Textbook of Ophthalmology (2021) PDF

Textbook of Ophthalmology Sanjeev Kumar Mittal, MS, FICO (Japan) Professor and Head Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Raj Kumar Agarwal, MS Consultant Ophthalmologist Saharanpur, Uttar Pradesh, India Thieme Delhi Stuttgart New Y...

Textbook of Ophthalmology Sanjeev Kumar Mittal, MS, FICO (Japan) Professor and Head Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Raj Kumar Agarwal, MS Consultant Ophthalmologist Saharanpur, Uttar Pradesh, India Thieme Delhi Stuttgart New York Rio de Janeiro Publishing Director: Ritu Sharma Development Editor: Dr Gurvinder Kaur Director-Editorial Services: Rachna Sinha Project Managers: Prakash Naorem, Jyothi Sriram Vice President, Sales and Marketing: Arun Kumar Majji Managing Director & CEO: Ajit Kohli Copyright © 2021 Thieme Medical and Scientific Publishers Private Limited. Thieme Medical and Scientific Publishers Private Limited. A - 12, Second Floor, Sector - 2, Noida - 201 301, Uttar Pradesh, India, +911204556600 Email: [email protected] www.thieme.in Cover design: Thieme Publishing Group Typesetting by RECTO Graphics, India Printed in India by Nutech Print Services 54321 ISBN: 978-93-88257-78-7 Important note: Medicine is an ever-changing science undergoing continual development. Research and clinical experience are continually expanding our knowledge, in particular, our knowledge of proper treatment and drug therapy. Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book. Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book. Every user is requested to examine carefully the manufacturers’ leaflets accompanying each drug and to check, if necessary, in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released in the market. Every dosage schedule or every form of application used is entirely at the user’s own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed. If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page. Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation without the publisher’s consent is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage. Dedicated to The Almighty Contents Preface Acknowledgments Note from the Authors Competency Mapping Chart 1. Anatomy and Embryology of the Eye 2. Vision– Its Physiology, Neurology, and Assessment 3. Optics and Refraction 4. Ocular Therapeutics 5. The Conjunctiva 6. The Cornea 7. The Sclera 8. The Uveal Tract 9. The Pupil 10. The Lens 11. The Glaucoma 12. Vitreous Humor 13. The Retina 14. The Optic Nerve 15. The Afferent (Sensory) System 16. The Efferent (Motor) System 17. Strabismus (Squint) 18. Ocular Tumors 19. Ocular Injuries 20. The Lids 21. The Lacrimal Apparatus 22. The Orbit 23. Ocular Manifestations in Neurological Disorders 24. Ocular Manifestations of Systemic Diseases 25. Cryotherapy and Lasers in Ophthalmology 26. Eye Surgery 27. Ocular Symptoms and Examination 28. Community Ophthalmology Index Preface The goal of this book is to provide a clinical overview of the major areas of ophthalmology in a simplified way. Although this book is essentially meant for undergraduate students, it will not only be of great use for Postgraduation aspirants but also serve as a foundation book for residents in ophthalmology. To make it more student friendly, illustrations, tables and flow charts have been generously used to give it the form of a conceptual book. We had started working on this book about 8 years ago. Now, we are happy to complete this and bring it to our readers. In fact, some part of the text is in more detail than required, but this feature of the book makes the text more attractive and explanatory in nature. The undergraduate course is not as extensive as the one earmarked for postgraduate entrance examinations. The contents of this book, however, cover the latter requirement. MBBS students should keep this fact in mind. Nevertheless, in spite of our efforts, the book is not likely to be free from human errors and mistakes. Therefore, any feedback and suggestions from the readers will be appreciated. Sanjeev Kumar Mittal, MS, FICO Raj Kumar Agarwal, MS (Japan) Acknowledgments With blessings of my parents, I, Dr. Sanjeev Kumar Mittal, acknowledge the motivation provided by my spouse Dr. Sunita Mittal and daughters Dr. Gauri Mittal and Pooja Mittal in writing this textbook of ophthalmology. This book owes its existence to the help, support, and inspiration of several people as well as the blessings of my parents. I, Dr. Raj Kumar Agarwal, would like to express my sincere gratitude toward my spouse Dr. Renu Agarwal and daughters Dr. Akshi Raj and Dr. Archi Raj in writing the book of ophthalmology. We extend our heartiest appreciation to our alma mater where we built a passion for teaching and writing. The students, too, have proved to be a perennial source of inspiration. The contributions of the entire publication team at Thieme and Ms. Yukti Tyagi toward compiling the manuscript are peerless. Sanjeev Kumar Mittal, MS, FICO Raj Kumar Agarwal, MS (Japan) Note from the Authors We thank our contributors, listed below, for offering valuable content contribution to the following book chapters: Chapter 2: Vision- Its Physiology, Neurology, and Assessment Sunita Mittal, MBBS, MD Additional Professor Department of Physiology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Gauri Mittal, MBBS MD Resident Department of Pharmacology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Chapter 4: Ocular Therapeutics S. S. Handu, MBBS, MD, DM Professor and Head Department of Pharmacology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India We thank the following fellow doctors for helping with providing clinical photographs: Chapters 5 and 6: The Conjunctiva and the Cornea Neeti Gupta, MBBS, MS, Fellow-Cornea LVPEI Associate Professor Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Chapter 11: The Glaucoma Ajai Agarwal, MBBS, MS, MAMS, FICS Additional Professor Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Chapter 13: The Retina Ramanuj Samantha, MBBS, MS, FICO Assistant Professor Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Chapter 17: Strabismus (Squint) Anupam, MBBS, MS Additional Professor Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Chapters 20 and 22: The Lids and the Orbit Rimpi Rana, MBBS, MS Senior Resident Department of Ophthalmology All India Institute of Medical Sciences Rishikesh, Uttarakhand, India Competency Mapping Chart Competency COMPETENCY Page No. Code The student should be able to Visual Acuity Assessment OP1.1 Describe the physiology of vision 15 OP1.2 Define, classify, and describe the types and 45, 718 methods of correcting refractive errors OP1.3 Demonstrate the steps in performing the 22 visual acuity assessment for distance vision, near vision, color vision, the pin hole test, and the menace and blink reflexes OP1.4 Enumerate the indications and describe the 59, 659, 680 principles of refractive surgery OP1.5 Define and enumerate the types and the 467 mechanism by which strabismus leads to amblyopia Lids and Adnexa, Orbit OP2.1 Enumerate the causes; describe and discuss 481, 519, the etiology, clinical presentations, and 522, 524, diagnostic features of common conditions 526, 532, of the lid and adnexa including Hordeolum 535, 539, externum/internum, blepharitis, preseptal 558, 574 cellulitis, dacryocystitis, hemangioma, dermoid, ptosis, entropion, lid lag, and lagophthalmos Competency COMPETENCY Page No. Code The student should be able to OP2.2 Demonstrate the symptoms and clinical 481, 519, signs of conditions enumerated in OP2.1 522, 524, 526, 532, 535, 539 OP2.3 Demonstrate under supervision clinical 553 procedures performed in the lid including: Bell’s phenomenon, assessment of entropion/ectropion, regurgitation test of lacrimal sac, massage technique in congenital dacryocystitis, and trichiatic cilia removal by epilation OP2.4 Describe the etiology and clinical 574 presentation; discuss the complications and management of orbital cellulitis OP2.5 Describe the clinical features on ocular 578 examination and management of a patient with cavernous sinus thrombosis OP2.6 Enumerate the causes and describe the 570, 578 differentiating features, clinical features, and management of proptosis OP2.7 Classify the various types of orbital tumors; 564, 569, 582 differentiate the symptoms and signs of the presentation of various types of ocular tumors OP2.8 List the investigations helpful in diagnosis 569, 582 of orbital tumors; enumerate the indications for appropriate referral Conjunctiva Competency COMPETENCY Page No. Code The student should be able to OP3.1 Elicit document and present an appropriate 85, 187 history in a patient presenting with a “red eye” including congestion, discharge, and pain OP3.2 Demonstrate document and present the 85 correct method of examination of a “red eye” including vision assessment, corneal luster, pupil abnormality, and ciliary tenderness OP3.3 Describe the etiology, pathophysiology, 89 ocular features, differential diagnosis, complications, and management of various causes of conjunctivitis OP3.4 Describe the etiology, pathophysiology, 98 ocular features, differential diagnosis, complications, and management of trachoma OP3.5 Describe the etiology, pathophysiology, 108 ocular features, differential diagnosis, complications, and management of vernal catarrh OP3.6 Describe the etiology, pathophysiology, 115 ocular features, differential diagnosis, complications, and management of pterygium OP3.7 Describe the etiology, pathophysiology, 536 ocular features, differential diagnosis, complications, and management of symblepharon Competency COMPETENCY Page No. Code The student should be able to OP3.8 Demonstrate correct technique of removal 499 of foreign body from the eye in a simulated environment OP3.9 Demonstrate the correct technique of Practical instillation of eye drops in a simulated environment Corneas OP4.1 Enumerate, describe, and discuss the types 127 and causes of corneal ulceration OP4.2 Enumerate and discuss the differential 127 diagnosis of infective keratitis OP4.3 Enumerate the causes of corneal edema 121 OP4.4 Enumerate the causes and discuss the 559 management of dry eye OP4.5 Enumerate the causes of corneal blindness 115, 121, 122, 123, 156, 161 OP4.6 Enumerate the indications and the types of 676 keratoplasty OP4.7 Enumerate the indications and describe the 140, 143, methods of tarsorrhaphy 151, 153, 536, 539, 563, 607 OP4.8 Demonstrate technique of removal of 499 foreign body in the cornea in a simulated environment OP4.9 Describe and discuss the importance and 676, 706 protocols of eye donation and eye banking Competency COMPETENCY Page No. Code The student should be able to OP4.10 Counsel patients and family about eye Practical donation in a simulated environment Sclera OP5.1 Define, enumerate, and describe the 165 etiology, associated systemic conditions, clinical features, complications, indications for referral, and management of episcleritis OP5.2 Define, enumerate, and describe the 167 etiology, associated systemic conditions, clinical features, complications, indications for referral, and management of scleritis Iris and Anterior Chamber OP6.1 Describe clinical signs of intraocular 177, 180 inflammation and enumerate the features that distinguish granulomatous from nongranulomatous inflammation; identify acute iridocyclitis from chronic condition OP6.2 Identify and distinguish acute iridocyclitis 177, 180 from chronic iridocyclitis OP6.3 Enumerate systemic conditions that can 177, 180 present as iridocyclitis and describe their ocular manifestations OP6.4 Describe and distinguish hyphema and 183, 505 hypopyon OP6.5 Describe and discuss the angle of the 2 anterior chamber and its clinical correlates Competency COMPETENCY Page No. Code The student should be able to OP6.6 Identify and demonstrate the clinical 180, 265, features, and distinguish and diagnose 288, 292, common clinical conditions affecting the 293, 298, anterior chamber 311, 716 OP6.7 Enumerate and discuss the etiology and the 265, 288, clinical distinguishing features of various 292, 293, glaucomas associated with shallow and 298, 311 deep anterior chamber; choose appropriate investigations and treatment for patients with above conditions OP6.8 Enumerate and choose the appropriate 177, 180 investigation for patients with conditions affecting the uvea OP6.9 Choose the correct local and systemic 187 therapy for conditions of the anterior chamber and enumerate their indications, adverse events, and interactions OP6.10 Counsel patients with conditions of the iris Practical and anterior chamber about their diagnosis, therapy, and prognosis in an empathetic manner in a simulated environment Lens OP7.1 Describe the surgical anatomy and the 218, 223 metabolism of the lens OP7.2 Describe and discuss the etiopathogenesis, 229, 230, stages of maturation, and complications of 231, 235, 241 cataract OP7.3 Demonstrate the correct technique of ocular 233, 244 examination in a patient with a cataract Competency COMPETENCY Page No. Code The student should be able to OP7.4 Enumerate the types of cataract surgery and 244, 686, 694 describe the steps, and intraoperative and postoperative complications of extracapsular cataract extraction surgery OP7.5 To participate in the team for cataract Practical surgery OP7.6 Administer informed consent and counsel Practical patients for cataract surgery in a simulated environment Retina and Optic Nerve OP8.1 Discuss the etiology, pathology, clinical 339, 341, features, and management of vascular 346, 351, occlusions of the retina 372, 375, 377, 378, 386 OP8.2 Enumerate the indications for laser therapy 337, 339, in the treatment of retinal diseases 341, 346, (including retinal detachment, retinal 351, 372, degenerations, diabetic retinopathy, and 375, 377, hypertensive retinopathy) 378, 386 OP8.3 Demonstrate the correct technique of 725 fundus examination, and describe and distinguish the funduscopic features in a normal condition and in conditions causing an abnormal retinal examination OP8.4 Enumerate and discuss treatment modalities 339, 341, in management of diseases of the retina 346, 351, 372, 375, 377, 378, 386, 701 Competency COMPETENCY Page No. Code The student should be able to OP8.5 Describe and discuss the correlative 392, 394, anatomy, etiology, clinical manifestations, 395, 403, diagnostic tests, imaging, and management 411, 415 of diseases of the optic nerve and visual pathway Miscellaneous OP9.1 Demonstrate the correct technique to 439 examine extraocular movements (uniocular and binocular) OP9.2 Classify, enumerate the types, methods of 450, 452, 459 diagnosis, and indications for referral in a patient with heterotropia/strabismus OP9.3 Describe the role of refractive error 45, 59, 450, correction in a patient with headache and 451, 453, 631 enumerate the indications for referral OP9.4 Enumerate, describe, and discuss the causes 728, 729, of avoidable blindness and the National 730, 731, 734 Programmefor Control of Blindness (including Vision 2020) OP9.5 Describe the evaluation and enumerate the 495 steps involved in the stabilization, initial management, and indication for referral in a patient with ocular injury Integration Human Anatomy AN30.5 Explain effect of pituitary tumors on visual 421 pathway Competency COMPETENCY Page No. Code The student should be able to AN31.3 Describe anatomical basis of Horner’s 593 syndrome AN31.5 Explain the anatomical basis of oculomotor, 596, 597, 598 trochlear, and abducent nerve palsies along with strabismus AN41.1 Describe and demonstrate parts and layers 1 of eyeball AN41.2 Describe the anatomical aspects of cataract, 257 glaucoma, and central retinal artery occlusion Physiology PY10.17 Describe and discuss functional anatomy of 15, 213, 257, eye, physiology of image formation, 259 physiology of vision including color vision, refractive errors, color blindness, physiology of pupil, and light reflex PY10.18 Describe and discuss the physiological 424 basis of lesion in visual pathway PY10.19 Describe and discuss auditory and visual 15 evoked potentials PY10.20 Demonstrate testing of visual acuity, color, 15 and field of vision in volunteer/ simulated environment Pathology PA36.1 Describe the etiology, genetics, 491 pathogenesis, pathology, presentation, sequelae, and complications of retinoblastoma Competency COMPETENCY Page No. Code The student should be able to Pharmacology PH1.58 Describe drugs used in ocular disorders 60, 280 General Medicine IM24.15 Describe and discuss the etiopathogenesis, 57, 154, 235, clinical presentation, identification, 372, 733 functional changes, acute care, stabilization, management and rehabilitation of vision, and visual loss in the elderly  Anatomy and CHAPTER 1 Embryology of the Eye Anatomy of Eyeball Blood Supply of Eyeball Innervation of Eyeball Embryology of Eyeball ▃ ▃ Anatomy of Eyeball (AN41.1) Each eyeball is situated in a bony cavity known as the orbit. It is protected by eyelids and soft tissues. In the orbit, it is suspended by extraocular muscles and their facial sheaths. Dimensions Anteroposterior diameter: at birth—17.5 mm; in adults—24 mm. Horizontal diameter: 23.5 mm. Vertical diameter: 23 mm. Shape Being flattened in vertical diameter, its shape resembles an oblate spheroid. Structure Eyeball consists of three coats (tunics, Fig. 1.1): 1. Outer fibrous coat. 2. Intermediate vascular coat (uveal tissue). 3. Innermost nervous layer (retina). Outer Fibrous Coat It consists of cornea and sclera. Cornea is the anterior 1/6th, transparent and avascular part of the fibrous coat. Sclera is the posterior 5/6th opaque part of the fibrous coat. The anterior part of the sclera is covered by a mucous membrane, the conjunctiva, which is reflected over the inner surface of the eyelids. The junction of sclera and cornea is called the sclerocorneal junction or limbus. Conjunctiva is firmly adherent at the limbus. Fig. 1.1 Tunics (coats) of eyeball. Abbreviations: Ant., anterior; Post., posterior. Intermediate Vascular Coat (Uveal Tissue) It consists of three parts: 1. Iris: It is the anterior most part of the uveal tissue. 2. Ciliary body: It extends from iris to ora serrata and is subdivided into two parts: anterior (pars plicata, 2 mm) and posterior (pars plana, 4 mm). 3. Choroid: It is the posterior most part of the uveal tissue. It lies in contact with sclera on its outer surface and with retina on its inner surface. Innermost Nervous Layer (Retina) It extends from optic disc to ora serrata. It ends abruptly just behind the ciliary body as a dentate border called ora serrata. It is concerned with visual functions. Segments The eyeball is divided into anterior and posterior segments (Fig. 1.2) by the lens, which is suspended from the ciliary body by fine delicate fibrils called zonules (suspensory ligaments of lens). Both anterior and posterior chambers communicate with each other through the pupil. Anterior Segment This includes structures anterior to the lens, that is, cornea, iris, lens, and part of ciliary body. The anterior segment is divided by the iris into an anterior chamber and a posterior chamber. Anterior Chamber (OP6.5) Boundaries: The posterior surface of cornea forms the anterior boundary, while the iris, part of ciliary body, and surface of lens in the pupillary area forms the posterior boundary of the anterior chamber. Depth: It is 2.5 mm in center. It is shallower in hypermetropes and deeper in myopes. It contains a clear watery fluid called aqueous humor (0.25 mL). Angle: Angle of anterior chamber is a peripheral recess of the anterior chamber through which drainage of aqueous humor takes place. Posterior Chamber It is a triangular space and contains aqueous humor. Boundaries: The posterior surface of iris and part of ciliary body forms the anterior boundary, while the lens, zonules, and ciliary body forms the posterior boundary. Fig. 1.2 Structure of eyeball. Both anterior and posterior chambers communicate with each other through the pupil. Posterior Segment This includes structures posterior to the lens, that is, vitreous humor, retina, choroid, and optic nerve. Vitreous humor is a gel-like material which fills the cavity behind the lens. The detailed anatomy of various parts of the eyeball and ocular adnexa (eyelids, lacrimal apparatus, and orbit) is described in respective chapters. ▃ ▃ Blood Supply of Eyeball The eye has two separate systems of blood vessels (Table 1.1): 1. Retinal vessels: These supply part of the retina. 2. Ciliary blood vessel: These supply rest of the eye.  Arterial Supply Both retinal and ciliary arteries branch from the ophthalmic artery, which is a branch of the internal carotid artery (ICA), and gives rise to the following branches (Fig. 1.3 and Fig. 1.4): Lacrimal artery: It supplies the lacrimal gland. Central retinal artery: Supplies the retina. Short posterior ciliary arteries (10–20 in number): Supply the uveal tract. Long posterior ciliary arteries (two in number). Muscular arteries: Supply four recti muscles which give rise to anterior ciliary arteries. Short posterior ciliary arteries pierce the sclera in a ring around the optic nerve and give rise to the intrascleral circle of Zinn. These end as choriocapillaris and supply the entire choroid. Long posterior ciliary arteries pierce sclera in horizontal meridian and pass forward in suprachoroidal space (between sclera and choroid), without giving any branch, reach ciliary muscle and form circulus arteriosus iridis major (major arterial circle of iris) with anterior ciliary arteries. It supplies ciliary processes and iris. The recurrent branches from the circle supply the anterior part of choriocapillaris. Branches from this major arterial circle run radially through the iris, which form a circular anastomosis near the pupillary margin called the circulus arteriosus iridis minor (minor arterial circle of iris). Anterior ciliary arteries give branches to the conjunctiva, sclera, and limbus. Central retinal artery supplies the inner layers of retina. Outer layers of retina are nourished by diffusion from choriocapillaris. Small anastomoses between vessels of uveal origin and central retinal artery connect the uveal and retinal circulations. Occlusion of one of the ciliary arteries usually does not produce dramatic effects because of arterial ring and manifold arterial supply to choriocapillaris. Venous Drainage Venous drainage of inner retina occurs via central retinal vein to superior ophthalmic vein after which the blood passes into cavernous sinus and out of the skull through internal jugular vein. Outer retinal layers are drained by vortex veins which drain into the superior ophthalmic vein. Table 1.1 Blood supply of the eyeball Part of the eye Arterial supply Venous drainage Iris and Long Vortex veins drain blood ciliary body posterior from whole of uveal tract Choroid ciliary except outer part of ciliary arteries and muscle which is drained by anterior anterior ciliary veins. ciliary arteries. Short posterior ciliary arteries. Retina: ♢ outer layers of By diffusion from retina ♢ inner layers of choriocapillaris central retinal Vortex veins via central retinal vein into retina artery. cavernous sinus. Fig. 1.3 Arterial supply of eyeball. Fig. 1.4 Ophthalmic artery and its branches. Uveal tract drains through three groups of ciliary veins, namely, short posterior ciliary veins, vortex veins, and anterior ciliary veins.  Short posterior ciliary veins receive blood only from sclera. They do not receive any blood from the choroid. Vortex veins (venae vorticosae): Small veins from uveal tract join to form four vortex veins, namely, superior temporal, inferior temporal, superior nasal, and inferior nasal veins. These pierce sclera behind the equator and drain into superior and inferior ophthalmic veins which, in turn, drain into cavernous sinus. As ophthalmic veins communicate with cavernous sinus, they act as a route by which infections can spread from outside to inside the cranial cavity. Vortex veins drain blood from whole of the uveal tract except outer part of ciliary muscle, which is drained by anterior ciliary veins. Veins from the outer part of ciliary body form a plexus, ciliary venous plexus, which drain into anterior ciliary veins. These receive blood from only outer part of ciliary muscle. ▃ ▃ Innervation of Eyeball Eyeball is innervated by both sensory and motor nerves. Sensory Nerve Supply It is derived from ophthalmic division of the trigeminal nerve (V1). It is purely a sensory nerve. It divides into three branches (Fig. 1.5): Nasociliary nerve. Lacrimal nerve. Frontal nerve. Long ciliary nerve (a branch of nasociliary nerve) is sensory to eyeball but may also contain sympathetic fibers for pupillary dilatation. Nasociliary nerve also gives off sensory root to ciliary ganglion. Motor Nerve Supply These nerves supply extrinsic (extra ocular muscles) and intrinsic muscles. Nerve Supply of Extrinsic Muscles (Extra Ocular Muscles) Mnemonic—LR6 (SO4)3, that is, lateral rectus is supplied by 6th nerve (Abducens nerve). Superior oblique is supplied by 4th nerve (Trochlear nerve), and rest of the muscles (i.e., superior rectus [SR], inferior rectus [IR], medial rectus [MR], and inferior oblique) are supplied by 3rd nerve (oculomotor nerve). Oculomotor nerve (III) divides into (Fig. 1.6): Superior branch: It innervates SR and levator palpebrae superioris (LPS). Inferior branch: It innervates MR, IR, inferior oblique (IO), and a branch to ciliary ganglion. Fig. 1.5 Ophthalmic nerve and its branches. Fig. 1.6 Oculomotor nerve and its branches. Abbreviations: LPS, levator palpabrae superioris; SR, superior rectus; IR, inferior rectus; MR, medial rectus; IO, inferior oblique muscle. Fig. 1.7 Course of nerve supply through ciliary ganglion. Abbreviations: LPS, levator palpabrae superioris; SR, superior rectus; IR, inferior rectus; MR, medial rectus; IO, inferior oblique muscle. Nerve Supply to Intrinsic Muscles (AN41.3) Ciliary muscle and sphincter pupillae are supplied by the 3rd nerve (Oculomotor nerve). Dilator pupillae is supplied by sympathetic fibers.  Ciliary Ganglion It is a parasympathetic ganglion of oculomotor nerve (III), as preganglionic parasympathetic fibers from branch of oculomotor nerve (III) synapse with postganglionic parasympathetic fibers within the ganglion. Postganglionic parasympathetic fibers leave the ganglion through short ciliary nerves which enter the eyeball around optic nerve. These innervate sphincter pupillae and ciliary muscle. A sensory root passes from the nasociliary nerve to eyeball through ganglion. These fibers are responsible for sensory innervations to all parts of the eyeball (Fig. 1.7). Third branch to ganglion is the sympathetic root and contains postganglionic sympathetic fiber from the superior cervical ganglion. These fibers reach the eyeball and innervate dilator pupillae muscle. These fibers also continue along short ciliary nerves. ▃ ▃ Embryology of Eyeball In general, there are three main stages in prenatal development of the eye: Period of embryogenesis. Period of organogenesis. Period of differentiation. Embryogenesis Three germ layers (ectoderm, mesoderm, and endoderm) are formed after a series of divisions and proliferations in fertilized ovum. Ectoderm overlying notochord becomes thickened to form neural plate (neuroectoderm). A ridge of cells (neural crest) develops along the edges of the neural plate. Neural crest cells subsequently migrate and give rise to various structures within the eye and orbit (Fig. 1.8a). Neural plate is converted to neural groove, which becomes deeper, and neural groove is converted into neural tube (Fig. 1.8b).  By the end of embryogenesis, the neural tube is divided into an enlarged cranial part which develops into three primary brain vesicles: prosencephalon (forebrain), mesencephalon (midbrain), and rhombencephalon (hind brain). The narrow caudal part becomes the spinal cord (Fig. 1.8c). Organogenesis The period of organogenesis begins after the 3rd gestational week. On the 22nd day of gestation, optic pits form as lateral outpouchings of prosencephalon (Fig. 1.8d). Failure of optic pit to develop into optic vesicle results in complete absence of an eye (true anophthalmia). On the 25th day of gestation, optic pits enlarge and form optic vesicles. Proximal part of optic vesicle becomes constricted and elongated to form optic stalk. Optic vesicles grow laterally and come in contact with overlying surface ectoderm (Fig. 1.1.8e). If insult to embryo occurs after outgrowth of optic vesicle, developmental arrest of ocular growth results in microphthalmos (small eye). Surface ectoderm overlying the optic vesicles become thickened to form lens placode on the 27th day. Lens placode undergoes invagination and is converted into lens vesicle. Simultaneously, wall of optic vesicle begins to invaginate and form a double-layered optic cup as a result of differential growth of the wall of vesicle (Fig. 1.8f and Fig. 1.8g). Lens vesicle becomes completely separated from the surface ectoderm on day 33 of gestation. Margins of the optic cup grow over upper and lateral sides of the lens to enclose it, but not on the inferior aspect of lens, resulting in a choroidal or fetal fissure under the surface of each cup and extend to the most proximal portion of the optic stalk. As developing neural tube is surrounded by mesoderm, this fetal fissure is the portal through which mesoderm enters the developing eye. Between the 5th and 7th weeks of gestation, fetal fissure closes and the globe is formed (Fig. 1.8h).  Embryonic fissure runs from optic nerve to margin of pupil (anterior part of optic cup). Incomplete closure of embryonic (choroidal) fissure around 5 to 8 weeks of gestation results in absence of the part of an ocular structure called coloboma. As embryonic fissure is inferior and slightly nasal, typical coloboma is inferonasal in location. If entire length of fissure is involved, coloboma is complete. If only part of fissure is involved, it may involve iris (iris coloboma), choroid (choroid coloboma), retina (retinal coloboma), and optic disc (disc coloboma). During development of optic cup and lens vesicle, the mesoderm surrounding optic vesicle gives rise to various vascular and orbital tissues. Differentiation Differentiation begins around 8th gestational week and occurs before the eye is fully functional. For macula, differentiation is completed after the birth. Various components of eyeball are derived from: Optic cup which develops from neuroectoderm (neural plate). Mesoderm surrounding optic vesicle. Lens placode (a specialized area of surface ectoderm). Fig. 1.8 (a–h) Optic cup with choroidal fissure. Optic Cup It is a double-layered embryonic tissue (Fig. 1.9 and Table 1.2).  Myelination of nerve fibers begins in the 8th month. It starts at chiasm and proceeds toward optic nerve to reach lamina cribrosa just before birth and stops there. Thus, in normal eyes, myelination stops at lamina cribrosa. If myelination extends beyond lamina cribrosa, nerve fibers of retina (axons of ganglion cells) also get myelinated. The opaque nerve fibers are called myelinated (medullated) nerve fibers. Fig. 1.9 Layers of optic cup. Abbreviation: RPE, retinal pigment epithelium. Table 1.2 Derivatives of optic cup Part of optic cup Derivative Outer layer of optic cup Anterior part of it continues The cells of outer layer contain forward in ciliary body and pigment granules iris as their anterior- pigmented epithelium. Posterior part of outer layer of optic cup forms RPE. Inner layer of optic cup Forms nervous layer of retina. Optic stalk It develops into optic nerve. Mouth of optic cup It becomes a round opening, the future pupil. Abbreviations: RPE, retinal pigment epithelium. Other coats of eyeball are derived from mesoderm surrounding the optic cup. Layers of mesoderm surrounding the optic stalk form the sheaths of optic nerve. Mesoderm Optic cup is completely surrounded by the mesoderm. This tissue soon differentiates into outer and inner layers (Fig. 1.10a). Outer layer (fibrous layer) is comparable with duramater and develops into sclera. Inner layer (vascular layer) of mesoderm is carried into the cup through the choroidal fissure and forms choroid, ciliary body, and iris. Part of this mesoderm which gets invaginated into optic cup forms the retinal vessels. Differentiation of mesoderm overlying the anterior aspect of eye is different. Vacuolization in mesoderm splits it into outer layer, which forms stroma and inner epithelium of cornea, and the inner layer, which forms stroma and blood vessels of iris and ciliary body. The anterior chamber forms between the two layers and correspond to the subarachnoid space of the brain (Fig. 1.10b). Lens Placode Lens placode is converted into lens vesicle which is lined by a single layer of cubical cells surrounded by the basal lamina. Cells in the anterior wall of vesicle remain cubical, while cells in the posterior wall of vesicle become elongated. The cavity of vesicle is eventually obliterated (Fig. 1.11). Development of Various Ocular Structures Development of Retina Retina is developed from two walls of optic cup (Table 1.3). Fig. 1.10 (a) Layers of optic cup. (b) Differentiation of mesoderm. Table 1.3 Development of retina Part of optic cup Derivative Outer layer of optic cup Anterior part of it continues The cells of outer layer contain forward in ciliary body and pigment granules. iris as their RPE. Posterior part of outer layer of optic cup forms RPE. Inner layer of optic cup Forms nervous layer of retina. Mouth of optic cup It becomes a round opening, the future pupil. Abbreviation: RPE, retinal pigment epithelium. Fig. 1.11 Differentiation of lens vesicle. Table 1.4 Development of optic nerve Part of optic stalk Derivative Outer layer of optic stalk It gives rise to lamina cribrosa which becomes permeated by collagen fibers  from sclera and choroid by 8th month. Inner layer of optic stalk It develops into glial cells which separate the axons into bundles. Table 1.5 Development of cornea and sclera Part Derivative Outer layer (fibrous layer) of It develops into sclera. mesoderm surrounding the optic cup Outer layer (fibrous layer) of It forms stroma and inner mesoderm anterior to optic cup epithelium of cornea. Surface ectoderm It forms superficial epithelium of cornea. Development of Optic Nerve The optic stalk develops into the optic nerve. The nerve fiber layer (Ganglion cell axons) migrate through the vacuolization of cells in the optic stalk (Table 1.4). The hyaloid artery in the central axis of optic nerve develops into central retinal artery. Optic nerve sheaths are formed from the layers of mesoderm surrounding the optic stalk. Myelination of nerve fibers begins in the 8th month. It starts at chiasm and proceeds toward optic nerve to reach lamina cribrosa just before birth and stops there. Thus, in normal eyes, myelination stops at lamina cribrosa. If myelination extends beyond lamina cribrosa, myelination of nerve fibers of retina (axons of ganglion cells) results. The opaque nerve fibers are called myelinated (medullated) nerve fibers. Development of Cornea and Sclera Development of cornea and sclera is briefly explained in Table 1.5. Development of Uveal Tissue Development of uveal tissue is briefly explained in Table 1.6. Table 1.6 Development of uveal tissue Part Derivative Inner layer (vascular layer) of It is carried into the cup mesoderm through the choroidal fissure and forms choroid, stroma, and blood vessels of iris and ciliary body. Neuroectodermally derived optic As the rim of optic cup cup rim grows anteriorly, it develops into two epithelial layers. The anterior epithelial layer becomes pigmented and is continuous with RPE posteriorly. The posterior epithelium remains nonpigmented and is continuous with the inner retinal layer of optic cup (i.e., nervous layer of retina). Sphincter and dilator pupillae muscles. Abbreviations: RPE, retinal pigment epithelium. Table 1.7 Derivatives of lens placode (Lens vesicle) Parts of lens placode Derivative Cells in anterior wall of lens Form lens epithelium. vesicles remain cubical Equatorial cells of anterior Form secondary lens fibers. epithelium Cells of posterior wall become Form primary lens fibers. elongated and lose their nuclei The basal lamina of lens vesicle Develops into lens capsule. Development of Lens Lens is developed from lens placode which is converted into lens vesicle (Table 1.7). Development of Vitreous Vitreous is derived from: Ectoderm—Ectodermal component is derived from optic cup (secondary vitreous). It is an avascular structure and surrounds the primary vitreous. Mesoderm—Mesoderm invades inside of optic cup through choroidal fissure. Here it forms hyaloid vessels (primary vitreous). Hyaloid artery extends toward and around lens vesicle and anastomoses with vessels in the vascular mesoderm. The Canal of Cloquet containing hyaloid artery is formed due to condensation between primary and secondary vitreous. Fate of hyaloid artery: In the 3rd trimester, hyaloid system begins to regress, except for the portion that supplies the retina as central retinal artery. Hyaloid artery in vitreous disappears but hyaloid canal in vitreous (through which the artery passes) persists. When secondary vitreous fills the cavity, primary vitreous with hyaloid vessels is pushed anteriorly and ultimately disappears. If primary vitreous fails to regress persistent hyperplastic primary vitreous (PHPV) results. Development of Accessory Structures of Eyeball  Eyelids develop from both surface ectoderm and mesoderm. Mesoderm gives rise to muscle and tarsal plates. Ingrowth of surface ectodermal cells from lids margins form tarsal glands and epithelial buds from lid margins form cilia. Conjunctiva and conjunctival glands develop from ectoderm lining the lids and globe. Lacrimal glands develop from a number of buds arising from the superolateral angle of the conjunctival sac. Nasolacrimal system (canaliculi, lacrimal sac, and nasolacrimal duct): Lacrimal drainage system develops from surface ectoderm. Nasolacrimal system becomes patent by the 6th month of gestation. Table 1.8 Important events in ocular embryogenesis Period after conception Event 22nd day Appearance of optic pits. 25th day Formation of optic vesicles from optic pit. 27th day Formation of lens placoid from surface ectoderm. 28th day Formation of embryonic (fetal) fissure. 5th week Lens pit forms and deepens into lens vesicle. Development of hyaloid vessels and primary vitreous. 6th week Closure of embryonic fissure. Differentiation of retinal pigment epithelium. Formation of secondary vitreous.  Appearance of eyelid folds and nasolacrimal duct. Formation of primary lens fibers. 7th week Formation of embryonic lens nucleus. Formation of sclera begins. 3rd month Differentiation of precursors of rods and cones. Development of ciliary body and anterior chamber. Eyelid folds lengthen and fuse. 4th month Regression of hyaloid vessels. Formation of major arterial circle of iris and iris sphincter muscle. Formation of eyelid glands and cilia. 5th month Eyelid separation begins. Differentiation of photoreceptors. 6th month Differentiation of dilator pupillae muscle. Nasolacrimal system becomes patent. Differentiation of cones. 7th month Differentiation of rods. Myelination of optic nerve. 8th month Completion of anterior  chamber angle formation. Hyaloid vessels disappear. 9th month Retinal vessels reach temporal periphery. Pupillary membrane disappears. After birth Development of macula. Extraocular muscles develop from mesoderm. In summary, the eye is formed from both ectoderm (neural and surface ectoderms) and mesoderm. Important events of development are listed in Table 1.8.  Vision–Its Physiology, CHAPTER 2 Neurology, and Assessment Introduction Visual Process Assessment of Visual Function Binocular Vision ▃ Introduction The light falling upon the retina stimulates the sensory nerve endings, rods and cones. Histologically, retina consists of 10 distinct layers including three layers of cell (Fig. 2.1). These are as follows: Layer of rods and cones– These are the receptors sensitive to light and serve as sensory nerve endings for visual sensations. The cell bodies of rods and cones form the outer nuclear layer (ONL). Fig. 2.1 Layers of retina. Layer of bipolar cells– This layer also includes horizontal cells, amacrine cells, and Muller’s cells. The cell bodies of these cells form the inner nuclear layer (INL). Layer of ganglion cells– They give rise to optic nerve fibers. The cell bodies of ganglion cells form the ganglion cell layer (GCL). Functionally, the retina can be subdivided into four regions, namely, optic nerve head (ONH), fovea, retina peripheral to fovea, and peripheral retina (Table 2.1). Photoreceptors The rods are mainly located in the periphery, whereas the cones occupy the central region (Table 2.2). ▃ Visual Process (OP1.1, PY10.17, PY10.19, PY10.20) It is the process by which our brain forms an image from light energy. Visual process can be divided into the following stages (Flowchart 2.1): Initiation of visual sensation. Transmission of visual impulse. Visual perception. Initiation of Visual Sensation The light falling upon retina causes two essential reactions: photochemical changes and electrical changes. The photochemical changes concern visual pigments, that is, pigments in rods and cones. The photochemical changes in rods and cones are similar but the changes in rhodopsin have been studied in detail. Rhodopsin absorbs light with a peak sensitivity of 505 nm (green light) (Flowchart 2.2). Rods are low-resolution detectors and consist of the following: Flowchart. 2.1 Stages of visual process. Table 2.1 The regional variations of sensory nerve endings Retinal region Features 1 Optic nerve head (Blind Receptors are absent, i.e., no rods spot) and cones. So, insensitive to light. 2 Fovea Only cones are present and hence it is responsible for visual acuity. At fovea, there is one-to-one correspondence between photoreceptors and ganglion cells. 3 Retina peripheral to fovea Here both cones and rods are present. 4 Peripheral retina Mainly rods are present. This region is responsible for perception of dim light. Table 2.2 Difference between rods and cones Rods Cones These are responsible for These are responsible for dim light vision (scotopic vision in bright light vision). These cannot detect (photopic vision) and color color. vision. These predominate in extra These predominate at fovea foveal region where many and there is one-to-one rods synapse with a bipolar correspondence between cell. Hence, receptive field is cones and bipolar cells. more with less resolution. Hence, resolution is more Rhodopsin (visual purple) is and visual acuity is better. the visual pigment present in There are three types of the rods. cones, each containing a specific pigment responsible  for color discrimination and normal daylight vision. An apoprotein, opsin (called scotopsin), to which the chromophore molecule (11-Cis-retinal) is attached. 11-Cis-retinal belongs to the carotenoid family. In the dark, it is in 11-cis form and gets converted to all-trans form in the presence of light. Retinal is derived from food sources. It is not synthesized in the body. On exposure to light, 11-Cis-retinal is converted into all-trans-retinal isomer through short-lived intermediate products. With this change, rhodopsin loses its color (bleaching of rhodopsin). The all-trans-retinal is converted to all-trans-retinol and reaches the liver via blood. In liver, it is converted to 11-Cis- retinol. This is transformed to 11-Cis-retinal and combines with opsin to form rhodopsin (regeneration of rhodopsin). If subject immediately goes into dark after a brief exposure to light, all-trans- retinal is directly converted to 11-Cis-retinal by isomerase in the retina. Only the first step in the bleaching sequence requires input of light. All subsequent reactions can proceed in the dark as well as in light. When the intensity of background illumination remains relatively constant, rates of visual pigment bleaching and regeneration are in balance. This equilibrium between bleaching and regeneration of visual pigment is called visual cycle. Electrical changes: The biochemical reactions result in generation of receptor potential. The process by which light energy is converted into receptor potential is known as phototransduction. Transmission of Visual Impulse The processing of visual information takes place at the following three levels: 1. At retina. 2. At LGB (lateral geniculate body). 3. At visual cortex. Flowchart. 2.2 Photochemical changes in rhodopsin (Rhodopsin cycle). The changes in electrical potential are transmitted through bipolar cells, ganglion cells, and optic nerve fibers to brain via visual pathway (visual pathway comprises optic nerves, optic chiasma, optic tracts, lateral geniculate bodies, optic radiations, and visual cortex in brain Flowchart 2.3). Processing at Retina Bipolar cells, horizontal cells, and amacrine cells participate in lateral inhibition (a form of inhibition in which activation of a particular neural unit is associated with inhibition of the activity of nearby units). Lateral inhibition prevents spreading of excitatory signal widely in the retina and improves the contrast of borders and edges of an object. Retinal ganglion cells are of two types: Magno cells (M cells). Parvo cells (P cells).  Magno cells are larger cells and concerned with black and white response, perception of movement, and rough sketch of the object. Parvo cells are smaller cells and predominate in the macular region. These cells are color sensitive and concerned with color vision and finer details of the object. Two separate pathways start from ganglion cells, one from parvo cells (parvocellular pathway) and another from magno cells (magnocellular pathway). Both pathways are involved in the parallel processing of the image. The action potentials (impulse) developed from these cells are conducted to lateral geniculate bodies (LGBs). Processing at Lateral Geniculate Body (LGB) The retina has point-to-point representation in a LGB. A LGB consists of six layers. Magnocellular pathway from magno cells terminate in layers 1 and 2 of LGB. Parvocellular pathway from parvo cells terminate in layers 3, 4, 5 and 6 of LGB. On each side, layers 1, 4 and 6 receive input from contralateral eye, while layers 2, 3 and 5 receive input from the ipsilateral eye. Flowchart. 2.3 (a, b) Algorithm for visual pathway. From LGB, two separate pathways project to the visual cortex. Magnocellular pathway from layers 1 and 2 carries signals for detection of movement, depth, and rough sketch of the object. Parvocellular pathway from layers 3, 4, 5, and 6 carry signals for color vision and finer details of the object (Fig. 2.2). Visual Perception (Processing at visual cortex) Visual cortex consists of two areas: Primary visual cortex or striate cortex which transforms information received from LGB and transmits it to the secondary visual cortex. Secondary visual cortex or extra striate cortex which transmits information received from primary visual cortex to the higher visual areas. Fig. 2.2 Processing of visual impulse at lateral geniculate body. Visual Sensations Visual sensations resulting from the stimulation of retina by light are of four types: Light sense.  Form sense. Sense of contrast. Color sense. Light Sense It is the perception of light in all its gradations of intensity. The intensity of light required to perceive it is called the light minimum. The light is no longer perceived if the intensity of light is reduced below the point of light minimum. The eye functions normally in a wide range of illumination by adjustment to such changes (called visual adaptation). Visual adaptation involves dark adaptation (adaptation to dim illumination) and light adaptation (adaptation to bright illumination). If we move from bright sun light into a dim light in the room, we cannot perceive the objects in the room until sometime has elapsed to adapt the amount of illumination by the eyes. The time taken to see in dim light is called dark adaptation time. The rods are much more sensitive to low illumination, so that rods are used in dim light at dusk (scotopic vision). The cones come into play in bright illumination (photopic vision). Bats have few or no cones; hence, it is a nocturnal animal. Squirrels have no rods and is therefore a diurnal animal. Human beings have rods and cones both. During dark adaptation, the following changes take place in the eye: Pupils dilate. Vision changes from cones to rods (photopic vision to scotopic vision). This is called Purkinje shift. Sensitivity of receptors to light increases. Photopigments are resynthesized and so their concentration increases. Since vitamin A is required for the synthesis of both rod and cone pigments, deficiency of this vitamin produces visual abnormalities. Visual acuity decreases. During light adaptation, the following changes take place in the eye: Pupils constrict. Vision changes from rods to cones (scotopic to photopic vision). Photopigments are bleached and so their concentration decreases.  Sensitivity of receptors to light decreases. This happens due to decreased concentration of photopigments. Visual acuity increases. Both the photoreceptors work together at the midrange of illumination, which is the mesopic range. Form Sense It is the ability which enables us to perceive the shape of objects. Cones play the major role in form sense, so it is most acute at the fovea having cones. It decreases very rapidly toward the periphery due to a decrease in the number of cones. Visual acuity is the ability to see fine details of objects in the visual field. Assessment of visual acuity is discussed in the latter part of this chapter. Sense of Contrast (Contrast Sensitivity) It is the ability to perceive slight changes in the luminance between the regions which are not separated by definite borders. It indirectly assesses the quality of vision as loss of contrast sensitivity may disturb the patient more than the loss of visual acuity. Color Sense It is the ability to distinguish between different colors excited by the light of different wavelengths. The appreciation of colors (color vision) is a function of cones. Therefore, it occurs only in photopic vision. In dark adapted eyes, where the rod function dominates, colored objects appear as gray differing in brightness. There are three types of cones with three different pigments which absorb wavelengths of light in the spectrum corresponding to red, green, and blue colors. The three pigments are: Pigment sensitive to red light (long wave pigment): It absorbs maximally in the yellow portion with a peak of 570 nm. The cone that contains this pigment is called “L” cone. Pigment sensitive to green light (middle wave pigment): It absorbs maximally the green portion of spectrum with a peak of 535 nm. The cone that contains this pigment is called “M” cone.  Pigment sensitive to blue light (short wave pigment): It absorbs maximally blue violet portion of spectrum with a peak of 445 nm. The cone that contains this pigment is referred to as “S” cone (Fig. 2.3). Any given cone pigment may be deficient or entirely absent. Deficiency of red pigment is called protanomaly (red weakness) and its entire absence is called protanopia (red blindness). Deficiency of green pigment is called deuteranomaly (green weakness) and its entire absence is called deutranopia (green blindness). Deficiency of blue pigment is called tritanomaly (blue weakness) and its entire absence is called tritanopia (blue blindness). Trichromats possess all three types of cones. Absence of one type of cone renders the individual dichromat, while absence of two types of cone renders the individual monochromat. The red, green, and blue colors are called primary colors. These in different proportions will give a sensation of white or any other color shades. Hence, normal color vision is called trichromatic. For any given color, there is a complimentary color which when mixed will produce white. If a person stops looking at a color, he or she may continue to see it for a short time (positive after image), or he or she may see its complimentary color (negative after image). When a colored light strikes the retina, the response of the cones depends on the color mixture. The response in the form of local potentials gets transmitted into the bipolar cells which, in turn, activates ganglion cells. The signals from the three cones after processing by the ganglion cells are conducted to LGB in three different ways: Fig. 2.3 Color sensitivity excited by the light of different wavelengths. Red green pathway via parvo cells. Blue yellow pathway via parvo cells. Luminance (white black) pathway via magno cells. The cells of LGB process the color sensation in a similar fashion as that of ganglion cells and conduct the impulses to primary visual cortex. Red– green and blue–yellow pathways take relay in the layers 3 to 6 (Parvo cells) and white–black take relay in layers 1 and 2 (Magno cells). The primary visual cortex contains clusters of color-sensitive neurons. The color information from these neurons is projected to area 37 (secondary visual cortex) which converts color input into the sensation of color. Theories of Color Vision The following theories have been proposed to explain the mechanism of color vision:  Young-Helmholtz theory (trichromatic theory). Hering theory (Opponent process theory). Young-Helmholtz Theory Postulates: There are three primary colors– red, green, and blue. There are three types of cones with different pigments, each maximally sensitive to one of the primary colors, although each color receptor also responds to the other two primary colors. All other colors are assumed to be perceived by combinations of these, that is, sensation of any given color is determined by the relative frequency of impulse reaching the brain from each of the three cone systems. This theory fails to explain the sensation of black color. It also has difficulty in explaining color confusion and complimentary color after images. Hering Theory The Hering theory assumes three sets of receptor systems: red–green, blue– yellow, and black–white. Each system is assumed to function as an antagonistic pair. The stimulation of one results in inhibition of the opposite receptor in the pair, for example, red light stimulates the red receptors and simultaneously inhibits the green. This concept can explain color contrast (if a piece of blue paper is laid up on a yellow paper, the color of each of them is heightened due to color contrast) and color blindness. The most widely accepted theory (stage theory) incorporates both theories which help in explaining how our color vision system works. 1. The first stage is the receptor stage. The trichromatic theory operates at the receptor level which consists of three photopigments. 2. The second stage is the neural processing stage for color vision in which signals are recorded into the opponent process form by the higher level neural system. ▃ Assessment of Visual Function Each eye must be tested separately throughout for all forms of visual perceptions (form sense, field of vision, light sense, and color sense). Visual perceptions can be assessed by: Subjective tests– These tests require the patient’s subjective expression of visual function which include: Assessment of visual acuity. Assessment of field of vision. Assessment of dark adaptation. Assessment of contrast sensitivity. Assessment of color vision. Objective tests– These tests are independent of patient’s expression and achieved by electrophysiological tests which include: Electroretinography (ERG). Electrooculography (EOG). Visual evoked potential (VEP). Subjective Tests Assessment of Visual Acuity (OP1.3) Visual acuity of the eye is an estimation of its ability to discriminate between two points. It must be tested both for distance and near. Distant visual acuity is tested by: Snellen’s Test Types The basic principle of Snellen’s test types is the fact that two objects can be perceived separately only when they subtend a minimum angle of 1 minute at the nodal point of the eye. The Snellen’s test type consists of a series of letters arranged in lines, each diminishing in size from above downward. Each letter is so designed that it can be placed in a square, the sides of which are 5 times the breadth of the constituent lines. Hence, at a given distance, whole letter subtends an angle of 5 minute at the nodal point of the eye. The letter of the top line subtends an angle of 5 minutes at the nodal point of eye if it is 60 m from the eye. The letters in subsequent lines subtend an angle of 5 minutes if they are 36, 24, 18, 12, 9, and 6 m away from the eye, but at 6 m, a 6/6 letters subtend an angle of 5 minutes, a 6/12 letter subtends 10 minutes, and a 6/60 letter subtends an angle of 50 minutes (Fig. 2.4). The illumination of chart should not fall below 20 foot candles. Recording of Visual Acuity The patient should be seated at a distant of 6 m from the chart. At this distance, the rays of light are practically parallel and accommodation is thus negligible. The patient is asked to read test types with each eye separately and the visual acuity is expressed as a fraction, in which the numerator is the distance of the chart from the patient (6 m) and denominator is the distance at which a person with normal vision ought to be able to read, for example, if a patient reads only the top line, his visual acuity will by 6/60 as a normal person ought to have read this line from a distance of 60 m, and when a patient reads the 7th (last) line of the chart, his visual acuity is recorded as 6/6 which is a normal person’s vision. When the top letter cannot be read, the patient is asked to move toward the chart till he reads the top line, for example, if he reads the top line from a 3 m distance, his visual acuity will be 3/60. If the patient cannot read the top letter even from a distance of less than 1 m, he is asked to count the fingers of the examiner and visual acuity is recorded as FC- 3′, FC- 1’. When the patient fails to count fingers, the examiner moves his or her hand and observes whether the patient appreciates hand movements (HMs) or not. If he or she appreciates HMs, his or her visual acuity is recorded as HM +ve. In absence of the recognition of HMs, see whether the patient can perceive the light, and the visual acuity is recorded as PL +ve or PL –ve. In illiterate individuals, “E” test types or Landolt broken ring (C) should be used. Fig. 2.4 (a) Snellen’s test types; (b) Landolt broken ring test; (c) The illiterate E test; (d) 20/20 Snellen’s letter. In U.S.A, metric system is not usually followed and values are converted to feet (6 m = 20 ft). Therefore, 6/6 becomes 20/20 and 6/60 becomes 20/200, etc. The Snellen’s fraction can also be expressed as a decimal (i.e., 6/6 = 1 and 6/12 = 0.5). Log MAR acuity The Bailey-Lovie chart is more accurate than Snellen’s test type and is the standard mean of visual acuity measurement. This records the minimum angle of resolution (MAR) which relates to the resolution required to resolve the elements of a letter. At 6 m, a 6/6 letters subtend an angle of 5 minutes and each limb of the letter has an angular width of 1 minute, and then an MAR of 1 minute is needed for resolution. A 6/12 (20/40) letter subtends 10 minutes of arc and each limb of the letter has an angular width of 2 minute, so an MAR of 2 minutes is needed for resolution. So, Snellen’s acuity is inverted and reduced to express MAR. Log MAR is simply the log of the MAR. Each line of the chart comprises five letters and the letter size changes by 0.1 Log MAR units per row. Thus, each letter can be assigned a score of 0.02. The final score takes account of every letter that has been read correctly. The Bailey-Lovie chart is used at 6 m testing distance.  For example, in Snellen’s visual acuity of 6/6, MAR of 1 minute is needed for resolution. Therefore, Log MAR score is 0.00 as the Log of MAR value of 1 minute is 0. For Snellen’s visual acuity of 6/60, MAR of 10 minute is needed for resolution. Therefore, Log MAR score is 1.00 as Log of MAR of 10 minute is 1. For Snellen’s visual acuity of 6/12, MAR of 2 minute is needed for resolution. Therefore, Log MAR score is 0.30 as Log of MAR of 2 minute is 0.301 (Fig. 2.5 and Table 2.3). Pinhole Test If the vision is subnormal, visual acuity is measured by asking the patient to read the letters through a pinhole. A pinhole is placed in front of the eye to be tested and the other eye is covered. The pinhole allows only central rays of light which are not refracted by the media. If the vision improves by two or more lines in the chart, it indicates an underlying refractive error. The visual acuity is assessed again with the correcting glasses. Fig. 2.5 LogMAR visual acuity chart. Table 2.3 Notations for recording visual acuity Visual acuity Visual acuity Decimal Log MAR (feet, 6 m = 20 (meter) equivalent equivalent ft) 6/60 20/200 0.10 +1.0 6/36 20/120 0.17 +0.8 6/24 20/80 0.25 +0.6 6/18 20/60 0.33 +0.5 6/12 20/40 0.5 +0.3 6/9 20/30 0.6 +0.2 6/6 20/20 1.00 0.00 6/5 20/16 1.20 −0.1 6/4 20/12.5 1.50 −0.2 The pinhole does not improve visual acuity in the presence of macular or optic nerve diseases. Visual Acuity in Hard/Dense Cataract In a totally opaque cataract, testing of visual acuity is not possible by Snellen’s chart/Bailey–Lovie chart. Visual acuity (likely to be regained after surgery) in the presence of dense cataract can be tested by: Laser interferometer. Potential acuity meter (PAM). Laser interferometer is based on the phenomenon of interference. Two pin-points of a laser light are focused which interferes with each other and form a diffraction pattern of parallel lines (light and dark fringes) on the retina. The change in the distance between these two pin-points result in the alteration of fringe pattern, and the visual acuity can be estimated by asking the patient to identify the orientation of progressively finer lines.  Potential acuity meter projects a tiny Snellen’s chart on to the retina. The small image of the chart passes through the defects in the media and the patient is required to read the alphabets. Testing of Visual Acuity in Infants and Young Children The preverbal children are tested by means of Optokinetic Nystagmus (OKN) drum and preferential looking behavior. Optokinetic Nystagmus (OKN) A white drum with vertical black stripes is rotated before the eyes. If vision is normal, the infant follows stripe with a slow motion. As this stripe disappears, the eyes switch suddenly back to pick up a new stripe, indicating that the infant can discriminate the stripe. By varying the distance between infant and drum or the breadth of stripes, the assessment of visual acuity can be made in children. Preferential Looking Behavior It is based on the fact that infants prefer to look at a pattern rather than a homogenous stimulus. The infants’ preference is quantified by incorporating the patterns which vary in stripe width. The test in common use include the Teller acuity cards, which consist of 17 of them with black stripes (gratings) of varying width, and Cardiff acuity cards, which consist of familiar pictures with variable outline width. Coarse greetings or pictures with wider outline are seen more easily than fine greetings or thin outline pictures. The grating size of the card can then be converted to the equivalent of Snellen’s visual acuity. Near visual acuity is tested by: Jaeger test types. Roman test types. In Jaeger test types, a series with print types of different sizes in increasing order is arranged and marked from 1 to 7. The patient acuity is recorded as J-1 to J-7 depending upon the print type he reads.  In Roman test types, the near vision is recorded as N6, N8, N10, N12, N18, and N36. The near vision is tested in good illumination keeping the chart at a reading distance of 14 to 16 inches (35–40 cm). Assessment of Field of Vision Visual fields is the space that one eye can see while remaining fixed. It is a three-dimensional area (not a flat plane) and may be described as “island of vision surrounded by a sea of darkness.” Binocular visual field is the visual field seen simultaneously with both eyes. Extent (of Monocular visual field) Superiorly 60° Nasally 60° Inferiorly 70–75° Temporally > 90° (100–110°) The extent is limited by brow superiorly, nose nasally, and the cheek inferiorly. The typical configuration of normal visual field, therefore, is horizontally oval with a shallow depression (Fig. 2.6). Divisions of Visual Field Visual field is divided into temporal and nasal halves by an imaginary vertical meridian drawn through fovea. It is also divided into superior and inferior halves by a horizontal meridian that passes from fovea to temporal periphery (Fig. 2.7). Fig. 2.6 Uniocular and binocular visual fields. Abbreviations: BS, blind spot; F, foveola of retina; ONH, Optic nerve head. Visual acuity is sharpest at foveola and decreases progressively toward periphery (nasal slope is steeper than temporal slope). This is described as hill of vision. At optic disc, there are no photo receptors. So, it is a nonvisual area and corresponds to normal blind spot. Blind spot is located 10 to 20 temporal to fixation and 1.5 degree below the horizontal meridian. Normally, a person is not aware of his blind spot because the corresponding area of other eye sees normally.  Absolute scotoma is an area of total visual loss. Even brightest and largest stimuli cannot be perceived in absolute scotoma. Relative scotoma is an area of partial visual loss, in which brighter or larger stimuli can be seen but smaller or dimmer targets cannot be seen. Blind spot has absolute scotoma corresponding to actual optic nerve head (Papilla) and relative scotoma surrounding the absolute scotoma which corresponds to the peripapillary retina. Measurement of Visual Fields 1. Confrontation test: It is a rough method of assessment. In this method, patient’s visual field is compared with that of the examiner; therefore, the examiner should have a normal visual field. The patient sits facing the examiner at a distance of approximately 2 feet and is asked to cover his left eye and told to look straight into the examiner’s left eye with his right eye. The examiner closes his right eye and moves his finger from the periphery in the plane half way between him and the patient. The patient is asked to tell as soon as he sees the finger; the finger is moved in various parts of the field. The test is repeated for the other eye in the same way. Thus, a rough assessment is made about the visual field of the patient. If any defect is indicated by confrontation test, it must be accurately recorded by perimeter. 2. Measurement of visual field on a flat surface: Measurement of visual field on a flat surface is called Campimetry. Black tangent screen remains the standard tool for campimetry which was introduced by Bjerrum (Bjerrum’s screen). It detects localized defects or scotomas in central and paracentral visual fields. The typical arcuate scotomas seen in glaucoma still bear Bjerrum’s name. Fig. 2.7 Division of visual field. Abbreviations: BS, blind spot; F, foveola of retina. 3. Measurement of visual field on a curved surface: Measurement of visual field on a curved surface is called Perimetry. Perimetry has largely replaced campimetry nowadays. The instrument used for perimetry is called perimeter (Flowchart 2.4). Both central and peripheral fields of vision can be recorded with perimeters. The perimeter is commonly a half sphere situated at the patient’s near point. The first perimeters were arc perimeters. Lister perimeter uses small round objects as test targets, while Aimark perimeter is a light projection arc perimeter. Goldmann hemispheric projection perimeter has a bowl-shaped screen. The target is projected onto the bowl and the stimulus value of test object can be varied by changing the size or intensity. Computer technology was combined with visual field testing in the mid-1970s, resulting in introduction of automated perimeters. Several automated perimeters were introduced but the two most widely used systems are octopus perimeter and Humphrey visual field analyzer. Automated perimetry is more accurate than manual and has largely replaced manual perimetry. Flowchart. 2.4 Types of perimeter. Advantages of Automated Perimetry Over Manual Perimetry Automated perimetry is quantifiable and repeatable. There is constant monitoring of fixation in automated perimetry. Reliability of test can be verified by false +ve and false –ve results immediately. Abnormal points are retested automatically. Typical stimuli used in perimetry are spots of light of various diameter (size) and intensity. The factors affecting the perception of stimulus include the following: Size of stimulus. Luminance of stimulus. Color of stimulus. Length of time the stimulus is presented. Contrast brightness of background and stimulus. Luminance is the intensity or brightness of a light stimulus. The luminance of a given stimulus at which it is perceived 50% of the time when presented statically is known as threshold sensitivity. The human eye needs about a 10% change in brightness to make out a difference between light stimuli. It is highest at fovea and decreases progressively from macula to periphery. The stimulus brighter than threshold intensity is called suprathreshold and the dimmer one is called subthreshold. Differential light sensitivity measures the degree by which the luminance of the target requires to exceed the background luminance in order to be perceived by the eye. Types of Perimetry—Perimetry Is of Two Types Kinetic perimetry. Static perimetry. Kinetic Perimetry In kinetic perimetry, a stimulus of a given size and intensity is moved from a nonseeing area to a seeing area until it is perceived. The stimulus is moved along various meridians and the point of perception is recorded on a chart. The points along different meridians (clock hours) are joined and an isopter is obtained for that stimulus size and intensity. Isopter, therefore, encloses an area within which a target of a given size and intensity is visible. As the size and luminance (intensity of a light stimulus) of a target is decreased, the area within which it can be perceived becomes smaller, so that a series of ever diminishing circles (called isopters) is formed. Using stimuli of different intensities, several different isopters can be plotted. The brightest target will have the largest isopter and the dimmest target will have the smallest isopter. Kinetic perimeter is a two-dimensional assessment of the boundaries of hills of vision. It can be performed by: Bjerrum’s tangent screen (campimetry). Lister perimeter. Goldmann perimeter. Static Perimetry In static perimeter, a nonmoving stimuli of varying luminance is presented in the same position. It is a three-dimensional assessment of the visual field, providing the assessment of the boundary of hill of vision (area) and of differential threshold sensitivity (height). Static perimeter can be performed by using suprathreshold or threshold stimuli. In suprathreshold static perimetry, visual stimuli of intensity above expected normal threshold value (suprathreshold) is presented in various locations in the visual field. Detected targets (stimuli) indicate grossly normal visual function, whereas failure to recognize the suprathreshold stimulus reflects the areas of decreased visual sensitivity. If suprathreshold intensity is too high, milder defects may be missed. Therefore, selection of appropriate suprathreshold intensity is important. This type of perimetry is used mainly for screening. If stimuli are not visible in any area, further evaluation with threshold stimuli should be conducted. Threshold static perimetry measures the value of threshold intensity at different locations in the visual field. The technique involves increase in the intensity of target light by large steps (4 dB) until threshold is crossed and then decreased in smaller steps (2 dB) to the point where it cannot be identified (staircase threshold determination strategy). It determines the patient’s threshold for that particular point. As threshold static perimetry represents quantitative assessment, it is the most accurate method of monitoring glaucomatous visual field defects. Static perimeter is usually carried out with computerized, automated perimeters: octopus perimeter and Humphrey visual field analyzer, as automated perimeters, use threshold static perimetry. Physiologic Influences on Visual Fields Pupil size: Miosis decreases threshold sensitivities in central and peripheral visual fields and exaggerate field defects, so pupil + 5.00 D Symptoms Asthenopic symptoms—Strain on ciliary muscle due to sustained accommodative effort produces asthenopic symptoms (eyestrain) which include eye ache, burning, watering, frontal headache, and eye fatigue. The asthenopic symptoms are noticed chiefly after prolonged near work and increase toward evening. Symptoms of eye strain may be absent if near work is avoided. Esophoria (latent convergent squint): Increased accommodative convergence due to continuous accommodation results in esophoria which further increases eye strain. Blurring of vision (near > distance) occurs when hypermetropia is not fully corrected by voluntary accommodative effort. It is associated with asthenopic symptoms due to sustained accommodative efforts. Inadvertent rubbing of eyes (due to eye strain) with dirty fingers may result in recurrent stye, chalazia, or blepharitis. Symptoms vary with the age of patient and the degree of hypermetropia. The accommodational reserve is good in younger patients and decreases among older ones. Mild hypermetropia in young individuals: It is easily compensated by accommodation. Thus, mild hypermetropia may not cause any  symptom in young individuals because of good accommodational reserve. Mild hypermetropia in older patients: Symptoms may appear because of decrease in accommodation in older patients. When high hypermetropia is present, especially in adults or older patients, it cannot be compensated by accommodation. Thus, there is marked blurring of vision for near and distance. Signs Eyeballs are usually small with small cornea. Anterior chamber is shallow than usual. Such an eye is predisposed to angle-closure glaucoma. Fundus: Disc is small and hyperemic and margins may be seen blurred. So, it may be confused with papillitis, a condition known as pseudopapillitis: ♢ Blood vessels may be unduly tortuous. ♢ Retina shows glistening appearance (a bright reflex), resembling a watered silk appearance. Complications of Untreated Hypermetropia If hypermetropia is left untreated, it can lead to complications such as: Convergent strabismus (due to excessive use of accommodation). Amblyopia (lazy eye). Recurrent styes and blepharitis (infections due to rubbing of eyes resulting from eye strain). Treatment Hypermetropia may be treated by: Spectacles. Contact lenses. Surgery. Spectacles  If there is no symptom or tendency to develop convergent squint, no spectacles are prescribed. Hypermetropia with asthenopia is corrected by convex lenses. As hypermetropia in children tends to decrease with advancing age, therefore, annual checkup is must for a possible change in glasses. Glasses must be used constantly. In young patients with active accommodation, undercorrection is advised. In older patients, accommodation is poor; all manifest hypermetropia becomes absolute and full correction is advised. Refraction is conducted under cycloplegia: ♢ In children horizontal curvature (normal rule). With the Rule Astigmatism When vertical curvature > Horizontal curvature, it is termed as astigmatism ‘with the rule’. Against the Rule Astigmatism When horizontal curvature > vertical curvature, it is termed as astigmatism “against the rule.” It occurs after cataract surgery through superior incision, in which vertical meridian flattens due to scarring. Irregular Astigmatism When surface of cornea is irregular, rays of light are refracted irregularly, leading to multiple foci in various positions, and completely blurred image is produced on retina. This condition is called irregular astigmatism. It is due to corneal opacities or scarring and cannot be corrected. It is also seen in keratoconus and lenticonus (Flowchart 3.3). Optics in Astigmatism A more curved meridian has greater refractive power and will focus the rays sooner. Let us suppose vertical curvature > horizontal curvature. So, vertical rays come to a focus sooner than horizontal and, instead of a focal point, rays will have two foci. The configuration of rays refracted through the astigmatic (toric) surface is called Sturm’s conoid. The distance between two foci is called focal interval of sturm. The focal interval is the degree or measure of astigmatism (Fig. 3.19). Table 3.5 explains the various types of astigmatism. Symptoms These depend upon the type and the degree of astigmatism. Symptoms include: Defect in visual activity. Distance vision is often found to be good in mixed astigmatism as circle of least diffusion falls upon or near retina. Distortion of objects. Asthenopic symptoms: ♢ Burning. ♢ Eye ache. Flowchart. 3.3 Astigmatism. Fig. 3.19 Sturm’s conoid. ♢ Headache. ♢ Eye fatigue. In smaller degree of astigmatism, defect in visual activity is minimal but asthenopia or eye strain is marked due to efforts of accommodation (to produce a circle of least diffusion upon retina); however, in higher degree of astigmatism, asthenopic symptoms are absent because no attempts are made to ameliorate the blurred vision. Signs Head tilt, especially in oblique astigmatism, in an attempt to bring the axes nearer to vertical and horizontal meridians. Half closure of lids as in myopes in an attempt to achieve the greater clarity of stenopaeic vision. Oval or tilted optic disc. Determination of Astigmatic Power and Axis It can be done with: Retinoscopy: It reveals power in two different axes. Keratometry: It measures corneal curvature in two different meridians. Jackson’s cross cylinders: To verify the power of cylinder in the optical correction. Astigmatic fan test: To confirm the power and axis of the cylindrical lenses. Table 3.5 Types of astigmatism Focal point of Type of Position of object rays astigmatism At position A: If retina is situated Vertical rays are at A: Rays from converging more both meridian focus than horizontal behind the retina, rays. So, shape of i.e., hypermetropia bundle of light in both meridian. rays, i.e., section The condition is will be horizontal compound oval or oblate hypermetropic ellipse. astigmatism. At position B: If a retina is Vertical rays come positioned at B: to a focus while Vertical meridian horizontal rays are will be emmetropic still converging. while horizontal So, bundle of light meridian will be rays, i.e., section hypermetropic. This of conoid will be a condition is called horizontal straight simple line. hypermetropic astigmatism. At position C: If the retina is Divergence of situated at C: vertical rays and Vertical meridian convergence of will be myopic. horizontal rays are Horizontal meridian equal. So, rays will be from both meridia hypermetropic. The meet forming a condition is called circle, known as mixed circle of least astigmatism. diffusion. At position D: If retina is situated Divergence of at D: Vertical vertical rays > meridian will be convergence of myopic. Horizontal horizontal rays. So, meridian will be bundle of rays will hypermetropic. The be vertical oval. condition is called mixed astigmatism. At position E: If retina is Vertical rays positioned at E: diverging and Vertical meridian horizontal rays will be myopic. come to a focus. Horizontal meridian So, shape of comes to a focus. bundle of light The condition is rays will be a called simple vertical straight myopic line. astigmatism. At position F: If retina is Divergence of positioned at F: vertical rays is Both meridians will more than that of be myopic. This horizontal rays. So, condition is called bundle of light compound myopic rays will be astigmatism.  vertical oval or prolate ellipse. Treatment Spectacles In small astigmatism (4 D is usually symptomatic and not tolerated. Anisometropia may be congenital or acquired. Types Anisometropia may be: Simple anisometropia: One eye is emmetropic while the other has a refractive error. Compound anisometropia: Both eyes are ametropic and have same type of refractive errors but different in magnitude, for example, myopia of −1 D and −3 D in two eyes. Mixed anisometropia: Both eyes are ametropic but one is myopic and the other is hypermetropic. It is also called antimetropia. Anisometropia and Binocular Vision In small degree of anisometropia, binocular vision is usually maintained. In anisometropia of >2.5D, fusion is not possible and binocular vision is disrupted. Vision is then uniocular. The eye with high- refractive error is suppressed and anisometropic amblyopia (partial loss of vision) results. When one eye is emmetropic or hypermetropic and other eye is myopic, emmetropic or hypermetropic eye is used for distance and myopic eye for near work. Both eyes have good visual activity (alternating vision). Before the glasses are prescribed, make sure that two eyes are functioning simultaneously. This can be assessed by the FRIEND test. FIN—is written in green letters. RED—is written in red letters.  Patient sits at a distance of 6 m wearing a diplopia goggle with red glass in front of right eye: If he or she reads FRIEND, he or she has binocular vision. If he or she reads RED or FIN persistently, he or she has uniocular vision. If he or she reads FIN at one time and RED at the other, he or she has alternating vision. Treatment Spectacles: Anisometropia up to 2.5 D is well-tolerated with spectacles. In high-degree of anisometropia, aniseikonia occurs with spectacles. So, spectacles are not readily acceptable because of difficulty in fusion of images. If full correction is not tolerated, each eye is under corrected. If eye has become amblyopic, patching of emmetropic eye is done and amblyopic eye is used with spectacles. Contact lenses eliminate aniseikonia. Surgery: LASIK in anisometropic patients. ▃ Correction of Refractive Errors (IM24.15) Refractive errors can be corrected with: Spectacles. Contact lenses. Refractive surgery. Spectacles Important aspects of spectacles are as follows: Material of lenses. Type of lenses. Fitting of lenses. Frames. Material of Lenses  Glass lenses: They are usually made of crown glass having RI of 1.52. For high myopes, high-index lenses (RI = 1.53–1.74) are used to minimize the thickness. Therefore, they are thin and light weight. Resilens or CR-39 plastic lenses are light-weight and made of allyl diglycol carbonate. They are often resistant to scratching.