Clinical Orthoptics E-Book

Fiona J. Rowe

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 714

Veröffentlichungsjahr: 2012

Beschreibung

Clinical Orthoptics has become established as a basic reference text providing fundamental information on anatomy, innervation and orthoptic investigation, plus diagnosis and management of strabismus, ocular motility and related disturbances. It is aimed at trainee ophthalmologists and orthoptic undergraduate students. Qualified orthoptists, general ophthalmologists and optometrists will also find valuable guidance in these pages.

In this edition, the author has maintained the goal of producing a user-friendly, clinically relevant and succinct book, while revising it to reflect a variety of developments in the field.

FEATURES

• Essential reading for students of orthoptics and ophthalmolology
• Now fully revised and updated
• Generously illustrated with photographs and line drawings
• Includes diagnostic aids, case reports, and helpful glossary

Leseprobe

Contents

Cover

Dedication

Title Page

Title Page

Preface

Acknowledgements

List of Figures

List of Tables

Section I

Chapter 1: Extraocular Muscle Anatomy and Innervation

Muscle pulleys

Ocular muscles

Innervation

Associated cranial nerves

Chapter 2: Binocular Single Vision

Worth's classification

Development

Retinal correspondence

Physiology of stereopsis

Fusion

Retinal rivalry

Suppression

Diplopia

Chapter 3: Ocular Motility

Saccadic system

Smooth pursuit system

Vergence system

Vestibular-ocular response and optokinetic response

Brainstem control

Muscle sequelae

Past-pointing

Bell's phenomenon

Chapter 4: Orthoptic Investigative Procedures

Visual acuity

Cover test

Ocular motility

Accommodation and convergence

Retinal correspondence

Fusion

Stereopsis

Suppression

Synoptophore

Aniseikonia

Fixation

Measurement of deviations

Hess charts

Field of binocular single vision

Uniocular field of vision

Measurement of torsion

Parks-Helveston three-step test

Diplopia charts

Bielchowsky phenomenon (dark wedge test)

Forced duction test

Forced generation test

Orthoptic exercises

Section II

Chapter 5: Heterophoria

Classification

Aetiology

Causes of decompensation

Esophoria

Exophoria

Hyperphoria/hypophoria

Alternating hyperphoria

Alternating hypophoria

Cyclophoria

Incomitant heterophoria

Hemifield slide

Investigation of heterophoria

Management

Chapter 6: Heterotropia

Esotropia

Factors necessary for development of binocular single vision

Constant esotropia with an accommodative element

Constant esotropia without an accommodative element

Accommodative esotropia

Relating to fixation distance

Exotropia

Hypertropia

Hypotropia

Cyclotropia

Dissociated vertical deviation

Dissociated horizontal deviation

Quality of life

Pseudostrabismus

Chapter 7: Microtropia

Terminology

Classification

Investigation

Management

Chapter 8: Amblyopia and Visual Impairment

Classification

Aetiology

Investigation

Management

Eccentric fixation

Cerebral visual impairment

Delayed visual maturation

PHACE syndrome

Chapter 9: Aphakia

Methods of correction

Investigation

Problems with unilateral aphakia

Management

Section III

Chapter 10: Incomitant Strabismus

Aetiology

Aid to diagnosis

Diplopia

Abnormal head posture

Chapter 11: A and V Patterns

Classification

Aetiology

Investigation

Management

Chapter 12: Accommodation and Convergence Disorders

Accommodative disorders

Presbyopia – physiological

Presbyopia – premature (non-physiological)

Accommodative insufficiency

Accommodative fatigue

Accommodative paralysis

Accommodative spasm

Accommodative inertia

Micropsia

Macropsia

Convergence anomalies

Convergence insufficiency

Convergence paralysis

Convergence spasm

Specific learning difficulty

Chapter 13: Ptosis and Pupils

Ptosis

Marcus Gunn jaw-winking syndrome

Lid retraction

Pupils

Chapter 14: Neurogenic Disorders

III (third) cranial nerve

IV (fourth) cranial nerve

VI (sixth) cranial nerve

Multiple sclerosis

Acquired motor fusion deficiency

Non-accidental injury

Premature visual impairment

Ophthalmoplegia

Chapter 15: Mechanical Paralytic Strabismus

Congenital cranial dysinnervation disorders

Brown's syndrome

Adherence syndrome

Moebius syndrome

Strabismus fixus syndrome

Thyroid eye disease

Orbital injuries

Blow-out fracture

Soft tissue injury

Supraorbital fracture

Naso-orbital fracture

Zygoma fracture

Conjunctival shortening syndrome

Retinal detachment

Cataract

Macular translocation surgery

Chapter 16: Myogenic Disorders

Thyroid eye disease

Chronic progressive external ophthalmoplegia

Myasthenia gravis

Myotonic dystrophy

Ocular myositis

Kearns–Sayre ophthalmoplegia

Chapter 17: Craniofacial Synostoses

Plagiocephaly

Brachycephaly

Scaphocephaly/dolichocephaly

Occipital plagiocephaly

Apert's syndrome

Craniofrontonasal dysplasia

Crouzon's syndrome

Pfeiffer syndrome

Saethre–Chotzen syndrome

Unicoronal syndrome

General signs and symptoms

Ocular signs and symptoms

Management

Chapter 18: Nystagmus

Aetiology

Classification

Investigation

Management

Chapter 19: Supranuclear and Internuclear Disorders

Saccadic movement disorders

Smooth pursuit movement disorders

Vergence movement disorders

Gaze palsy

Optokinetic movement disorders

Vestibular movement disorders

Brainstem syndromes

Skew deviation

Ocular tilt reaction

Ocular investigation

Management options

Section IV: Appendices

Diagnostic Aids

Investigation considerations

Cover test pointers

Cover test results

Ocular movement pointers

Abbreviations of Orthoptic Terms

DIAGRAMMATIC ABBREVIATIONS

Diagrammatic Recording of Ocular Motility

Diagrammatic Recording of Nystagmus

Glossary

Case Reports

Concomitant strabismus

Incomitant strabismus

Index

Dedication

This book is dedicated to my family

This edition first published 2012 © 1997, 2004 by Blackwell Publishing Ltd © 2012 by Wiley-Blackwell

Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley's global Scientific, Technical and Medical business with Blackwell Publishing.

Registered office:John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

Editorial offices:9600 Garsington Road, Oxford, OX4 2DQ, UK The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK 2121 State Avenue, Ames, Iowa 50014-8300, USA

First edition published 1997 by Blackwell Science Second edition published 2004 by Blackwell Publishing Ltd Third edition published 2012 by Wiley-Blackwell

For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell.

The right of the author to be identified as the author of this work has been asserted in accordance with the UK Copyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

Library of Congress Cataloging-in-Publication Data

Rowe, Fiona J. Clinical orthoptics / Fiona J. Rowe.—3rd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4443-3934-5 (pbk. : alk. paper) I. Title. [DNLM: 1. Ocular Motility Disorders–Outlines. 2. Craniosynostoses–Outlines. 3. Orthoptics–methods–Outlines. 4. Strabismus–Outlines. WW 18.2] 617.7'62–dc23 2011037444

A catalogue record for this book is available from the British Library.

Preface

Clinical Orthoptics has become established as a basic reference text providing fundamental information on anatomy, innervations and orthoptic investigation, plus diagnosis and management of strabismus, ocular motility and related visual disturbances. As with previous editions, the third edition is not designed to provide in-depth discussion of the content as it is recognised that this can be found in other excellent texts, in systematic reviews and in journal literature.

Following the revision of previous editions, this third edition, in addition to many of the original illustrations, contains new figures, tables and flowcharts designed to enhance the written text. Reference and further reading lists for each chapter have been extended and include up-to-date literature.

The layout of the text remains similar to that of the previous edition. Section I concentrates on anatomy and innervations of extraocular muscles including muscle pulley systems and associated cranial nerves. Ocular motility and orthoptic investigative techniques have been updated to include new assessments and reference to normative data. Section II refers to concomitant strabismus and Section III to incomitant strabismus. There has been considerable revision to add new information on conditions not previously included. A new chapter on craniofacial synostosis syndromes has been added. Section IV includes an updated list of abbreviations and glossary of definitions with additions to the information provided on diagnostic aids, flowcharts and illustrative case reports.

Acknowledgements

Thanks are due to my colleagues and undergraduate students at the University of Liverpool, whose discussions provoke enquiry and understanding of orthoptics. Thanks are due to Addenbrooke's Hospital, Cambridge, for permission to use patient photographs and to the patients and parents for their consent to use these images. The glossary incorporates terminology from the British and Irish Orthoptic Society, and thanks are due to the Society for permission to use the glossary terminology. Finally, a thank you to the team at Wiley-Blackwell, the publisher, for their input to this text.

List of Figures

1.1Orbital apex1.2Extraocular muscles1.3Medial rectus action1.4Lateral rectus action1.5Superior rectus action1.6Inferior rectus action1.7Superior oblique action1.8Inferior oblique action1.9Extraocular muscle insertions1.10Cardinal positions of gaze – position of main action of extraocular muscles2.1Projection in normal retinal correspondence2.2Projection in abnormal retinal correspondence2.3Projection in heteronymous diplopia2.4Projection in homonymous diplopia2.5Horopter2.6Right convergent strabismus with suppression2.7Right convergent strabismus with pathological diplopia2.8Right convergent strabismus with paradoxical diplopia3.1Saccadic eye movement control pathways3.2Smooth pursuit eye movement control pathways3.3Vergence eye movement control pathways3.4Vestibulo-ocular and optokinetic response control pathways3.5Sagittal cross section of brainstem; schematic representation3.6Coronal cross section of brainstem; schematic representation3.7Sagittal view of cortical areas; schematic representation4.1Optics of visual acuity4.2Forced choice preferential looking4.3Teller cards4.4LogMAR test4.5LEA symbols4.6Snellen test4.7Sheridan Gardiner test4.8Kay's pictures4.9Cardiff acuity cards4.10Vistech chart4.11LEA contrast numbers4.12Heidi contrast faces4.13Hypermetropia4.14Myopia4.15Astigmatism4.16Occluders4.17Fixation targets4.18Cover/uncover test in manifest strabismus4.19Cover/uncover test in latent strabismus4.20Alternate cover test4.21Rotation of the eye4.22Optokinetic nystagmus Drum4.23RAF rule4.24Flipper lenses4.25Bagolini glasses4.26Results with Bagolini glasses4.27Worth's four lights test4.28Risley prism (a): Prism bars and loose prisms (b)4.29Response to overcome a base out prism4.30Lang two pencil test4.31Frisby stereotest4.32FD2 stereotest4.33Lang stereotest4.34TNO stereotest4.35Titmus/Wirt stereotest4.36Randot stereotest4.37Sbisa bar4.38Amsler chart4.39Synoptophore4.40Optics of the synoptophore4.41Maddox slides4.42Simultaneous perception slides4.43Fusion slides4.44Stereopsis slides: (a) gross stereopsis; (b) detailed stereopsis4.45Angle kappa4.46Angle kappa slide assessment4.47Fixation4.48Fusion response with 4 dioptre prism test4.49Suppression scotoma response with 4 dioptre prism test4.50Prism position4.51Hirschberg's corneal reflections4.52Maddox rod4.53Maddox wing4.54Hess screen4.55Lees screen4.56Arc perimeter4.57Goldmann perimeter4.58Octopus perimeter4.59Six vectors for uniocular rotations4.60Objective assessment of torsion4.61Diplopia chart of IV nerve palsy4.62Diplopia chart of VI nerve palsy4.63Bar reading4.64Stereograms5.1Post-fixational blindness6.1Classification of esotropia6.2Infantile esotropia6.3Intermittent fully accommodative esotropia6.4Intermittent convergence excess esotropia6.5Classification of exotropia6.6Constant exotropia6.7Intermittent distance exotropia6.8Hypertropia6.9Pseudostrabismus8.1Neutral density filter bar11.1A pattern11.2V pattern14.1Right III nerve palsy14.2Hess chart of right III nerve palsy14.3Hess chart of left inferior rectus palsy14.4Hess chart of right inferior oblique palsy14.5Left IV nerve palsy14.6Hess chart of left IV nerve palsy14.7Field of binocular single vision of left IV nerve palsy14.8Right VI nerve palsy14.9Hess chart of right VI nerve palsy14.10Field of binocular single vision of right VI nerve palsy15.1Duane's retraction syndrome15.2Hess chart of Duane's retraction syndrome15.3Field of binocular single vision of Duane's retraction syndrome15.4Right Brown's syndrome15.5Hess chart of right Brown's syndrome15.6Field of binocular single vision of right Brown's syndrome15.7Thyroid eye disease15.8Hess chart of thyroid eye disease15.9Hess chart of unilateral thyroid eye disease15.10Field of binocular single vision of thyroid eye disease15.11Left orbital floor fracture15.12Hess chart of left orbital floor fracture15.13Hess chart of right medial wall fracture15.14Field of binocular single vision of left orbital floor fracture18.1Nystagmus; early onset18.2Nystagmus; late onset18.3Nystagmus velocity19.1Hess chart of right internuclear ophthalmoplegia19.2Field of binocular single vision of right internuclear ophthalmoplegia19.3Internuclear ophthalmoplegia and one and a half syndrome – site of lesionsChart 1Eso-deviationsChart 2Exo-deviationsChart 3Microtropia

List of Tables

1.1Primary, secondary and tertiary muscle actions4.1Age-related visual acuity norms10.1Differences between congenital and acquired defects10.2Differences between neurogenic and mechanical defects10.3Torticollis differential diagnosis14.1Differences of superior oblique and superior rectus palsy14.2Differences of unilateral and bilateral superior oblique palsy

SECTION I

1

Extraocular Muscle Anatomy and Innervation

This chapter outlines the anatomy of the extraocular muscles and their innervation and associated cranial nerves (II, V, VII and VIII).

There are four rectus and two oblique muscles attached to each eye. The rectus muscles originate from the Annulus of Zinn, which encircles the optic foramen and medial portion of the superior orbital fissure (Fig. 1.1). These muscles pass forward in the orbit and gradually diverge to form the orbital muscle cone. By means of a tendon, the muscles insert into the sclera anterior to the rotation centre of the globe (Fig. 1.2).

The extraocular muscles are striated muscles. They contain slow fibres, which produce a graded contracture on the exterior surface, and fast fibres, which produce rapid movements on the interior surface adjacent to the globe. The slow fibres contain a high content of mitochondria and oxidative enzymes. The fast fibres contain high amounts of glycogen and glycolytic enzymes and less oxidative enzymes than the slow fibres. The global layer of the extraocular muscles contains palisade endings in the myotendonous junctions, which are believed to act as sensory receptors. Signals from the palisade endings passing to the central nervous system may serve to maintain muscle tension (Ruskell 1999, Donaldson 2000).

Muscle pulleys

There is stereotypic occurrence of connective tissue septa within the orbit and stereotypic organisation of connective tissue around the extraocular muscles (Koornneef 1977, 1979). There is also stability of rectus extraocular muscle belly paths throughout the range of eye movement, and there is evidence for extraocular muscle path constraint by pulley attachment within the orbit (Miller 1989, Miller et al. 1993, Clark et al. 1999). High-resolution MRI has confirmed the presence of these attachments via connections that constrain the muscle paths during rotations of the globe (Demer 1995, Clark et al. 1997). CT and MRI scans have shown that the paths of the rectus muscles remain fixed relative to the orbital wall during excursions of the globe and even after large surgical transpositions (Demer et al. 1996, Clark et al. 1999). It is only the anterior aspect of the muscle that moves with the globe relative to the orbit.

Figure 1.1 Orbital apex.

Figure 1.2 Extraocular muscles.

Histological studies have demonstrated that each rectus pulley consists of an encircling ring of collagen located near the globe equator in Tenon fascia attached to the orbital wall, adjacent extraocular muscles and equatorial Tenon fascia by sling-like bands, which consist of densely woven collagen, elastin and smooth muscle (Demer et al. 1995, Porter et al. 1996). The global layer of each rectus extraocular muscle, containing about half of all extraocular muscle fibres, passes through the pulley and becomes continuous with the tendon to insert on the globe. The orbital layer containing the remaining half of the extraocular muscle fibres inserts on the pulley and not on the globe (Demer et al. 2000, Oh et al. 2001, Hwan et al. 2007). The orbital layer translates pulleys while the global layer rotates the globe through its insertion on the sclera. The inferior oblique muscle also has a pulley that is mechanically attached to the inferior rectus pulley (Demer et al. 1999).

The general arrangement of orbital connective tissues is uniform throughout the range of human age from foetal life to the tenth decade. Such uniformity supports the concept that pulleys and orbital connective tissues are important for the mechanical generation and maintenance of ocular movements (Kono et al. 2002).

Ocular muscles

Medial rectus muscle

This muscle originates at the orbital apex from the medial portion of the Annulus of Zinn in close contact with the optic nerve. It courses forward for approximately 40 mm along the medial aspect of the globe and penetrates Tenon's capsule roughly 12 mm from the insertion. The last 5 mm of the muscle are in contact with the eye and the insertion is at 5.5 mm from the limbus with a width of 10.5 mm. The muscle is innervated by the inferior division of the III nerve, which enters the muscle on its bulbar side. Its function is adduction of the eye (Fig. 1.3).

Figure 1.3 Medial rectus action.

Lateral rectus muscle

This muscle arises by two heads from the upper and lower portions of the Annulus of Zinn where it bridges the superior orbital fissure. It courses forward for approximately 40 mm along the lateral aspect of the globe and crosses the inferior oblique insertion. It penetrates Tenon's capsule at roughly 15 mm from the insertion and the last 7–8 mm of the muscle is in contact with the eye. The insertion is at 7 mm from the limbus with a width of 9.5 mm. The muscle is innervated by the VI nerve, which enters the muscle on its bulbar side. Its function is abduction of the eye (Fig. 1.4).

Figure 1.4 Lateral rectus action.

Superior rectus muscle

This muscle arises from the superior portion of the Annulus of Zinn and courses forward for approximately 42 mm along the dorsal aspect of the globe forming an angle of 23° with the sagittal axis of the globe. Superiorly, it is in close contact with the levator muscle. It penetrates Tenon's capsule at roughly 15 mm from the insertion and the last few mms of the muscle are in contact with the eye. The insertion is at 7.7 mm from the limbus with a width of 11 mm. The muscle is innervated by the superior division of the III nerve, which enters the muscle on its bulbar side. Its functions are elevation, intorsion and adduction of the eye (Fig. 1.5).

Figure 1.5 Superior rectus action. The course of the superior rectus is at an angle of 23° to the medial wall of the orbit. Actions in adduction are principally intorsion and adduction; in the primary position, actions are elevation, intorsion and adduction; action in abduction is principally elevation.

Figure 1.6 Inferior rectus action. The course of the inferior rectus is at an angle of 23° to the medial wall of the orbit. In adduction, the actions are principally extorsion and adduction; in the primary position, actions are depression, extorsion and adduction; action in abduction is principally depression.

Inferior rectus muscle

This muscle arises from the inferior portion of the Annulus of Zinn and courses forward for approximately 42 mm along the ventral aspect of the globe forming an angle of 23° with the sagittal axis. It penetrates Tenon's capsule roughly 15 mm from the insertion and the last few millimetres of the muscle are in contact with the eye as it arcs to insert at 6.5 mm from the limbus. The width of insertion is 10 mm. The muscle is innervated by the inferior division of the III nerve, which enters the muscle on its bulbar side. Its functions are depression, extorsion and adduction of the eye (Fig. 1.6).

Superior oblique muscle

This muscle originates from the orbital apex from the periosteum of the body of the sphenoid bone, medial and superior to the optic foramen. It courses forward for approximately 40 mm along the medial wall of the orbit to the trochlea (a V-shaped fibrocartilage that is attached to the frontal bone). The trochlear region is described by Helveston et al. (1982).

The muscle becomes tendonous roughly 10 mm posterior to the trochlea and is encased in a synovial sheath through the trochlea. From the trochlea, it courses posteriorly, laterally and downwards forming an angle of 51° with the visual axis of the eye in the primary position. It passes beneath the superior rectus and inserts on the upper temporal quadrant of the globe ventral to the superior rectus. Its insertion is fanned out in a curved line 10–12 mm in length. The muscle is innervated by the IV nerve that enters the muscle on its upper surface roughly 12 mm from its origin. Its functions are intorsion, depression and abduction of the eye (Fig. 1.7).

Figure 1.7 Superior oblique action. The course of the superior oblique tendon is at an angle of 51° to the medial wall of the orbit. Action in adduction is depression; in the primary position, actions are depression, intorsion and abduction; in abduction, action is intorsion.

Inferior oblique muscle

This muscle arises from the floor of the orbit from the periosteum covering the anteromedial portion of the maxilla bone. It courses laterally and posteriorly for approximately 37 mm, forming an angle of 51° with the visual axis. It penetrates Tenon's capsule near the posterior ventral surface of the inferior rectus, crosses the inferior rectus and curves upwards around the globe to insert under the lateral rectus just anterior to the macular area. The muscle is innervated by the inferior division of the III nerve that enters the muscle on its bulbar surface. Its functions are extorsion, elevation and abduction of the eye (Fig. 1.8).

Figure 1.9 illustrates the muscle insertions in relation to the anterior segment of the eye. Figure 1.10 illustrates the positions of main action of each extraocular muscle and Table 1.1 illustrates all primary, secondary and tertiary muscle actions.

Figure 1.8 Inferior oblique action. The course of the inferior oblique is at an angle of 51° to the medial wall of the orbit. Action in adduction is elevation; actions in the primary position are elevation, extorsion and abduction; in abduction, action is extorsion.

Figure 1.9 Extraocular muscle insertions. SR, superior rectus; MR, medial rectus; LR, lateral rectus; IR, inferior rectus.

Figure 1.10 Cardinal positions of gaze – position of main action of extraocular muscles.

Levator palpebral superioris

This muscle originates from the under surface of the lesser wing of sphenoid bone above and in front of the optic foramen by a short tendon that blends with the origin of the superior rectus. It runs forward and changes directly from horizontal to vertical at the level of the equator of the globe. At approximately 10 mm above the superior margin of the tarsus, it divides into anterior and posterior lamellae. The anterior lamellae form the levator aponeurosis that is inserted into the lower third of the entire length of the anterior surface of the tarsus. Its fibres extend to the pre-tarsal portion of the orbit and skin. The posterior lamellae form Muller's muscle that is attached inferiorly to the superior margin of the tarsus.

Table 1.1 Primary, secondary and tertiary extraocular muscle actions.

Innervation

The extraocular muscles are innervated by the III, IV and VI nerves.

III nerve

The III nerve (third/oculomotor) supplies the superior rectus, inferior rectus, medial rectus, inferior oblique and levator muscles. Its visceral fibres innervate the ciliary muscle and sphincter pupillary muscle that synapse in the ciliary ganglion.

The nuclei are in the mesencephalon at the level of the superior colliculus. There is an elongated mass of cells that form the nuclei. Peripheral motor neurones innervate multiply innervated extraocular muscle fibres and central motor neurones innervate single innervated muscle fibres. Dorsal nucleus fibres pass to the ipsilateral inferior rectus, intermediate nucleus fibres pass to the ipsilateral inferior oblique, ventral nucleus fibres pass to the ipsilateral medial rectus, paramedian nucleus fibres pass to the contralateral superior rectus, central caudal nucleus fibres pass to both levator muscles, and the anterior median/Edinger-Westphal nucleus contains the parasympathetic fibres (Bienfang 1975). The nerve fibres emerge from the mesencephalon ventrally where they are closely associated with the posterior cerebellar and superior cerebral arteries. The nerve courses forward through the subarachnoid space to pierce the dura mater at the posterior clinoid process and enter the cavernous sinus.

The third cranial nerve pathway is supplied by branches of the basilar artery including the superior cerebellar arteries, posterior cerebral arteries, mesencephalic perforating arteries, collicular and accessory arteries in the midbrain; the thalamoperforating arteries supplemented by the superior cerebellar artery, posterior communicating artery and posterior cerebral artery in the proximal nerve pathway; and inferior cavernous sinus arteries, medial posterior choroidal artery and tentorial arteries in the distal nerve pathway (Marinkovic & Gibo 1994, Cahill et al. 1996).

IV nerve

The IV nerve (fourth/trochlear) supplies the superior oblique. The nucleus lies in the mesencephalon at the level of the inferior colliculus. The nerve fibres decussate (although about 3% do not decussate but retain ipsilateral projection) and emerge from the brainstem dorsally. The nerves curve around the brainstem and course forward through the subarachnoid space to pierce the dura mater and enter the cavernous sinus.

The fourth cranial nerve pathway is in close association or contact with branches of the basilar artery in the midbrain including the superior cerebellar artery, vernian artery and collicular artery. It is supplied by posterior cerebral artery and posterior communicating artery in its proximal pathway and by the internal carotid artery, medial posterior choroidal artery and tentorial arteries in the distal pathway (Marinkovic et al. 1996, Yousry et al. 2002).

VI nerve

The VI nerve (sixth/abducens) supplies the lateral rectus. The nucleus is situated in the pons in the floor of the IV ventricle near the midline, medial to VIII nucleus and proximal to the paramedian pontine reticular formation. The medial longitudinal fasciculus lies medial to the nucleus. The nerve fibres emerge from the brainstem ventrally and course forward and laterally over the petrous tip of the temporal bone and under the petrosphenoid ligament. The nerve pierces the dura mater to enter cavernous sinus. The nerve divides into two distinct trunks along its pathway between the brainstem and the lateral rectus muscle.

The sixth cranial nerve pathway is supplied with branches of the basilar artery including the anterior inferior cerebellar artery, posterior inferior cerebellar artery, pontomedullary artery and accessory arteries in the pons and clivus region. The distal pathway is supplied by the internal auditory artery, anterolateral artery and tentorial artery (Marinkovic et al. 1994, Yousry et al. 1999).

Common nerve pathways

The III, IV and VI nerves course forward together in the lateral aspect of the cavernous sinus entering the orbit through the superior orbital fissure. The III and VI nerves enter within the muscle cone.

The III nerve divides into the superior and inferior divisions. The superior division enters the superior rectus on its bulbar surface and passes through the muscle to terminate in the levator muscle. The inferior branch supplies the medial rectus, inferior rectus, and then passes beneath the optic nerve to the floor of the orbit and terminates in the inferior oblique. The terminal branch also sends a short branch to the ciliary ganglion. The VI nerve passes forward and laterally to enter the lateral rectus bulbar surface. The IV nerve enters through the superior orbital fissure laterally and superior to the Annulus of Zinn. It passes anteriorly and medially crossing the III nerve, levator muscle and superior rectus, and enters the superior oblique on its orbital surface.

Associated cranial nerves

Autonomic nerves

These nerves supply smooth muscles and source ganglia. Smooth muscles include the muscular blood vessels, Muller's muscle, pulley smooth muscle, sclera myofibroblasts and choroidal smooth muscle (Demer et al. 1997). Source ganglia include the pterygopalatine ganglion, ciliary ganglion and superior cervical ganglion.

Proprioceptive nerves

These nerves consist of palisade endings and spindles. Palisade endings innervate myotendonous cylinders at the termination of each multiply innervated global layer fibre in the rectus extraocular muscles (Lienbacher et al. 2011). Spindles are composed of several orbital layer myofibres and have nerve terminals within a very thin capsule.

II nerve

The II (optic) nerve serves the sensory function of vision. Its pathway commences in the eye at the receptor cells in the retina. There is a complex arrangement of nuclei and processes from three layers of photoreceptors, bipolar cells and ganglion cells. There are in the region of 1.2–1.5 million retinal ganglion cells and 105 million photoreceptors with an average ratio of 1 retinal ganglion cell to 100 photoreceptors. At the fovea, the ratio is 1:1 for retinal ganglion cells to photoreceptors.

Retinal ganglion cells include midget (parvocellular), parasol (magnocellular), koniocellular and other cells. Midget ganglion cells are responsible for slow conduction of impulses with low temporal resolution and require high contrast stimuli. Parasol ganglion cells are responsible for fast conduction of impulses with high temporal resolution and requiring low contrast stimuli. Midget cells have colour selectivity whereas parasol cells have little or no colour selectivity. Koniocellular cells have moderate conduction velocity and moderate sensitivity to light and spatial resolution. They have some colour selectivity and may have a role in motion detection and visual attention. Other cells include light reflex ganglions and photosensitive neurones.

Retinal ganglion cells pass in nerve fibre bundles to the optic discs and pass from each eye to the intracranial cavity along the optic nerves. The optic nerves merge in the optic chiasm where there is crossing of nasal retinal fibres. Ipsilateral temporal and contralateral nasal fibres pass along the optic tracts to the lateral geniculate nuclei where the first synapse of retinal nerve fibres occurs. The post-synaptic fibres then pass via the optic radiations to the visual cortex. The visual cortex (V1) occupies the calcarine sulcus in the occipital lobe and is the primary visual area.

V nerve

The V nerve (fifth/trigeminal) serves sensory and motor functions and the nuclei extend through the pons down into the medulla. The sensory nerve has three branches.

Sensory nerves

The ophthalmic division serves the sensory function to the lacrimal gland, conjunctiva, forehead, eyelids, anterior scalp and mucous membranes of the nose. The sensory fibres pass through the superior orbital fissure to the cavernous sinus and pass inferiorly to the trigeminal ganglion, which is located under the cavernous sinus in Meckel's cave (a groove in the skull). Fibres pass from the ganglion posteriorly to the pons to the trigeminal nuclei.

The maxillary division serves the sensory function to the cheeks, upper gums and teeth and lower eyelids. The sensory fibres pass through the foramen rotundum, underneath the cavernous sinus to the trigeminal ganglion and then onto the nuclei in the pons.

The mandibular division serves the sensory function to the teeth, gums of the lower jaw, pinna of ears, lower lip and tongue. The sensory fibres pass through the foramen ovale underneath the cavernous sinus to the trigeminal ganglion and then onto the nuclei in the pons.

Motor nerves

Motor fibres of the V nerve serve the muscles of mastication. The motor nuclei are located in the pons near the seventh nerve nuclei and aqueduct. Nerve fibres leave ventrally and medially and pass anteriorly to the trigeminal ganglion, through the foramen ovale to the muscles of mastication.

VII nerve

The VII nerve (seventh/facial) serves sensory and motor functions. The VII nerve has central connections to the motor face area of the cerebral cortex and the nuclei are divided into upper and lower halves. Corticobulbar fibres double decussate for the upper face but there is single decussation for lower face fibres.

Sensory fibres

Ganglion cells supply taste buds in the palate and tongue and sensory fibres are also present in the skin, in and around the external acoustic meatus. Fibres pass to the geniculate ganglion situated in the internal auditory meatus and pass back to the pons.

Motor fibres

The nuclei are located in the lateral part of the pons and fibres loop around the abducens nuclei, forming the facial colliculus, before leaving the pons ventrally. Fibres pass anteriorly and enter the internal auditory meatus. The nerve enters a narrow bony canal above the labyrinth and descends to the stylomastoid foramen where a branch supplies the stapedius muscle. It leaves the skull and supplies the facial muscles (frontal, zygomatic, buccal, mandibular marginal and cervical branches).

VIII nerve

The VIII nerve (eight/auditory) serves the sensory function of hearing and balance.

Cochlear nerve (hearing)

Receptor cells are hair cells in the organ of Corti. Fibres pass from the spiral ganglion along the Cochlear nerve through the internal auditory meatus to the cisterna pontis, to the inferior cerebellar peduncle and to the cochlear vestibular nuclei in the pons/medulla.

Vestibular nerve (balance)

Receptor cells are hair cells in the utricles, saccules and semicircular canals. Fibres pass from Scarpa's ganglion along the vestibular nerve through the internal auditory meatus to the cisterna pontis and to the vestibular nuclei in the pons/medulla. Within the internal auditory meatus, the vestibular and cochlear nerves are in close association with the facial nerve. Within the acoustic foramen and intracranial cavity, these nerves are closely associated with both the sixth and facial nerves.

References

Bienfang DC. Crossing axons in the third nerve nucleus. Investigative Ophthalmology and Visual Science. 1975; 14: 927–31.

Cahill M, Bannigan J, Eustace P. Anatomy of the infranuclear blood supply to the intracranial oculomotor nerve. British Journal of Ophthalmology. 1996; 80: 177–81.

Clark RA, Miller JM, Demer JL. Location and stability of rectus muscle pulleys. Muscle paths as function of gaze. Investigative Ophthalmology and Visual Science. 1997; 38: 227–40.

Clark RA, Rosenbaum AL, Demer JL. Magnetic resonance imaging after surgical transposition defines the anteroposterior location of the rectus muscle paths. Journal of American Association for Paediatric Ophthalmology and Strabismus. 1999; 3: 9–14.

Demer JL, Clark RA, Miller JL. Magnetic resonance imaging (MRI) of the functional anatomy of the inferior oblique (IO) muscle. (ARVO abstract). Investigative Ophthalmology and Visual Science. 1999; 40(4): S772.

Demer JL, Miller JM, Poukens V. Surgical implications of the rectus extra ocular muscle pulleys. Pediatric Ophthalmology and Strabismus. 1996; 33: 208–18.

Demer JL, Miller JM, Poukens V, Vinters HV, Glasgow BJ. Evidence for fibromuscular pulleys of the recti extra ocular muscles. Investigative Ophthalmology and Visual Science. 1995; 36: 1125–36.

Demer JL, Oh SY, Poukens V. Evidence for active control of rectus extra ocular muscle pulleys. Investigative Ophthalmology and Visual Science. 2000; 41: 1280–90.

Demer JL, Poukens V, Miller JM, Micevych P. Innervation of extraocular pulley smooth muscle in monkey and human. Investigative Ophthalmology and Visual Science. 1997; 38: 1774–85.

Donaldson IM. The functions of the proprioceptors of the eye muscles. Philosophical Transactions of the Royal Society of London Series B Biological Sciences. 2000; 355: 1685–754.

Helveston EM, Merriam WW, Ellis FD, Shellhamer RH, Gosling CG. The trochlea: a study of the anatomy and physiology. Ophthalmology. 1982; 89: 124–33.

Hwan Lim K, Poukens V, Demer J. Fascicular specialisation in human and monkey rectus muscles: evidence for anatomic independence of global and orbital layers. Investigative Ophthalmology and Visual Science. 2007; 48: 3089–97.

Kono R, Poukens V, Demer JL. Quantitative analysis of the structure of the human extra ocular muscle pulley system. Investigative Ophthalmology and Visual Science. 2002; 43: 2923–32.

Koornneef L. New insights in the human orbital connective tissue; result of a new anatomical approach. Archives of Ophthalmology. 1977; 95: 1269–73.

Koornneef L. Orbital septa: anatomy and function. Ophthalmology. 1979; 86: 876–80.

Lienbacher K, Mustari M, Ying HS, Buttner-Ennever JA, Horn AK. Do palisade endings in extraocular muscles arise from neurons in the motor nuclei? Investigative Ophthalmology and Visual Science. 2011; 52: 2510–19.

Marinkovic S, Gibo H. The neurovascular relationships and the blood supply of the oculomotor nerve: the microsurgical anatomy of its cisternal segment. Surgical Neurology. 1994; 42: 505–16.

Marinkovic SV, Gibo H, Stimec B. The neurovascular relationships and the blood supply of the abducent nerve: surgical anatomy of its cisternal segment. Neurosurgery. 1994; 34: 1017–26.

Marinkovic S, Gibo H, Zelic O, Nikodijevic I. The neurovascular relationships and the blood supply of the trochlear nerve: surgical anatomy of its cisternal segment. Neurosurgery. 1996; 38: 161–69.

Miller JM. Functional anatomy of normal human rectus muscles. Vision Research. 1989; 29: 223–40.

Miller JM, Demer JL, Rosenbaum AL. Effect of transposition surgery on rectus muscle paths by magnetic resonance imaging. Ophthalmology. 1993; 100: 475–87.

Oh SY, Poukens V, Demer JL. Quantitative analysis of extra ocular muscle global and orbital layers in monkey and human. Investigative Ophthalmology and Visual Science. 2001; 42: 10–6.

Porter JD, Poukens V, Baker RS, Demer JL. Structure function correlations in the human medial rectus extra ocular muscle pulleys. Investigative Ophthalmology and Visual Science. 1996; 37: 468–72.

Ruskell GL. Extraocular muscle proprioceptors and proprioception. Progress in Retinal and Eye Research. 1999; 18: 269–91.

Yousry I, Camelio S, Wiesmann M, Schmid UD, Moriggl B, Brückmann H, Yousry TA. Detailed magnetic resonance imaging anatomy of the cisternal segment of the abducent nerve: Dorello's canal and neurovascular relationships and landmarks. Journal of Neurosurgery. 1999; 91: 276–83.

Yousry I, Moriggl B, Dieterich M, Naidich TP, Schmid UD, Yousry T. MR anatomy of the proximal cisternal segment of the trochlear nerve: neurovascular relationships and landmarks. Radiology. 2002; 223: 31–38.

Further reading

Apt L. An anatomical evaluation of rectus muscle insertions. Transactions of the American Ophthalmological Society. 1980; 78: 365–75.

Bach-y-Rita P. Neurophysiology of extraocular muscle. Investigative Ophthalmology. 1967; 6: 229–34.

Bjork A. Electrical activity of human extrinsic eye muscles. Experientia. 1952; 8: 226–7.

Brandt DE, Leeson CR. Structural differences of fast and slow fibers in human extraocular muscle. American Journal of Ophthalmology. 1966; 62: 478–87.

Duke-Elder S, Wybar KC. The anatomy of the visual system. System of Ophthalmology, Volume 2. St. Louis, MO, Mosby-Year Book, Inc. 1961.

Howe L. Insertion of the ocular muscles. Transactions of the American Ophthalmological Society. 1902; 9: 668–78.

Scobee RC. Anatomic factors in the etiology of strabismus. American Journal of Ophthalmology. 1948; 31: 781–95.

Sevel P. The origins and insertions of the extraocular muscles : development, histologic features and clinical significance. Transactions of the American Ophthalmological Society. 1986; 84: 488–526.

Souza-Dias C, Prieto-Diaz J, Uesegui CF. Topographical aspects of the insertions of the extraocular muscles. Journal of Pediatric Ophthalmology and Strabismus. 1986; 23: 183–9.

2

Binocular Single Vision

Binocular single vision is the ability to use both eyes simultaneously so that each eye contributes to a common single perception.

Normal binocular single vision occurs with bifoveal fixation and normal retinal correspondence in everyday sight. Abnormal binocular single vision occurs in the absence of bifoveal fixation usually with abnormal retinal correspondence in everyday sight.

Worth's classification

Binocular single vision can be classified into three stages:

1. Simultaneous perception and superimposition

2. Fusion

3. Stereoscopic vision

Simultaneous perception is the ability to perceive simultaneously two images, one formed on each retina. Superimposition is the simultaneous perception of the two images formed on corresponding areas, with the projection of these images to the same position in space. This may occur whether the correspondence is normal or abnormal. If fusion is absent, two similar images are seen as separate but superimposed and no fusion range is demonstrable.

Fusion may be sensory or motor. Sensory fusion is the ability to perceive two similar images, one formed on each retina, and interpret them as one. Motor fusion is the ability to maintain sensory fusion through a range of vergence, which may be horizontal, vertical or cyclovergence. Stereoscopic vision is the perception of the relative depth of objects on the basis of binocular disparity.

Development

The initial ocular position in the human neonate (Rethy 1969) is often one of divergence. In the early postnatal period, divergence decreases towards a binocular coincidental position resulting in similar visual stimulation of each eye, which in turn facilitates firing of binocular driven cells/neurones in the striate cortex (Hubel & Wiesel 1968), and once the straight position is attained, this is maintained preferentially. The globes are approximately 73% of adult size in infancy and the lens is relatively less convex. The size of eye (lens and cornea) renders the eye hypermetropic, which is overcome by amplitude of accommodation. Other developments include accommodation, ocular muscles and nerve supply, visual pathway and foveal development. Binocular single vision is dependent on retinal correspondence and disparity. Eighty percent of the striate cortex neurones are driven from either eye (binocular driven cells) whilst 10% are driven by the right eye only and 10% by the left eye only (Hubel & Wiesel 1968).

Some sensory and motor binocular associations exist in the visual system of the newborn. The binocular reflexes relate to the development of binocular single vision on the basis of continued use of the visual system. Postural reflexes are inborn and must be present if binocular single vision is to develop:

a. Static reflexes compensate for changes in position of the head relative to the body.

b. Statokinetic reflexes compensate for changes in head position relative to space.

Fixation reflexes form the mechanism from which binocular vision develops:

a. The primary fixation reflex achieves foveal fixation in either eye and is present at birth.

b. The refixation reflex allows foveal refixation from target to target and maintenance of foveal fixation on a moving target. This develops from 6 to 8 weeks of age. Most neonates are capable of locating and briefly fixing a moving target, and the eyes can move in a coarsely conjugate fashion. Thus, the refixation reflex, although unstable, appears to be present at birth, despite the fact that in the first months of life the fovea is still poorly differentiated.

c. The conjugate fixation reflex, where the eyes learn to move together during versions, is the first reflex by which the eyes move binocularly and develops from 2 to 3 weeks of age.

d. The disjugate fixation reflex allows binocular vision to be maintained through the range of vergence movements that follow changes of fixation distance and develops from 2 to 3 months of age.

e. The corrective fusion reflex allows binocular vision to be maintained under conditions of stress, such as overcoming prisms in clinical testing situations, and develops from 3 to 6 months of age.

f. Kinetic reflexes maintain binocular single vision through controlled accommodation and convergence.

The newborn does not converge the eyes, but the attempt to converge may be seen as early as 1 month after birth. The macula is poorly developed at birth with incomplete migration of retinal ganglion cells from the foveal area. Saccadic eye movements are poorly controlled, and several movements are required to achieve foveation. By 5–6 weeks of age, the conjugate fixation reflex is developed, and the two eyes conjugately fix an object and follow it over a considerable range for at least a few seconds. Density of cones in the fovea increases with myelination of nerve fibres in the visual pathway. Smooth pursuit eye movement and colour vision develop from 2 months. Accommodation develops rapidly from 2–3 months and approaches the same levels of accuracy as adults (Horwood & Riddell 2004). Optokinetic nystagmus is asymmetrical up to 3 months with absent nasal to temporal movement, after which there is progression to symmetrical motion processing by the age of 6 months (Bosworth & Birch 2007). By 6 months, the conjugate movements of binocular vision become accurate and convergence is well developed. By 6–8 months, a fusional movement can be detected by placing a small prism over either eye.

A critical period occurs in the development of the visual system during which the visual system is susceptible to abnormal visual input (Daw 1998). The period of normal visual development is up to 5 years of age.

Retinal correspondence

This concerns the retinal areas of each eye that have the same visual direction during binocular vision.

Normal retinal correspondence

This is a binocular condition in which the fovea and areas on the nasal and temporal side of one retina correspond to and have, respectively, common visual directional sensitivity with the fovea and temporal and nasal areas of the retina of the other eye. Normal retinal correspondence is the normal state in which the visual direction of each fovea is the same (Flom & Weymouth 1961, Flom & Kerr 1967) (Fig. 2.1).

Figure 2.1 Projection in normal retinal correspondence with normal binocular single vision. Stimulation of corresponding points in both eyes results in localisation of the stimulus in the same direction in space. Both fovea, FL and FR, are corresponding points as are points on temporal and nasal retinas, TL and NR, NL and TR.

Abnormal retinal correspondence

This is a binocular condition in which there is a change in visual directional sensitivity such that the fovea of the fixing eye has a common visual directional sensitivity with an area other than the fovea of the deviating eye (Burian 1951). The pairing of all retinal areas is similarly changed. The condition may occur whichever eye is used for fixation (Fig. 2.2).

Figure 2.2 Projection in abnormal retinal correspondence with right esotropia. O is the fixation target. FL and FR are the fovea of both eyes and P is the pseudofovea of the right eye. FL and P are corresponding points as the right eye undergoes sensory adaptation with abnormal retinal correspondence. Stimulation of these corresponding points results in a single perception of the fixation target.

Harmonious abnormal retinal correspondence is present where the angle of anomaly is equal to the objective angle, and the subjective angle is zero. Unharmonious abnormal retinal correspondence is present where the angle of anomaly is different from the objective angle. The angle of anomaly is the difference between the objective and subjective angles of deviation. Abnormal retinal correspondence is present in constant manifest strabismus usually of a small angle less than 20 prism dioptres.

Physiology of stereopsis

The locations of all points in space that are imaged on corresponding retinal points are termed the horopter. Panum's space is a narrow band around the horopter within which object points give rise to binocular single vision. Objects are seen as single even though the object stimulates slightly disparate retinal elements.

Panum's area is the retinal area surrounding one corresponding retinal point within which disparity of correspondence may occur, whilst maintaining binocular single vision. Binocular single vision is the result not of a rigid point-to-point correspondence but of a point-to-area relationship. The amount of foveal image disparity that permits fusion is small, and disparity increases gradually from the fovea to the periphery. Panum's area is narrow at the fixation point and widens towards the periphery. The horizontal area at the fovea is approximately 6–10 minutes, and this increases towards the periphery measuring approximately 30–40 minutes at 12° from the fovea. It may be larger than this as moving random-dot stereograms have shown fusion of disparities of 2°–3° (Hyson et al. 1983, Erkelens & Collewjin 1985, Piantanida 1986). Increases can be related to anatomical and physiological differences known to exist between the foveal cone system and the rod and cone system of the peripheral retina. The increase in Panum's area parallels the increase in size of the retinal receptive fields. Performance with motor skills is related to the level of stereoacuity in that performance is considerably worse in the absence of stereopsis (O’Connor et al. 2010).

Physiological diplopia

This is a type of diplopia that exists in the presence of binocular vision. It consists of the appreciation that a near object appears double when a distant object is fixated (heteronymous or crossed diplopia), and a distant object appears double when a near object is fixated (homonymous or uncrossed diplopia) (Figs. 2.3 and 2.4).

Figure 2.3 Projection in heteronymous diplopia. X is the fixation target, which is seen as a single image by the corresponding fovea FL and FR. O is an object between the fixation target and the eyes that stimulates non-corresponding temporal retinal points, TL and TR, resulting in crossed physiological diplopia.

Figure 2.4 Projection in homonymous diplopia. X is the fixation target seen as a single image by the corresponding foveal points, FL and FR. O is an object further away than the fixation target that stimulates non-corresponding nasal retinal points, NL and NR, resulting in uncrossed physiological diplopia.

All objects outside Panum's space give rise to physiological diplopia. Physiological diplopia indicates that the patient is capable of using both eyes and is not suppressing one eye.

Fixation disparity

Fixation disparity is a phenomenon that occurs in binocular single vision in which the image is seen singly despite a slight underconvergence or overconvergence of the visual axes; the fixation target is imaged on slightly disparate retinal points within Panum's area. There is an apparent displacement of uniocularly observed details of targets whose other details are fused binocularly.

The phenomenon can be demonstrated clinically when targets, which have mainly identical features but also contain some dissimilar features, are presented to the eyes. Fusion occurs for the identical features, but a displacement occurs for the dissimilar features in the direction of the projection of the existing heterophoria.

Fixation disparity may be involved in the maintenance of binocular single vision. Disparity of retinal images causes fusional movements. At the end of a fusional movement, not all the disparity is annulled; a small disparity remains, which acts as an error signal. The residual fixation disparity may control the direction and strength of the innervation that maintains the new binocular position.

When visual objects are fused by being imaged on horizontally disparate points, within Panum's space, stereopsis results. The greater the horizontal disparity, the greater the depth effect. A vertical disparity produces no stereoscopic effect (Fig. 2.5).

Figure 2.5 Projection in stereopsis. O is the fixation target, which projects directly to the fovea of the left eye. This should also project directly to the right eye. However, due to slight under- or overconvergence of the right eye, direct stimulation may not occur, resulting in fixation disparity. In this figure, there is slight overconvergence of the right eye with stimulation of a point just nasal to the fovea. As this point falls within Panum's area, the stimuli to either eye are fused, resulting in a single image of the fixation target.

Local stereopsis occurs where localised features of objects are extracted from a visual scene and assigned relative depth values, indicating that one feature is further away from another. Global stereopsis occurs where the perception of whole objects in stereoscopic depth is achieved.

Monocular clues are important in the estimation of the relative distance of visual objects and are active in monocular as well as binocular vision. These clues are the result of experience:

Motion parallax: Targets further away move more in the horizontal plane than nearer targets.Linear perspective: Objects of the same size decrease in size the further away they are.Overlapping contours: Overlap in images determines which is in front or behind the other.Distribution of highlights and shadows.Size of known objects: When size is known, the relative distance can be determined.Aerial perspective: Knowledge of colours and hues.

Fusion

Central fusion occurs when the images of an object are perceived by each fovea, and the area surrounding them, and are unified. This produces bifoveal binocular single vision with fusion. The highest levels of stereoacuity are associated with central fusion. Peripheral fusion results from unification of images outside the central region. Gross stereopsis is associated with peripheral fusion. Central and peripheral fusion usually function simultaneously. A patient's sensory status is considered crucial to the long-term stability of a successful surgical outcome. Fusion serves as the glue to maintain alignment (Burian 1941, Kushner & Morton 1992, Morris et al. 1993). It indicates the patient's ability to control their latent tendency for the eyes to drift. In order for fusion to occur, the images presented to each eye must be similar in size, brightness and sharpness. Peripheral fusion contributes significantly to the maintenance of binocular single vision (Bielchowsky 1935). If this is destroyed, even while maintaining good central vision, disruption of binocularity occurs.

When measured with large field stimuli, 8° of motor cyclovergence has been demonstrated in normals (Guyton 1988). Therefore, individuals can use this ability to fuse torted images without diplopia. This ability derives from the receptive fields in the peripheral retina being large compared to those in the central retina. This amount of motor cyclovergence combined with the 8° of sensory cyclofusion allows norms to fuse up to 16° of cyclodisparity.

Retinal rivalry

When dissimilar images are presented to corresponding retinal areas, fusion becomes impossible and retinal rivalry occurs. When dissimilar targets are presented to each eye, the patient will see one target, then the other, or a mosaic of contours, but not both simultaneously. Retinal rivalry is a physiological finding in binocular single vision and is distinct from suppression as it indicates a state of fluctuation between competing components. Retinal rivalry may also be produced by differences in colour and unequal illumination.

Suppression

Suppression is the mental inhibition of visual sensations of one eye in favour of those of the other eye when both eyes are open. This may occur in binocular single vision and commonly in manifest strabismus.

Physiological suppression is present in binocular single vision. Blurred images are suppressed when concentrating on one particular object. Pathological suppression is present in manifest strabismus and may alternate with alternating deviations (Fig. 2.6).

Figure 2.6 Projection in right esotropia with suppression. O is the fixation target, which stimulates the fovea of the left eye and a nasal retinal point of the right eye. The nasal retinal point is suppressed, which ensures a single perception of the fixation target.

Suppression may occur with interocular blur, suspension, binocular retinal rivalry or permanent suppression. Interocular blur arises where there is a significant difference in blur or contrast between the two eyes such as with anisometropia, unequal amplitude of accommodation or asymmetric accommodation. Suspension relates to physiological suppression during physiological diplopia. Binocular retinal rivalry with differences from either eye in object size or shape prevents fusion. This can be exclusively dominant, in which one image swaps with the other and back; mosaic dominant, in which small interwoven retinal patches alternate; or luminance, which involves colour rivalry. Permanent suppression occurs where the individual is unable to see the object. Suppression occurs at a cortical level and may involve inhibitory interaction between neighbouring ocular dominance columns (Sengspiel et al. 1994).

The area and density of suppression will vary according to the type of strabismus (Harrad 1996). A defined small central suppression scotoma exists in microtropia whereas larger angle strabismus shows an elliptical shaped scotoma extending horizontally, particularly in esotropia. Suppression can be more extensive involving the entire hemifield as has been reported in exotropia (Jampolsky 1955).

Suppression typically develops in childhood strabismus. There is an issue as to whether adults can truly develop suppression. Inattention to diplopia and true suppression are different, but probably related, adaptive sensory strategies and additive factors other than the age of the patient may be involved (McIntyre & Fells 1996). Development of ‘suppression’ has been reported in adults with thyroid eye disease (Fells 1979), following retinal detachment surgery (Wright et al. 1999) and keratoconus (Sherafat et al. 2001). In adult onset strabismus, patients are seen to have a poor prognosis with regard to the ability to learn to suppress or ignore diplopia. Patients can have persistent troublesome diplopia that can be difficult or impossible to alleviate. An ability to develop suppression as an adult or an inattention to the diplopic image may reflect an element of plasticity in the mature binocular visual system.

Diplopia and confusion are not appreciated where suppression is present. Confusion is the simultaneous appreciation of two superimposed images due to the stimulation of corresponding retinal points by two different images. Binocular single vision is not present with pathological suppression, and suppression obstructs attempts to obtain binocular single vision.

Diplopia

Pathological binocular diplopia results from the presence of a manifest ocular deviation and is the simultaneous appreciation of two separate images caused by the stimulation of non-corresponding points by one object. It may be horizontal, vertical or torsional, or any combination.

Figure 2.7 Projection in right esotropia with normal retinal correspondence and pathological diplopia. O is the fixation target, which stimulates non-corresponding points of the left fovea and right nasal retina. The nasal retina projects temporally, resulting in uncrossed pathological diplopia.

Figure 2.8 Projection in right esotropia with paradoxical diplopia. With abnormal retinal correspondence, there is sensory adaptation of the strabismic eye such that the pseudofovea and the fovea of the other eye become corresponding points. The retinal area between the fovea and pseudofovea of the strabismic eye, which was originally nasal retina, takes on the sensory function of temporal retina. With redirection of the strabismic eye, non-corresponding points are stimulated (FL and Q), resulting in crossed paradoxical diplopia.

Heteronymous diplopia is crossed binocular diplopia associated with exotropia in which the image of the fixation object is received on the temporal area of the retina of the deviating eye and is projected nasally. Homonymous diplopia is uncrossed binocular diplopia associated with esotropia in which the image of the fixation object is received on the nasal area of the retina of the deviating eye and is projected temporally (Fig. 2.7).

Paradoxical diplopia is pathological binocular diplopia in which heteronymous diplopia occurs in esotropia or homonymous diplopia occurs in exotropia (Fig. 2.8).

References

Bielchowsky A. Congenital and acquired deficiencies of fusion. American Journal of Ophthalmology. 1935; 18: 925.

Bosworth RG, Birch EE. Direction-of-motion detection and motion VEP asymmetries in normal children and children with infantile esotropia. Investigative Ophthalmology and Visual Science. 2007; 48: 5523–31.

Burian HM. Anomalous retinal correspondence : its essence and its significance in diagnosis and treatment. American Journal of Ophthalmology. 1951; 34: 237–53.

Daw NW. Critical periods and amblyopia. Archives of Ophthalmology. 1998; 116: 502–5.

Erkelens CJ, Collewjin H. Eye movements and steropsis during dichoptic viewing iof moving randon-dot stereograms. Vision Research. 1985; 25: 583–8.

Fells P. Confusion, diplopia and suppression. Transactions of Ophthalmic Society of UK. 1979; 99: 386–90.

Flom MC, Kerr KE. Determination of retinal correspondence. Multiple testing results and the depth of anomaly concept. Archives of Ophthalmology. 1967; 77: 200–13.

Flom MC, Weymouth F. Retinal correspondence and the horopter in anomalous correspondence. Nature. 1961; 89: 34–6.

Guyton DL. Ocular torsion: sensorimotor principles. Graefes Archives of Clinical and Experimental Ophthalmology. 1988; 226: 241–5.

Harrad R. Psychophysics of suppression. Eye. 1996; 10: 270–3.

Horwood AM, Riddell PM. The development of convergence and accommodation. British and Irish Orthoptic Journal. 2004; 1: 1–9.

Hubel DH, Wiesel TN. Receptive fields and functional architecture of monkey striate cortex. Journal of Physiology (London). 1968; 195: 215–43.

Hyson MT, Julesz B, Fender DH. Eye movements and neural remapping during fusion of misaligned random-dot stereograms. Journal of Optical Society of American Association. 1983; 73: 1665–73.

Jampolsky A. Characteristics of suppression in strabismus. Archives of Ophthalmology. 1955; 54: 683–96.

Kushner BJ, Morton GV. Postoperative binocularity in adults with longstanding strabismus. Ophthalmology. 1992; 99: 316–9.

McIntyre A, Fells P. Bangerter foils: a new approach to the management of pathological intractable diplopia. British Orthoptic Journal 1996, 53: 43–47.

Morris RJ, Scott SE, Dickey CF. Fusion after surgical alignment of longstanding strabismus in adults. Ophthalmology. 1993; 100: 135–8.

O’Connor AR, Birch EE, Anderson S, Draper H, FSOS research group. The functional significance of stereopsis. Investigative Ophthalmology and Vision Science. 2010; 51: 2019–23.

Piantanida TP. Stereo-hysteresis revisited. Vision Research. 1986; 26: 431–7.

Sengspiel F, Blakemore C, Kind PC, Harrad R. Interocular suppression in the visual cortex of strabismic cats. Journal of Neuroscience. 1994; 14: 6855–71.

Sherafat H, White JEW, Pullum KW, Adams GGW, Sloper JJ. Anomalies of binocular function in patients with longstanding asymmetric keratoconus. British Journal of Ophthalmology. 2001; 85: 1057–60.

Wright LA, Cleary M, Barrie T, Hammer HM. Motility and binocularity outcomes in vitrectomy versus scleral buckling in retinal detachment surgery. Graefe's Archives of Clinical and Experimental Ophthalmology. 1999, 237: 1028.

Further reading

Asher H. Suppression theory of binocular vision. British Journal of Ophthalmology. 1953; 37: 37–49.

Awaya S, Nozaki H, Hoh T, Harada K. Studies of suppression in alternating constant exotropia and intermittent exotropia : with reference to the effects of fusional background. In: Moore S, Mein J. and Stockbridge L. (eds) Orthoptics, Past, Present and Future. Miami, Symposia Specialists. 1976; pp. 531–46.

Bagolini B, Capobianco NM. Subjective space in comitant squint. American Journal of Ophthalmology. 1965; 50: 430–42.

Barlow HB, Blakemore C, Pettigrew JD. The normal mechanisms of binocular depth discrimination. Journal of Physiology (London)