Ocular motility




CONCOMITANT ESOTROPIA


In a comitant deviation the angle is the same, or nearly the same, for all positions of gaze; the two types are non-accommodative and accommodative.


Non-accommodative


Early-onset (infantile)


Presentation





  • Before the age of 6 months.



Signs





  • Large and stable angle with no significant refractive error.



  • Fixation may be alternating in the primary position with cross fixation in side-gaze ( Figs 14.1 and 14.2 ).




    Fig. 14.1



    Fig. 14.2



Look for





  • Latent and manifest-latent nystagmus.



  • Inferior oblique overaction may be present initially or develop later.



  • Dissociated vertical deviation (DVD) which often develops by the age of 3 years.



Differential diagnosis ( Table 14.1 )




Table 14.1

Differential diagnosis of early-onset esotropia








  • Congenital bilateral sixth nerve palsy



  • Secondary (sensory) esotropia (see Figs 14.3 and 14.5 )



  • Nystagmus blockage syndrome in which convergence dampens a horizontal nystagmus



  • Duane syndrome types I and III (see Figs 14.16 and 14.17 )



  • Möbius syndrome



  • Strabismus fixus



Basic near


Presentation





  • After the age of 6 months.



Signs





  • Straight for distance and esotropia for near.



  • Normal or low AC/A ratio and normal refraction.



Distance


Presentation





  • Early adult life.



Signs





  • Intermittent or constant esotropia for distance, and minimal or no deviation for near.



  • Myopia is common.



Microtropia


Presentation





  • May be spontaneous or following surgery for a large deviation.



Signs





  • Very small angle that may not be apparent on cover testing.



  • Central suppression scotoma of the deviating eye.



  • Abnormal retinal correspondence (ARC) with reduced stereopsis and variable peripheral fusional amplitudes.



  • Anisometropia and amblyopia are common.



Acute (late onset)


Presentation





  • At about 5 years of age with sudden onset of diplopia and esotropia.



Signs





  • Esotropia for distance and near.



  • Normal motility.



  • Normal refraction.



Differential diagnosis





  • Sixth nerve palsy.



Sensory (secondary)


Pathogenesis





  • Unilateral congenital or early-onset reduction in visual acuity which interferes with or abolishes fusion.



Look for





  • Opacity of the media such as cataract.



  • Optic atrophy or optic nerve hypoplasia.



  • Colobomatous microphthalmos ( Fig. 14.3 ).




    Fig. 14.3



  • Macular scarring from toxoplasmosis ( Fig. 14.4 ).




    Fig. 14.4



  • Retinoblastoma ( Fig. 14.5 ).




    Fig. 14.5



Convergence spasm


Presentation





  • Usually in adult life as an intermittent phenomenon which is usually hysterical.



Signs





  • Esotropia and bilateral miosis ( Fig. 14.6 ).




    Fig. 14.6



  • Pseudo-myopia due to accommodative spasm.



Cyclic


Presentation





  • Alternating manifest esotropia lasting 24 hours followed by normal binocularity for 24 hours.



Signs





  • Large deviation but diplopia is unusual.



  • Fusional amplitudes are subnormal or absent.



Consecutive


Cause





  • Surgical overcorrection of exotropia.



Refractive accommodative


The AC/A ratio is normal and esotropia is a physiological response to excessive hypermetropia. Presentation is usually between 2 and 3 years of age.


Fully accommodative


Signs





  • Esotropia without correction ( Fig. 14.7A ).




    Fig. 14.7A



  • Straight after correction of hypermetropia ( Fig. 14.7B ).




    Fig. 14.7B



Partly accommodative


Signs





  • Esotropia without correction ( Fig. 14.8A ).




    Fig. 14.8A



  • Angle is reduced but not eliminated after correction of hypermetropia ( Fig. 14.8B ).




    Fig. 14.8B



Non-refractive accommodative


Refraction is normal but the AC/A ratio is high so that a unit increase of accommodation is accompanied by a disproportionately large increase in convergence.


Convergence excess


AC/A ratio is high due to increased accommodative convergence.


Signs





Hypoaccommodative convergence excess


AC/A ratio is high due to weak accommodation.


Signs





  • Remote near point of accommodation.



  • Straight for distance.



  • Esotropia for near.



Pseudo-esotropia


Epicanthic folds and broad nasal bridge


This may simulate or accentuate an esotropia.


Signs





  • Symmetric corneal light reflexes are central or slightly displaced nasally ( Fig. 14.10 ).




    Fig. 14.10



  • No deviation on cover-uncover test.



Negative angle kappa


Signs





  • The corneal light reflexes are displaced temporally as may occur in high myopia.



Narrow interpupillary distance


This may occur in hypotelorism in which there is narrow separation of the orbits as a result of skull malformation or failure of brain development.




CONCOMITANT EXOTROPIA


Constant (early onset)


Presentation





  • Often at birth.



Signs





  • Normal refraction.



  • Large and constant angle.



  • DVD may be present.



Look for





  • Neurological anomalies.



Intermittent (basic)


Presentation





  • Around 2 years of age with exophoria breaking down to exotropia.



Signs





  • Straight with BSV at times ( Fig. 14.11A ).




    Fig. 14.11A



  • Divergent with suppression at other times ( Fig. 14.11B ).




    Fig. 14.11B



Classification




  • a.

    Distance (divergence excess) – angle is greater for distance.


  • b.

    Near (convergence insufficiency) – angle is greater for near.


  • c.

    Non-specific – angle is the same for distance and near.



Sensory (secondary)


Pathogenesis





  • Monocular visual impairment by acquired lesions such as cataract ( Fig. 14.12 ) or other opacities of the media.




    Fig. 14.12



Consecutive


Presentation





  • In adult life either in an amblyopic eye or following surgery for esotropia.



Signs





  • Large and constant deviation ( Fig. 14.13 ).




    Fig. 14.13



Microexotropia


Presentation





  • In isolation or in association with a primary intermittent or constant exotropia.



Look for





  • Amblyopia and anisometropia.



Hypertelorism


Signs





  • Congenital anomaly in which there is wide separation of the orbits often associated with shallow orbits as in Crouzon syndrome.



  • Gross exotropia ( Fig. 14.14 ).




    Fig. 14.14



Pseudo-exotropia




  • a.

    Positive angle kappa without ocular anomalies in which the corneal light reflexes are displaced nasally giving a false impression of an exotropia.


  • b.

    Positive angle kappa is caused by macular heterotopia (e.g. dragged macula in retinopathy of prematurity – Fig. 14.15 ) with temporal displacement of the fovea and consequent nasal displacement of the corneal light reflexes.




    Fig. 14.15





CONGENITAL SYNDROMES


Duane retraction syndrome type 1


Signs (left eye)





  • Primary position – straight or slight esotropia ( Fig. 14.16A ).




    Fig. 14.16A



  • Abduction is absent or limited and is accompanied by widening of the palpebral fissure ( Fig. 14.16B ).




    Fig. 14.16B



  • Adduction is normal or mildly limited and is accompanied by retraction of the globe and narrowing of the palpebral fissure ( Fig. 14.16C ).




    Fig. 14.16C



Duane retraction syndrome type 2


Signs





  • Primary position – straight or slight exotropia.



  • Abduction is normal or slightly limited.



  • Adduction is limited.



Duane retraction syndrome type 3


Signs (left eye)





  • Primary position – straight or slight esotropia ( Fig. 14.17A ).




    Fig. 14.17A



  • Abduction ( Fig. 14.17B ) and adduction ( Fig. 14.17C ) are both limited.




    Fig. 14.17B



    Fig. 14.17C



  • All three types of Duane syndrome may be associated with up-shoot of the affected eye on adduction and occasionally a down-shoot.



Brown syndrome


Signs (left eye)





  • Primary position – straight ( Fig. 14.18A ).




    Fig. 14.18A



  • Limited elevation in adduction ( Fig. 14.18B ).




    Fig. 14.18B



  • Limited elevation on upgaze ( Fig. 14.18C ).




    Fig. 14.18C



  • Normal left elevation in abduction ( Fig. 14.18D ).




    Fig. 14.18D



  • Absence of left superior oblique overaction.



Causes ( Table 14.2 )




Table 14.2

Causes of Brown syndrome







  • 1.

    Congenital




    • Idiopathic



    • Congenital click syndrome – impaired movement of the superior oblique tendon through the trochlea



  • 2.

    Acquired




    • Trauma to the trochlea or superior oblique tendon



    • Tendonitis associated with rheumatoid arthritis, pansinusitis and scleritis




Monocular elevator deficit


Signs (right eye)



Jun 6, 2019 | Posted by in OPHTHALMOLOGY | Comments Off on Ocular motility

Full access? Get Clinical Tree

Get Clinical Tree app for offline access