Visual Fields Via the Visual Pathway, Second Edition

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Visual Fields via the Visual Pathway SECOND EDITION

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Visual Fields via the Visual Pathway SECOND EDITION

Fiona Rowe

University of Liverpool, UK

CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2016 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Version Date: 20151020 International Standard Book Number-13: 978-1-4822-9965-6 (eBook - PDF) This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright. com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-forprofit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com

This book is dedicated to my family. “Family is not an important thing; it is everything.” Michael J. Fox

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Contents

List of figures 

xv

Prefacexxi Acknowledgements 

xxiii

Disclosure xxv About the author 1

2

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Field of vision and visual pathway 1 General anatomy of the visual system 1 Visual field defect types 5 Altitudinal visual field defect 5 5 Arcuate visual field defect Constriction/diffuse defect 6 Hemianopia 6 Quadrantanopia 6 Scotoma 8 Sector-shaped (wedge) visual field defect 8 Parameters and variables in visual field assessment 14 References 16 Further reading 17 Methods of visual field assessment 19 Perimetry 19 Flicker perimetry 20 Frequency Doubling Technology (FDT) 20 Short-Wavelength Automated Perimetry (SWAP) 20 High-pass resolution perimetry 21 Saccadic Vector Optokinetic Perimetry (SVOP) 21 Standard perimetry 22 Presentation of visual field data 23 Goldmann perimeter 23 Humphrey automated perimeter 24 Octopus 900 perimeter 26 Patient set-up 27 Kinetic perimetry 29 Static perimetry 30

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viii Contents

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Screening programmes 30 Threshold programmes 31 Reliability indices 32 Global indices and analysis options 33 Printout options 38 Humphrey perimetry printouts 39 Octopus perimeter printouts 42 Detection of visual field defect and detection of change 46 Stato–kinetic dissociation 59 References 59 Further reading 63 Programme choice 65 Choice of perimeter 65 Static versus kinetic perimetry 65 Perimetry options for assessment of children 67 Screening versus threshold static perimetry 67 Full versus partial 30-degree central programmes 67 Macular and central threshold programmes 69 Colour perimetry 69 Peripheral programmes 72 Esterman strategy 73 Visual standards for safe driving 74 Interpretation 77 Choice of driving visual field assessment 77 Inter-perimeter comparisons 82 Kinetic perimetry 82 Static perimetry 82 References 90 Further reading 92 Ocular media 93 Introduction 93 Cornea 93 Anatomy 93 Pathology 93 Congenital abnormalities 93 Acquired abnormalities 94 Associated signs and symptoms 95 Anterior chamber 95 Anatomy 95 Pathology 95 Associated signs and symptoms 95 Lens 95 Anatomy 95 Pathology 96 Congenital abnormalities 96 Acquired abnormalities 96 Associated signs and symptoms 96

Contents ix

Posterior chamber 96 Pathology 97 Congenital abnormalities 97 Acquired abnormalities 97 Associated signs and symptoms 97 Visual field defects 97 References 101 Further reading 101 5 Retina 103 Anatomy 103 Pathology 105 Congenital abnormalities 105 Acquired abnormalities 105 Hereditary dystrophies 105 Retinal degeneration 105 Retinal detachment 106 Retinal inflammation/infection 106 Retinal toxicity 107 Tumours 107 Vascular abnormalities 107 Associated signs and symptoms 108 Fundus appearance 108 Pupil abnormalities 109 Visual perception 109 Visual acuity 109 Visual field defects 109 Retinal degeneration 110 Retinal dystrophy 110 Retinal infection/inflammation 110 Retinal toxicity 111 Retinal tumours 111 Vascular abnormalities 111 Choice of visual field assessment 115 References 115 Further reading 116 6 Optic nerve 119 Anatomy 119 Pathology 120 Congenital abnormalities 120 Coloboma 120 Drusen (hyaline bodies) 120 Glaucoma 120 Morning glory syndrome 120 Myelinated nerve fibres 121 Optic disc pit 122 Optic nerve hypoplasia 122 Tilted disc 125

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Acquired abnormalities 125 Compression 125 Glaucoma 129 Hereditary abnormalities 129 Inflammatory neuropathy 129 Oedema 130 Optic atrophy 130 Toxic optic neuropathies 131 Vascular abnormalities 131 Associated signs and symptoms 134 Anterior segment appearance 134 Colour vision 134 Contrast sensitivity 134 Fundus appearance 134 Ocular appearance 134 Pupil abnormalities 136 Visual perception 137 Visual acuity 138 Visual field defects 138 Congenital abnormalities 138 Coloboma 138 Drusen 139 Myelinated nerve fibres 139 Optic disc pit 139 Optic nerve hypoplasia 139 Tilted disc 140 Acquired abnormalities 140 Glaucoma 140 Inflammation 144 Oedema 156 Toxic neuropathy 172 Trauma 172 Tumours 172 Vascular abnormalities 179 Choice of visual field assessment 179 References 188 Further reading 192 Optic chiasm 195 Anatomy 195 Pathology 195 Craniopharyngioma 196 Glioma 196 Hydrocephalus 196 Inflammation/Infection 196 Meningioma 196 Multiple sclerosis 198 Pituitary tumour 198 Trauma 198 Vascular abnormalities 198

Contents xi

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Associated signs and symptoms 201 General signs 201 Ocular defects 201 Cranial nerve palsy/ocular deviation 203 Hemifield slide phenomenon 203 Optic atrophy 204 Postfixational blindness 204 Proptosis 204 See saw nystagmus 204 Sensory abnormalities 204 Visual acuity 204 Visual field defects 205 Craniopharyngioma 205 Glioma and meningioma 206 Hydrocephalus 207 Infection/inflammation 207 Multiple sclerosis 208 Pituitary adenoma 208 Vascular abnormalities 215 Choice of visual field assessment 215 References 226 Further reading 228 Optic tract 231 Anatomy 231 Pathology 231 Craniopharyngioma 232 Meningioma 232 Multiple sclerosis 232 Pituitary tumours 232 Trauma 232 Vascular abnormalities 232 Associated signs and symptoms 232 General signs 232 Optic atrophy 235 Pupil abnormalities 235 Visual field defects 235 Congruous visual field loss 235 Incongruous visual field loss 235 Choice of visual field assessment 236 References 241 Further reading 241 Lateral geniculate body 243 Anatomy 243 Pathology 244 Associated signs and symptoms 244 Optic atrophy 244 Pupil abnormalities 244 Sensory loss 245 Visual field defects 245

xii Contents

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Choice of visual field assessment 245 References 248 Further reading 249 Optic radiations 251 Anatomy 251 Pathology 251 Associated signs and symptoms 252 Eye movement abnormalities 252 Hemiparesis 256 Optic atrophy 256 Pupil abnormalities 258 Reading difficulties 258 Sensory abnormalities 258 Visual processing 258 Achromatopsia 258 Agnosia 258 Alexia 259 Depth impairment 259 Prosopagnosia 259 Simultanagnosia 259 Visual hallucinations 259 Visual neglect 259 Visual field defects 259 Parietal lobe lesion 260 Temporal lobe lesion 260 Choice of visual field assessment 260 References 285 Further reading 287 Visual cortex 289 Anatomy 289 Pathology 290 Space-occupying lesions 290 Trauma 290 Vascular abnormalities 290 Associated signs and symptoms 290 Cerebral achromatopsia 290 Cortical blindness 290 Optic atrophy 293 Preservation of visual acuity 293 Pupil abnormalities 293 Riddoch phenomenon and blind sight 293 Sensory abnormalities 294 Visual hallucinations 294 Visual field defects 294 Altitudinal visual field defects 294 Checkerboard visual field defects 294 Homonymous hemianopia 294 Bilateral homonymous hemianopia 294

Contents xiii

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Unilateral homonymous hemianopia 294 Homonymous quadrantanopia 296 Macular involvement 298 Macular hemianopia 298 Macular sparing 298 Scotomas 307 Temporal crescent defect or sparing 307 Choice of visual field assessment 311 References 324 Further reading 326 Differential diagnosis 327 Age 327 Congruity 327 Eye movement generation 329 Fundus and anterior segment abnormalities 330 Optic atrophy 330 Ocular motility abnormalities 330 330 Pupil abnormalities Sensory abnormalities 330 Type of visual field defect 331 Visual acuity 331 Visual field defect progression 331 Visual perception 332 References 334 Visual field artefacts and errors of interpretation 337 Esterman programme assessment 337 Fatigue 337 Hysterical/functional visual loss and malingering 338 Learning curve 340 Lens rim defects 340 Observer interpretation 340 Ocular variables 341 Patient instruction and set-up 341 Patient positioning 342 Performance difficulties 344 Refractive errors 346 Reliability indices 347 References 353 Further reading 356 Glossary of terms in visual field assessment

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Index 365

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List of figures*

CHAPTER 1

  1.1 Hill of vision. 2   1.2 Normal extent of field of vision. 3   1.3 Afferent visual pathway. 4   1.4 Altitudinal visual field defect. 5   1.5 Arcuate visual field defect. 7   1.6 Constriction/diffuse defect. 8  1.7 Hemianopia. 9  1.8 Quadrantanopia. 11  1.9 Scotoma. 13 1.10 Sector-shaped (wedge) visual field defect. 15 CHAPTER 2

  2.1 Saccadic Vector Optokinetic Perimetry (SVOP) perimeter.   2.2 SVOP targets.   2.3 Goldmann perimeter.   2.4 Octopus 900 perimeter.   2.5 Humphrey visual field analyzer.   2.6 Henson 9000 perimeter.   2.7 Henson threshold result. ZATA standard printout for left eye.   2.8 Henson suprathreshold result.   2.9 Map of Goldmann kinetic isopters. 2.10 Luminance values (decibels). 2.11 Octopus 900 isopter boundaries. 2.12 Kinetic assessment strategy. 2.13 Global indices. 2.14 Calculation of global indices. 2.15 Total deviation versus pattern devia­tion.





21 22 22 22 23 23 25 26 27 28 29 30 35 36 36

2.16 Glaucoma hemifield test location of comparative areas. 2.17 Box plot representation. 2.18 Bebie curve representation. 2.19 Cluster analysis. 2.20 Polar analysis. 2.21 Humphrey three-in-one printout. 2.22 Humphrey single-field analysis print­out. 2.23 Humphrey overview printout. 2.24 Humphrey change analysis printout. 2.25 Humphrey glaucoma change probability printout. 2.26 Humphrey-guided progression analysis printout. 2.27 Octopus 900 four-in-one printout. 2.28 Octopus 900 seven-in-one printout. 2.29 Octopus 900 series display. 2.30 Octopus 900 trend printout. 2.31 Octopus 900 cluster trend printout. 2.32 Octopus 900 polar trend printout. 2.33 Stato–kinetic dissociation.

37 37 38 38 38 39 41 43 44 46 49 51 52 53 54 55 56 57

CHAPTER 3

  3.1   3.2   3.3   3.4   3.5   3.6   3.7

Choice of perimeter; general indications. 24-2 strategy. 30-2 strategy. 32 strategy. Low vision central strategy. G1 strategy. G2 strategy.

66 68 68 68 69 69 70

*Unless otherwise stated the right visual field is displayed above the left visual field result or to the right side of the left visual field result. Note: The blind spot appears on the right side of central fixation within the right visual field and on the left side of central fixation within the left visual field.

xv

xvi  List of figures

  3.8   3.9 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 3.25

10-2 strategy. 70 Macula strategy. 70 M strategy. 70 Macula threshold visual field assess­ment. 71 Full field 120 strategy. 73 Peripheral 68 and 60-4 strategies. 74 07 strategy. 74 Low vision periphery strategy. 74 Binocular Esterman programme. 75 Monocular Esterman programme. 76 European Commission guidelines. 76 Esterman visual field assessment; hemia­nopia. 78 Esterman visual field assessment; quadrantanopia. 79 Esterman and Goldmann perimeter visual field assessments; sector retinitis pigmentosa. 80 Esterman and Octopus perimeter visual field assessments; superior quadrantanopia. 81 Kinetic perimetry comparison. 83 Kinetic and static perimetry compari­son. 85 Static perimetry comparison. 87

CHAPTER 4

  4.1 Anterior segment appearance; herpes simplex virus. 94   4.2 Anterior segment appearance; anterior uveitis. 95   4.3 Anterior segment appearance; catar­act. 96   4.4 Humphrey perimeter visual field assess­ment; cataract. 98   4.5 Humphrey perimeter visual field asses­­sm ­ ent; corneal dystrophy. 99   4.6 Octopus perimetry visual field assessment; glaucoma and cataract. 100 CHAPTER 5

  5.1 Retinal and optic disc topography schematic.   5.2 Fundus appearance of retinitis pigmen­tosa.   5.3 Fundus appearance of macular drusen.   5.4 Fundus appearance of HIV infection.   5.5 Fundus appearance of toxoplasmosis.

104 105 106 106 106

  5.6 Fundus appearance of cytomegalo­v irus. 106   5.7 Fundus appearance of choroidal melanoma. 107   5.8 Fundus appearance in diabetic retinopathy. 107   5.9 Fundus appearance of post-laser treatment for diabetic retinopathy. 107 5.10 Fundus appearance of central retinal artery occlusion. 108 5.11 Fundus appearance of central retinal vein occlusion. 108 5.12 Humphrey perimeter visual field assessment; macular degeneration. 110 5.13 Humphrey perimeter visual field assess­­ment; macular drusen. 111 5.14 Humphrey perimeter visual field assessment; retinitis pigmentosa. 114 5.15 Humphrey perimeter visual field assessment; toxoplasmosis. 114 5.16 Humphrey perimeter visual field assessment; retinopathy. 115 CHAPTER 6

  6.1 Fundus appearance of coloboma. 120   6.2 Optic nerve drusen. 121   6.3 Fundus appearance of morning glory syndrome. 125   6.4 Fundus appearance of myelinated nerve fibres. 125   6.5 Fundus appearance of optic disc pit. 125   6.6 Fundus appearance of tilted optic discs. 126   6.7 Crowded orbital apex in thyroid eye disease. 126   6.8 Fundus appearance in optic nerve meningioma. 126   6.9 Bilateral optic nerve meningioma. 127 6.10 Fundus appearance in glaucoma. 129 6.11 Fundus appearance in optic neuritis. 130 6.12 Fundus appearance in early papilloedema. 131 6.13 Fundus appearance in acute papilloedema. 131 6.14 Fundus appearance in chronic papilloedema. 131 6.15 Fundus appearance in vintage papilloedema. 131 6.16 Fundus appearance of optic atrophy. 132

List of figures  xvii

6.17 Fundus appearance in nutritional toxicity. 133 6.18 Optical coherence tomography in glaucoma. 135 6.19 Humphrey perimeter visual field assess­ment; optic disc drusen. 139 6.20 Humphrey perimeter visual field assessment; myelinated nerve fibres. 140 6.21 Humphrey and Goldmann perimeter visual field assessment; optic nerve hypoplasia. 141 6.22 Schematic representation of nerve fibre bundle loss. 143 6.23 Perimeter visual field assessment; paracentral scotomas (glaucoma). 143 6.24 Perimeter visual field assessment; arcuate defects (glaucoma). 145 6.25 Perimeter visual field assessment; nasal steps (glaucoma). 148 6.26 Humphrey perimeter visual field assessment; asymmetrical visual field loss (glaucoma). 150 6.27 Perimeter visual field assessment; asym­metrical visual field loss (glaucoma). 152 6.28 Humphrey perimeter visual field assessment; dissimilar patterns of visual field loss (glaucoma). 156 6.29 Humphrey perimeter visual field assess­ment; central scotoma (optic neuritis). 157 6.30 Humphrey perimeter visual field assessment; caecocentral scotoma 158 (optic neuritis). 6.31 Perimeter visual field assessment; arcuate defect (optic neuritis). 158 6.32 Humphrey perimeter visual field assessment; generalised constriction 160 (optic neuritis). 6.33 Perimeter visual field assessment; reduced sensitivity (optic neuritis). 161 6.34 Humphrey perimeter visual field assessment; bilateral visual field loss (optic neuritis). 163 6.35 Humphrey perimeter visual field assessment; bilateral visual field loss (optic neuritis). 164

6.36 Humphrey perimeter visual field assessment; atypical visual field loss (optic neuritis). 6.37 Humphrey perimeter visual field assessment; inflammation. 6.38 Humphrey perimeter visual field assessment; early papilloedema. 6.39 Humphrey perimeter visual field assessment; acute papilloedema. 6.40 Humphrey perimeter visual field assessment; chronic papilloedema. 6.41 Humphrey perimeter visual field assessment; chronic papilloedema. 6.42 Perimeter visual field assessment; optic atrophy. 6.43 Humphrey perimeter visual field assessment; progressive papilloedema. 6.44 Goldmann perimeter visual field assessment; papilloedema. 6.45 Humphrey perimeter visual field assessment; papilloedema. 6.46 Humphrey perimeter visual field assessment; unilateral optic nerve meningioma. 6.47 Humphrey perimeter visual field assessment; thyroid eye disease. 6.48 Humphrey perimeter visual field assess­ment; thyroid eye disease. 6.49 Humphrey perimeter visual field assessment; altitudinal defect (vascular). 6.50 Humphrey perimeter visual field assessment; nerve fibre bundle defects (vascular).

165 166 168 168 170 172 173 176 178 179 184 185 186 187 187

CHAPTER 7

  7.1   7.2   7.3   7.4   7.5   7.6   7.7   7.8

Neuroimaging of normal pituitary area. 196 Neuroimaging of craniopharyngioma. 196 Optic chiasm glioma. 197 Neuroimaging of hydrocephalus. 198 Pituitary adenoma. 199 Pituitary apoplexy. 200 Internal carotid artery aneurysm. 202 Humphrey perimeter visual field assessment; craniopharyngioma. 206   7.9 Humphrey perimeter visual field assessment; craniopharyngioma. 207

xviii  List of figures

7.10 Humphrey perimeter visual field assessment; glioma. 7.11 Humphrey perimeter visual field assessment; hydrocephalus. 7.12 Humphrey perimeter visual field assessment; pituitary adenoma. 7.13 Pituitary adenoma. 7.14 Humphrey perimeter visual field asses­sment; pituitary adenoma. 7.15 Humphrey perimeter visual field assessment; pituitary adenoma. 7.16 Pituitary adenoma. 7.17 Pituitary adenoma. 7.18 Pituitary adenoma. 7.19 Pituitary adenoma. 7.20 Pituitary adenoma. 7.21 Pituitary adenoma. 7.22 Pituitary adenoma.

208 210 210 211 212 214 215 218 219 222 223 224 225

CHAPTER 8

  8.1 Craniopharyngioma.   8.2 Internal carotid artery aneurysm.   8.3 Humphrey perimeter visual field assessment; migraine.   8.4 Humphrey perimeter visual field assessment; meningioma.   8.5 Goldmann perimetry visual field assessment; vascular infarct.

233 234 236 237 240

CHAPTER 9

  9.1 Schematic lateral geniculate body structure.   9.2 Goldmann perimeter visual field assessment; sector defect.   9.3 Goldmann perimeter visual field assessment; sector defect.

244 246 247

CHAPTER 10

10.1 10.2 10.3 10.4 10.5 10.6 10.7

Vascular infarct. Vascular infarct. Vascular infarct. Arteriovenous malformation. Primary space-occupying lesion. Meningioma. Humphrey perimeter visual field assessment; vascular haemorrhage.

252 253 254 255 256 257 261

10.8 Goldmann perimeter visual field assessment; vascular infarct. 10.9 Vascular infarct. 10.10 Humphrey perimeter visual field assessment; trauma. 10.11 Humphrey perimeter visual field assessment; space-occupying lesion. 10.12 Space-occupying lesion. 10.13 Space-occupying lesion. 10.14 Vascular infarct. 10.15 Perimeter visual field assessment; vascular infarct. 10.16 Humphrey perimeter visual field assessment; arteriovenous malformation. 10.17 Vascular infarct. 10.18 Humphrey perimeter visual field assessment; space-occupying lesion. 10.19 Humphrey perimeter visual field assess­ment; space-occupying lesion. 10.20 Vascular infarct.

264 265 266 267 269 271 274 276 280 281 282 283 285

CHAPTER 11

11.1 Vascular infarct. 11.2 Vascular infarct. 11.3 Perimeter visual field assessment; consecutive vascular infarcts. 11.4 Perimeter visual field assessment; bilateral vascular infarcts. 11.5 Humphrey perimeter visual field assessment; vascular haemorrhage. 11.6 Perimeter visual field assessment; vas­cular infarct. 11.7 Humphrey perimeter visual field assessment; vascular haemorrhage. 11.8 Vascular infarct. 11.9 Humphrey perimeter visual field assessment; vascular infarct. 11.10 Vascular infarct. 11.11 Goldmann perimeter visual field assessment; temporal crescent loss. 11.12 Goldmann perimeter visual field assessment; spared temporal crescent.

291 292 295 297 299 306 308 314 317 317 322 323

CHAPTER 12

12.1 Visual pathway and outline of visual field defects.

328

List of figures  xix

CHAPTER 13

13.1 Goldmann perimeter visual field assessment; functional defect. 13.2 Goldmann perimeter visual field assessment; functional defect. 13.3 Octopus perimeter visual field assessment; functional result. 13.4 Humphrey perimeter visual field assessment; lens rim defect. 13.5 Humphrey perimeter visual field assessment; lens rim defect. 13.6 Humphrey perimeter visual field assessment; lens rim defect. 13.7 Humphrey perimeter visual field assessment; ptosis.

338 339 339 342 345 345 346

13.8 Eye position. 13.9 Head position representation. 13.10 Goldmann perimeter visual field assessment; refractive scotoma. 13.11 Humphrey perimeter visual field assessment; fixation losses. 13.12 Humphrey perimeter visual field assessment; high false-negative score. 13.13 Humphrey perimeter visual field assessment; high false-positive score (normal visual field). 13.14 Humphrey perimeter visual field assessment; high false-positive score (abnormal visual field).

346 347 348 349 350 351 352

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Preface

Visual Fields via the Visual Pathway, Second Edition presents the varying visual field deficits occurring with lesions of the visual pathway. This second edition expands the content to consider further types of perimetry and update existing perimetry information. The Octopus 900 perimetry, introduced since the first edition, features alongside Goldmann and Humphrey perimeters. Further additions to clinical case scenarios are included, maintaining a key illustrative feature of the original edition. The main content is, as per the original edition, structured such that the visual pathway is traced anatomically from front to back and each section of the visual pathway has its own dedicated chapter. The chapters are clearly structured and comprise an outline of anatomy, pathology and signs and symptoms, plus visual field defects specifically associated with that part of the visual pathway. Each chapter is supplemented by numerous

illustrations of visual field results, neuroimaging scans and/or line drawings: colour plates of associated fundus images are also provided. In addition chapters are provided on the basic theory of visual field assessment, methodology, aids to differential diagnosis, artefacts of visual field results and a glossary of terms used in visual field assessment. References and further reading lists are provided for each chapter containing key articles and up-to-date literature. This textbook has been written to provide a guide for the multidisciplinary eye care team, including ophthalmologists, orthoptists, optometrists, ophthalmic technicians and ophthalmic nurse practitioners, as well as the wider multidisciplinary medical team, including neurologists, neurosurgeons and endocrinologists. Its clinical content for both text and illustrations is particularly relevant for the practitioner.

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Acknowledgements

I wish to express my sincere thanks to colleagues at the University of Liverpool for their continuous support. I also thank Carmel Noonan for help in improving the quality of a number of images. I am grateful to Carl Zeiss AG (Humphrey Instruments) for permission to reproduce illustrations on programme results, to Haag Streit AG for permission

to reproduce illustrations on programme grids, to Professor David Henson for permission to reproduce illustrations for the Henson 9000 perimeter and to i2eye Diagnostics for permission to reproduce illustrations for the Saccadic Vector Optokinetic Perimetry perimeter.

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Disclosure

Dr. Fiona Rowe has no financial or commercial interest in either the Goldmann perimeter, Humphrey visual field analyzer or Octopus 900 perimeter.

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About the author

Dr. Fiona Rowe qualified as an orthoptist in 1990 and has maintained combined clinical and academic research activity since then. She currently is a Reader in health services research at the University of Liverpool, an NIHR Research Fellow and until recently, was Director of Research for the British and Irish Orthoptic Society. She is associate editor-in-chief for the journal Strabismus, associate editor for BMC Ophthalmology, chair of the regional AHP research network, Cochrane Eyes and Vision group editor and a mentor for the National Institute of Health Research health services research scheme. Her particular research interests include acquired brain injury, visual field evaluation and control of ocular alignment. Research projects include chief investigator for the Vision In Stroke (VIS) study,

Visual Impairment in Stroke; Intervention Or Not (VISION) trial and Impact of Visual Impairment after Stroke (IVIS) programme. Other projects include evaluating the impact of knowledge of visual impairment to the treatment choices made by therapists in the care of stroke patients, comparison of therapy options for hemianopic visual field loss, evaluation of binocular vision in acquired brain injury, evaluation of ward-based visual impairment assessment and the comparison of static and kinetic perimetry strategies. Dr. Rowe is the author of two textbooks: Clinical Orthoptics and Visual Fields via the Visual Pathway, co-author on four book chapters, and has presented and published her research extensively. Further research details can be found on http:// pcwww.liv.ac.uk/~rowef/index.htm.

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1 Field of vision and visual pathway Visual field assessment is the process by which the boundaries of the visual field are plotted and the field within the peripheral boundaries is determined to be intact. The term perimetry derives from the word perimeter and denotes the mapping of the boundary or outer perimeter of the field of vision. Campimetry is a further term used in visual field assessment but denotes the assessment of the visual field on a flat surface. Assessment of the visual field has been undertaken in varying ways since the blind spot was first documented by Mariotte in the seventeenth century. The outer boundaries of the visual field were assessed by Young and Purkinje in the nineteenth century. However, the first clinical measurement of the visual field was not made until the 1850s by von Graefe. Varying methodologies have been developed for the assessment of the field of vision since the nineteenth century. In 1889, Bjerrum introduced a tangent screen for the assessment of the visual field which currently retains his name. This predominantly assessed the central visual field. The Arc perimeter was introduced by Aimark in the 1930s which had the advantage of being able to plot the peripheral visual field. This was followed by the introduction of the Goldmann perimeter in 1945 which today, although no longer in manufacture, remains in widespread use and continues to be of considerable clinical value. The Friedmann perimeter was the first quantitative static measurement introduced in 1966 and assessed the central visual field. Automated perimetry was introduced in the 1970s with the subsequent development of a myriad of different automated perimeters with many testing programmes which today provide accurate and reliable visual fields

with the advantage of statistical analysis of results and computer storage of patient files. The automated perimeters most commonly in current use in hospital practice are the Humphrey field analyzer (Humphrey Systems, Dublin, CA, USA) and Octopus 900 perimeter (Haag Streit Int, Koeniz, Switzerland).

GENERAL ANATOMY OF THE VISUAL SYSTEM The hill of vision is a map of the visual sensitivity across the visual field usually in three dimension. A one-dimensional representation usually takes a horizontal section bisecting the optic disc and fovea (Figure 1.1). The central peak of the hill equates to the fovea and is typically the area of highest sensitivity. Sensitivity decreases towards the periphery of the visual field (Hart and Burde 1983). The normal monocular visual field extends 50–60 degrees superiorly, 60 nasally, 70–75 inferiorly and 90–100  temporally (Kanski and ­ McAllister 1989; Stamper et al. 1999). The extent of visual field will vary with stimulus size and the extent measured with a Goldmann I4e or ¾  mm white target is usually regarded as indicative of the peripheral visual field (Figure 1.2). As the optic disc has no retinal photoreceptors, it forms the blind spot of the visual field (Armaly 1969). The visual field is produced by retinal stimulation of each eye and relates to what is seen by the individual whilst maintaining steady fixation, that is the perceived vision of an individual. Retinal images are projected to a position opposite the area of retina stimulated, for example, objects that stimulate nasal retina are situated in the temporal 1

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Figure 1.1  Hill of vision. Map of visual field is usually in three-dimension but is represented here in onedimension for right and left eyes. The central peak has the highest sensitivity and represents the fovea. Sensitivity decreases towards the periphery of the visual field.

General anatomy of the visual system  3

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Figure 1.2  Normal extent of field of vision. Goldmann chart plotted with a I4e target showing the peripheral boundary of the visual field and the blind spot. The extent of peripheral boundary is age dependent; for example (a) 20-year old, (b) 60-year old.

4  Field of vision and visual pathway

visual field and objects that stimulate inferior ­retina are situated in the superior visual field. A high percentage of nerve fibres arise from the macular area of the retina and pass directly to the optic disc (papillomacular bundle). Nerve fibres located further temporally in the peripheral retina (nasal field of vision) must arc above and below the macular fibres to enter the optic disc superiorly and inferiorly. Nerve fibres on the nasal side of the optic disc (temporal field of vision) pass directly to the nasal border. Once in the optic nerve the macular fibres move to a central position with superior retinal fibres above and inferior retinal fibres below. Temporal and nasal nerve fibres retain their temporal and nasal location within the optic nerve. On reaching the optic chiasm, the temporal nerve fibres maintain their temporal position whilst nasal nerve fibres (both central and peripheral) decussate. Ipsilateral temporal nerve fibres and contralateral nasal nerve fibres regroup in the optic tracts but again with superior fibres retaining a more superior location to the inferior fibres.

Nerve fibres are distributed in a complicated multi-layered arrangement in the lateral geniculate nucleus of the lateral geniculate body with macular fibres distributed throughout the nucleus. Ipsilateral and contralateral peripheral nerve fibres are located in different layers of the nucleus. There  is a synapse of nerve fibres in the lateral geniculate body. Fibres leaving the lateral geniculate body fan out to form the optic radiations, many of which pass directly posterior to the visual cortex. A proportion, however, initially passes anteriorly and laterally before turning posterior towards the visual cortex. Within the striate visual cortex (area V1), the macular fibres terminate on the tip of the occipital lobe (occipital pole) whilst the more peripheral fibres terminate more anteriorly. The most peripheral fibres relating to the monocular crescent of each eye are the most anteriorly represented. Superior fibres are on the upper lip of the calcarine fissure whilst inferior fibres are on the lower lip. Figure 1.3 represents the afferent visual pathway.

Retina

Optic nerve Optic chiasm Optic tract Lateral geniculate body

Optic radiations

Visual cortex

Figure 1.3  Afferent visual pathway. Visual pathway from retina to visual cortex.

Visual field defect types  5

ischaemic optic neuropathies. The defect precisely respects the horizontal meridian. The sharp horizontal separation occurs because there is a clear demarcation between superior and inferior nerve fibres temporal to the macula and nasal to the optic disc (Figure 1.4). Severe hypotension, sudden haemorrhage and rapid development of anaemia may be responsible for simultaneous bilateral ischaemic optic neuropathies with altitudinal visual field defects. They may also be due to bilateral symmetric involvement at a cortical level including bilateral lesions affecting the occipital lobe (Heller-Bettinger et al. 1976; Miller and Newman 1999).

VISUAL FIELD DEFECT TYPES There are a number of different types of visual field defects along with a number of classification schemes that have been proposed for use in clinical studies. Such classification schemes ­t ypically divide visual field defects into retinal and­ non-retinal nerve fibre bundle defect types and have largely been used in research studies for glaucoma, ocular hypertension and optic n ­ euritis (Brusini 1996; Keltner et al. 1994; Keltner et al. 2003). Examples of retinal nerve fibre layer defects include arcuates, nasal steps and paracentral scotomas whereas examples of non-­ retinal nerve fibre layer defects include hemianopia and ­quadrantanopia. The frequently occurring visual field defects are described below.

Arcuate visual field defect This is caused by selective damage to the superior or inferior retinal nerve fibre bundles as they enter the optic nerve head and is typical of glaucoma. However, such visual field defects are also seen with papilloedema and in optic neuritis, ischaemic

Altitudinal visual field defect This involves two quadrants of either the superior or inferior visual field and is typically seen in HAAG-STREIT INTERNATIONAL

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Figure 1.4  Altitudinal visual field defect. (a) Superior altitudinal defect involving inferior retinal nerve fibres; (b) inferior altitudinal defect involving superior retinal nerve fibres. (Continued)

6  Field of vision and visual pathway

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Figure 1.4 (Continued)  Altitudinal visual field defect. (a) Superior altitudinal defect involving inferior ­retinal nerve fibres; (b) inferior altitudinal defect involving superior retinal nerve fibres.

optic neuropathy and congenital optic disc drusen (Figure 1.5). Temporally, the defect is narrow because all of the nerve fibre bundles converge on the optic disc. The defect spreads out on the nasal side but typically arcs over central fixation. All complete arcuate scotomas extend to the horizontal meridian producing a nasal step assuming there is differing involvement of the superior and inferior visual fields.

Constriction/diffuse defect A diffuse depression or constriction of the visual field can be caused by many conditions such as cataract, pupil miosis, glaucoma and incorrect refractive correction. In static perimetry, this appears as a reduction in decibel values across the visual field. In kinetic perimetry, this appears as constricted isopters (Figure 1.6).

Hemianopia A hemianopia is a defect involving one half of the visual field. A heteronymous hemianopia involves opposite sides of the visual field (e.g. lesions of the optic chiasm typically produce bitemporal heteronymous hemianopias). A homonymous ­ hemianopia involves the same side of the visual field in each eye (e.g. lesions of the retrochiasmal pathways typically produce homonymous ­hemianopias) (Figure 1.7).

Quadrantanopia This is a defect involving a quadrant of each visual field. Heteronymous quadrantanopia in­ volves opposite sides of the visual field and either superior or inferior quadrants. Homonymous quadrantanopias involve the same side of the visual field in each eye and either superior or inferior quadrants.

Visual field defect types  7

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Figure 1.5  Arcuate visual field defect. (a) Superior arcuate defect with inferior nasal step; (b) inferior ­arcuate defect.

8  Field of vision and visual pathway

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Figure 1.6  Constriction/diffuse defect. Reduced area of visual field.

These may be produced by temporal, parietal or occipital lobe lesions (Figure 1.8).

Scotoma A scotoma is an absolute or relative area of depressed visual sensitivity surrounded by normal vision. In an absolute scotoma all vision is lost, whereas in a relative scotoma a variable amount of vision remains. Scotomas may be central, paracentral or caecocentral in type (Figure 1.9). A central scotoma only involves fixation (Figure  1.9a). The scotoma can be relative or absolute depending on the severity of the lesion. A central scotoma typically occurs in optic neuritis although it can also be caused by ischaemic and compressive optic nerve lesions. A paracentral scotoma (Figure 1.9b) involves an area of visual field away from fixation and tends to be elongated circumferentially along the course of the optic nerve fibres within the central 30 degrees. It may be seen in glaucoma or lesions affecting the optic disc such as papilloedema.

A caecocentral scotoma (Figure 1.9c) extends from fixation to the blind spot and is caused by disease of the papillomacular bundle. It typically occurs in toxic optic neuropathies and Leber’s optic neuropathy. Congenital optic disc pits associated with serous detachment of the macula may also produce a similar defect. Bilateral caecocentral scotomas may be due to toxic amblyopia, optic neuritis, Leber’s optic neuropathy or intrinsic optic nerve tumours. Scotomas can be caused by retro-chiasmal visual pathway lesions in which bilateral homonymous scotomas occur in the left or right visual field and in the central, paracentral or peripheral visual field ‒ see Chapter 11.

Sector-shaped (wedge) visual field defect These visual field defects start as small scotomas on the temporal side of the visual field and typically end as complete sectorial loss (Figure 1.10).

Visual field defect types  9

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Figure 1.7  Hemianopia. (a,b) Bitemporal hemianopia; (c,d) homonymous hemianopia.

(Continued)

10  Field of vision and visual pathway

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Figure 1.7 (Continued)  Hemianopia. (a,b) Bitemporal hemianopia; (c,d) homonymous hemianopia.

Visual field defect types  11

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Figure 1.8  Quadrantanopia. (a,b) Superior homonymous quadrantanopia; (c,d) inferior ­homonymous quadrantanopia.(Continued)

12  Field of vision and visual pathway

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Figure 1.8 (Continued)  Quadrantanopia. (a,b) Superior homonymous quadrantanopia. (c,d) inferior homonymous quadrantanopia.

Visual field defect types  13

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o e 70 ire ur id lin 255 270 285 300 e s this pa chan 240 h Für Seitenwechsel t ss e g e ge ng Zeiger hier durchführen r I’i r de han lo n d e c ô t é, To c dex a x pa n i r ic i Correction : s w in g Object

e,

P fa

Relat. Intens. dB 210 1 0,0315 15 2 0,100 10 Object mm2 3 0,315 5 4 1,00 0 0 1/16 a 0,40 4 I 1/4 b 0,50 3 II 1 c 0,63 2 III 4 d 0,80 1 IV 16 e 1,00 0 v 64 Printed in Switzerland 940–2414

30

OS.

OD.

sph ⁐

Refraction :

◦ ◦

cyl

Visus:

(a) HAAG-STREIT INTERNATIONAL

120

105

90 70 60

135

75

60

Nomen: Datum:

45

50

150

30

40 30 165

15

20 10

180

90 80

70

60

50

40

30

20

10 20

10

30

40

50

60

70

80 90

0

10 20

195

mm Diameter pupillae

40

60

Relat. Intens.

4 3 2 1 e dc b ae d c ba ed c b a edc b a dB 0 1 2 3 4 5 6 7 8 9 10111213141516171819 315 0 e line I d i II s is 300 III theng th e g o IV han al To c dex V

70 re u r c 240 255 270 285 pa ha Für Seitenwechsel sse n g e Zeiger hier durchführen r I’i r de n d e c ô t é, x pa in r ici s win g

OS.

,

225

330

Object

50

Po i fa

Relat. Intens. dB 210 1 0,0315 15 2 0,100 10 Object mm2 3 0,315 5 4 1,00 0 0 1/16 a 0,40 4 I 1/4 b 0,50 3 II 1 c 0,63 2 III 4 d 0,80 1 IV 16 e 1,00 0 v 64 Printed in Switzerland 940-2414

345

30

OD.

Correction : Refraction :

sph ⁐

cyl

◦ ◦

Visus:

(b)

Figure 1.9  Scotoma. (a) Central Involvement of central fixation only. (b) Paracentral. Defects are located within 30 degrees of central fixation. (c) Caecocentral. Central fixation is involved with extension of the defect to the blind spot. (Continued)

14  Field of vision and visual pathway

HAAG-STREIT INTERNATIONAL

120

105

90 70 60

135

75

60

Nomen: Datum:

45

50 150

30

40 30

165

15

20 10

180 90 80

70

60

50

40

30

20

10

10

20 30

40

50

60

70

80 90 0

10 20

195

345

30

Relat. Intens. dB 1 0,0315 15

210

2 0,100 10 Object 5 0 4 3

c 0,63 d 0,80 e 1,00

2 III 1 IV 0 v

330

50

mm

3 0,315 4 1,00 a 0,40 b 0,50

mm Diameter pupillae

40

2

1/4

1 4 16 64

225

60

315

70 e, ine re u r c 240 255 270 285 300 sid his l pa h a e Für Seitenwechsel t h ss e n g e t ge long Zeiger hier durchführen r I’i r de han c nd To c dex a ex p ôté, in ar i ci s w in g Correction: Object

1/16

Po i fa

0 I II

OS.

Printed in Switzerland 940–2414

OD.

Relat. Intens.

4 3 2 1 e d c b a e d c b a e d c b a e d c b a dB 0 1 2 3 4 5 6 7 8 9 10111213141516171819 0 I II III IV V

Refraction:

sph ⁐

cyl

◦ ◦

Visus:

(c)

Figure 1.9 (Continued)  Scotoma. (a) Central Involvement of central fixation only. (b) Paracentral. Defects are located within 30 degrees of central fixation. (c) Caecocentral. Central fixation is involved with extension of the defect to the blind spot.

PARAMETERS AND VARIABLES IN VISUAL FIELD ASSESSMENT There are a number of parameters that must be considered when undertaking quantitative visual field assessment as follows: 1. Luminance intensity 2. Size of stimulus 3. Anatomical features 4. Interference with perception of stimuli 5. Patient ability 6. Examination technique The sensitivity of the visual field is expressed in luminance or light intensity units. Luminance ­intensity is the light intensity of an optical source which can be seen by the human eye. Luminance units may be measured in candelas which is a unit of luminance recognized by the International System

of Units (SI). The luminance of a surface source can be measured per square metre (cd/m2). Light intensity may also be expressed as an apostilb which is an absolute unit of  light measurement equal to 0.1 millilamberts (1 cd/m2 equals 3.14 asb). This is an older unit of measurement no longer used as an SI unit. The range of retinal light sensitivity measured by visual field assessment is expressed in log units with a base of 10. In perimetry, stimuli intensity for visual field assessment is represented in decibel ­values which equal 1/10th of a log unit (10 dB equals 1 log unit) and allows larger numbers to be expressed as smaller numerical units. Therefore, changes in ­sensitivity are more easily detected (0 dB = 1000 apostilb = 318.4 cd/m2; Table 1.1). Perimeters generate light of varying intensities using neutral density filters over a maximally omitting bulb. The different intensities are graded in decibel values as an inverted logarithmic scale. The luminous intensity of the stimulus in automated

Parameters and variables in visual field assessment  15

120

105

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Nomen: Datum:

45

50 150

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20 10

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30 20

10 20

10

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10 20

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30

Relat. Intens. dB 1 0,0315 15

2 0,100 10 Object

2 III 1 IV 0 v

1/4

1

60

225

1/16

315

4 16 64

OS.

Printed in Switzerland 940–2414

OD.

Relat. Intens.

4 3 2 1 e d c b a e d c b a e d c b a e d c b a dB 0 1 2 3 4 5 6 7 8 9 10111213141516171819 0 I II III IV V

70 e , ne re u r c id li 240 255 270 285 300 pa ha e s this Für Seitenwechsel h sse n g e t ge long Zeiger hier durchführen r I’i r de han c nd To c dex a ex p ôté, n i a r ici s w in g Correction : Object

c 0,63 d 0,80 e 1,00

0 I II

Po i fa

5 0 4 3

330

50

mm2

3 0,315 4 1,00 a 0,40 b 0,50

mm Diameter pupillae

40

210

Refraction :

sph ⁐

cyl

◦ ◦

Visus:

Figure 1.10  Sector-shaped (wedge) visual field defect. Temporal defect extending to the blind spot.

Table 1.1  Luminance intensity Candela/ metre2

Apostilb

Decibel

3,184

10,000

0

318.4

1,000

10

31.84

100

20

3.18

10

30

0.3

1

40

0.03

0.1

50

Luminance Brightest

Dimmest

visual field assessment may be altered from 0 to 51 dB (brightest to dimmest) providing a wide range of brightness levels for stimuli to completely assess the threshold of all visual field areas. The relative luminance between background and stimulus will alter sensitivity. Goldman and Octopus 900 perimeters generate a maximum stimulus luminance of 1000 apostilbs equating to 0  dB. The Humphrey

automated perimeter generates a maximum stimulus luminance of 10,000 apostilbs equating to 0 decibels. In Goldmann and Humphrey perimetry, the background illumination is set at 31.5 apostilb and, for Octopus 900 perimetry, is set at 31.4 apostilb. This standard calibration is necessary for test/ retest repeatability. The area of retina stimulated will provide different responses to stimuli, that is peripheral retinal responses have lower luminance sensitivity than central retinal. The size of stimulus can be varied in that stimuli can be presented in sizes I to V in both automated and manual perimetry. Sizes range from 0.56 mm to 9.03 mm diameter and ¼ mm2 to 64 mm2 area (Table 1.2). Size III stimulus is standardly set for automated perimetry (4 mm2). The size of stimuli remains constant in automated perimetry thereby providing consistent stimuli. Stimulus size is varied during testing in kinetic perimetry when plotting peripheral and central isopters. There are a number of external variables that must be considered with regard to the visual field

16  Field of vision and visual pathway

Table 1.2  Size and intensity of targets in kinetic perimetry Stimulus V4e IV4e III4e II4e I4e I3e I2e I1e

Apostilb

Decibel value

Target area (mm2)

Target diameter (mm)

1000 315 100 31.5 10 3.15 1 0.315

0 5 10 15 20 25 30 35

64 16 4 1 ¼ ¼ ¼ ¼

9.03 4.51 2.26 1.13 0.56 0.56 0.56 0.56

Note: These eight standard stimuli are frequently used to allow continuity of testing and interpretation.

result. These include anatomical features of the face (e.g. prominent brow or nose), interference with ocular media and perception of stimuli (e.g. ptosis, miotic pupil, uncorrected refractive error, cataract), attention and age of the patient, and technique of the examiner (explanation of the test and patient set-up) (Haas et al. 1986; Johnson et al. 1989). Protruding facial features such as lids and brows  may provide a spurious visual field defect often in the superior visual field. Where there is ptosis, the lid should be taped to prevent the lid blocking stimuli presentation. Miosis depresses the visual field and can exaggerate the size and depth of existing visual field defects. Pupil diameter less than 2 mm produces visual field loss in the form of generalised depression of sensitivity as pupil constriction dims both the intensity of the stimulus and the intensity of the background by reducing the incident light reaching the retina. This is a problem when assessing patients on miotics for glaucoma (Lindenmuth et al. 1989; Mikelberg et al. 1987). Refractive errors if uncorrected can result in refractive scotomas with enlarged blind spots and enlargement of other visual field defects. There is also a depression of sensitivity in the visual field (Goldstick and Weinreb 1987; Weinreb and Perlman 1986). Defocus effectively enlarges the stimulus size but will reduce the luminance (Atchison 1987; Henson and Morris 1993). Refractive errors greater than 1 dioptre should be corrected and the prescription given according to the patient’s age and instrument optics. Incorrect spectacle corrections can also cause artefacts due to reduced light sensitivity which may produce local or generalised visual field loss.

Abnormalities that interfere with media clarity reduce illumination and therefore sensitivity within the visual field will be generally depressed and existing visual field defects exaggerated (Drance et al. 1967; Guthauser and Flammer 1988; Guthauser et al. 1987; Jaffe et al. 1986). Age gradually depresses the visual field sensitivity. Light-difference sensitivity decreases with age partly due to age-related loss of nerve fibres (Balazsi et al. 1984) and increased condensation of the media.

REFERENCES Armaly MF. (1969) The size and location of the normal blind spot. Archives of Ophthalmology. 82; 182‒201. Atchison DA. (1987) Effect of defocus on visual field measurement. Ophthalmic and Physiological Optics. 7; 259‒65. Balazsi AG, Rootman J, Drance SM, Schulzer M, Douglas GR. (1984) The effect of age on the nerve fibre population of the human optic nerve. American Journal of Ophthalmology. 97; 760‒6. Brusini P. (1996) Clinical use of a new method for visual field damage classification in glaucoma. European Journal of Ophthalmology. 6; 402‒7. Drance SM, Berry V, Hughes A. (1967) Studies on the effects of age on the central and peripheral isopters of the visual field in normal subjects. American Journal of Ophthalmology. 63; 1667‒72.

Further reading  17

Goldstick BJ, Weinreb RN. (1987) The effect of refractive error on automated global analysis program Gel. American Journal of Ophthalmology. 104; 229‒32. Guthauser U, Flammer J. (1988) Quantifying visual field damage caused by cataract. American Journal of Ophthalmology. 106; 480‒4. Guthauser U, Flammer J, Niesel P. (1987) Relationship between cataract density and visual field damage. Documenta Ophthalmologica Proceedings Series. 49; 39‒41. Haas A, Flammer J, Schneider U. (1986) Influence of age on the visual fields of normal subjects. American Journal of Ophthalmology. 101; 199‒203. Hart WM Jr, Burde RM. (1983) Three-dimensional topography of the central visual field. Sparing of foveal sensitivity in macular ­disease. Ophthalmology. 90; 1028‒38. Heller-Bettinger I, Kepes JJ, Preskorn SH, Wurster JB. (1976) Bilateral altitudinal anopia caused by infarction of the calcarine cortex. Neurology. 26; 1176‒9. Henson DB, Morris EJ. (1993) Effect of uncorrected refractive errors upon central visual field testing. Ophthalmic and Physiological Optics. 13; 339‒43. Jaffe GJ, Alvarado JA, Juster RP. (1986) Agerelated changes of the normal visual field. Archives of Ophthalmology. 104; 1021‒5. Johnson CA, Adams AJ, Lewis RA. (1989) Evidence for a neural basis of age-related visual field loss in normal observers. Investigative Ophthalmology. 30; 2056‒64. Kanski J, McAllister J. (1989). Glaucoma A colour manual of diagnosis and treatment. London, UK: Butterworths. Keltner JL, Johnson CA, Spurr JO, Beck RW, Group ONS. (1994) Visual field profile of optic neuritis. Archives of Ophthalmology. 112; 946‒53. Keltner JL, Johnson CA, Cello KE, Edwards MA, Bandermann SE, Kass MA, Gordon MO, OHTS group. (2003) Classification of Visual Field Abnormalities in the Ocular Hypertension Treatment Study. Archives of Ophthalmology. 121; 643‒50.

Lindenmuth KA, Skuta GL, Rabbani R, Musch DC. (1989) Effect of pupillary constriction on automated perimetry in normal eyes. Ophthalmology. 96; 1289‒301. Mikelberg FS, Drance SM, Schutzer M, Wijsman K. (1987) The effect of miosis on visual field indices. Documenta Ophthalmologica Proceedings Series. 49; 645‒9. Miller NR, Newman NJ. (1999) Walsh and Hoyt’s Clinical NeuroOphthalmology. The Essentials, 5th edition. Baltimore, MD: Williams & Wilkins. Stamper R, Lieberman M, Drake M. (1999) Diagnosis and Therapy of the Glaucomas. St. Louis, MO: CV Mosby. Weinreb RN, Perlman JP. (1986) The effect of refractive correction on automated perimetric thresholds. American Journal of Ophthalmology. 101; 706‒9.

FURTHER READING American Academy of Ophthalmology. (1996) Automated perimetry. Ophthalmology. 103; 1144‒51. Anderson DR. (1992) Automated Static Perimetry, 1st edition. St. Louis, MO: CV Mosby. Armaly MF. (1969) Ocular pressure and visual fields: A 10-year follow-up study. Archives of Ophthalmology. 81; 25‒40. Driver and Vehicle Licensing Agency (DVLA). For medical practitioners. At a glance guide to the current medical standards of fitness to drive. November 2014 edition. Swansea, UK: Driver’s Medical Group, DVLA. Autzen T, Work K. (1990) The effect of learning and age on short-term fluctuation and mean sensitivity of automated static perimetry. Acta Ophthalmologica. 68; 327‒30. Fankhauser F, Enoch JM. (1962) The effect of blur on perimetric thresholds. Archives of Ophthalmology. 86; 240‒51. Field Analyzer Owner’s Manual. (1991) Humphrey Instruments Inc. (Carl Zeiss Group). Gonzalez de la Rosa M, Pareja A. (1997) Influence of the fatigue effect on the mean deviation measurement in perimetry. European Journal of Ophthalmology. 7; 29‒34.

18  Field of vision and visual pathway

Haley MJ. (1987) The Field Analyzer Primer, 2nd edition. San Leandro, CA: Zeiss Humphrey systems. Herse PR. (1992) Factors influencing normal perimetric thresholds. Investigative Ophthalmology and Visual Science. 33; 611‒7. Heuer DK, Anderson DR, Feuer WJ, Gressel MG. (1987) The influence of refraction ­accuracy on automated perimetric threshold ­measurements. Ophthalmology. 94; 1550‒3. Hoyt WF, Tudor RC. (1963) The course of papillary temporal retinal axons through the anterior optic nerve. A Nanta degeneration study in the primate. Archives of Ophthalmology. 69; 503‒7. Johnson C, Nelson-Quigg JM. (1993) A prospective three year study of response properties of normal subjects and patients during automated perimetry. Ophthalmology. 100; 269‒74. Katz J, Sommer A, Witt K. (1991) Reliability of visual field results over repeated testing. Ophthalmology. 98; 70‒5. Kline LB, Foroozan R. (2012) NeuroOphthalmology Review Manual, 7th edition. Thorofare, NJ: Slack Inc.

Enoch JM. (ed). (1979) Perimetric standards and perimetric glossary of the International Council of Ophthalmology. The Hague/Boston/London: Concilium Ophthalmologicum Universale. Reitner A, Tittl M, Ergun E, BaradaranDilmaghani R. (1996) The efficient use of perimetry for neuro-ophthalmic diagnosis. British Journal of Ophthalmology. 80; 903‒5. Rowe FJ. (1998) Visual field analysis with Humphrey automated perimetry. Part I and II. Eye News. Vol 4, No 6 and Vol 5 No 1. Rowe FJ. (1999) Idiopathic Intracranial Hypertension. Assessment of Visual Function and Prognosis for Visual Outcome. PhD Thesis. Anglia Ruskin University, Cambridge, UK. Sarkies N. (1987) Neurological visual fields. British Orthoptic Journal. 44; 15‒24. Townsend JC, Selvin GJ, Griffin JR, Comer GW. (1991) Visual Fields – Clinical Case Presentations. Oxford, UK: Butterworth-Heinemann. Werner EB, Adelson A, Krupin T. (1988) Effect of patient experience on the results of automated perimetry in clinically stable glaucoma patients. Ophthalmology. 95; 764‒7. Zalta AH. (1989) Lens rim artefact in automated threshold perimetry. Ophthalmology. 96; 1302–11.

2 Methods of visual field assessment PERIMETRY Visual field assessment may be undertaken by a variety of methods. These include a qualitative estimation of the visual field through comparison of the patient’s visual field to that of the examiner, and quantitative measurement of the visual field through standard white-on-white target detection, colour detection, motion detection, form resolution and gaze tracking methods. Such perimetry methods typically are operated under photopic visual conditions at high light levels (day time) in which there are luminance levels greater than 3 cd/m2. Scotopic visual conditions occur at low ambient light levels (night) in which there are luminance levels less than 0.003 cd/m2. Mesopic visual conditions are ‘in between’ at luminance levels of 0.003–3 cd/m2. Furthermore some perimeter tests target specific functional sub-pathways that subserve different aspects of vision and whose physiological properties are distinct (McBride and Rowe 2014). Standard achromatic perimetry (white-on-white) often detects visual field loss only when a substantial number of retinal ganglion cells are already lost (Kerrigan-Baumrind et  al. 2000). By using function-specific perimetry, it is proposed that earlier visual field loss detection, particularly for glaucoma, can be achieved (Quigley et  al. 1988). The M (magnocellular) pathway consists of larger retinal ganglion cells that are mainly linked with visual perception and respond predominantly to motion and coarse outlines. They are regarded as insensitive to colour stimuli in balanced luminance conditions, respond to high contrast sensitivity and resolve higher temporal and lower spatial

frequencies (Liu et al. 2006; Silva et al. 2005). The K (koniocellular) pathway consists of smaller, sparse retinal ganglion cells that are sensitive to short wavelengths (S/blue cones) (Liu et al. 2006; Shipp 2006; Silva et  al. 2005). The spatial and temporal resolutions of the K pathway overlap with M and P pathways. The P (parvocellular) pathway consists of small retinal ganglion cells that are sensitive to colour (particularly red/green), respond predominantly to fine details and to lower contrast sensitivity. They resolve lower temporal and higher spatial frequencies (Liu et al. 2006; Silva et al. 2005). It is possible to isolate responses from the M, P and K pathways by using different test stimuli. Strategies to isolate the P and K pathways include the use of coloured, high contrast, small stimuli, whereas strategies to isolate the M pathway include the use of stimuli that are colour neutral and have high temporal and low spatial frequencies such as large, fast motion reversal, low contrast targets (Xu et al. 2001). Approximately 80% of ganglion cells are parvocellular, 5% are koniocellular and 15% are magnocellular, which react to temporally modulated stimuli. The Humphrey automated field analyzer, Octopus 900 perimeter and Goldmann perimeter will be addressed specifically throughout this text for purposes of description and illustrations of visual field defects as these perimeters are most commonly used in hospital eye clinics for visual field assessment. However, a brief overview of other perimetry methods is provided for information. Confrontation may be used during a patient’s clinical examination as a very basic indication of the visual field. It has been found to be reliable for acute bedside assessment but less so for follow-up 19

20  Methods of visual field assessment

and where some recovery has taken place (Cassidy et  al. 1999). However, Townend et  al. (2007) reported that substantial visual field loss such as hemianopia is likely to be underestimated by confrontation and automated perimetry is more sensitive. In practice, for assessment of the visual field at the bedside, confrontation remains a realistic test choice. Confrontation is performed in photopic lighting with the patient and examiner facing each other. The patient closes one eye and fixates on the examiners nose. The examiner introduces a target from the periphery into each quadrant of the field. The examiner may hold a 10- to 20-mm white pin as the target but in addition may use his/her fingers as targets and the number of fingers seen in each quadrant can also be documented. A red pin may be used to compare colour contrast in the central field and in each quadrant. One confrontation method is as follows. To first assess the peripheral boundary of the visual field, the patient is asked to continue looking at the examiner’s nose and to say ‘yes’ when they are aware of a target moving in their outer vision. Using the white-mounted target, slowly move this in from the periphery from the following ‘clock’ positions: first 12, 3, 6 and 9 o’clock in random order followed by 1, 2, 4, 5, 7, 8, 10 and 11 o’clock positions in random order. If a visual field defect is found, additional positions are assessed to further outline the boundary of the field defect. Additional positions should be perpendicular to the defect boundary. The central visual field is then assessed. The patient continues to look at the examiner’s nose and is asked whether they can see all parts of the examiners face or whether part or one side of the face appears more blurred or faded than the rest. The patient should consider whether right versus left eyes, mouth versus forehead, right versus left ears are seen equally well to further qualify their responses. Next, compare finger counting in each quadrant. Hold both hands up (with fingers closed), one hand positioned to the outer side of each of the patient’s eyes. Briefly raise one or two fingers from one hand and ask the patient to say whether fingers were raised and if so, how many were seen (Welsh 1961). Repeat this with both hands held in the lower quadrants below the

patient’s cheek level. Finally, briefly raise fingers on both hands and ask the patient how many are seen in total.

Flicker Perimetry Flicker perimetry is based on an optical illusion that when a small stimulus region is flickered in counter phase at a high temporal frequency against a background of random dots, an edge or border is perceived (Horn et al. 2014; Reznicek et al. 2014). Typically the stimulus is a 5° area with flicker at a frequency of 10–15 Hz resulting in a grey circle being seen against a mean luminance background. This method is used to evaluate temporal visual function alongside spatial resolution and contrast sensitivity and targets the M pathway. Flicker perimetry can be undertaken using perimeters such as the Octopus 600 (Haag Streit AG, Koeniz, Switzerland).

Frequency Doubling Technology (FDT) FDT is based on an optical illusion that when a low spatial frequency sinusoidal grating (< 1 cycle/ degree) undergoes high temporal counter phase flickering at 15 Hz or greater, gratings appear to double to twice their actual spatial frequency (Kelly 1966; Soliman et al. 2002). Essentially there is a rapid contrast reversal in which light bars become dark and vice versa. The frequency doubling phenomenon is thought to be mediated by a subset (5%) of ganglion cells within the M pathway called M cells (Maddess and Henry 1992; Sample et al. 2000) that have larger diameter axons making them more prone to damage in early glaucoma (Anderson and Johnson 2003; Glovinsky et al. 1991; Johnson and Samuels 1997). FDT can be undertaken using perimeters such as the Humphrey Matrix (Carl Zeiss AG, Dublin, CA) and Octopus 300 perimeter (Haag Streit AG).

Short-Wavelength Automated Perimetry (SWAP) SWAP visual field assessment is based on the principle that larger ganglion cells within the retina are selectively damaged during early glaucoma

Perimetry 21

(Demirel and Johnson 2001; Johnson et al. 1993). Ten per cent of these larger ganglion cells belong to the blue-yellow pathway: part of the K pathway (Dacey and Lee 1994). The blue-yellow conditions of SWAP isolate the S cone system (short-wavelength cones), reduce the participation of other cone systems (red – long wavelength and green – medium wavelength) and saturate the rods activity through the adaptation to yellow light (Delgado et al. 2002; Wild et al. 2006). SWAP can be performed on the Humphrey Visual Field Analyzer and the Octopus perimeter. A Goldman size V target (1.74° diameter) is used with a blue filter placed over the source of light allowing only light with a peak transmission of 440 nm through. The white background light is replaced by yellow light illuminated at 100 cd/m 2 in the perimeter bowl. The targets are presented for 200 msec in all test locations and the test is performed within the central 30° of the visual field. SWAP has not been introduced routinely into clinical practice due to a number of factors: clinicians are not united on a definition of abnormality criteria; the effect of the ageing lens on results; lengthy test time; patient fatigue and patient dislike of the test and the large intra- and inter-subject variability even with normal subjects, which make it difficult to define an abnormal field (McBride and Rowe 2014; Moss et al. 1995).

ring at each individual location is reached (Frisen 1993; Wall et  al. 1991, 2004). Steps are made in 1 decibel (dB) increments.

Saccadic Vector Optokinetic Perimetry (SVOP) SVOP (i2eye Diagnostics, Edinburgh, United Kingdom) uses eye tracking to detect the natural saccadic eye responses of gaze shifts towards stimuli in the visual field when they are seen by the patient (Fleck et  al. 2012) (Figure 2.1). The patient is asked to look at a series of white dots or small pictures (Figure 2.2). The perimeter uses an eye tracker to monitor the patient’s eye movement responses to these visual stimuli presented at predetermined visual field locations on a display

High-pass resolution perimetry High-pass resolution perimetry may also be termed Ring perimetry and uses ring-shaped targets of different sizes to determine resolution over the central 30° of the visual field. This form of perimetry aims to find the smallest test target that can be detected in a given location within the visual field. Background luminance is set at 20 cd/m 2 . The test targets consist of a bright circular core surrounded by darker borders with ring core luminance at 25 cd/m 2 and ring border luminance at 15 cd/m 2 . A ‘vanishing optotype’ property is achieved as the average luminance of the target and the background are equal. The test includes 14 different sizes of target presented at 50 different locations within the central visual field. The rings are reduced or increased in stepped size until the patient’s threshold for detection of the

Figure 2.1  Saccadic Vector Optokinetic Perimetry (SVOP) perimeter. (Courtesy of i2eye Diagnostics, Edinburgh, United Kingdom.)

22  Methods of visual field assessment

Figure 2.2  SVOP targets. (Courtesy of i2eye Diagnostics, Edinburgh, UK.)

screen. A decision algorithm makes an automated decision on whether the stimuli have been seen or not based on the direction of any detected eye movements (Murray et  al. 2009). This method is reported as particularly useful for childhood perimetry assessment.

Standard perimetry Visual field assessment may be manual, automated or semi-automated. Manual perimetry may use a kinetic and/or static technique and perimeters include Goldmann perimetry (Figure 2.3), Octopus 900 perimetry (Figure 2.4), Friedmann perimetry and Bjerrum screens. Automated perimetry predominantly uses a static technique and perimeters include the Humphrey field analyzer (Figure 2.5), Octopus 900 perimeter, Henson 9000 perimeter (Figure 2.6), Dicon perimeter, Octopus 300/600 perimeter and Medmont perimeter. Specifications for Goldmann, Humphrey and Octopus 900 perimeters are outlined in Table 2.1. Smaller sized perimeters such as the Henson 9000 and Octopus 300 or 600 models are typically used more in community and optometric practice than in hospital eye clinic practice but offer a range of suprathreshold and threshold programmes as well as flicker and frequencydoubling options. Furthermore they provide reliable and repeatable visual field results and their printout options are similar in presentation

Figure 2.3  Goldmann perimeter.

Figure 2.4  Octopus 900 perimeter.

Presentation of visual field data  23

(a)

 

(b)

Figure 2.5  Humphrey visual field analyzer. (a) Humphrey 7 series and (b) Humphrey 8 series.

PRESENTATION OF VISUAL FIELD DATA Data presentation may be in different forms.

Figure 2.6  Henson 9000 perimeter. (Courtesy of Professor David Henson, University of Manchester, UK.)

to Humphrey and Octopus 900 perimeters (Figures 2.7 and 2.8). Automated perimetry may use a kinetic technique in which preset vectors at preset speeds run as a defined testing programme. Such perimeters include the Humphrey field analyzer and Octopus 900 perimeter. Semi-automated perimetry uses an automated testing programme coupled with examiner intervention during the test to add further vectors to refine and evaluate suspicious areas of the visual field.

1. Map of isopters (Figure 2.9). This is used to document the area of visual field and isopters are assessed with targets of differing size and luminance. This mode of presentation is used to display visual field results obtained with kinetic perimetry. 2. Luminance values (decibels; Figure 2.10). Values are plotted at different points within the field of vision, which measure differential light sensitivity (thresholds) at those points across the visual field. These decibel values are converted to a greyscale map and given statistical values when compared to age-matched normal results. This mode of presentation is used to display visual field results with static automated perimetry.

Goldmann perimeter The Goldmann perimeter is a spherical projection perimeter (Figure 2.3), which incorporates a system that allows direct registration of the target position. The bowl has a radius of 30 cm and illumination of the bowl is constant and uniform. The target used to determine the boundaries and

24  Methods of visual field assessment

Table 2.1  Perimetry specifications Goldmann perimeter

Humphrey field analyzer

Octopus 900 perimeter

Bowl

Spherical 30 cm

Aspheric 18–30 cm

Spherical 30 cm

Background luminance

31.5 apostilb 10 cd/m2

31.5 apostilb 10 cd/m2

31.4 apostilb 10 cd/m2

Stimulus size

Goldmann I–V

Goldmann I–V

Goldmann I–V

Stimulus duration

Operator dependent

200 msec

100-infinite msec

Stimulus luminance for 0 dB value

4,800 apostilb

10,000 apostilb

4,000–10,000 apostilb

Range

0–40 dB

0–51 dB

0–47 dB

Strategies

Kinetic

4-2 and 3-1 step SITA standard SITA fast Kinetic (750i 840, 850 and 860)

4-2-1 step Dynamic Tendency oriented Kinetic

Fixation control

Monitored by examiner

threshold of the visual field is projected onto the inside of the bowl. The target can be altered in size and luminous intensity and both kinetic and static examination of the central and peripheral visual field can be achieved. There are six target sizes from the largest size V to the smallest size O (64, 16, 4, 1, ¼ and 1/16 mm2) with a difference of 5 dB between each target size. Size O is generally not used as its results are inconsistent. There are two sets of grey filters to change the stimulus intensity (luminance). The first set includes four grey filters: 1.0, 0.315, 0.1 and 0.0315. The second set contains five grey filters: 1.0, 0.8, 0.63, 0.5 and 0.4. The filters allow a change of target intensity in 1 dB steps. The bowl luminosity is set to 31.5 apostilb and the brightness of the target is set to 1000 apostilb. These factors should be set by calibration and therefore provide a standardized examination at each test as the adaptive state of the eye is the same at each examination. The visual field can be compared over a variable time period in the knowledge that the examination conditions have remained constant. A V4e target calibrated at 1000 apostilb equates to 0 dB. The instrument is handled from the examiner’s side and the fixation of the patient’s eye can be

Blink control, pupil position control, automated eye tracking

constantly checked through a reticulated telescope. It is important to continuously assess patient fixation to ensure reliability of patient responses. The patient should be instructed to continually look towards the central fixation target.

Humphrey automated perimeter The Humphrey automated perimeter is a sensitive and highly precise assessor of visual field. It is a single unit, fully automatic, computerized, projection perimeter (Figure 2.5). The background illumination is 31.5 apostilb, which is set as a standard by the International Perimetric Society and is the same as for Goldmann and Octopus perimetry. The Humphrey automated perimeter uses stimuli that are projected onto the bowl area and which are varied in luminosity over a range of 51 dB. The stimulus size can be varied but not during a test. The size is set before the test programme is run (Heijl and Patella 2002). A Goldmann size III target size is usually used by default, which is considered small enough to detect small scotomas (Flammer et  al. 1983) but large enough to be relatively unaffected by residual refractive errors (Sloan 1961). The Humphrey perimeter can incorporate a kinetic

Presentation of visual field data  25

Record Num 10 Age 79 Time 13:50:00 Left RX Plano VA R 6/6 L 6/6

Ex, Ample dob 22/07/1930 Date 08/06/2010 Right RX Plano Pupil Diameter R 3 L 3 LEFT EYE

Threshold Test Goldmann lll White Stimulus Background 10 cd/m2

30

30

17

14

13

5

25

26

25

20

24

22

26

27

26

28

25

25

26

14

25

26

29

31

30

28

27

22

19

25

20

29

29

31

31

28

27

23

24

27

27

29

29

30

29

27

27

29

27

28

27

28

24

26

22

27

Threshold dB (0=3183cd/m2)

-8

-12 -13 -20

-7 -11 -12 -19

Presentations Fovea

-7

-3

-4

-4

-2 -12

0

-2

-2 -5 -5

1

1

-1 0

-2 -3 -1

-1

0

0

-2

-1

-2

1

-3 -2

-6

0

-1 -1 -2

-2 -2

-3

-8

-4

-5

-1

-2 -4

-2

-5

-5

-3 -13

0

-3

-2

0

-1

-3

-3 -6 -6

-2

-1 1

-3

-2

-2

0

0

-2 -1 -2

-2

-1 -1

-4

-3 -4

-2

-2

-1

-1 -1

-3

-1 -1

-3

-2

-3

0

-4

-3

-7

-1

-1 -3

0 0

-1

-4

Total Defect dB

Pattern Defect dB

30

30

0

-1

54

Fixation Losses False Positives False Negatives

2/11 0/0 0/6

Mean Defect

-3.17 dB p