth ventricle. Association Ataxia T, cerebral whipple s disease. AE of OMA is usually not determined (idiopathic). long-term prognosis of children born with OMA The head thrusts associated with OMA typically diminish over time, but tend not to completely disappear. ?? true improvement versus an adaptive compensatory mechanism to mask the head thrust.
  • 82. 3-Ocular flutter • Intermittent burst-like, back to back saccadic in Purely • • • • • • horizontal plane with high frequency, low amplitude. No intersaccadic latency aggravated by change posture , attempt to fixation. Recovering from opsoclonus. Isolated OF in MS, Cerebellar signs. Voluntary OF in 8% of population in attempt to converge Dorsal midbrain lesion so associated with vertical gaze palsy (parinaud s syndrome).
  • 83. 4- Opsoclonus Myoclonus (OMS) • Eye : Opsoclonus (rapid, involuntary, chaotic, • • • • multidirection (horizontal ,vertical and torsional), unpredictable, conjugate fast eye movements without intersaccadic intervals). Myoclonus (jerky limbs) , fascial twitches , eye blinking, ataxia , (truncal , appendicular) . PPRF Called Dancing limb Dancing eye syndrome. MS, Hyperosmolar ketoacidosis, viral encephalitis. Drugs lithium,phyention, amitriptyline,cocaine.
  • 84. OMS • Paraneoplastic etiology: SCC of lung, ovarian, • • • • • breast CA, 50% of children with OMS have neuroblastoma , in 2% of children with neuroblastoma . Antineuronal abs anti Hu, Ri, Yo, Ma1 and antiamphyphyisin abs. ttt: propranolol, verapamil, clonazepam. Tumour removal. IVIG in idiopathic and postinfectious. Brain stem lesion (MB, Pons)
  • 85. 5- Ocular bobbing • Spontaneous, vertical, Sudden conjugate rhythmic • • • • downward jerk of the eyes followed by a slow return to the mid position. paralysis of horizontal conjugate gaze. pontine hemorrhage (comatosed). Atypical OB: intact horiz conj g (acute cerebellar hge, metabolic enceph, obst hydrocephalus). Reverse OB: fast movement is upward followed by delayed slow return (TS, EBV encephalitis).
  • 86. Social Impact • One major difficulty individuals suffering from nystagmus • • • • face is the lack of knowledge about the disorder, from the outside community. In conversation, sufferers with involuntary head movement may cause people to think they are disagreeing with what they are saying. Reading speed is likely to be affected because of the extra time and effort it takes to scan words. Some people are unable to get their driver’s license. People with the disorder find it difficult to play sports, especially those involving good hand to eye coordination.
  • 87. Nystagmus and alcohol • In police work, testing for horizontal gaze nystagmus is one of a battery of field sobriety tests used by officers to determine whether a suspect is driving under the influence of alcohol. • The test involves observation of the suspect's pupil as it follows a moving object, noting lack of smooth pursuit, distinct and sustained nystagmus at maximum deviation, and the onset of nystagmus prior to 45 degrees. • published by the National Highway Traffic Safety Administration.
  • 88. tullio’s phenomenon • sound-induced subjective and objective responses. The subject may feel sensations of unsteadiness, imbalance or vertigo, associated with disturbances of oculomotor and postural control. • TP is provoked by very loud sound if physiological. It is pathological if it is provoked by normal sounds. Changes to the functioning and/or the morphology of the labyrinth should be looked for in patients with the pathological form: decreased thresholds for the acoustically evoked vestibular potentials, SC dehiscence, traumatic lesions of the labyrinth, ligament hyperlaxity.
  • 89. tullio’s phenomenon • Tullio’s phenomenon (TP) is a pattern of sound-induced imbalance symptoms, motor responses of the eyes (nystagmus), head (myogenic responses) and other spinal neuron synkinesis (postural sway).It may be physiological or pathological. • Pathological Tullio’s phenomenon is characterised by subjective and objective sonovestibular symptoms resulting from abnormal hypersensitivity to normal sounds of the vestibular end organs secondary to morphological changes in vibration and pressure transmission between the external and the inner ear.