■''^^i'lf 
 
 
 THE LIBRARY 
 
 OF 
 
 THE UNIVERSITY 
 
 OF CALIFORNIA 
 
 LOS ANGELES 
 
 GIFT OF 
 Mrs. Clifford B. Walker 
 

 
 
 
 
 
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 LECTURES 
 
 ON 
 
 THE HUMAN EYE 
 
 IN ITS 
 
 NORMAL AND PATHOLOGICAL CONDITIONS 
 
 BY 
 
 ADOLF ALT, M. D. 
 
 Lecturer on Ophthalmology and Otology in the Trinity Medical School 
 Toronto, Canada 
 
 WITH 95 ILLUSTRATIONS BY THE AUTHOR 
 
 NEW YORK 
 
 G. P. P U T N A M • S S O N S 
 
 182 Fifth Avenue 
 
 1880.
 
 Coi'VRjGHT, 1880, Bv G. P. Putnam's Sons, New York.
 
 Biomedical 
 Library 
 
 WvV 
 lot 
 
 DEDICATION. 
 
 THIS BOOK IS DEDICATED TO THE MEMORY OF MY FATHER, 
 
 DETTMAR ALT, 
 
 LATE PHYSICIAN IN MANNHEIM, AND HIS FRIENDS, MY HIGHLY- 
 ESTEEMED TEACHERS, 
 
 DR. TH. VON DUSCH, 
 
 PROFESSOR AT HEIDELBERG, AND 
 
 DR. H. KNAPP, 
 
 OF NEW YORK, FORMERLY PROFESSOR AT HEIDELBERG. 
 
 635920
 
 PREFACE. 
 
 The histological conditions of the human eye have 
 of late received a good deal of attention, and their 
 study has been opened to a wider circle by a number 
 of atlases, -which, like the one published conjointly by 
 Pagenstecher & Genih, and another by Becker^ can 
 boast of an excellent execution. 
 
 A book treating systematically on this subject, 
 and especially on the histological conditions of the 
 pathological human eye, whose execution and price 
 would allow it to be of usefulness to every one in- 
 terested in this matter, has been to this day a want 
 often felt. 
 
 For quite a number of years I have been engaged 
 in collecting for my own instruction, microscopical 
 specimens of normal and pathological eyes. This 
 material for examination, especially its pathological 
 part, has by the kindness of Dr. H. Knapp, of New 
 York, and a great many other colleagues, to whom 
 my sincerest thanks are due, become so large, that I 
 think it in season to give the results of my researches 
 to the medical public in systematic order. I have 
 confined myself, however, in this book entirely to 
 the eye-ball itself, and have left the accessory parts 
 to be treated at a later period, when I shall be 
 better able to do so than I can at present, on ac- 
 count of the scarcity of material which is at my 
 disposal. Furthermore, I have given especial atten- 
 tion to the pathological conditions of the eye-ball. 
 This I thought only natural, as with regard to the
 
 Vi PREFACE. 
 
 normal conditions I could bring forward but little 
 that was new ; and I could doubtlessly presume that 
 all my readers would be more or less acquainted 
 with these. 
 
 All of the illustrations are drawn from my own 
 specimens, and I have anxiously tried to copy only 
 what I really saw without being influenced by pre- 
 conceived ideas. 
 
 I have thought it unnecessary to enlarge the book 
 by an elaborate record of all the authors and articles 
 I consulted, when studying up this subject, as a sum- 
 mary of them may be found in Graefe & Saemisch's 
 cyclopedia. I have endeavored, however, to do jus- 
 tice to every author whose opinion I stated, confirmed, 
 or disagreed with, by adding the name in brackets. If 
 in consequence of having only my own comparatively 
 small library at my disposal, I should have unconsci- 
 ously omitted some, or been mistaken with regard to 
 others, I beg herewith the pardon of the persons of- 
 fended. Since the German manuscript, of which this 
 book is a translation, was finished during November, 
 1878, of course I could not take into account the lit- 
 erature of this year. 
 
 This book is an elaboration of the notes written 
 down while lecturing on the subject under consid- 
 eration, at the New York Ophthalmic and Aural 
 Institute in 1876 and 1877. Since these lectures 
 were kindly and forbearingly received by my audi- 
 ence, I may, perhaps, venture to hope that they will 
 also find readers who will peruse them in the same 
 spirit. And if this book should be able to en- 
 large the interest already taken in the study of the 
 histology of the finest human organ, and to act as a 
 new stimulus to renewed strife to fill up the chasms
 
 PREFACE. 
 
 yet unfilled in our knowledge, what labor I had to 
 bestow on it will be amply repaid. 
 
 My sincerest thanks are due to Dr. T. R. Pooley, 
 of New York, who has kindly undertaken the revision 
 of the manuscript and proofs of my volume with a view 
 to the correction, as far as practicable, of any errors 
 of style or expression. 
 
 The Author. 
 
 Toronto, Canada, August, 1879.
 
 CONTENTS. 
 
 PAGE 
 
 Preface i 
 
 I. Cornea. 
 
 1. Normal conditions I 
 
 2. Pathological conditions 1 1 
 
 A . Keratitis and its results 1 1 
 
 a. Infiltration of the cornea I3 
 
 b. Purulent Keratitis i6 
 
 0. Abscess of the cornea i6 
 
 y3. Ulcer of the cornea 19 
 
 y. Keratomalacia 22 
 
 The Results of Keratitis. 
 
 a. Formation of scars and pannus 23 
 
 3. Anterior synechias 25 
 
 c. Prolapsus iridis and granuloma iridis traumaticum 29 
 
 d. Keratoconus e cicatrice and staphyloma cornese 29 
 
 e. Pterygiam 30 
 
 B. Injuries of the cornea, their mode of healing and results 31 
 
 a. Injuries without retention of a foreign body 31 
 
 b. Wounds with retention of a foreign body 36 
 
 c. Burns with lime 37 
 
 C. Regressive metamorphoses 3S 
 
 D. Tumors of the cornea 3S 
 
 II. Sclerotic. 
 
 1. Normal conditions 39 
 
 2. Pathological conditions 42 
 
 A. Sclerilis and its results 42 
 
 a. Infiltration-scleritis 42 
 
 b. Purulent scleritis 43 
 
 The Results of Scleritis. 
 
 a. Formation of scars 44 
 
 b. Prolapse and incarceration of iris, ciliary body, choroid, retina, 
 
 crystalline lens and vitreous body in the sclerotic 45 
 
 c. Hypertrophy of the sclerotic 45 
 
 d. Atrophy of the sclerotic and ectasy (staphyloma of the sclerotic). . 46 
 
 1. The anterior staphyloma of the sclerotic 47 
 
 0. The corneo-scleral staphyloma 47 
 
 /?. The ciliary staphyloma 48 
 
 2. The equatorial staphyloma of the sclerotic 49 
 
 3. The posterior staphyloma of the sclerotic 49
 
 X CONTENTS. 
 
 PAGE 
 
 B. Injuries to the sclerotic and their results 51 
 
 a. Wounds without subsequent retention of a foreign body 51 
 
 b. Wounds with subsequent retention of a foreign body 53 
 
 C. Tumors of the sclerotic 54 
 
 III. Conjunctiva Bulbi and the Episcleral Tissue. 
 
 1. Normal conditions 55 
 
 2. Pathological conditions 57 
 
 A. Conjunctivitis and its results 58 
 
 a. Conjunctivitis catarrhalis, episcleritis, phlyctaenula 58 
 
 b. Conjunctivitis blennorrhoica (purulenta, gonorrhoica), ulcer of the 
 
 conjunctiva 59 
 
 c. Conjunctivitis crouposa and diphtheritica 61 
 
 d. Conjunctivitis trachomatosa 61 
 
 The Results of Conjunctivitis. 
 
 B. Injuries to the conjunctiva and their results 63 
 
 1. Wounds without retention of a foreign body 63 
 
 2. Wounds with subsequent retention of a foreign body 64 
 
 3. Bums with lime - 64 
 
 C. Tumors of the conjunctiva bulbi and episcleral tissue 65 
 
 a. Lymphangiectasia and serous cysts 65 
 
 b. Granuloma (polypus) 66 
 
 c. Dermoid and lipomatous tumors 67 
 
 d. Fibroma and osteoma 69 
 
 e. Papilloma, melanoma and melanocancroid new-formations 69 
 
 f. Leucosarcoma and melanosarcoma 71 
 
 g. Epithelioma 74 
 
 IV. Iris. 
 
 r. Normal conditions 81 
 
 2. Pathological conditions 84 
 
 A. Iritis and its results 84 
 
 a. Iritis serosa (sero-fibrinosa, haemorrhagica) 8.1 
 
 b. Iritis fibrinosa (plastica) 87 
 
 c. Iritis purulenta (parenchymatosa) 89 
 
 The Results of Iritis. 
 
 a. Synechise of the iris 91 
 
 b. Atrophy of the iris 92 
 
 B. Injuries to the iris and their results '. 93 
 
 C. Tumors of the iris 97 
 
 a. Granuloma traumaticum 97 
 
 b. Melanoma 97 
 
 c. Leucosarcoma and melanosarcoma 98 
 
 V. Corpus cimare. 
 
 1. Normal conditions 99 
 
 2. Pathological conditions 103 
 
 A. Cycliiis and its results 103
 
 CONTENTS. xi 
 
 PAGK 
 
 a. Cyclitis serosa , 103 
 
 b. Cyclitis fibrinosa (plastica) 105 
 
 c. Cyclitis purulenta (parenchymntosa) 109 
 
 The Results of Cyclitis. 
 
 a. Cyclitic membranes iii 
 
 b. Atrophy 113 
 
 c. Staphyloma 113 
 
 B. Injuries to the ciliary body and their results 113 
 
 C. Tumors of the ciliary body 115 
 
 a. Myoma 115 
 
 b. Sarcoma 115 
 
 VI. Choroidea. 
 
 1. Normal conditions 116 
 
 2. Pathological conditions 120 
 
 A. Pathological changes of the pigmented epithelium 120 
 
 B. Choroiditis and its results 125 
 
 a. Choroiditis serosa (sero-fibrinosa) 125 
 
 b. Choroiditis fibrinosa (plastica) 127 
 
 c. Choroiditis purulenta (parenchymatosa). ... % 130 
 
 The Results of Choroiditis. 
 
 a. Detachment of the retina and vitreous body 133 
 
 b. I^iquefaction of the vitreous body 134 
 
 c. Glaucomatous excavation of the optic papilla 134 
 
 d. Atrophy ; synechia between retina and choroid, and pigmentation 
 
 of the former 134 
 
 e. Ossification 135 
 
 /. Staphyloma 136 
 
 C. Injuries to the choroid and their results 136 
 
 D. Tumors of the choroid 138 
 
 a. Cystoid formations 138 
 
 b. Granuloma 138 
 
 c. Sarcoma 138 
 
 VII. Opticus. 
 
 1. Normal conditions 142 
 
 2. Pathological conditions 146 
 
 a. CEdema of the optic nerve and papilla 147 
 
 b. Vaginitis nervi optici 149 
 
 c. Neuritis interstitialis nervi optici 150 
 
 d. Neuritis medullans nervi optici 152 
 
 Results of the affections detailed in the foregoing 153 
 
 Glaucomatous atrophy and excavation, and atrophy of the optic 
 nerve caused by embolism 155 
 
 Hzemorrhages in the ocular part of the optic nerve and hsematogene- 
 ous pigmentation 156 
 
 Tumors of the ocular part of the optic nerve 157
 
 xii CONTENTS. 
 
 PAGE 
 
 VIII. Retina. 
 
 1. Normal conditions 159 
 
 2. Pathological conditions i68 
 
 A. CEdema of the retina i68 
 
 B. Inflammatory processes in the retina and their results 169 
 
 a. Retinitis albuminurica 169 
 
 b. Retinitis interstitialis diffusa (atrophica) 174 
 
 c. Retinitis purulenta 177 
 
 C. Changes in the structure of the retinal blood-vessels, haemorrhages 
 
 and detachment of the retina 1 78 
 
 The Results of Retinitis. 
 
 D. Injuries to the retina and their results ,00 182 
 
 E. Tumors of the retina 183 
 
 a. Fibroma 183 
 
 b. Small-celled medullary sarcoma (glioma) 183 
 
 IX. Lens Crystai.linea. 
 
 r. Normal conditions 187 
 
 2. Pathological conditions 190 
 
 A. Cataracts formed within an intact lens-capsule 190 
 
 B. Injuries to the lens-capsule and lens-substance, and their results. . 194 
 
 X. Vitreous Body and Zonula Zinnii. 
 
 1. Normal conditions of the vitreous body 198 
 
 2. Pathological conditions of the vitreous body 199 
 
 A. Liquefaction of the vitreous body (synchisis) 200 
 
 B. Plastic hyalitis 201 
 
 C. Purulent hyalitis 202 
 
 Zonula Zinnii. 
 
 1. Normal conditions 203 
 
 2. Pathological conditions 204
 
 ILLUSTRATIONS. 
 
 PAGE 
 
 Fig. I. (i) The interfibrillar canals. (2) Interlamellar canals and lacunoe. 
 
 N. Nerve-sheath filled with the injection-fluid 5 
 
 Fig. 2. Corneo-scleral margin. C. Cornea. S. Sclerotic. CS. Schlemm's 
 canal. D. Descemetic mcmljrane. I. Iris. Lp. The fibres of the liga- 
 mentum pectinatum with endothelial cells adhering to them 8 
 
 Fig. 3. Isolated fibres of the ligamentum pectinatum. The endothelial cells 
 
 are shrunken and appear as darker swellings 9 
 
 Fig. 4. Cavity of an abscess in the cornea, after the contents have become 
 
 absorbed 18 
 
 Fig. 5. Proliferation of the endothelium of Descemet's membrane, observed 
 
 in a case of corneal abscess with hypopyon iS 
 
 Fig. 6. Ulcer of the cornea; its ground and walls filled with round-cells, 
 
 the surrounding epithelium proliferating 19 
 
 Fig. 7. Healed corneal ulcer. The loss of substance filled with new-formed 
 
 connective-tissue into which tlie epithelial layer sends papillary offsets. 21 
 
 Fig. 8. Deposits of lime in the cornea of a staphylomatous eye 24 
 
 Fig. 9. Anterior .synechia between cornea and iris. The endothelium of 
 Descemet's membrane forming a layer of spindle-shaped cells around 
 the place where iris and cornea are united 26 
 
 Fig. 10. Anterior synechia l:)etween cornea and vitreous body 28 
 
 Fig. II. Staphyloma of the cornea, with hypertrophy of the latter 30 
 
 Fig. 12. Section through a pterygium in a meridional direction. Pi. Ptery- 
 gium. A. Corneal lamellae raised by the pterygium. B. Bowman's 
 layer. C. Normal corneal lamellae 31 
 
 Fig. 13. Equatorial section through a pterygium. Pt. Pterygium. S. Scler- 
 otic (corneo-scleral margin). E. Encapsuled conjunctival epithelium, 
 undergoing regressive metamorphoses 32 
 
 Fig. 14. A healing corneal wound four days after it was inflicted 33 
 
 Fig. 15. Showing how the stump of the iris may be caught in the corneal 
 
 wound after iridectomy 35 
 
 Fig. 16. Pigmented cystoid formation in the cornea 36 
 
 Fig. 17. Eye-lash embedded in scar-tissue within the cornea, and sur- 
 rounded by epitheloid cells. C. Eye-lash 37 
 
 Fig. 18. Blood-vessels of the sclerotic from a wounded eye in the process of 
 phthisis bulbi. A. Proliferation of the endothelial cells, i. Giant- 
 cells. B. Transformation into connective-tissue 46 
 
 Fig. 19. Corneo-scleral staphyloma, i. New insertion of the iris which 
 adheres to Descemet's membrane by means of a tissue formed from the 
 endothelial cells. 2. The ectatic part ; the membrana Descemetii has 
 disappeared 48 
 
 Fig. 20. Ciliary staphyloma. Ciliary body adherent to the sclerotic and 
 
 atrophic. Beginning ectasia 49
 
 xiv ^LL USTRA TIONS. 
 
 PAGE 
 
 Fig. 21. Posterior staphyloma from a myopic eye. Choroid and sclerotic 
 
 adhere to each oiher and are atrophic 50 
 
 Fig. 22. Scar in the sclerotic 52 
 
 Fig. 23. A small piece of iron embedded in the sclerotic 53 
 
 Fig. 24. Trachoma-granule from the bulbar conjunctiva. Blood-vessels in- 
 jected with a stained fluid. L. Enlarged lymph-canals 62 
 
 Fig. 25. Crystalline lens dislocated under the conjunctiva and there encap- 
 
 suled 64 
 
 Fig. 26. Lymphangiectasia of the bulbar conjunctiva 66 
 
 Fig. 27. Granuloma (polypus) of the bulbar conjunctiva 67 
 
 Fig. 28. Dermoid tumor of the bulbar conjunctiva 6S 
 
 Fig. 29. Partially pigmented epithelial papillae from a dermoid tumor of 
 
 the bulbar conjunctiva 71 
 
 Fig. 30. Meianosarcoma of the bulbar conjunctiva. I. Shows how the pig- 
 mented cells creep along the blood-vessels of the conjunctiva and upon 
 
 Bowman's layer under the epithelium of the cornea 73 
 
 Fig. 31. Epithelioma of the bulbar conjunctiva 75 
 
 Fig. 32. Epithelioma of the bulbar conjunctiva, i. Epithelial cylinder filled 
 
 with round cells. 2. Epithelial cylinders ending in round-cellcylinders. 
 
 Fig. 33. Epithelioma of the bulbar conjunctiva. The tissue of the cornea 
 
 is changed into one consisting of long fine spindle-cells 78 
 
 Fig. 34. Epithelioma of the bulbar conjunctiva. The tumor has perforated 
 the cornea, and is spreading upon the surface and into the parenchyma 
 
 of the iris. C. Cornea. I. Iris . . 78 
 
 Fig. 35. Epithelioma of the bulbar conjunctiva. An anterior ciliary artery 
 surrounded by epithelial cells. Nests of epithelial cells in the tissue of 
 
 the ciliary body 79 
 
 Fig. 36. Serous iritis. The pupillary edge of the iris is adherent to the 
 anterior lens-capsule. The peripheral parts of the iris are protruding 
 
 into the anterior chamber (crater-shaped iris) 85 
 
 Fig. 37. Hsemorrhagic iritis (with spongy exudation). Haemorrhages in 
 the parenchyma of the iris. In the anterior chamber lies a fibrinous 
 
 and a gelatinous exudation 87 
 
 Fig. 38. Plastic iritis. Pupillary membrane 88 
 
 Fig. 39. Plastic iritis. New-formed connective-tissue upon the anterior 
 surface of the iris. This tissue is lamellar and contains blood-vessels. 
 
 H. A large haemorrhage 89 
 
 Fig. 40. Purulent ii itis 90 
 
 Fig. 41. New-formed connective-tissue uniting the posterior surface of the 
 
 iris with the anterior lens-capsule after plastic iritis 92 
 
 Fig. 42. Iritis chronica. Atrophy of the iris and colloid metamorphosis of 
 
 its anterior endothelial coat 93 
 
 Fig. 43. So-called cyst of the iris, formed after an injury to the cornea. The 
 walls of the cyst are formed by Decemet's membrane, the atrophic iris 
 and some new-formed connective-tissue, and lined with the endothelium 
 
 of the anterior chamber 95 
 
 Fig. 44. Incarcerated iris. Small prolapse of the iris into a corneal wound 
 
 covered with new-formed connective-tissue and epithelium gft
 
 ILLUSTRATIONS. XV 
 
 PAGE 
 
 Fig. 45. Traumatic granuloma of the iris after this membrane has prolapsed. 
 Gr. Granuloma. C. Cornea. D. Descemet's membrane. Ir. Iri^. Cc. 
 Ciliary body. LK. Lens-capsule 98 
 
 Fig. 46. Ciliary body from a myopic eye 100 
 
 Fig. 47. Ciliary body from an hypermetropic eye 100 
 
 Fig. 48. Sero-fibrinous cyclilis. Amorphous fibrine, containing numerous 
 
 round-cells, lies upon the posterior lens-capsule 104 
 
 Fig. 49. Serous cyclitis. The exudation lies in the tissue of the ciliary 
 
 body itself, and presses the muscular fibres apart 105 
 
 Fig. 50. Plastic cyclitis. Cyclitic membrane upon the posterior lens-capsule. 
 
 Theposterior chamber is obliterated. Lens and iris are pressed forward . 106 
 
 Fig. 51. Plastic cyclitis. Shows how the cells of the retinal layer of the 
 ciliary body are changed into spindle-cells and aid in the formation of 
 a cycliiic membrane 107 
 
 Fig. 52. Plastic cyclitis. Tubular excrescences of the pigmented (uveal) 
 
 layer of the ciliary body 107 
 
 Fig. 53. Plastic cyclitis. The same tubular excrescences. The younger 
 
 ones as yet unpigmented 108 
 
 Fig. 54. Plastic cyclitis. Cyclitic membrane. Detachment of the ciliary body. 109 
 
 Fig. 55. Purulent cyclitis no 
 
 Fig. 56. Gumma of the ciliary body. I. Iris. L. Lens. G. Gumma. Cm. 
 
 Cyclitic membrane in 
 
 Fig. 57. Plastic cyclitis from an eye with anterior phthisis. The cyclitic 
 membrane is very considerably shrunken, and brings the ciliary bodies 
 nearly in contact with each other II2 
 
 Fig. 58. Hypertrophy of the ciliary muscle in a case of cyclitis ... 113 
 
 Fig. 59. Isolated rupture of the ciliary body. The eye was enucleated on 
 account of hsemophthalmus. The tissue of the ciliary body was per- 
 fectly filled with blood. (The latter has not been drawn, to show the 
 rupture better) 1 14 
 
 Fig. 60. Primary melanosarcoma of the ciliary body 115 
 
 Fig. 6r. Normal entrance of the optic nerve into the eye-ball. i. A blood- 
 vessel coming from the choroid and entering the retina iiS 
 
 Fig. 62. Thickened and hardened intercellular substance from the pig- 
 mented epithelial layer, lying upon the lamina vitrea of the choroid. 
 The pigmented epithelial cells have been brushed off I2i 
 
 Fig. 63. Vitreous bodies upon the lamina vitrea of the choroid ; i, contain- 
 ing lime I2i 
 
 Fig. 64. Formation of osseous tissue in the vitreous bodies of the lamina 
 
 vitrea choroidese 122 
 
 Fig. 65. Tumor-like new formation of pigmented and unpigmented cell- 
 cylinders, starting from the uveal layer of the ciliary body and neigh- 
 boring choroid 123 
 
 Fig. 66. Pigmentary retinitis. Pigmented cell-cylinders going over in such 
 cylinders without pigment. Blood-vessel changed into connective- 
 tissue 124 
 
 Fig. 67. Pigmentary retinitis. Pigment in the perivascular sheath of a 
 
 retinal blood-vessel 125
 
 xvi ILL US TRA TIONS. 
 
 PAGE 
 
 Fig. 68. Plastic choroiditis. Fibro-cellular exudation in the tissue of the 
 
 choroid 128 
 
 Fig. 69. Plastic choroiditis. Adhesion between retina and choroid 129 
 
 Fig. 70. Plastic choroiditis. Pigmentation of the retina 129 
 
 Fig. 71. Purulent choroiditis 130 
 
 Fig. 72. Tubercle of the choroid 131 
 
 Fig. 73. Osseous tissue, with marrow in the choroid 132 
 
 Fig. 74. Parenchymatous hsemorrhage splitting the choroid into two layers, 
 
 caused by contusion of the eye-ball 136 
 
 Fig. 75. Granulation-tissue starting from the wounded choroid 137 
 
 Fig. 76. Cystoid formation in the choroid 138 
 
 Fig. 77. From a chondrosarcoma of the choroid, i. Sarcoma-cells. 2. 
 Cartilage-tissue ; in its centre. 3. Remains of the vitreous body 
 changed into delicate, myxomatous tissue. 4. Connective-tissue sur- 
 rounding the cartilage-tissue ... 140 
 
 Fig. 78. Osseous tissue formed in a sarcomatous tumor of the choroid 141 
 
 Fig. 79. Shows how the double-contoured nerve-fibres of the optic nerve 
 
 are changed into non-medullated ones in an hypermetropic eye 145 
 
 Fig. 80. Shows how the double-contoured nerve-fibres of the opticus are 
 
 changed into non-medullated ones in a myopic eye 145 
 
 Fig. 81. Qidema of the intervaginal space and optic papilla, i. The en- 
 larged intervaginal space. 2. Spaces in the optic papilla filled with serum. 148 
 Fig. 82. Fibrinous vaginitis of the optic nerve. I. Intervaginal space 
 
 obliterated by new-formed connective-tissue. Optic nerve atrophic . . . 149 
 Fig. 83. Interstitial inflammation of the optic nerve. Longitudinal section. 151 
 Fig. 84. Interstitial inflammation of the optic nerve. Transverse section . . 151 
 Fig. 85. Atrophic excavation of the optic papilla filled with a delicate con- 
 nective-tissue formed in the neighboring vitreous body 154 
 
 Fig. 86. Very deep glaucomatous excavation. Atrophy of the optic nerve . 156 
 Fig. 87. From an atrophic optic nerve. Hypertrophy of the connective- 
 tissue, M'hich contains some pigment. The nerve- fibres are broken up 
 
 into a grumous substance 157 
 
 Fig. 88. Granuloma of the optic papilla 1158 
 
 Fig. 8g. Cystoid degeneration of the retina near the ora serrata 166 
 
 Fig. 90. Albuminuric retinitis, i. Nerve fibre layer, considerably thickened 
 
 through sclerosed hypertrophic nerve fibyes. 2. Haemorrhage 171 
 
 Fig. 91. Albuminuric retinitis. I. Outer granular layer. 2. Inner granular 
 layer. 3. Cavity filled with fil^rine. 4. Cavity filled with cells con- 
 taining fat-granules. Both cavities containing, moreover, peculiar struc- 
 tures of varying size, which coalesce and refract the light very strongly. 
 
 Some fat-granule cells lie in the outer granular layer 172 
 
 Fig. 92. Detached and perfectly atrophied retina. Capillaries changed into 
 
 cylinders of amorphous lime 180 
 
 Fig. 93. Anterior polar cataract. The apex of the cone is formed by a 
 lamellar, dim tissue, without any cellular elements. The basis consists 
 
 of lime and fat 194 
 
 Fig. 94. Connective-tissue within the ruptured lens-capsule 196 
 
 Fig. 95. Osseous tissue formed within the ruptured lens-capsule 197
 
 THE HUMAN EYE. 
 
 I. 
 
 CORNEA. 
 
 I. Normal Conditions. 
 
 The tissue of the cornea consists of the following parts, 
 viz., the epithelium, Reicherfs or, as it is commonly styled, 
 Bowman s layer, the parenchyma, Descemef s membrane and 
 its endothelium, blood and lymphatic vessels and nerves. 
 
 The epithelial layer of the cornea viewed from the surface 
 presents a delicate mosaic, formed of cells some of which 
 angular, and others round. Each of these cells possesses a 
 large, round or oval nucleus, in which usually several nucleoli 
 may be seen. A small amount of cementing substance 
 unites the cells with each other, and can be easily demon- 
 strated by staining the cornea with nitrate of silver or chloride 
 of gold. 
 
 In teased specimens of this superficial part of the corneal 
 epithelium we frequently find such cells lying on their edge. 
 They then appear considerably broader around the nucleus, 
 not unlike the blood-corpuscles of the amphibia {Waldeyer). 
 
 These flattened cells form several layers. 
 
 Beneath them follow several layers of cells, characterized 
 by being less flattened and bearing offsets. Of these we 
 have again two distinct kinds. The one bear small offsets all 
 over their surface — serrated cells — and the other have only 
 one, two or three broader offsets on their inner surface. The 
 small offsets of the former, which lie more superficially, in- 
 terlace with each other. The large offsets of the latter, which 
 lie nearer to Bowman s layer, dip into the interstitia between 
 the cells of the underlying layer. Each of these cells again
 
 2 THE HUMAN' E YE. 
 
 has a large round or oval nucleus with several nucleoli. 
 I often also found in this layer cells with two nuclei and 
 smaller ones of apparently recent date. The same cementing 
 substance which unites the cells of the superficial layer, is 
 also found between these. 
 
 The innermost part of the epithelium is formed of one 
 single layer, called the basal layer. Its cells are long and 
 cylindric or club-shaped. Their form, however, varies greatly. 
 Sometimes they are broader in their outer and sometimes in 
 their inner part ; some are cone-shaped, while others have one 
 or two notches, in which the neighboring cells fit. They 
 all have a round or oval nucleus with nucleoli ; some of them 
 also have two nuclei {Waldeyer). These cells, too, are united 
 by the same cementing substance, and thus all the different 
 layers of the epithelium are united into one. 
 
 Waldeyer is of the opinion, that the new formation of 
 epithelial cells takes place in the basal and middle layers. 
 The corneal epithelium, however, consists altogether of living 
 cells, as even the most superficial ones have a nucleus, and I 
 therefore see no sufficient reason for denying to one of these 
 layers the ability of producing new cells, y. Arnold's experi- 
 ments on the regeneration of epithelial defects of the cornea, 
 moreover, decidedly prove that the new formation takes 
 place in all the layers. 
 
 Under the epilhelium of the cornea lies Reicherfs or 
 Bowman s layer. This appears as a vitreous layer, which is, 
 however, not distinctly separated from the underlying paren- 
 chyma. A high magnifying power shows it to be somewhat 
 striated, and we may split it into fibrillae by a number of 
 chemical agents {Waldeyer^. I never found cells in this 
 layer in its normal condition. Boivmans layer cannot be 
 readily and evenly separated from the underlying paren- 
 chyma, as fibres springing from it pass into the latter, and 
 vice versa. They can be readily traced between the lam- 
 ellae of the parenchyma. They also were first described 
 by Bowman. 
 
 At the periphery of the cornea Bozvmatis layer is split 
 up into its fibrillar, and these pass over into the conjunc- 
 tival tissue.
 
 CORNEA. 2 
 
 Waldeyers opinion that Bowman s layer is condensed 
 parenchyma of the cornea, and not a separate membrane, is 
 certainly correct. In the following we shall have to state 
 additional reasons for this assertion. 
 
 Some few authors maintain that the outer surface of 
 Bowman s layer bears small elevations in which the cells of 
 the basal layer of the epithelium are said to fit. 
 
 The parenchyma proper of the cornea consists of the 
 stroma, embedded in which lies a system of lymphatic canals, 
 the cellular elements, blood vessels and nerves of the cornea. 
 
 The stroma of the corneal parenchyma is transparent and 
 formed of exceedingly fine fibrillae, which are united by a 
 cementing substance. When isolated the fibrillae appear 
 wavy, but otherwise in no way different from connective tissue 
 fibrillae. I have never found elastic fibrillae among them 
 {Henle). The best agent to split the cornea into these fibrillae, 
 is a ten per cent, solution of common salt {Schweigger-Seidel). 
 Sometimes I obtained a good view of them in situ by stain- 
 ing the cornea with logwood. It then became evident that 
 the fibrillae intersect each other at all possible angles, and 
 not at right angles only, as Waldeyer and others maintain. 
 
 These finest fibrillae of the corneal stroma are united into 
 fascicles, and several of these fascicles together form a lamella. 
 The lamellae lie mostly parallel to the surface of the cornea, 
 from which rule exceptions are rare. 
 
 Fibrills, fascicles and lamellae are united with each other 
 by a protaplasmatic cementing substance, which is seen as a 
 fine homogeneous light streak between them, and has some- 
 times a granular appearance. We have thus an interfibrillar, 
 an interfascicular and an interlamellar but always the same 
 cementing substance. 
 
 Embedded in this substance, furthermore, are von Reck- 
 lingJiausen s corneal canals. It is well known that, by stain- 
 ing the living cornea with nitrate of silver or chloride of gold, 
 these canals are easily demonstrated. Logwood and carmine 
 do not answer this purpose very well. Berlin blue some- 
 times, but not constantly, yielded me as good pictures as 
 gold or silver. In a plain view of the cornea thus stained, 
 we see a system of fine canals which intersect each other at
 
 4 THE HUMAN E YE. 
 
 very varying angles, and which form here and there a larger 
 cavity, which is called a lacuna. In transverse sections of 
 the cornea we see that this system of canals (like the lamellae) 
 runs mostly in a direction parallel to the outer surface of the 
 cornea, and that the lacunae are arranged in rows lying, of 
 course, in the same direction. The small canals, however, 
 which unite the lacunae of the larger canals with each other, 
 pass through the corneal parenchyma at very different angles. 
 In transverse sections taken from hardened specimens the 
 lacunae appear lens-shaped. From the plain views of a 
 stained living cornea we know, however, that their shape 
 varies considerably, according to the number of canals which 
 are in connection with them. 
 
 The caliber of the canals and lacunae is by no means uni- 
 form. As a rule, however, as pointed out by von Reckling- 
 hausen and confirmed by Waldeyer, the canals and lacunae 
 which lie nearest to Bowman's layer are the narrowest, 
 while those lying nearest to Descemefs membrane are the 
 widest. The same rule holds good with regard to the thick- 
 ness of the lamellae in these parts of the cornea. Waldeyer 
 and other authors before and with him have drawn the at- 
 tention to these facts, and to the probability that the cornea 
 consists of a conjunctival, a sclerotical and a choroideal 
 part. We would thus find the widest canals and lacunae in 
 the choroideal and the smallest in the conjunctival part of 
 the cornea. 
 
 Another means of demonstrating this system of canals 
 and lacunae, is to inject into them a colored fluid. Bowman 
 while experimenting on the cornea of animals obtained by 
 such injection a system of straight canals, which he called 
 corneal tubes. As far as my experiments show, these corneal 
 tubes do not belong to the human cornea. Waldeyer suc- 
 ceeded in injecting a colored fluid into the interlamellar and 
 interfascicular canals. Since I could not procure Waldeyer s 
 fluids in the proper condition, I made my injections with a 
 saturated solution of Berlin blue. I thus not only obtained 
 injections of the canals lying in the interlamellar and inter- 
 fascicular cementing substance (as Waldeyer)^ but, moreover, 
 a system of blue lines corresponding exactly with the ar-
 
 CORNEA. 5 
 
 rangement of the fibrillae, as I had sometimes occasion to 
 see it after staining the cornea with logwood. These lines 
 (See Fig. i) were arranged in 
 fascicles intersecting each other 
 at various angles. I think, if I 
 am not mistaken, that I have 
 thus injected also the interfibril- 
 lae canals, which, of course, were 
 somewhat enlarged by the pres- 
 sure exerted upon them during 
 the injection. This system of in- 
 terfibrillar canals is in direct con- ^ ^igr- 1. d) The interfibniiar canals. (2, 
 
 Interlamellar and lacunre. N. Nerve- 
 nection with the interfascicular sheath filled with the injection-fluid. 
 
 and interlamellar canals, and all of them, as we shall see 
 later on, are in direct communication with the canals en- 
 closing the corneal nerves. (See Fig i.) 
 
 Kuehne and others describe this system of canals as being 
 filled with a continuous protoplasmatic substance. Most au- 
 thors, however, resent this opinion. Von Recklinghausen and 
 others after him, whose opinion I, too, share, maintain that 
 these canals contain the nutritive (lympathic) fluid. 
 
 The canals have no walls of their own ( Waldeyer). Con- 
 trary statements seem to be erroneous. 
 
 Besides the nutritive fluid, which fills the canals through- 
 out, they contain three different kinds of cells, viz : fixed cor- 
 neal cells, wandering (lymphatic) cells, and pigmented cells. 
 
 The. fixed cells of the cornea, as they have been called by 
 Co/mheim, lie in the lacunae. Such a cell, however, never 
 altogether fills the lacuna, in which it lies. They mostly 
 adhere to one wall of the lacuna, and fill only about two- 
 thirds of it. The cells appear as protoplasmatic bodies with 
 an oval or round nucleus, usually containing several nucleoli. 
 The protoplasma is very granular around the nucleus. Wal- 
 deyer succeeded in isolating these cells, and described them as 
 very thin, completely flattened bodies, having a few short 
 offsets. I have never been able to isolate them. I, how- 
 ever, frequently found their nucleus perfectly hidden by the 
 granular protoplasma, which fact would prove that these cells 
 are not always flat, but sometimes thicker around their nucleus.
 
 6 THE HUMAN EYE. 
 
 Besides the agents recommended by Waldeyer and com- 
 monly used in studying these parts, I can recommend the 
 staining of the cornea with eosine {Dreschfeld), an aniline 
 color which is highly fluorescent. This fluorescence causes 
 the outlines of the cells, etc., to be exceedingly well defined. 
 
 The offsets of a fixed corneal cell reach only a very small 
 distance into the canals which communicate with the lacuna 
 in which it lies. 
 
 A number of undoubted observations are on record which 
 prove the contractility of the fixed corneal cells, and Waldeyer 
 lately has seen them move about along the walls of the lacuna. 
 
 The pigmented cells which we sometimes find in the per- 
 iphery of the cornea (especially in the eyes of negroes) are 
 perfectly identical with these unpigmented fixed corneal cells. 
 Their granular pigment is enclosed in the protoplasma, leav- 
 ing the nucleus free. 
 
 Besides the fixed cells we always find in the cornea a 
 number of wandering (lymphatic) cells. They differ in no 
 way from those found in other organs, and they wander 
 along the preformed corneal canals, and not promiscuously 
 through the tissue. This is proven beyond doubt by Gener- 
 sicJts experiments, who brought living cornese into the lymph- 
 sacs of frogs. 1 have often repeated this experiment, and 
 . always with the same result, that is of finding the immigrated 
 lymph-cells filHng only the corneal canals. The same is seen 
 in the earlier stages of inflammation of the cornea, when the 
 structure of its parenchyma has not yet been destroyed. 
 
 The connection between fixed and wandering cells in the 
 corneal parenchyma is not yet clearly defined. I can fully 
 confirm the opinions of earlier authors, that fixed cells can 
 become wandering ones. Whether, however, wandering cells 
 can become fixed ones, is as yet an open question. 
 
 The parenchyma of the cornea is covered on its inner 
 surface by Desccmcfs membrane. This membrane is a per- 
 fectly homogeneous, vitreous membrane, and is about two- 
 thirds the thickness of Bozvnians layer. I cannot agree with 
 those authors who state it to have in transverse sections 
 a striated appearance. No more can I concur in Waldeyer s 
 opinion, who says that Descemefs membrane cannot readily
 
 CORNEA. 7 
 
 be separated from the corneal parenchyma. Pathological 
 specimens have taught me that a perfect detachment of this 
 membrane is possible. Walb had also occasion to describe 
 such a case. 
 
 Descemef s membrane is moreover an elastic membrane. 
 In a previous paper I have stated its tendency to wind itself 
 up in a spiral way from specimens of the animal eye. I can 
 add now that I am in possession of specimens from the 
 human eye in which Descemef s membrane is detached and 
 shows three and four spiral windings. This detachment and 
 the tendency to wind itself up spirally seem to me to prove 
 that, unlike Bowman s layer, this membrane is really a sep- 
 arate structure, and not condensed corneal parenchyma, 
 as Waldeyer seems to think. This similarity between Des~ 
 cemet" s membrane and the vitreous membrane of the choroid, 
 besides other similarities mentioned later, seems to confirm 
 the opinion that the inner portion of the cornea is really its 
 choroideal part. 
 
 The inner surface of Descemef s membrane is covered 
 by a single layer of endothelial cells. These cells are not as 
 regular and uniform in shape and size in the human eye as they 
 usually are in the eyes of animals. They are five or six in num- 
 ber, angular, or round, and have a round or eliptical, sometimes 
 bean-shaped nucleus, with one or more nucleoli. In trans- 
 verse sections they often appear so flat that the thin layer is 
 only recognized with difficulty, in other eyes they appear as 
 large cuboid cells with a round nucleus. They are united 
 by a cementing substance, not different from the one de- 
 scribed in other parts of the cornea. In the angles between 
 two or three neighboring cells, we frequently find stomata. 
 Near the periphery of Descemef s membrane I nearly always 
 find, like Henle, the " vitreous warts," which were first describ- 
 ed by Hassal. I found them several times even in children's 
 eyes, which proves that the opinion of Waldeyer and others 
 who consider these " warts," to be a change caused by old 
 age only is erroneous. They are round, vitreous bodies, 
 sometimes granular, mostly perfectly homogeneous. Some- 
 times two or more of them coalesce, just as we shall describe 
 later on of the vitreous (colloid) bodies of the lamina vitrea
 
 8 
 
 THE HUMAN E YE. 
 
 of the choroid. They generally push the adjacent endothel- 
 ial cells aside, and alter their shape accordingly. They are 
 seldom as large as the endothelial cells, are very hard, and 
 resist all chemical agents. 
 
 At the corneo scleral-margin, the region where cornea 
 and sclerotic pass over into each other, the tissues show cer- 
 tain characteristic alterations. 
 
 Fig. 2. Corneo-scleral margin. C. Cornea. S. Sclerotic. OS. Schlemm's canal. D. Des- 
 cemet's membrane. I. Iris. Lp. The fibres of the ligamentum pectinatum with endo- 
 thelial cells adhering to them. 
 
 The corneal epithelium passes directly over into the con- 
 junctival epithelium. The fibres into \\\{\c\i Bowman s layer, 
 is, split up and the anterior lamellae of the corneal paren- 
 chyma together enter the subconjunctival (episcleral) tissue 
 in such a way that these two parts cannot be separated with- 
 out tearing the fibres. (This is the so-called conjunctival 
 part of the cornea.)
 
 CORNEA. g 
 
 The bulk of the corneal lamellae terminate in the lam- 
 ellae and fibres of the sclerotic, from which they are not his- 
 tologically, but chemically, different. The corneal canals also 
 are continuous with those of the sclerotic {Waldeyer). (This 
 is the scleral part of the cornea). 
 
 Descemefs membrane and the adjacent lamellae undergo 
 very important changes in this region. Waldeyer, when de- 
 scribing these parts, states that none of the previous illus- 
 trations gave an exact picture of these conditions, and I 
 must add that his own does not do so either. The illustra- 
 tion herewith given (See Fig. 2) shows these conditions still 
 better. It is drawn from a specimen taken from the myopic 
 eye of an adult. We here plainly see that Descemefs mem- 
 brane and the adjacent lamellae are split up into fibres, which 
 are partially lost in the tendon and connective tissue of the 
 ciliary muscles and partially in the tissue of the iris. Ad- 
 herent to these fibres are a number of endothelial cells which 
 appear very similar to those covering the posterior surface 
 of Descemefs membrane. Between the fibres are open cavi- 
 ties and canals which com- 
 municate on one side with 
 the anterior chamber, on the 
 other with Schlemtns canal. 
 This system of cavities and 
 canals is called Font ana s 
 spaces. While in the ani- 
 mal eye these spaces are 
 covered by what has been 
 
 styled the " iris-trabeculae " '''^•S- isolated fibres of the ligamentum pec- 
 -' tinatum. The endothelial cells are shrunken 
 
 (Irisbalken), such trabeculae and appear as darker swellings. 
 
 springing from the iris are not found in the human eye. 
 The network of fibres formed in this region through the 
 splitting up of Descemefs membrane, has been called the 
 ligamentum pectinatum. In hardened specimens it can be 
 detached with the periphery of Descemefs membrane, and we 
 then find what Fig. 3 illustrates ; a network of coarse con- 
 nective-tissue fibres, which refract the light strongly, and 
 have therefore a peculiar sclerotic appearance, to which 
 a number of endothelial cells are adherent. This network
 
 lO THE HUMAN EYE. 
 
 passes over into Desceniefs membrane on one side, on the 
 other, as stated above, in the iris and ciliary body. Its 
 outer part terminates in a fascicle of circular equatorial 
 fibres, forming a ring which has received the name of the 
 posterior terminal ring {Gre^izring). Besides this there ex- 
 ists, but less constantly, an anterior terminal ring nearer the 
 place where Descemef s membrane begins to be split up into 
 fibres. 
 
 The blood-vessels of the cornea He only in its most periph- 
 eral parts, and form a small border at the corneo-scleral 
 margin which varies in breadth from one to two and a half 
 mm. This difference in breadth is found in nearly every 
 individual cornea. 
 
 These corneal blood-vessels come from the anterior ciliary 
 arteries, and anastomose with the marginal blood-vessels of 
 the conjunctiva, which have the same origin. The superficial 
 arterial branches of the marginal blood-vessels very soon, 
 after having entered the cornea, end in a capillary network 
 which forms the so-called marginal loops of the cornea. Leber, 
 in Graefe and SaemiscJis cyclopedia, gives an excellent illus- 
 tration of these blood-vessels. I frequently found, however, 
 that these terminal loops when injected with a colored fluid 
 have little cone or diverticle-like offsets, in the direction 
 towards the centre of the cornea, which are, perhaps, remains 
 of the foetal praecorneal blood-vessels, and certainly must be 
 of great importance for the pathological new-formation of 
 blood-vessels in this membrane. In the inner layers of the 
 cornea the capillary network passes over into comparatively 
 broad veinous branches. The blood is carried by them to 
 the episcleral and then into the anterior ciliary veins. 
 
 The blood-vessels of the cornea are histologically in no 
 way different from others. 
 
 At the corneo-scleral margin from forty to forty-eight 
 larger nerve-branches enter the posterior layers of the corneal 
 tissue. They come partially from the anterior ciliary, and 
 partially from the conjunctival nerves. Very soon after 
 their entrance into the cornea they lose their double contour. 
 They then branch off and form what is called the " narrow 
 stroma-plexus." From this plexus smaller branches run for-
 
 CORNEA. 1 1 
 
 ward, and just. behind Bowman s layer split again into axis- 
 cylinders and axis-fibrillae, which pierce Bowman's layer and 
 form the " sub-epithelial plexus " around the basis of the basal 
 layer of the corneal epithelium. From this plexus again 
 fibrillae spring forward into the anterior parts of the epithe- 
 lium and there form between the flattened cells the terminal, 
 " intra-pithelial " plexus. Whether this is really the terminal 
 plexus, and in what way the fibrillae end, is as yet an open 
 question. Kuehne and others say that they end in the cells. 
 Coh7iheim states that they have a special terminal nodule 
 lying upon the external surface of the epithelium. Other 
 authors maintain a free ending between the cells. My own 
 specimens did not allow me a deciding opinion with regard 
 to this point. 
 
 I can, however, confirm the statement of others that the 
 larger nerve-branches lie in a system of canals which are 
 sometimes lined with flat endothelial cells. Where the 
 larger nerves are split up into their branches, an endothelial 
 cell is often found lying on the nerve itself, these have 
 been mistaken for ganglionic cells. There are, however, 
 no ganglionic cells to be found in the cornea, in which opin- 
 ion I agree with Waldeyer. In specimens which have been 
 stained with chloride of gold, the axis-fibrillae always appear 
 varicose. Waldeyer is of the opinion that this varicosity is 
 artificially produced, and does not exist during life, an 
 opinion put forth before him by Engelmann. 
 
 It has been stated before that the system of canals in 
 which the nervous fibres are embedded is in direct communi- 
 cation with the lympathic canals of the cornea, which is 
 proven by injecting the latter with a colored fluid. (See 
 Fig. I.) 
 
 2. Pathological Conditions. 
 A . Keratitis and its Results. 
 
 The large majority of the facts collected in the following 
 pages is derived from examinations of human eyes.
 
 12 THE HUMAN EYE. 
 
 To whatever degree a cornea is inflamed, we find it 
 to contain more cells than in the normal condition. These 
 additional cells are chiefly round-cells and partially small 
 spindle-shaped ones. They are the same formative cells 
 which are called either wandering or lymphatic, and are 
 identical with the emigrated white blood-corpuscles as we 
 find them in the beginning in every inflamed tissue. 
 
 CoJinhcim and his pupils maintain that these cells are 
 all emigrated ones from the marginal blood-vessels of the 
 cornea. According to Boettcher and others they are simply 
 the products of the proliferating cells of the corneal paren- 
 chyma. My own examinations of the inflamed human cornea 
 and experiments on the cornea of animals, force me to agree 
 with those authors who believe that the additional cells, in such 
 an inflamed cornea take their origin from both these points, 
 viz., from the blood-vessels and the fixed (and wandering) 
 cells. {Strieker, Norris, Fuchs, etc.) 
 
 I am, furthermore, convinced by my own experimental 
 researches that the process of emigration of cells from the 
 marginal blood-vessels precedes the process of proliferation 
 of the cells of the corneal parenchyma. I once saw, for 
 instance, a cornea perfectly filled with round-cells only three 
 hours after a superficial injury. These cells could not possi- 
 bly have been the result of proliferation of the corneal cells, 
 and therefore could only be immigrated ones from the blood- 
 vessels. These immigrated cells lie, as a rule, at first in the 
 corneal canals, not in the lacunae. Only when the process of 
 proliferation begins in the fixed corneal cells, we find more 
 than one cell in the lacunae. 
 
 I have seen fixed corneal cells, which in this second stage 
 contained three and four nuclei. If the process of inflamma- 
 tion does not stop here, the cells soon become so numerous 
 that the tissue of the cornea suffers under the pressure and 
 becomes gradually mortified. This necrosis of the corneal 
 tissue may be confined to a small intraparenchymatous space 
 (abscess) or may reach the surface (ulcer). 
 
 Whilst in the normal cornea, as we stated above, the 
 wandering cells lie in the corneal canals only and not in the 
 stroma, the latter cannot resist their vital power any longer
 
 CORNEA. 
 
 13 
 
 in the later periods of inflammation, and we then see that the 
 new-formed cells traverse the stroma of the cornea in all 
 directions, totally disregarding the corneal canals. 
 
 We have in the following pages to speak of two different 
 degrees of inflammation of the cornea, viz., infiltration-kera- 
 titis and purulent keratitis. These two kinds are, however, 
 different only in degree; but they are histologically distinct 
 enough from each other. Under these two heads we can, 
 furthermore, place all the manifold kinds of keratitis which 
 the clinicists can and must consider separately, and the 
 histological conditions do not allow us to speak of more 
 than these two kinds of inflammation of the cornea. 
 
 a. Infiltratio7i of the Cornea. 
 
 The characteristic feature of infiltration of the cornea 
 is the immigration (very rarely also the new formation) of 
 round-cells into the parenchyma of the cornea. This immi- 
 gration never leads to a perfect destruction of the latter, and 
 only very rarely alters it at all. 
 
 The infiltration is usually confined to only a circumscribed 
 part of the cornea, and never involves its entire thickness. 
 
 We find histologically, at first, only a number of round- 
 cells filling the canals of the diseased part of the cornea. 
 Later on we sometimes also see signs of proliferation in the 
 fixed corneal cells. The round-cells lie chiefly in the inner 
 layers of the cornea, and infiltration-keratitis but seldom 
 affects the lamellae which lie next to Bowmart s layer. 
 When the infiltration is confined, as is the rule, to the inner 
 parts of the cornea, the epithelium remains unaltered ; if it 
 affects the lamellae nearer the surface, the epithelium is 
 always found in a pathological condition. It appears micros- 
 copically in toto irregular and lacks its normal lustre and 
 smoothness ; microscopically we find its cells very irregular in 
 shape, granular and much enlarged, so that the whole of the 
 epithelial layer covering the infiltrated portion of the par- 
 enchyma is somewhat thickened. This thickening may 
 furthermore be due to serous imbibition or to proliferation 
 and new formation of these cells. The corneal lamellae sur- 
 rounding the infiltrated part appear in no way altered.
 
 14 
 
 THE HUMAN E YE. 
 
 Infiltration may heal by absorption of the immigrated 
 cells which may or may not be preceded by the formation 
 of new blood-vessels. These blood-vessels spring from the 
 marginal vessels nearest the infiltrated part. J. Arnold has 
 described the way in which this new-formation takes place, 
 and I can fully endorse his views. At first we find small 
 protoplasmatic offsets growing from the marginal blood- 
 vessels, nearest the diseased part, which grow thicker as they 
 grow farther into the corneal tissue. Gradually the central 
 part of these solid offsets becomes hollow, and we find later 
 on a protoplasmatic tube, with endothelium filled with a few 
 blood-corpuscles. Carmalt and Strieker saw new blood-ves- 
 sels being formed out of fixed corneal cells. They, however, 
 stand alone in this experience. 
 
 This new formation of blood-vessels generally begins in 
 the innermost layers of the cornea. Later on we sometimes 
 find blood-vessels in the superficial layers too. The latter 
 is the rule in cases of superficial infiltration. The new- 
 formation of blood-vessels is sometimes accompanied by 
 hypertrophy of the conjunctival tissue at the corneal mar- 
 gin, and the latter is then found to grow in between the 
 epithelium and Bowman s layer, and to be filled with round- 
 cells and new-formed blood-vessels. This interposed tissue 
 has lately been styled pannous. 
 
 During the process of recovery, the new-formed blood- 
 vessels either disappear or in rare cases, remain persistent. 
 If the latter is the case, the larger ones generally have a well- 
 defined adventitia. 
 
 Infiltration, as stated above, but very rarely alters the 
 corneal parenchyma, and, as a rule, leaves no trace behind. 
 In rare cases it leaves a scar. This is, however, always the 
 case when infiltration results, goes in the purulent form 
 of keratitis with partial destruction of the corneal tissue. If 
 the infiltration concerns the corneo-scleral tissue, it some- 
 times produces sclerosis of the involved parts, which is then 
 the result of the new-formation of translucent connective 
 tissue between the normal, transparent lamellae and subse 
 quent obliteration of the involved corneal canals. This pro- 
 cess is not to be confounded with that of the formation of a
 
 CORNEA. 
 
 15 
 
 scar, since the new formation here does not replace destroyed 
 tissue. Such a new formation of only translucent tissue 
 takes place also around those blood-vessels which remain 
 persistent, and is the cause of the grayish color of these parts. 
 
 We must enumerate under the type of infiltration-kera- 
 titis the following forms which clinicists consider as sep- 
 arate diseases, viz., corneal infiltration, parenchymatous 
 keratitis (which does not, as a rule, show any alteration of 
 the corneal parenchyma), pannous or vascular keratitis, 
 phyctaenular keratitis and some forms of traumatic kera- 
 . titis (results of cuts inflicted by sharp or ragged-edged 
 instruments.) 
 
 Among the forms of the clinically so-called parenchyma- 
 tous keratitis there is one characterized by a network of 
 systems of lines which are distinct from the grayish, infiltrated 
 surrounding parts of the cornea, and cross each other at 
 different angles. This network always lies in the superficial 
 layers, and is seen when the narrow canals in the superficial 
 layers are especially filled with round cells. 
 
 Phyctaenula, according to Iwanoff, is a circumscribed 
 infiltration of Bowman s layer, and always confined to the 
 parts surrounding a nerve-branch, piercing into the epithelial 
 layer. This simple local infiltration generally results in 
 local purulent keratitis, with loss of substance and the forma- 
 tion of a scar. 
 
 Among the forms of traumatic keratitis one has always 
 been of special interest to ophthalmologists. It has been 
 called striped keratitis (Streifige keratitis). This form of 
 infiltration-keratitis is found after injuries (mostly opera- 
 tive) on the corneo-scleral tissue. We find in such cases, 
 besides the general dimness of the parts surrounding the 
 wound, a number (generally from 10 to 12) grayish stripes, 
 which start from the wound in a radiating direction towards 
 the centre of the cornea, and after nearly reaching it are 
 bent in the form of arches and disappear in the normal 
 tissue. In order to find the real cause of this strange pic- 
 ture, I made a large number of parenchymatous injections at 
 the corneo-scleral margin of animal and human eyes, and I 
 came to the conclusion that these stripes are represented by
 
 l6 THE HUMAN EYE. 
 
 the larger nerve-canals when they are in a state of infiltra- 
 tion. This explanation seems to be the more plausible, 
 since, we know that at the corneo-scleral junction, from forty 
 to forty-eight nerves enter the corneal tissue, and our 
 operative wounds comprise, from one-fourth, to one-third 
 of the corneal periphery. Moreover, we never see striped 
 keratitis after wounds inflicted upon the centre of the cor- 
 nea, where no large nerve-canals exist. 
 
 Infiltration-keratitis usually heals without leaving a trace, 
 sometimes it causes sclerosis, of the involved parts, as above 
 stated, and in rare cases (except in phlyctsenula) it leads 
 to purulent keratitis with its results. Infiltration-keratitis 
 is furthermore constantly found accompanying purulent 
 keratitis, and then involves the tissue surrounding the parts 
 suffering from the purulent form of inflammation. 
 
 I have never found Descemefs membrane or its endothe- 
 lium, altered in cases of infiltration-keratitis. This form also 
 very rarely causes an inflammation of the tissue of the iris. 
 
 b. Purulent Keratitis. 
 
 The characteristic feature of the purulent form of kera- 
 titis is, that the increase of the cellular elements in the cor- 
 nea is such, as to destroy the corneal tissue. This holds good 
 whether the process involve only a superficial part of the 
 corneal tissue or be deeper seated, whether only a part or the 
 whole of the cornea be destroyed. 
 
 We can distinguish three forms of purulent keratitis, viz. : 
 abscess, ulcer and kerato-malacia. 
 
 c. Abscess of the Cornea. 
 
 Abscess of the cornea is that form of purulent keratitis 
 which always takes its origin, in the deeper layers of the 
 cornea, and which may remain altogether confined to them, 
 and never reach the surface of this membrane. 
 
 In this form of inflammation we always find a more or 
 less roundish, flattened part of the corneal tissue filled with 
 innumerable round-cells. The pressure exerted by these 
 cells upon the stroma of the cornea leads to mortification 
 and fatty degeneration of the involved parts, and thus a pus-
 
 CORNEA. 
 
 17 
 
 cavity is formed. This cavity has generally the shape of 
 a flattened globe, or is ovoid, with corroded walls. Some- 
 times trabeculae may be found springing from one side of the 
 cavity and reaching to the opposite wall. The cavity itself 
 is perfectly filled with round-cells, which often surround a 
 central nucleus of fatty (cheesy) detritus. The corneal tissue 
 surrounding the abscess is in a state of infiltration, and gen- 
 erally most so on that side of the abscess which lies nearest 
 the corneo-scleral margin. 
 
 In this stage the process may heal, without involving 
 more than the parts originally attacked. The healing 
 process always begins with the formation of blood-vessels, 
 from the corneo-scleral margin in the way above mentioned. 
 When the detritus and the cells are absorbed the walls of 
 the abscess may simply heal together or the cavity may 
 become partially or totally filled up with new-formed, (of 
 course only translucent) connective-tissue. The blood-ves- 
 sels may become atrophic and disappear or remain persistent. 
 
 As a rule, however, the process does not heal at this stage. 
 More cells immigrate and are formed by proliferation of the 
 old ones in the original cavity and the adjoining tissue, and 
 thus more and more of the parenchyma, is destroyed. It 
 may thus happen that the destruction of the tissue reaches 
 to the outer surface — that is, a deep ulcer may be formed. 
 In rare cases, when the abscess lies directly next to Desce- 
 mefs membrane, this may also be destroyed, and the abscess 
 thus opens into the anterior chamber, which may lead to 
 the formation of an anterior synechia, when the abscess lies 
 near the corneo-scleral margin. Moreover, the abscess can 
 lead to a total perforation of the cornea and open at the 
 same time upon the anterior and posterior surface of this 
 membrane. 
 
 If the abscess does not perforate either Bowmafi s Id^y^r or 
 Descemefs membrane, and its contents are not readily ab- 
 sorbed, the cavity may still be found after all the inflam- 
 matory symptoms have disappeared. It may then appear as 
 a cystoid formation in the cornea. (See Fig. 4.) 
 
 Corneal abscess is very frequently accompanied by the 
 formation of pus in the anterior chamber, which is called
 
 i8 
 
 THE HUMAN EYE. 
 
 hypopyon. There are three ways in which the formation of 
 hypopyon may take place. Since the corneal canals, as we 
 have seen above, communicate directly in the ligamentum 
 
 Fig. 4.— Cavity of an abscess in the cornea, after the contents have been perfectly absorbed. 
 
 pectinatum (through Fontanels canals) with the contents of 
 the anterior chamber, the cells may wander into the latter 
 through the former ; and this is probably the most common 
 way in which, the formation of hypopyon occurs. Fur- 
 thermore, if the abscess lies near Descemefs membrane the 
 structure of this membrane, becomes pathologically changed. 
 It becomes dim, and often two and three times thicker than 
 in the normal condition. This change is soon followed by 
 alterations in the endothelial layer. Its cells grow larger and 
 
 begin to proliferate, 
 
 and the new-formed 
 more or less roundish 
 cells lie at first in lit- 
 tle clusters on the 
 posterior surface of 
 Descemei' s membrane. 
 
 Fig. 5. — Shows proliferation of the endothelium of Des- Later Oil thev beCOmC 
 cemefs membrane, in a case of corneal abscess 1 r 11 
 
 with hypopyon. detachcd and fall to 
 
 the bottom of the anterior chamber. (See Fig. 5). If the 
 abscess lies near the corneo-scleral margin, the iris and ciliary 
 body frequently become inflamed also, and the inflammation 
 of these parts is then the third means of the formation of pus
 
 CORNEA. 
 
 19 
 
 in the anterior chamber. Hypopyon thus formed contains, 
 as a rule, some fibrinous matter. 
 
 If the abscess leads to the formation of an ulcer or to 
 total perforation of the cornea, it is the final cause of more 
 serious results, of which we shall have to speak later on. 
 
 b. Ulcer of the Cornea. 
 
 Every loss of substance of the cornea, caused by purulent 
 inflammation, and reaching to the surface, is an ulcer, whether 
 the pathological process began originally on the surface itself, 
 or involved at first the deeper layers only, and attacked the 
 superficial ones at a later period. 
 
 The process of ulceration begins, as a rule, from the sur- 
 face of the cornea, although, as just mentioned, it may also 
 begin in the deeper layers. We mostly find at first an infil- 
 
 FiG. 6. — Ulcer ofthe cornea ; its ground and walls lined with round-cells, the surrounding 
 epithelium proliferating. 
 
 tration of the lamellae lying next to Bowman'' s layer. The 
 number of cells is rapidly increased, and Bowman s layer as 
 well as the epithelium are raised, and the latter begins to 
 decay. The destruction is generally first noticed in its most 
 superficial layers, and only gradually takes up the remaining 
 ones. Meanwhile the attacked lamellse and finally Bowman's 
 layer also become destroyed, a4;id thus an ulcer is formed. 
 Its base is covered with pus, its walls are ragged, and the 
 adjoining corneal tissue is filled with a large number of round 
 cells, which decrease nearer the periphery of the cornea.
 
 20 TTTE HUMAN E YE. 
 
 The epithelium surrounding the ulcer is also in a pathologi- 
 cal condition. It becomes very much thickened in conse- 
 quence of the proliferation of its cells, especially in its middle 
 layers. The new-formed cells are nearly all serrated ones. 
 In some specimens I found the proliferation going on also in 
 the flattened (superficial) cells and in the basal layer. (See 
 Fig. 6.) 
 
 The conditions are entirely the same when the ulcer is 
 the result of a previous abscess of the cornea. 
 
 In this stage the process may stop and the ulcer heal. 
 If it progresses, the parts surrounding it become more and 
 more infiltrated and also destroyed, in the manner described 
 above. 
 
 A strange change takes place in the direction of the 
 lamellae, which form the base and walls of the ulcer. They 
 become bent towards the surface at an angle of about forty- 
 five degrees. This is probably the result of mechanical in- 
 fluences. 
 
 If the ulcer no longer progresses, its bottom cleanses 
 itself and its margins lose their ragged appearance. At the 
 same time, if the ulcer is not entirely superficial, a new-for- 
 mation of blood-vessels from the cornea-scleral margin takes 
 place, as has been previously described. It seems that in 
 these cases new vessels lie, as a rule, in the more superficial 
 layers of the cornea. Otherwise they differ in no way from 
 the new-formed blood-vessels we found during the healing 
 process of an abscess. 
 
 The third stage of the disease, the reparation of the loss 
 of substance, is ushered in by a marked proliferation of the 
 epithelium, which sometimes very rapidly grows over the 
 whole area of the ulcer. I am not certain whether one 
 special layer of the epithelium is the active one in this pro- 
 cess, but it seems to me that all the layers take an active 
 part in it. The new-formed epithelial cells vary greatly in 
 shape and size; they are mostly roundish, sometimes cylinder 
 and spindle-shaped. , 
 
 As soon as the epithelium begins to grow, a new and at 
 first very delicate connective-tissue, which is filled with a 
 great number of cells, is formed upon the ulcer. The epi-
 
 CORNEA. 
 
 21 
 
 thelium, however, always covers the loss of substance before 
 the new-formed tissue has reached the level of the surface of 
 the cornea. 
 
 This new-formed tissue afterwards becomes much denser 
 and tougher. Since Bowman s layer is never regenerated as 
 such, the epithelium is no longer supported in the normal 
 way, and grows into the new-formed connective-tissue in the 
 shape of papillae of different size. (See Fig. 7.) The margins 
 of Bowmajts layer around the original loss of substance are 
 generally bent inward, and the new-formed tissue lies often 
 on their outer surface, without, however, producing a thick- 
 ening of the cornea. When the new-formed tissue is per- 
 fectly dense it appears somewhat lamellar, like the normal 
 
 Fig. 7. — Healed corneal ulcer. The loss of substance filled with new-formed connective- 
 tissue into which the epithelial layer sends papillary offsets. 
 
 corneal tissue. The lamellse are, however, much smaller than 
 the normal ones, and are not arranged as regularly as these, 
 but intersect each other at obtuse angles. The fascicles 
 which form the new lamellae are also much smaller, and show, 
 even a long time after the healing process has been com- 
 pleted, a much larger amount of cellular elements than the 
 normal surrounding corneal tissue. The new-formed blood- 
 vessels disappear, as a rule, or they may remain persistent. 
 
 The new-formed tissue is, as is well known, only trans- 
 lucent, and, although it generally clears up somewhat when 
 the process of reparation is over, it never becomes trans- 
 parent. 
 
 If the progress of the ulcer does not stop in the way we
 
 22 THE HUMAN E YE. 
 
 just described, it destroys more and more of the corneal tissue, 
 and finally leads to perforation of Descemefs membrane. 
 Before this membrane is perforated, however, it is generally 
 pressed forward and protrudes towards the surface of the 
 cornea, a condition which has been called myocephalon or 
 keratocele. This protrusion of Descemefs membrane may be 
 caused by the normal intra-ocular pressure ; but it is, how- 
 ever, usually increased. 
 
 If Descemefs membrane be thus perforated, the aqueous 
 humor flows off, and the iris may become either simply at- 
 tached to the cornea or prolapse into the wound-canal, which 
 conditions we shall have to describe more fully later on. 
 
 With the microscope we are always able to detect a 
 former ulcer by the following conditions : the irregular thick- 
 ness of the epithelial layer, the partial absence of BoivmarCs 
 layer, and the translucent, irregularly lamellated scar-tissue, 
 with its abnormal number of cellular elements. 
 
 Sometimes we find srhall particles of metallic substances 
 in this scar-tissue, which have been brought there by the use 
 of metallic collyriums. Saeinisch also found cavities filled 
 with colloid substance. 
 
 xA.ll the different forms of ulcers, as distinguished by cHni- 
 cists, show these same histological conditions. The parasites, 
 which in recent times have been considered of great impor- 
 tance in the formation of every disease, have, of course, also 
 been found in the cornea. I have never been able to con- 
 sider them as the important agents they are thought to be 
 by others, at least in diseases of the eye. 
 
 y. Keratomalacia. 
 
 It is the characteristic feature of keratomalacia, that the 
 deleterious new-formation of cells concerns and destroys the 
 whole of the corneal tissue. 
 
 In all other points this process is the same as has just 
 been described. The whole of the corneal tissue becomes 
 mortified and is thrown off. The ensuing loss of substance 
 is repaired through tissue growing from the surrounding con- 
 junctiva and episclera. When the loss is thus perfectly re- 
 paired by the newly-formed connective-tissue, we find what
 
 CORNEA. 
 
 23 
 
 has been styled by clinicists phthisis anterior, namely, a 
 grayish, translucent connective-tissue in the place of the 
 cornea, which is either flat or, as often happens in a later stage 
 through morbid changes in the interior of the eyeball, drawn 
 inward. 
 
 Although it is not out of place to consider abscess, ulcer 
 and keratomalacia as three different and distinct types of 
 inflammation of the corneal tissue, I will here again state 
 that from an abscess an ulcer may originate, and that kerato- 
 malacia may as well be the result of an abscess as of an ulcer. 
 
 In all of these inflammatory processes of the corneal tis- 
 sue the conjunctiva and episclera are more or less altered. 
 The purulent form of keratitis often cause inflammatory pro- 
 cesses in the tissue of the iris sometimes of the whole uveal 
 tract, and in a small number of cases causes panophthalmitis. 
 
 The Results of Keratitis. 
 
 a. Formation of Scars and Panniis. 
 
 Losses of substance, which concern only the epithelial 
 layer, and leave the substantia propria of the cornea intact, 
 usually heal, without leaving a trace. If, however, the 
 smallest particle of the corneal tissue itself is destroyed, 
 scar-tissue is formed to repair the loss. This newly-formed 
 tissue is only translucent, and according to the degree in 
 which it lacks transparency, we call it clinically nebecula, 
 macula or leuconia of the cornea. It is evident from this 
 that as a rule only the purulent forms of keratitis will pro- 
 duce persistent alterations in the corneal tissue. 
 
 As above stated infiltration keratitis may lead to sclerosis 
 of the cornea, and this is mostly the case when infiltra- 
 tion lies near to or at the corneo-scleral margin. This 
 sclerosis has erroneously been called interstitial keratitis. As 
 already stated, the sclerosis is caused by the new-formation of 
 connective-tissue between the normal lamellae of the sub- 
 stantia propria of the cornea, which obliterates the corneal 
 canals, which by retracting reduces the quantity of fluid
 
 24 
 
 THE HUMAN E YE. 
 
 in the tissue of the lamellae and produces atrophy. This 
 new-formed tissue is formed from the fixed and wandering 
 corneal cells, and the sclerosed tissue, furthermore, is dis- 
 tinguished from scar-tissue by its want of cellular elements. 
 
 Nebecula, macula and leucoma are clinical names for 
 the same histological condition, namely, scar-formation in 
 the tissue of the cornea. The way in which these scars are 
 formed has been described above under the head of Purulent 
 Keratitis. Besides the cavities filled with colloid and metal- 
 lic deposits which were mentioned at the same place, deposits 
 of lime are not infrequently found in such scars, and they 
 consist of granules which are round or shell-like. (See Fig. 8.) 
 
 Fig. 8.— Deposits of lime in the cornea of a staphylomatous eye. 
 
 They lie mostly in the anterior parts of the cornea, directly 
 under the epithelium, and I think they begin in the blood- 
 vessels, whose ramifications are often beautifully shown by 
 these deposits. It is not improbable that ossification of the 
 cornea described by Stellwag was in reality nothing but such 
 deposits of lime. 
 
 In phthisis anterior and large scars of the cornea the epi- 
 thelium is often very much altered. It is found mostly horny 
 or in a state of colloid metamorphosis. 
 
 Here we should mention, what is called a facette. Al- 
 though I never had the occasion to examine a facette mi- 
 croscopically, it may be deduced from clinical observation 
 that in such cases the loss of substance is covered by epithe- 
 lium only, without the new-formation of connective-tissue. 
 The peculiarity of a facette is therefore that the loss of sub-
 
 CORNEA. 
 
 25 
 
 Stance is in reality never filled up again, although covered 
 with epithelium, and this is why it hardly ever shows any 
 dimness. 
 
 The formation of what is called pannus of the cornea has 
 been spoken of before. I have here only to mention the 
 conditions of persisting pannus. In pannous corneae we 
 find large blood-vessels with a well-developed adventitia 
 and capillary blood-vessels. It is always easy to trace their 
 origin back to the vessels of the corneo-scleral margin. 
 Where they lie in normal corneal tissue they appear sur- 
 rounded by a new-formed tissue, which when young is fine 
 and cellular, and later on becomes tough and bare of cells. 
 This tissue causes the dimness of the cornea which always 
 accompanies the pannus. Small hemorrhages are not rare 
 in this tissue, and may be found also in vascular scar-tissue. 
 
 As has been stated above. Bowman's layer, when once 
 destroyed, is never regenerated ; the same holds good for 
 Descemef s membrane. The latter is, however, never de- 
 stroyed to the same extent as the former, and, if the 
 cornea has been perforated upon its outer or inner surface, 
 Descemefs membrane, is always found drawn into the canal 
 of the perforation, and adhere it to its walls. 
 
 b. Anterior Synechicz, 
 
 Anterior synechias are very frequently the result of puru- 
 lent keratitis, when the latter has led to perforation. The 
 name anterior synechise is usually applied only to the adhe- 
 sions of the iris to the cornea ; there are, however, as well 
 anterior synechiae of the crystalline lens, or, if the lens is 
 wanting, of the vitreous body. 
 
 In anterior synechia of the iris, this membrane may 
 simply adhere with its anterior surface to the posterior sur- 
 face of the cornea, or the iris may have been drawn more or 
 less far into the canal of the perforation, and having grown 
 together with the corneal tissue may there be incarcerated. 
 If the anterior surface of the iris only is adherent to the pos- 
 terior surface of the cornea, this adhesion need not necessarily 
 have taken place at the site of the perforation, but may
 
 26 
 
 THE HUMAN EYE. 
 
 also He in the neighborhood of the latter. The endothelium 
 of Descemefs membrane and the anterior surface of the iris 
 are always wanting- in these places, and is replaced by a 
 small layer of tissue, consisting of long delicate spindle- 
 shaped cells, which are transformed endothelial cells. That 
 this is really the case is readily proven in specimens where 
 the adhesion has only partly been accomplished. The 
 endothelial cells then are seen to be partly enlarged, or to 
 have one or two offsets, while others are already spindle- 
 
 FiG. q.— A nterior synechia between cornea and iris. The endothelium of Descemet's mem- 
 brane forming a layer of spindle-shaped cells around the place where iris and cornea 
 are united. 
 
 shaped. Sometimes these endothelial cells are also found to 
 undergo a regressive metamorphosis, and colloid degenera- 
 tion is comparatively the most frequent one. 
 
 If the iris has been drawn into the canal of the perfora- 
 tion and there become adherent, it is after some time impos- 
 sible to make out the exact line where the tissue of the iris 
 is united to that of the cornea, as they coalesce perfectly. 
 (See Fig. 9.) The pigmented cells of the parenchyma of the 
 iris and the blood-vessels of the latter grow into the cornea,
 
 CORNEA. 
 
 27 
 
 and minute particles of pigment, freed by the destruction of 
 tlie cells, are seen to be thrown some distance into the neigh- 
 boring corneal tissue, and there remain stationary. In the 
 beginning of this process cornea and iris are full of lymphatic 
 cells, which later on disappear. 
 
 Desceniefs membrane is in these cases generally drawn 
 with the iris into the canal of the perforation, and sometimes 
 its ends are bent inward upon the iris. In the first case the 
 endothelial cells help in the formation of the scar-tissue, and 
 can no longer be distinguished. In the second case the en- 
 dothelial cells are found transformed into spindle-cells, as 
 described above, and they form a small layer of delicate 
 tissue in the angles, where Descemefs membrane is bent 
 backward upon the iris and upon the latter. 
 
 The two different kinds of anterior synechia of the iris, viz., 
 simple adhesion and incarceration, are found in all parts of the 
 cornea. Their histological conditions are always the same. 
 
 Anterior synechiae between the crystalline lens and cornea 
 are very much rarer. They are generally combined with an- 
 terior synechia of the iris, or in rare cases seen without the 
 former. They are furthermore mostly found in eyes suffering 
 from staphyloma of the cornea. In all of the cases which I 
 had occasion to examine, the crystalline lens was cataractous. 
 Sometimes the anterior capsule of the crystalline lens was 
 simply adherent to the inner orifice of the canal of a perfora- 
 tion, without being ruptured ; sometimes the capsule was 
 ruptured, and new-formed connective-tissue had grown into 
 it. O. Becker states that in cases of anterior polar cataract, 
 we have a right to diagnose an intra-uterine perforation of 
 the cornea with anterior synechia of the crystalline lens. 
 
 Although it is probable that anterior synechiae between 
 the vitreous body and the cornea, especially in eyes from 
 which the crystalline lens has been removed by an operation 
 or an injury, are more frequent than we know of, I only once 
 had an opportunity to examine such a specimen. (See 
 Fig. 10.) 
 
 The specimen is taken from an eye enucleated on account 
 of ciliary staphyloma. The following are the histoolgical 
 conditions.
 
 28 THE HUMAN EYE. 
 
 Nearly in the centre of the cornea the above described 
 results of ulceration and perforation are to be seen. The 
 crystalline lens is wanting. The vitreous body is healed in 
 
 Fig. io. — Anterior synechia between cornea and vitreous body. 
 
 the form of a cone into the scar-tissue of the cornea. It is 
 here transformed into connective-tissue and perfectly coa- 
 lesces with the corneal scar. The wound-lips of Descejnefs 
 membrane lie upon the iris, and can be traced farther back- 
 ward than would be possible if they had simply been bent 
 backward. A new-formation of vitreous substance must 
 therefore have taken place. The surface of the conical pro- 
 lapse of the vitreous body has a network of delicate fibrills, 
 in the meshes of which a number of oval and bean-like cells 
 with an oval and finely granulated nucleus are embedded. 
 The cells of this network pass gradually over into the en- 
 dothelial cells oi Descemefs membrane, and are probably de- 
 rived from them. The posterior part of the vitreous body is 
 liquefied. (Similar pictures are drawn, {o\ instance, in Iwan- 
 off's experiments on the detachment of the vitreous body.) 
 
 Anterior synechiae of the iris and vitreous body are of 
 course very apt to cause chronic inflammation of the in- 
 volved parts, which are continuously dragged upon in the act 
 of accommodation. The anterior synechiae of the crystalline 
 lens can have the same effect by continuous pressure upon 
 the iris. These conditions are therefore very frequently the 
 origin of the perfect destruction of the so diseased eye, and 
 of sympathetic affection of its fellow. 
 
 Anterior synechiae of the iris are moreover sometimes the
 
 CORNEA. 29 
 
 origin of the so-called cysts of the iris, which will be treated 
 of later on. 
 
 c. Prolapsus iridis and granuloma iridis traumaticum. 
 These will be spoken of in Chapter IV. 
 
 d. Keratoconus e cicatrice and staphyloma cornece. 
 
 Since purulent keratitis, as has been above stated, mostly 
 produces irritation or even inflammation of the uveal tract, 
 it is often combined with an increase of intra-ocular pres- 
 sure. The new-formed scar-tissue is therefore (the more so 
 as the supporting layer of Bowman is wanting) frequently not 
 strong enough to retain the normal curvature of the cornea. 
 
 If the scar lies in or very near the centre of the cornea, 
 and there is no anterior synechia, the intra-ocular pressure 
 may stretch the tissues more symmetrically, and thus pro- 
 duce a conical cornea (keratoconus.) (Keratoconus, which 
 is sometimes seen as an humory malformation and without a 
 scar of the cornea, does not belong here.) We find in these 
 cases at a later period the radius of the whole cornea consid- 
 erably shortened and the cornea, especially the central scar 
 and Descemefs membrane, which is mostly unruptured, very 
 much thinned. If the keratoconus is so large that the lids 
 can no longer perfectly cover its apex, the epithelial layer 
 upon it is often transformed into horny scales. 
 
 This conical stretching of the cornea may become sta- 
 tionary at any time ; it can, however, also progress until 
 it leads to a spontaneous rupture of the eye and subsequent 
 phthisis, with its dangerous consequences. 
 
 If the cornea has been perforated and a partial or total 
 anterior synechia of the iris or a synechia between iris, crys- 
 talline lens and cornea has been the result, the intra-ocular 
 pressure frequently causes the formation of a partial or total 
 staphyloma of the cornea. The name staphyloma of the 
 cornea can therefore only be applied to those cases where 
 the iris at least is adherent to the stretched and bulging scar- 
 tissue of the cornea — that is, where an adherent leucoma 
 yields to the intra-ocular pressure. We find, therefore, in 
 these cases not only the corneal scar, but also the iris, unduly
 
 30 
 
 THE HUMAN EYE. 
 
 Stretched. The latter membrane often becomes so atrophic 
 that it is represented only by a thin layer of pigment upon 
 the posterior surface of the cornea. The cornea is mostly 
 attenuated in the same way as into keratoconus and atrophic ; 
 in rare cases, however, hypertrophic, and even sometimes to 
 a high degree. (See Fig. ii.) Manz stated that he found 
 
 Fig. II. — Staphyloma of the cornea, with hypertrophy of the latter. 
 
 in cases of staphyloma of the cornea an abnormally large 
 number of serrated epithelial cells. From what has been 
 stated above, it is evident that this condition is not peculiar 
 to staphyloma only. If the staphyloma is so large that the 
 lids can no longer cover it, its epithelial layer is often found 
 horny or in colloid metamophosis. Deposits of phosphate 
 of lime are not very rare in such staphylomatous corneae. 
 
 e. Pterygitan. 
 
 The formation of pterygium of the conjunctiva may be 
 caused by a marginal ulcer of the cornea. This happens in 
 the following way. The marginal ulcer causes infiltration 
 and swelling of the adjacent parts of the conjunctiva, a fold 
 of which comes into contact with the corneal ulcer, and grad- 
 ually becomes adherent to its walls and bottom. That this 
 may be really the case was proven in a case which I have 
 described elsewhere, by the fact that Bowman s layer was 
 severed from the periphery of the corneal tissue and bent 
 backward upon itself. Furthermore, I found the conjunc-
 
 CORNEA. 
 
 31 
 
 tival epithelium incarcerated between the conjunctival tissue 
 of the pterygium and the ground of the corneal ulcer, and in a 
 state of colloid degeneration. The whole of the tissue of the 
 pterygium, which grows like a wedge into the corneal tissue, 
 is merely unaltered conjunctiva, and we shall therefore have 
 more to say upon this subject in the chapter treating on this 
 membrane, the more so, since pterygium is not always caused 
 by a marginal ulcer of the cornea. (See Figs. 12 and 13.) 
 
 Fig, 12 —Section through a pterygium in a meridional direction. Pt. Pterygium. A. Cor- 
 neal lamellx raised by the pterygium. B. Bowman's layer. C. Normal corneal lamellae. 
 
 B. Injuries to the Cornea, their Mode of Healing 
 
 AND THEIR RESULTS. 
 
 a. Injuries without the retention of a foreign body. 
 
 Injuries of the cornea which entail a loss of substance of 
 this membrane, always lead to the formation of an ulcer, if 
 ever so small, and heal in the same manner. They fall there- 
 fore under the head of purulent keratitis. They are rents or 
 scratches, and such injuries by which a segment is cut off from 
 the surface of the cornea. The conditions are different when
 
 32 
 
 THE HUMAN E YE. 
 
 the cut is linear or an instrument has been thrust through 
 the cornea and only severed the continuity of the tissue, 
 without causing a loss of substance. 
 
 Let us first examine those conditions which are found when 
 an uncomplicated cut has been inflicted upon the cornea. This 
 
 ft .. 
 
 S 
 
 Fig. 13. — Equatorial section through a pterygium. Pt. Pterygium. S. Sclerotic (corneo- 
 scleral margin). E. Encapsuled conjunctival epithelium undergoing regressive meta- 
 morphoses. 
 
 cut may involve only a part of the cornea or perforate its whole 
 thickness, the healing process will be essentially the same. 
 
 As soon as three hours after the cornea has thus been cut, 
 the lips of the wound may be found infiltrated with round- 
 cells (cl. Infiltration of cornea.) These cells can only be immi- 
 grated ones, and cannot as yet be considered as resulting from 
 a proliferation of the fixed corneal cells. Very soon after- 
 wards (in eight or ten hours) a fibrinous substance is exuded 
 into the canal of the wound, which is soon also invaded by 
 the round-cells. The epithelium margin of Bozvman s layer 
 and they very soon after the injury has been inflicted, appear 
 bent inward, and two or three days afterward the epithelial 
 cells are seen to proliferate into the wound-canal. It seems 
 that the new epithelial cells take their origin from the 
 basal layer and the serrated cells ; they lack, however, the
 
 CORNEA. 
 
 33 
 
 typical shape. (See Fig. 14.) While this proliferation of 
 the epithelial cells takes place, the fibrinous exudation 
 in the wound-canal is transformed into connective-tissue, 
 which at first is very delicate and filled with Cells, and later 
 on becomes denser and denser, and loses the numerous cells 
 
 Fig. 14. — A healing corneal wound four days after it was inflicted. 
 
 accordingly. At this period of the healing process the 
 epithelium generally fills the outer third of the wound- 
 canal. If the wound has pierced the whole thickness of the 
 cornea, the wound-lips o{ Descemef s membrane are, as a rule, 
 at first projecting into the anterior chamber in consequence 
 of the pressure exerted upon them by the fibrinous ex- 
 udation. This condition, although declared to be final by 
 Becker, is, however, not stationary. As soon as the new- 
 formed scar-tissue begins to shrink, the lips of the wound of 
 Descemefs membrane are dragged into the wound-canal. 
 This condition remains stationary, and the wound-lips of this 
 membrane are never reunited. The endothelial cells cover- 
 ing them begin also very frequently to proliferate, and then 
 take part in the formation of the scar-tissue. 
 
 When the scar-tissue thus formed becomes dense and 
 consolidated, the epithelial cells which had entered the 
 wound- canal partly disappear again, and we then find only a 
 small offset dipping through Bowman s membrane into the 
 corneal parenchyma in the shape of an epithelial papilla. 
 Sometimes the proliferation of epithelial cells is so considera-
 
 34 
 
 THE HUMAN EYE. 
 
 ble that secondary cylinders are seen to start from this pri- 
 mary papilla and grow into the adjacent parts of the corneal 
 tissue, just as we shall later on find it when we treat of the 
 epitheliomatous growths of the cornea. These secondary 
 cylinders, however, never remain stationary, and have always 
 disappeared when the scar is perfectly consolidated. 
 
 Every uncomplicated wound of the cornea (which does 
 not cause the formation of an ulcer) heals in the way just de- 
 scribed, and the histological conditions are so typical that we 
 can never err in the diagnosis. 
 
 From these facts, gleaned from the study of the healing 
 process of corneal wounds, it is quite possible to explain the 
 way in which a corneal fistula may be formed. I have never 
 had the occasion to examine such a fistula. But, if we as- 
 sume that the epithelium may grow through the whole of 
 the wound-canal, or that the fibrinous exudation is by some 
 cause or other not transformed into connective-tissue, we 
 easily understand that the intra-ocular pressure, especially 
 if it is somewhat increased, can re-open the canal. Corneal 
 fistulae are, as a rule, temporarily closed, until the anterior 
 chamber is refilled and the intra-ocular pressure reestablished, 
 when the fistule is again opened. It is true, a corneal fistula 
 is very rarely, if ever, observed after a wound, but is generally 
 the result of an ulcer which has led to perforation of the cor- 
 nea. The ulcers in these cases are, however, as a rule, so 
 small that their healing process is probably not greatly at 
 variance with the one after a perforating wound. 
 
 Wounds which lie in the corneo-scleral border heal some- 
 what differently, especially when accompanied by prolapse 
 of the iris. In the latter case the conditions greatly or alto- 
 gether resemble those found after purulent keratitis with sub- 
 sequent anterior synechia of the iris, and need not be dwelled 
 upon again here. 
 
 Corneo-scleral wounds generally gape more than those in 
 the centre do, and therefore the fibrinous exudation found 
 between the wound-lips is generally larger, and the healing 
 process is therefore more protracted. The fibrine, more- 
 over, generally protudes over the outer surface of the cornea, 
 and the epithelium here rarely grows into the wound-canal.
 
 CORNEA. 
 
 35 
 
 The epithelial cover for the new-formed scar-tissue is two- 
 thirds derived from the conjunctival epithelium. Since these 
 wounds lie close to, or even sever the marginal blood-vessels 
 of the cornea, new blood-vessels are, as a rule, formed during 
 the healing process. Striped keratitis, which mostly accom- 
 panies the healing of such corneo-scleral wounds, has been 
 more extensively treated of under the head of Infiltration- 
 Keratitis. 
 
 Corneo-scleral wounds are most frequently caused by 
 operations, especially iridectomy. When examining such 
 eyes we find, nearly invariably, some part of the iris incar- 
 cerated in the wound. The cause of this fact is certainly 
 that the stump of the iris is comparatively too long or the 
 corneo-scleral wound lies too peripheric in comparison with 
 the length of the iris-stump. (See Fig. 15.) If the stump 
 of the iris, for instance, were as long 
 as S in Fig. 15, and the corneo-scleral 
 section lay in A, an incarceration of the 
 former in the latter would be nearly 
 impossible, while if the section lay 
 in B, the stump could very easily 
 be thrown between the inner lips of 
 the section and there become retained. 
 
 In other cases not the stump but 
 neighboring parts of the iris become 
 incarcerated. It will be hardly possi- 
 ble to evade this ; but it might be ren- 
 dered less frequent by making the 
 corneal section no larger than the F'«- 's.-stump of iris after in- 
 
 *-" dectomy. Mode in whicti it be- 
 
 COloboma of the iris. comes entangled in the corneal 
 
 These incarcerations of the iris are 
 frequently the cause of the formation of a kind of partial 
 staphyloma, which is generally described as cystoid or ectatic 
 scar. 
 
 In all of these cases we find pigment-molecules in the 
 corneal canals adjoining the section. Sometimes also in- 
 tact living pigmented cells from the iris wander into the 
 cornea, and are there retained. These may, later on, pro- 
 liferate and lead to the formation of a corneal cyst, which
 
 36 
 
 THE HUMAN E YE. 
 
 is lined by an irregular layer of pigmented endothelial cells 
 and filled with a serum-like fluid. (Fig i6.) 
 
 It has been stated above that complicated corneal and 
 corneo-scleral wounds may produce the same effects as pur- 
 
 FiG. i6. — Pigmented cystoid formation in the cornea. 
 
 ulent keratitis. We must therefore also enumerate them 
 among the factors which may lead to total destruction of the 
 affected and sympathetic affections of the other eye. 
 
 In rare cases corneal wounds, instead of healing by sim- 
 ple infiltration, produce an excessive proliferation of cells, 
 and finally necrosis of the lips of the wound. The conditions 
 are then the same as in keratomalacia. 
 
 b. Wounds ivith the Retention of a Foreign Body. 
 
 A foreign body, if retained in the cornea after having 
 wounded it, always produces, unless it be minutely small, a 
 more or less circumscribed purulent keratitis, and is cast 
 off with the pus. 
 
 Very small particles of metal only, and sometimes lime- 
 salts, are permanently retained in the cornea. They are, 
 however, mostly brought there by the use of eye-washes 
 after the infliction of injury, and do not cause it. 
 
 Besides these inorganic foreign bodies, organic ones ate 
 sometimes thrust into the cornea when the wound is in- 
 flicted (or during ulcerative processes), and it seems that 
 they are retained without producing a lasting inflammatory
 
 CORNEA. 
 
 37 
 
 reaction. Among them are the particles of pigment and pig- 
 mented cells, as above mentioned, parts of Descemefs mem- 
 brane, or the capsule of the crystalline lens and ciliae. The 
 latter are always embedded in scar-tissue. The ciliae are 
 generally found to be surrounded by a layer of epitheloid or 
 typical epithelial cells. (See Fig. 17.) 
 
 Fio. 17.— Eye-lash embedded in scar-tissue witliin the cornea, and surrounded by epitheli- 
 oid cells. C. Eye-lash. 
 
 c. Burns with Lime. 
 
 Among the injuries inflicted upon the cornea, burns with 
 lime are not very rare. Gouvia made a number of experi- 
 ments to study their exact conditions. According to his 
 statements, the epithelial cells and the adjoining lamellae of 
 the cornea become perfectly infiltrated with lime, and thus 
 become necrotic. They are then thrown off by a circum- 
 scribed purulent keratitis, and the healing process is the same 
 as after this affection. 
 
 Such burns of the cornea are very frequently combined 
 with similar injuries to some part of the conjunctiva, especially 
 that of the lids. Since the conjunctival ulcer in such cases 
 generally lies just opposite to the corneal ulcer, the two 
 surfaces frequently heal together. This condition is called
 
 38 
 
 THE HUMAN EYE. 
 
 symblepharon, if only a part of the conjunctiva and cornea 
 are united. Extensive burns may cause the whole of the 
 conjunctival surface of the eye-lids to become united with 
 the eye-ball, which condition has received the name of an- 
 chyloblepharon. 
 
 C. Regresssive Metamorphoses. 
 
 The regressive metamorphoses which are observed in the 
 cornea (besides those found in scar-formations) are xerosis 
 cornese and arcus senilis. 
 
 Xerosis corneae is the result of insufficient moistening of 
 the corneal epithelium, and is caused by conjunctival diseases 
 or a protrusion of the eye-ball of such a degree that the lids 
 cannot cover it. The epithelium becomes irregular in appear- 
 ance and grayish, and under the microscope is found to be 
 horny and dying. This metamorphosis may even reach the 
 basal layer of the epithelium. 
 
 Arcus senilis corneae, the marginal dimness of the cornea 
 which is found chiefly in old people, is caused by fatty de- 
 generation of the lamellae and fixed corneal cells, as His and 
 Canton have described. 
 
 D. Tumors of the Cornea. 
 
 Although a large number of so-called tumors have been 
 described in literature, I know of no real corneal tumors, and 
 am forced to doubt the corneal origin of these tumors, the 
 more, since hardly any of them involved the corneal tissue 
 alone. So-called corneal tumors generally originate in the 
 episcleral tissue, and will be described more at length under 
 that head. 
 
 Among these tumors have been mentioned : papillomata, 
 dermoid, sarcomatous and cancroid tumors, fibromata, and 
 lately a granuloma of the cornea has been drawn by Pagen- 
 stecher and Genth, which I think must be considered as a 
 granuloma of the iris.
 
 II. 
 
 SCLEROTIC. 
 I. Normal Condi noNS. 
 
 The tissue of the sclerotic is fibrillar, like that of the cor- 
 nea. The fibrillae, however, are not so transparent. They are 
 united into fascicles, which interlace with each other without 
 the regularity and parallelism so characteristic of the cornea. 
 Here and there also elastic fibrillae may be found enclosed 
 in the fascicles. There are some more regularly arranged 
 fascicles in the anterior part of the sclerotic near ScJilemms 
 canal, and around the optic papilla, which run in an equa- 
 torial direction (circular fascicles). 
 
 The same cementing substance, we met with in the cornea, 
 unites the fibrillae of the sclerotic with each other into fas- 
 cicles, and these again with each other into layers. 
 
 Furthermore, we find similar lymphatic canals embedded 
 in the cementing substance of the sclerotic as we do in the 
 cornea. In consequence of the irregular arrangement of the 
 sclerotic fascicles it is, however, difficult to get as nice a view 
 of these canals as in the cornea. It is, however, possible and 
 my own researches support Waldeyer s statements on this 
 point, that parts of these canals can be seen by staining the 
 sclerotic carefully with nitrate of silver. The best specimens 
 are obtained from the parts of the sclerotic adjoining the 
 cornea. The sclerotic canals have, moreover, also lacunae, 
 containing fixed cells. The latter are identical with those of 
 the cornea in shape and situation. They are flat oval bodies, 
 with an oval nucleus, and have generally small offsets. By far 
 the most of these sclerotic cells are unpigmented. There are, 
 however, some pigmented ones to be found in every sclerotic 
 around the entrance of the optic nerve. In the eyes of the 
 white races they are but rarely found in the anterior portion 
 of the sclerotic near the corneo-scleral margin, while they are 
 never wanting in the eyes of the negroes.
 
 40 
 
 THE HUMAN E YE. 
 
 Besides the unpigmented and pigmented fixed cells, the 
 sclerotic also contains a comparatively small number of 
 wandering (lymphatic) cells, which are in no way different 
 from those found in other tissues. 
 
 The tendons of the external ocular muscles, and the ex- 
 ternal sheaths of the optic nerve insert themselves into the 
 sclerotic. The former reach this membrane at very acute 
 angles, and may be seen entering in the shape of a wedge, 
 Loewig states that the tendons of the recti muscles, after 
 having entered the sclerotic, form meridional (longitudinal) 
 fibres, while the oblique muscles are said by the same author 
 to form equatorial (circular) fibres. 
 
 The sheaths of the optic nerve, after coalescing with the 
 sclerotic, form part of the equatorial fibres which are found 
 nearly regularly around the entrance of the optic nerve in 
 this membrane. The lymphatic space, which is enclosed 
 between the sheaths of the optic nerve (intervaginal space), 
 is sometimes, especially in myopic eyes {Von Jaeger), found 
 to enter the sclerotic, severing it thus somewhat into two 
 layers. 
 
 Earlier authors unanimously described a large round hole 
 in the sclerotic, through which the optic nerve was said to 
 enter the eye-ball. Such a hole, however, does not exist. 
 The bundles of nerve fibres which constitute the optic nerve, 
 do not pierce the sclerotic in toto, but more or less separately, 
 so that, if the nerve-fibres could all be removed, the sclerotic 
 in this place would have the appearance of a sieve, which has 
 given to it the name of lamina cribrosa. 
 
 The inner surface of the sclerotic is covered with a layer 
 of thin flat endothelial cells, which are quadrangular or poly- 
 gonal. They may be easily brought to view by staining with 
 nitrate of silver. This endothelial layer is, however, not per- 
 fectly continuous, since it is pierced by a considerable number 
 of fibres, which unite the sclerotic with the choroid. Endo- 
 thelial cells are also found lying upon these fibres. 
 
 The exterior surface of the sclerotic is covered with the 
 loose episcleral tissue, the fibres of which enter and spring 
 from the sclerotic. Where this tissue surrounds Tennons 
 space it is covered with a very thin layer of endothelial cells.
 
 SCLEROTIC. 
 
 41 
 
 Anteriorly this episcleral tissue passes over into the conjunc- 
 tiva bulbi. 
 
 At the corneo-scleral margin the fibres and lymphatic 
 canals of the cornea go over into the fibres and canals of the 
 sclerotic. In transverse sections of this part of the eye-ball 
 we always find a number of vessels. Leber described them as 
 a venous plexus. Although I do not doubt the existence of 
 such a venous plexus, I must agree, on the other hand, with 
 Schwalbe and Waldeyer, who maintain the existence of the so- 
 called Schlemms canal, besides the venous plexus of Leber. 
 The latter is generally the largest of the vessels, and lies 
 nearest the inner surface of the sclerotic. It is lined with a 
 layer of endothelial cells, and the corneo-scleral fibres which 
 form its inner wall, are fenestrated in the manner above re- 
 ferred to. The anterior chamber and its endothelium are 
 therefore in more or less direct communication with ScJileniins 
 canal and its endothelial lining. While it is easy to fill the 
 venous plexus by injecting the blood-vessels with a colored 
 fluid, I was never able to inject ScJilemni s canal from this 
 side. It is, however, comparatively easy to fill it by injecting 
 a tinted fluid into the anterior chamber. I must further state, 
 with Waldeyer, that I never yet found blood, which is hardly 
 ever wanting in the vessels of the venous plexus, in this 
 vessel : 
 
 The blood-vessels of the sclerotic proper come from the 
 anterior and posterior ciliary arteries. Waldeyer states that 
 they are all surrounded by a sheath, called by him, " perithe- 
 lium-sheath." 
 
 The nerves of the sclerotic, according to Helfreich, are 
 arranged in a similar manner to those of the cornea. His 
 statement has not yet been confirmed by others. My own 
 researches, by staining the sclerotic with chloride of gold and 
 osmic acid, have not been successful. 
 
 The vorticous veins (4, 5 or 6) perforate the tissue of the 
 sclerotic at an acute angle, from before backwards. They are 
 surrounded by a lymphatic sheath, as are the ciliary arteries 
 and nerves, passing through the sclerotic, which opens into 
 the suprachoroidal space on one side and Tennons space on 
 the other side. The cilary nerves, while passing through
 
 42 THE HUMAN E YE. 
 
 their canals in the sclerotic, are frequently accompanied by 
 posterior ciliary arteries, which is of great importance in the 
 pathological processes observed in these organs. 
 
 2. Pathological Conditions 
 
 A. Scleritis and its Results. 
 
 Scleritis, like keratitis, is histologically characterized by a 
 larger number of round-cells, which may leave the fibres of 
 the sclerotic intact, and only separate them slightly from each 
 other, or may entirely destroy them. True, scleritis is, it 
 seems, never a primary disease, unless caused by an injury; 
 it seems to be always caused by an inflammatory process in 
 the neighboring tissues. There are two kinds of scleritis, 
 viz., infiltration-scleritis, and purulent-scleritis. The large 
 number of blood-vessels piercing the sclerotic are in such cases 
 of inflammation hyperaemic, and sometimes new blood-vessels 
 are seen to spring from them. Infiltration-scleritis is always 
 of a chronic character, and by aggravation may become puru- 
 lent. 
 
 a. hifiltratioti-Scleritis. 
 
 Infiltration-scleritis is always found in the parts of the 
 sclerotic which are pierced by blood-vessels. It affects the 
 fibres of the sclerotic comparatively little, if at all. The 
 primary diseases leading to it are corneal affections, iritis, 
 iridocyclitis, not purulent choroiditis, and intra-ocular new- 
 formations. From this it is evident, that we shall find infil- 
 tration-scleritis chiefly, or perhaps only, at the corneo-scleral 
 margin, and where the vasa vorticosa, the posterior and 
 anterior and ciliary arteries perforate the sclerotic. We then 
 find these blood-vessels in a state of hyperaemia, and fre- 
 quently, in higher degrees of inflammation, always new-formed 
 vessels starting from them and entering the tissue of the 
 sclerotic. The interstices between the fibres of this latter 
 membrane are filled with round-cells. I am, however, not 
 able to state whether these cells (like those found in the cornea 
 during keratitis) are immigrated as well as proliferated ones
 
 SCLEROTIC. 43 
 
 from the fixed scleral cells. It is certainly very probable that 
 they also come from both sources. Infiltration-scleritis gen- 
 erally involves the whole thickness of the sclerotic, and may 
 reach into the episcleral tissue. 
 
 When the primary disease heals, the scleritis generally 
 also disappears, without leaving a trace. In other cases, how- 
 ever, if the primary disease is of a very chronic kind, the 
 sclerotic begins to become stretched and atrophic (staphy- 
 loma), or a new-formation of connective-tissue takes place 
 between its fibres, which leads to an hypertrophic condition, 
 such as we find, for instance, in the sclerotic of phthisical eye- 
 balls. Wounds of the sclerotic also heal with the symptoms 
 of infiltration-scleritis. (See later on.) 
 
 b. Piirulcnt Scleritis. 
 
 The characteristic feature of purulent scleritis, is an abund- 
 ance of round-cells, which causes a rapid destruction of the 
 fibres of the sclerotic. This kind of scleritis also attacks by 
 preference the placet where the sclerotic is pierced by blood- 
 vessels and nerves. Purulent scleritis generally originates 
 from purulent affections of the uveal tract, and is one of the 
 symptoms of purulent panophthalmitis. It may also be 
 caused by foreign bodies. I have never had occasion to see 
 a genuine abscess such as we find in the cornea in the scler- 
 otic. Purulent panophthalmitis is sometimes incorrectly 
 called scleral abscess. 
 
 Since purulent scleritis is, as a rule, caused by purulent 
 affections of the uveal tract, it is not astonishing that it 
 chiefly (and often only) involves the inner layer of the scler- 
 otic. In consequence of circumscribed abscess-like cell-aggre- 
 gations in the choroid, which mostly perforate the lamina 
 vitrea and enter the vitreous body, a very small part of the 
 sclerotic may become ulcerated. In such a place the puru- 
 lent inflammation may then cause an excessive new-formation 
 of connective-tissue, which may grow through the choroid 
 and retina into the vitreous body. 
 
 The inflammation, however, does not always remain con- 
 fined only to such a circumscribed part, or to the inner layers 
 of the sclerotic, but the new-formation of cells, and with it
 
 44 
 
 THE HUMAN E YE. 
 
 necrosis of the sclerotic tissue, may progress, until this mem- 
 brane becomes perforated on its outer surface. Such perfora- 
 tions usually happen in the region of the equator of the 
 globe, where the vasa vorticosa pierce the sclerotic. 
 
 Although this kind of inflammation of the sclerotic is 
 generally chronic, it is in rare cases found to run its 
 course in a very acute manner. In these cases the new- 
 formation of cells is so excessive, that the destruction of the 
 fibres of the sclerotic cannot go hand in hand with it. Con- 
 sequently this membrane must become very much thick- 
 ened, and may, therefore, be mistaken for total staphyloma 
 of the sclerotic. 
 
 I had the opportunity to examine such an eye, which was 
 enucleated in a homoeopathic eye-hospital with the diagnosis 
 of total staphyloma of the sclerotic, and was shown to me as 
 a highly interesting and rare case of acute staphyloma with 
 hypertrophy of the sclerotic. It is true, to the naked eye 
 the sclerotic appeared to be about six times as thick as a 
 normal one. The microscope, however, revealed at once an 
 immense number of round-cells which lay between the fibres 
 of the sclerotic in the episcleral tissue, and pressed these 
 fibres, which were not as yet necrotic, far apart. 
 
 In case the sclerotic becomes perforated in a circumscribed 
 spot, the pus escapes on its outer surface, and choroid and 
 retina become adherent to the scar-tissue, which afterwards 
 closes the perforation. The result of such a perforation, with 
 subsequent synechia between sclerotic, choroid and retina, 
 may be staphyloma. 
 
 As was above stated, purulent scleritis is chiefly found 
 in the parts surrounding the blood-vessels and nerves which 
 pass through it ; and this inflammation may, too, become 
 the cause of sympathetic affections in the fellow-eye. 
 
 The Results of Scleritis. 
 a. Formation cf Scars. 
 
 Scars in the sclerotic are only found in consequence of 
 purulent scleritis. The conditions are then the same as when
 
 SCLERO TIC. 
 
 45 
 
 the sclerotic has been pierced by an injury, and will be treated 
 of under that head. 
 
 b. Prolapse and Incarceration of Iris, Ciliary Body, Choroid, 
 Retina, Crystalline Lens and Vitreous Body in the Sclerotic. 
 
 These conditions will also be spoken of in the chapter on 
 injuries of the sclerotic. 
 
 c. Hypertrophy of the Sclerotic. 
 
 A chronic inflammatory process of the whole eye-ball, 
 or of the uveal tract, frequently causes chronic infiltra- 
 tion-scleritis leading to new-formation of connective-tissue, 
 which produces a hypertrophic condition of the sclerotic. 
 From the fact that it is impossible at a later period of these 
 affections to find cellular elements in the hypertrophied con- 
 nective-tissue, and since, moreover, the lymphatic canals and 
 their lacunae are then more or less obliterated, we may with 
 some probability conclude that the fixed cells of the sclerotic 
 take an active part in the new-formation of this connective- 
 tissue. It is not impossible, however, that they are destroyed 
 only during the period of retraction of the new-formed tissue. 
 In spite of this retraction, the sclerotic sometimes remains 
 considerably thickened. This hypertrophic condition of the 
 sclerotic always precedes total phthisis of an eye-ball, and 
 the process leading to it begins, without exception, in the 
 posterior parts of the sclerotic, around the entrance of the 
 optic nerve. 
 
 The blood and lymphatic vessels become obliterated, and 
 this again results in grave disturbances in the nutrition of 
 the interior of the eye-ball. Later on, the hypertrophy pro- 
 gresses more and more towards the corneo-scleral margin, and 
 in the highest degrees of phthisis of the globe nearly the 
 whole of the sclerotic is equally thickened. It frequently 
 happens that while this is going on, inflammatory processes 
 in the interior of the globe, which produce shrinking, force 
 the sclerotic to fold itself. The episcleral tissue in such cases 
 is also nearly always inflamed, and takes an active part in 
 the new-formation of connective-tissue, and sometimes Ten- 
 nons space thus becomes perfectly obliterated.
 
 46 
 
 THE HUMAN EYE. 
 
 In examining two eyes which were enucleated in conse- 
 quence of gun-shot wounds, and were in the earher stages of 
 phthisis, I had an opportunity to find alterations in the pos- 
 terior ciliary blood-vessels within the sclerotic, which show 
 that these blood-vessels not only become obliterated by 
 pressure exerted upon them by the shrinking new-formed 
 connective-tissue, but that they may, moreover, take an active 
 part in this new-formation. I found the endothelium of these 
 vessels in a high degree of proliferation. Its cells were en- 
 larged and had several nuclei, and they filled the whole of the 
 lumen of each vessel so altered. In some of them I also 
 found giant-cells with from six to fifteen nuclei. While most 
 
 Fig. i8. — Blood-vessels of the sclerotic from a wounded eye in the process of phthisis bulbi. 
 A. Proliferation of the endothelial cells, i. Giant-cells. B. Transformation into con- 
 nective-tissue. 
 
 of the changed endothelial cells appeared round and vesicle- 
 like, some of them had one or two offsets, and passed gradu- 
 ally over into the spindle shape. (See Fig. i8.) 
 
 d. Atrophy of the Sclerotic and Ectasy {Staphyloma of the 
 
 Sclerotic). 
 
 Both kinds of scleritis (but especially infiltration scler- 
 itis) very frequently produce staphyloma of the sclerotic.
 
 SCLERO TIC. 
 
 47 
 
 The characteristic features of this affection are atrophy and 
 stretching of the scleral tissue. Although synechias between 
 the sclerotic and some part of the uveal tract are very fre- 
 quent in cases of such staphyloma, they are not always 
 found, and are therefore not essential. This atrophy and 
 ectasy may concern only a part of the sclerotic or the whole 
 of it. We have therefore a total and a partial staphyloma 
 sclerae. 
 
 Total staphyloma of the sclerotic is but seldom observed, 
 and then it forms only a part of the total ectasy of the eye- 
 ball. We find, in these eyes, an abnormal extenuation and 
 stretching of the sclerotic, which may occasionally be com- 
 bined with adhesions between this membrane and the uveal 
 tract. Even where such adhesions are wanting, the uveal 
 tract shows varying pathological alterations. All the blood- 
 vessels which either nourish the sclerotic or only pass through 
 it become, as a rule, obliterated. Also the nerves gradually 
 disappear, but generally much later than the blood-vessels. 
 
 Partial scleral staphyloma is of frequent occurrence, and 
 a characteristic feature of it is, that we nearly always find 
 an adhesion between the uveal tract and the bulging part of 
 the sclerotic. It may, of course, be found in any part of the 
 sclerotic. The following are the three kinds most frequently 
 observed. 
 
 I. Anterior Staphylo7na of the Sclerotic. 
 
 Concerns those parts of the sclerotic which lie in front 
 of the equator of the eye-ball. There are two varieties, 
 viz.^ corneo-scleral and ciliary staphyloma. 
 
 a. Corneo-Scleral Staphyloma {^formerly called Intercalar- 
 Staphylojna). 
 
 This form of staphyloma lies in the beginning just at the 
 corneo-scleral margin. In all such cases which I have ex- 
 amined, I found iritis or iridocyclitis either to be present, or 
 unmistakable signs that they had existed. The periphecal 
 parts of the iris are united to the corneo-scleral tissue by a 
 fine layer of newly-formed connective-tissue, which is formed
 
 48 
 
 THE HUMAN EYE. 
 
 by the proliferating endothelial cells of Desceniei's membrane 
 and the anterior surface of the iris. In consequence of this 
 adhesion of the anterior surface of the peripherical part of 
 the iris with the corneo-scleral tissue, Fontanas spaces become 
 obliterated. During the progress of the new-formation the 
 ligamentum pectinatum and the periphery of Descemefs 
 membrane are obliterated, and since the soft tissue of the 
 iris cannot replace the resistance which is lost with the dis- 
 appearance of Descemefs membrane, these parts become 
 gradually stretched and atrophied. Their blood-vessels and 
 lymphatic canals are found obliterated. 
 
 The stretching of these parts (where the iris is adherent 
 to the corneo-scleral tissue gradually, removes the free part 
 of the iris from the ciliary body. If the affection progresses 
 still farther, more and more of the anterior surface of the iris 
 becomes adherent to Descemefs membrane and more and 
 more of the latter membrane is destroyed. This leads, of 
 course, to a gradual diminution of the area of the free iris, 
 and the size of the anterior chamber, and furthermore to 
 dilation of the pupil, which is alway sobserved in such eyes. 
 (See Fig. 19.) 
 
 Fig. 19. — Corneo-scleral staphyloma, i. New insertion of the iris which adheres to Des- 
 cemefs membrane by means of a tissue formed from the endothelial cells. 2. The 
 ectatic part ; the membrana Descemetii has disappeared. 
 
 b. Ciliary Staphyloma. 
 
 Ciliary staphyloma concerns the ciliary region only, and 
 involves the ciliary body and the part of the sclerotic cover- 
 ing it. The affection takes its origin from a chronic cyclo-
 
 SCLERO TIC. 
 
 49 
 
 sderitis. This leads to an adhesion between the ciliary body 
 and the sclerotic, and to atrophy and stretching of these parts. 
 The muscular tissue of the ciliary body disappears totally in 
 the later stages of this process, and we frequently find only a 
 layer of pigmented cells lining the bulging parts, as the re- 
 mains of this body. The staphyloma is often bounded ante- 
 riorly by some atrophic ciliary processes, while posteriorly it 
 slopes gradually down into the more or less normal equato- 
 rial region. The blood-vessels and lymphatic canals of the 
 involved parts are, of course, again found to be obliterated 
 and the nerves atrophied. (See Fig. 20 ) 
 
 Fig. 2o.— Ciliary staphyloma. Ciliary body adherent to the sclerotic and atrophic. Be- 
 ginning ectasia. 
 
 Both of these two kinds of anterior staphyloma of the 
 sclerotic are frequently seen to travel around the whole of 
 the circumference of the eye-ball, and have therefore been 
 called *' annular " staphylomata. 
 
 2. Equatorial Staphyloma of the Sclerotic. 
 
 This form of scleral staphyloma lies either just in the 
 equator of the globe or a little behind it. It is caused by 
 chronic chorio-scleritis leading to adhesion between choroid 
 and sclerotic and atrophy, and is mostly found just where, in 
 the normal eye, a vorticous vein passes through the sclerotic. 
 The histological conditions are the same as in the other forms 
 of scleral staphyloma. 
 
 3. Posterior Staphyloma of t]ie Sclerotic. 
 
 Is the result of a chronic sclerochorioiditis, which, 
 however, does not always leads to an adhesion, and which 
 is nearly without exception confined to region of the optic
 
 50 
 
 THE HUMAN E YE. 
 
 nerve and macula lutea. Sometimes it is caused by a con- 
 genital defect. Since the point of direct vision (the 
 macula lutea) is gradually more and more removed from the 
 anterior surface of the globe in consequence of the staphy- 
 loma, it influences vision in a very important way, viz., it 
 makes the eye myopic. The histological conditions are also 
 here in no way different from what has been described above. 
 (See Fig. 21.) 
 
 Fig. 21.— Posterior staphyloma from a myopic eye. Ciioroid and sclerotic adhere to each 
 other and are atrophic. 
 
 All these different varieties of staphyloma of the sclerotic 
 may at any time become stationary. In rare cases they pro- 
 gress, until the eye becomes ruptured. In this way, and 
 in consequence of changes in the interior of the eye-ball, 
 such staphylomata lead to total destruction of the organ. 
 Staphylomata also usually cause an increase of the intra- 
 ocular pressure (glaucoma), with all its consequences. This 
 is probably due to the alterations in the uveal tract, and 
 especially to the obliteration of so many lymphatic canals 
 and blood-vessels, by which the veinous blood and lymphatic 
 fluids ought to be carried out of the eye. Glaucoma is chief- 
 ly caused by anterior and equatorial scleral staphylomata. 
 Since in posterior staphyloma the choroid is less frequently 
 found to adhere to the sclerotic, and it is generally confined 
 to a smaller part of the eye ; and, moreover, seems rather 
 to influence the entrance than the exit of the blood from 
 the eye-ball, glaucoma is but seldom found these eyes. 
 This latter argument seems especially to be proven by 
 the experiments of Kniess, which led this author to the 
 conclusion, that the lymphatic fluids in the eye-ball run
 
 SCLEROTIC. t\ 
 
 from behind forward. I cannot, however, agree with the 
 views of the same author when he finds the universal 
 cause of glaucoma in the obliteration of Fontanas spaces 
 As I have stated, glaucoma is frequently found as a conse- 
 quence of all these different kinds of staphyloma, especially 
 anterior scleral staphylomata, I have, however, examined 
 quite a number of glaucomatous eyes which showed no oblit- 
 eration of Fontanas spaces, that is, no corneo-scleral staphy- 
 loma. 
 
 The great influence exerted by all forms of scleral 
 staphyloma upon the nerves of the affected eye makes it 
 evident that they are frequently the cause of sympathetic 
 affections of the fellow-eye. 
 
 Several authors have observed deposits of lime in the 
 sclerotic, and even osseous formations, in consequence of 
 chronic scleritis have been described. Coccins and others 
 found a fatty degeneration of the sclerotic analogous to the 
 arcus senilis of the cornea. I never have seen any one of 
 these affections. 
 
 B. Injuries to the Sclerotic and their Results. 
 
 a. Wounds ivitJiout Subsequent Retention of a Foreig7i Body. 
 
 We have to speak under this head of ruptures of scler- 
 otic and wounds caused by cutting instruments. 
 
 The healing process after the infliction of such injuries to 
 the sclerotic greatly resembles those observed in the cornea 
 under similar circumstances. Very soon after the injury has 
 been received the blood-vessels become hypersemic, and the 
 edges of the lips are infiltrated with round-cells. We then 
 find the same histological conditions as in genuine infiltration- 
 scleritis. Somewhat later a fibrinous exudation into the canal 
 of the wound takes place, and this, too, becomes filled with 
 round-cells, and is gradually transformed into connective-tissue. 
 The new-formed tissue then becomes denser and begins to 
 shrink. This scar-tissue nearly always runs in a direction which 
 is different from the general one of the fibres of the sclerotic, 
 and therefore always admits of an easy diagnosis with the mi- 
 croscope. (See Fig. 22.) The result is the same whether
 
 52 
 
 THE HUMAN E YE. 
 
 Fig. 2J — Scar in the sclerotic. 
 
 the instrument pierces the whole thickness of the sclerotic 
 or only a part of it, or when purulent processes have pro- 
 duced perforation or partial ulceration of this membrane. 
 
 As purulent processes, 
 which lead to perforation 
 of the sclerotic, are, as a 
 rule, finished as such as 
 soon as the perforation 
 has taken place, we then, 
 usually find, only the 
 symptoms of infiltration- 
 scleritis. The healing process is in such cases as described 
 above. 
 
 Since, however, an injury or rupture of the sclerotic but 
 seldom occurs, which does not also at the same time affect 
 at least one of the neighboring membranes, the healing-pro- 
 cess may be a more complicated one, and, in fact, is so in most 
 cases. If the injury has been inflicted from the outside, at 
 least the conjunctiva bulbi must also be wounded ; but the 
 injury may just as well pierce all the internal membranes of 
 the globe and the vitreous body. If the wound of the scle- 
 rotic is received from its inner surface, the inflicting instru- 
 ment must have passed through nearly all the remaining 
 parts of the eye before reaching it. In this way a great 
 many variations and complications may be observed during 
 the healmg process. The most frequent complication is the 
 prolapse, and afterwards incarceration in the sclerotic of the 
 iris, the ciliary body or choroid. The histological conditions 
 in these cases are the same as those we found in incarcera- 
 tion of the iris in the cornea. In rare cases one of these 
 parts of the uveal tract may simply become adherent to 
 the wound in the sclerotic. Furthermore, we may find 
 the crystalline lens, the retina and the vitreous body pro- 
 lapsing into the scleral wound. If the injury did not at the 
 same time rupture the capsule of the crystalline lens, the 
 latter may escape in toto through the wound, and remain 
 lodged under the conjunctiva. If the capsule has been rup- 
 tured, the same may take place, or the crystalline lens, after 
 prolapsing into the scleral wound, may there become adher-
 
 SCLEROTIC. 
 
 53 
 
 ent. During the healing process the lens-substance is then, 
 as a rule, absorbed, and later on we find only the capsule 
 embedded in the scar. If prolapse of the retina has oc- 
 curred, this membrane always takes part in the formation of 
 the scar-tissue, and its nervous elements disappear. The 
 vitreous body, also, where it is caught in the wound, is trans- 
 formed into connective-tissue, and becomes adherent to the 
 scar. 
 
 When the injuring instrument reaches the sclerotic from 
 its inner surface, it must, as stated, have pierced the vitreous 
 body, retina and choroid before reaching the sclerotic. We 
 therefore find in such cases all these parts adherent to the 
 sclerotic, whether the injury concerns the whole or only a 
 part of the thickness of this membrane. 
 
 Whenever the uveal tract has also been injured, or has 
 only prolapsed into the wound of the sclerotic, we find mole- 
 cules of pigment in the lymphatic canals of the sclerotic ad- 
 joining the wound. Haemorrhages of varying size of the 
 wound-lips are of frequent occurrence, and are absorbed 
 during the healing process. 
 
 b. Wounds with Subsequent Retention of a Foreign Body. 
 
 Since the scleral tissue is a great deal more tolerant of 
 injuries than the tissue of the cornea, we 
 very frequently find foreign bodies embed- 
 ded in the sclerotic without causing any 
 serious reaction. Where such reaction 
 takes place, a circumscribed purulent scler- 
 itis ensues, during which the foreign body 
 is thrown off with the pus. 
 
 The more common result is, that in 
 consequence of chronic infiltration-scleritis 
 new-formation of connective-tissue takes 
 place, in which the foreign body becomes 
 embedded. All the injured membranes 
 take part in the formation of this tissue. 
 (See Fig. 23.) 
 
 Scars in the sclerotic may become ec- 
 tatic and lead to scleral staphyloma. f''^/ !^r'f?''^'P ^°'^>' 1?"' 
 
 ^ J emDedded in the sclerotic.
 
 54 
 
 THE HUMAN E YE, 
 
 Since most of the scleral injuries at the same time involve 
 a part of the uveal tract, they may produce sympathetic 
 affections of the fellow-eye. 
 
 C. Tumors of the Sclerotic. 
 
 Fibroma, sarcoma and osteoma of the sclerotic have been 
 described. They were all found at the corneo-scleral margin, 
 and certainly were tumors of the episcleral tissue.
 
 III. 
 
 CONJUNCTIVA BULBI AND EPISCLERAL 
 
 TLSSUE. 
 
 I. Normal Conditions. 
 
 The epithelium which covers the conjunctiva bulbi is 
 always thicker near the cornea-scleral margin than it is farther 
 backward. The peculiar superficial epithelial layer of the con- 
 junctiva palpebrarum, consisting of cylinder and cone-shaped 
 cells, is more and more changed into a layer of flat cells, like 
 the superficial layer of the corneal epithelium, the nearer it 
 comes to the corneo-scleral margin, and we find nearest the 
 cornea several layers of flat cells with an oval nucleus, which 
 frequently have one or two nucleoli. The more cuboid epi- 
 thelial cells of the inner layer of the conjunctiva palpebrarum 
 remain very much the same, until they join the basal layer 
 of the corneal epithelium. Near the corneo-scleral margin 
 we find at first a small, then rapidly increasing intermediate 
 layer, consisting of the same forms of cells which we found in 
 the middle layer of the corneal epithelium. Just where the 
 conjunctiva joins the cornea — that is, where Botvmans layer 
 of the cornea begins — the epithelium forms two or three pa- 
 pillae, which dip into the underlying tissue. 
 
 The so-called mucous-cells peculiar to the epithelium 
 of the conjunctiva are especially numerous upon the con- 
 junctiva bulbi. They are to be considered as metamor- 
 phosed epithelial cells {Waldeyer), and are large, round, 
 vesicle-like bodies. When viewed from above they ap- 
 pear as round circles, and seem to contain a transparent 
 fluid. In transverse-sections they show the same shape as 
 the " goblet-cells " of the intestinal tract, and are found to 
 have their base in the basal layer of the epithelium. 
 
 Among the cells of the basal layer, nearer the cornea and 
 the middle layers, I found frequently cells with two nuclei or 
 cells which show evident signs of being of a recent date. It
 
 56 THE HUMAN EYE. 
 
 appears therefore that the regeneration of the epethelial cells 
 of the conjunctiva takes place in the same way as it does in 
 the cornea. 
 
 Under this epithelium lies a tissue which by clinicists is 
 usually considered to form two layers, viz., the subconjunc- 
 tival and the episcleral tissue. Histologically such a separa- 
 tion does not exist. There is only one conjunctival or 
 episcleral tissue, and we may yield to the clinicists only so 
 far as to call the part of this tissue which lies close to the 
 sclerotic, episcleral, and the part just under the epithelium, 
 subconjunctival. Near to, and just at the corneo-scleral 
 margin, the possibility of even such an ideal separation is 
 wanting. 
 
 The conjunctival tissue is formed by a network of fine 
 connective-tissue fibres and elastic fibrillae. 
 
 The meshes of this network of fibres are comparatively 
 wide, except just under the epithelium and upon the sclero- 
 tic, where they become smaller and the tissue denser. This 
 condensation is caused by additional fibres coming from 
 Bowman s layer and the sclerotic, which enter the conjunc- 
 tiva. I observed above, that the fibres of the conjunctival 
 tissue enter the sclerotic. Within the meshes of the con- 
 junctiva lie a number of cells of two distinct kinds. The 
 first are flat cells and nuclei, which are adherent to the fibres, 
 probably belong to the class of endothelial cells, and are 
 comparatively rare. The second are lymphatic cells, sus- 
 pended in the fluid which fills the interstices, and generally 
 lie together in small clusters. These cells are more numer- 
 ous in the conjunctiva than in other tissues, and give it the 
 typical structure of what by older anatomists was called 
 adenoid tissue. I have never seen lymphatic follicles in 
 the normal human zox\]\xr\zX\v^{Waldeyer). 
 
 Small clusters of fat-cells have also been found by Wal~ 
 deyer in the conjunctival tissue. 
 
 The small yellowish tumor which is so frequently seen on 
 the inner or outer side of the cornea-scleral margin, in that 
 part of the conjunctiva bulbi which lies just behind the pal- 
 pebral fissure, has wrongly been called Pinguecula, as it was 
 thought to consist of fat-tissue. Scemisch changed this name
 
 CONJUNCTIVA BULB! AND EPISCLERAL TISSUE. 57 
 
 into " palpebral fissure-spot " (Lidspaltenfieck). The little 
 tumor consists chiefly of very dense connective-tissue, 
 which contains scarcely any blood-vessels or cells, and is 
 covered by a strangely thick layer of epithelial cells. I 
 always found among these epithelial cells such a large num- 
 ber of serrated ones that the condition was very similar to 
 that of an epithelial tumor. The erroneous opinion, that 
 this tumor consisted of fat-tissue, was first corrected by 
 Weller and Robin. 
 
 The blood-vessels of the conjunctiva all come from the 
 anterior ciliary blood-vessels. Their structure has nothing 
 peculiar. They are very numerous, especially in the sub- 
 conjunctival tissue, and the veins have a comparatively wide 
 lumen. The capillary blood-vessels which lie under the epi- 
 thelium form an irregular network with small interstices. 
 Contrary to Wa/dej/er, I cannot find any papillae {Gefasspa- 
 pillen) in the conjunctiva bulbi. 
 
 The nerves of the conjunctiva bulbi first form a net- 
 work of non-medullated fibres under the epithelium {J. Ar- 
 7iold) and then enter the latter. Longworth has lately been 
 able to prove beyond doubt, that these nerves really end 
 in peculiar little bulbous structures (Endkolben), as first de- 
 scribed by Krause and denied by a large number of exam- 
 iners, especially J. A rno/d and Waldeyer. 
 
 The lymphatic vessels of the conjunctiva are {Waldeyer 
 and others) in direct communication with the corneal and 
 scleral canals, which is a very important fact in pathological 
 processes. 
 
 2. Pathological Conditions. 
 
 Before speaking of the different kinds of inflammation of 
 the conjunctiva, I would like here to mention that kind of 
 oedema of the conjunctiva which is clinically known as in- 
 filtration-oedema, and is found so frequently after operations 
 and wounds near the cornea-scleral margin, especially when 
 the conjunctival wound is healed and the corneo-scleral or 
 scleral one as yet only partly, or not at all closed. In conse- 
 quence of the peculiar structure of the conjunctival tissue
 
 58 THE HUMAN EYE. 
 
 with its network of open canals, the fluids coming from the 
 cornea and anterior chamber can, of course, easily escape into 
 it. Histologically we find only the meshes filled with lym- 
 phatic fluid, and more or less distended. 
 
 Similar conditions are found in cases of so-called sub- 
 conjunctival haemorrhage. Whether such a haemorrhage was 
 caused by an injury or came on spontaneously, we simply find 
 the meshes and canals of the conjunctival tissue filled with 
 blood and distended. The blood gradually becomes absorbed, 
 and leaves, only in rare cases, some pigment behind. It is very 
 probable, but as yet not proven by histological examination, 
 that pathological alterations in the walls of the conjunctival 
 blood-vessels give rise to these haemorrhages. 
 
 A. Conjunctivitis (of the Conjunctiva Bulbi) and its 
 
 Results. 
 
 When examining into the different forms of inflammation 
 of the conjunctiva bulbi, we find the same forms we meet 
 with in other mucous membranes, viz., catarrhal, blennorr- 
 hoic, croupous and diphtheritic conjunctivitis. Such an in- 
 flammation of the conjunctiva bulbi is nearly always only 
 a symptom of inflammation of the whole conjunctiva. This 
 is, however, not the case with two types of inflammation 
 which are not among those just enumerated, viz., phlyc- 
 tenular conjunctivitis and clinically so-called episcleritis, which 
 are, as a rule, local diseases. A farther form of inflammation, 
 but rarely observed in the conjunctiva bulbi, is trachoma. 
 
 a. Conjunctivitis Catarrhalis, Episcleritis, PklyctcB?iula. 
 
 Catarrhal inflammation of the conjunctiva bulbi is ob- 
 served only when the whole of the conjunctiva is subject to 
 a catarrhal inflammation. The blood-vessels in such cases are 
 very hyperaemic. Thus an increased transudation, at first of 
 the serous fluid of the blood, and later of white blood-corpu- 
 scles into the meshes of the conjunctival tissue is caused, which 
 is accompanied by an increased secretion from the mucous- 
 cells. This condition can heal perfectly by removal of the 
 hyper-secretion from the conjunctival surface and by ab- 
 sorption, or it may become chronic. In rare cases new-forma-
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 59 
 
 tion of connective-tissue in the conjunctiva may take place 
 during the process of such a chronic catarrhal conjunctivitis. 
 
 The disturbances in the circulation caused by the considera- 
 ble degree of hyperaemia always found incases of conjunctivi- 
 tis, may also lead to affections of the cornea, or, as is frequently 
 the case, to hyperaemia of the iris. While the latter is often 
 found complicating with an acute catarrhal conjunctivitis, the 
 former affections result more frequently from a chronic one. 
 
 Clinicists make a distinction between catarrhal conjunc- 
 tivitis and episcleritis. They maintain that in the latter the 
 conjunctival tissue nearest to the sclerotic is the seat of the in- 
 flammation. As far as I know, cases of such clinically diag- 
 nosticated episcleritis have not yet been examined with the 
 microscope. Where episcleritis is a primary disease (and not 
 secondary to inflammation of the sclerotic, etc.), it is, as a rule, 
 a local and very chronic affection. In rare cases it may travel 
 all around the cornea and cause internal complications, such 
 iritis is, choroiditis, and even neuro-retinitis. Episcleritis is 
 always accompanied by a local catarrhal conjunctivitis, and 
 there is probably no catarrhal conjunctivitis of a more serious 
 degree which is not combined with, or causes some degree of 
 episcleritis. 
 
 Another local form of inflammation of the conjunctiva, 
 which is, however, as a rule, combined with a local, often even 
 with a general catarrhal conjunctivitis, is phlyctenula. 
 
 As far as I know, phlyctenula of the conjunctiva have 
 not yet been histologically examined. The process is clini- 
 cally, however, so similar to that in the cornea, that we 
 shall probably not be very far from the truth in assuming 
 that we here also find a sub-epithelial infiltration with round 
 cells. This infiltration may later on, be again absorbed, or 
 lead to the destruction of the epithelium above it, and thus 
 cause the formation of a superficial ulcer. The phlyctenula 
 may appear singly or we may find a number at the same time. 
 A variety of this affection is the so-called miliary phlyctenula. 
 
 b. Conjunctivitis Blejtnorrhoica {purulenta, gonorrhoica), Ulcer 
 of the Conjunctiva. 
 
 In blennorrhoic conjunctivitis, the characteristic secretion
 
 6o THE HUMAN E YE. 
 
 is at first muco-purulent, later on, entirely purulent. Blennorr- 
 hoic conjunctivitis of the conjunctiva bulbi is nearly always 
 caused by an inflammation of the same nature of the whole 
 conjunctiva, and probably always combined with an inflam- 
 mation of the episcleral tissue. 
 
 The conjunctival blood-vessels are, in these cases, always 
 highly hyperaemic, and this hyperaemia is followed by the 
 emigration and new-formation of numerous round-cells. 
 These symptoms are combined with oedema and swelling of 
 the conjunctiva, which again cause stasis in the veinous blood- 
 vessels and passive oedema, and thus a circuliis vitiosus is 
 formed. The infiltration and new-formation of round-cells 
 are followed by a lively proliferation of the epithelial cells, 
 and it seems later they not only allow the pus-cells to pass 
 through them, but themselves take an active part in the 
 formation of the pus. During this process small superficial 
 ulcers are frequently formed. Such small ulcers heal by 
 proliferation of the surrounding epithelium, and it seems that 
 all the layers take an active part in this restorative process. 
 The same healing-process, combined with a local blennorrhoic 
 conjunctivitis, is observed after the breaking of the pustule 
 formed by a phlyctenula. 
 
 After having lasted some time, blennorrhoic conjunctivitis 
 generally goes over into the catarrhal form, which may soon 
 lead to the normal condition or become chronic. Such a 
 chronic catarrhal conjunctivitis after blennorrhoea often pro- 
 duces trachoma. 
 
 Serious cases of blennorrhoea of the conjunctiva are nearly 
 without exception combined with inflammatory processes in 
 the cornea, which may lead to partial or total destruction of 
 this membrane, or even of the whole eye-ball. It is as yet 
 an unsettled question whether these complications originate 
 in an inoculation of pus-cells into the corneal-tissue, or only 
 in impaired nutrition, or in both combined. It seems to me, 
 however, that the latter is the most probable. 
 
 As a result of blennorrhoic conjunctivitis (especially when 
 combined with ulcus corneae), we find the formation of ptery- 
 gium, as I have already above stated. 
 
 The swelling of the papillae, which is so conspicuous in the
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 6 1 
 
 conjunctiva of the lids, in cases of blennorrhoea, is not ob- 
 served in the conjunctiva of the bulbus, since, as stated, it has 
 no papillae. 
 
 c. Conjunctivitis Crouposa and Diphtheritica. 
 
 Although these two forms of conjunctivitis do not seem 
 to have been as yet histologically examined, their analogy 
 with the same forms of inflammation in other mucous mem- 
 branes will help to explain the conditions. We therefore 
 probably find in croupous conjunctivitis that a fibrino-puru- 
 lent exudation is deposited upon the surface of the conjunc- 
 tiva, without implicating the epithelial layer. Croupous 
 membranes, taken from the conjunctiva, consist invariably 
 of a dense network of fibrinous threads, among which round- 
 cells lie in large quantity. The same exudation is probably 
 found in diphtheritic conjunctivitis ; but here it materially 
 involves the epithelium and the underlying tissue. The 
 croupous exudation, therefore, when cast off, leaves only an 
 inflamed conjunctiva behind, while the diphtheritic membrane 
 is never cast off without causing a deep ulcer. 
 
 The croupous as well as the diphtheritic form of inflamma- 
 tion are only rarely found to involve the bulbar conjunctiva. 
 When healing they go over into a blennorrhoic, and this later 
 on into a catarrhal conjunctivitis, which may either soon lead 
 to the normal condition or become chronic. In the latter case 
 they may, too, produce trachoma. 
 
 Both these kinds of conjunctivitis often result in destruc- 
 tion of the cornea, or even of the whole eye-ball. 
 
 d. Conjunctivitis Trachomatosa. 
 Although trachoma is frequently the result of chronic 
 catarrhal, blennorrhoic, or in some cases croupous and diph- 
 theritic conjunctivitis, it is also observed as a primary dis- 
 ease. It is only found in the bulbar conjunctiva, after it has 
 affected the whole of the remaining conjunctiva. My own 
 examinations of trachomatous conjunctiva have taught me 
 that its characteristic feature is the formation of tubercle-like 
 aggregations of round-cells. These clusters of round-cells are 
 more or less globe-shaped, and force the surrounding tissue 
 (which is also filled with round-cells; aside, at the same time
 
 62 
 
 THE HUMAN E YE. 
 
 compressing its fibres in such a way, that a number of authors 
 thought the granules were surrounded by a membrana pro- 
 pria, and were hypertrophic lymph-folHcles. But there are no 
 lymph-follicles in the human bulbar conjunctiva, and the ap- 
 parent membrana propria is, as stated, formed by the com- 
 pressed fibres of the conjunctival tissue. If the blood-ves- 
 sels of the conjunctiva are injected with some tinted fluid, it 
 
 Co 
 
 Fig. 24. — Trachoma-granule from the bulbar conjunctiva. Blood-vessels injected with a 
 stained fluid. L. Enlarged lymph-canals. 
 
 is easily seen that they pass through these accumulations of 
 round-cells. (See Fig. 24.) Besides the blood-vessels, I always 
 found enlarged lymphatic vessels in and around the granules. 
 
 These granules may reach the corneo-scleral margin, and 
 sometimes they are even found to lie in the corneal tissue 
 near this place. 
 
 Trachomatous conjunctivitis is usually a chronic affection, 
 and produces a hyper-secretion of mucous, or the secretion 
 of a muco-purulent fluid. The granules may undergo fatty 
 degeneration, and thus be absorbed, or they are transformed 
 into a tough connective-tissue {Preuss). This new-formed 
 tissue causes the obliteration of blood-vessels and lymph 
 canals and destruction of the mucous-cells. The latter 
 leads to xerosis of the cornea. Corneal affections are, more- 
 over, very frequent complications in cases of trachomatous 
 conjunctivitis. It produces, however, comparatively seldom 
 internal affections or the perfect destruction Df the eye-ball. 
 
 The Results of Conjunctivitis, viz., Argyrosis, Xerosis, and 
 
 Pterygium. 
 Argyrosis of the conjunctiva is not caused by the con-
 
 CONJUNCTIVA BULB! AND EPISCLERAL TISSUE. g^ 
 
 junctivitis itself, but by a too prolonged use of the chief rem- 
 edy employed in its treatment — nitrate of silver. This condi- 
 tion, according to Jiinge, is due to the precipitation of the 
 silver in the epithelium and the superficial layers of the con- 
 junctival tissue. 
 
 Xerosis conjunctivae we call an affection which is caused 
 by the dryness of the conjunctiva and the transformation of 
 its epithelial cells into horny scales. This process may be 
 combined with the formation of scar-tissue in the conjunctiva 
 or exist without it (xerosis parenchymatosa and xerosis sim- 
 plex), and originates in a want of moisture dependant upon 
 chronic forms of conjunctivitis, especially trachoma. The 
 mucous-cells are found either undergoing a colloid metamor- 
 phosis or altogether destroyed. Xerosis conjunctivae is 
 generally accompanied by the same affection of the cornea. 
 
 Pterygium, as stated above, may originate in a marginal 
 ulcer of the cornea, combined with blennorrhoic conjunctiv- 
 itis. I have, however, learned by clinical observation that 
 it may just as well be caused by catarrhal conjunctivitis 
 (especially in the acute form), without the existence of an 
 ulcer. 
 
 B. Injuries to the Conjunctiva and their Results. 
 
 I . Injuries zvithout the Retention of a Foreign Body. 
 
 Injuries to the conjunctiva, without retention of a foreign 
 body, ^re either cuts, rents or scratched wounds. The cuts 
 we observe on the bulbar conjunctiva are chiefly those caused 
 by an operation. If the tissue has simply been severed heal- 
 ing by primary intention, generally takes place and no trace 
 is left behind. If the cut, however, causes a loss of sub- 
 stance, or for some reason the wound-lips are not allowed to 
 become well applied to each other, the healing process occurs 
 by secondary intention. We then find, similar to those condi- 
 tions seen after a corneal wound, an exudation of a fibrinous 
 nature covering the loss of substance, or between the wound- 
 lips, which is gradually transformed into connective-tissue, 
 and then covered by new-formed epithelium. In the new- 
 formation of the latter, all the layers seem to participate.
 
 64 
 
 THE HUMAN E YE. 
 
 If the wound lies at the corneo-scleral margin, it is, as stated 
 above, covered to the larger extent by the conjunctival, to 
 the smaller by the corneal epithelium. 
 
 2. Wounds with Subsequent Retention of a Foreign Body. 
 
 If a foreign body remains in the conjunctiva after having 
 pierced only the epithelium and the layers under it, it nearly 
 always produces a general catarrhal and a local blennorrhoic 
 conjunctivitis. The latter leads to the formation of an ulcer 
 around the foreign body, which then is thrown off with the 
 pus, and the ulcer heals in the usual way. 
 
 If the foreign body has entered the deeper layers of the 
 conjunctiva, and is small enough to remain embedded there, 
 it is usually soon surrounded by dense connective-tissue 
 capsule, which is the result of chronic conjunctivitis. Among 
 such foreign bodies we find little pieces of wood, iron or stone. 
 
 Fig. 25. Crystalline lens dislocated under the conjunctiva and there encapsuled. 
 
 Lenses dislocated under the bulbar conjunctiva produce the 
 same results. (See Fig. 25.) 
 
 3. Burns with Lime. 
 
 Burns of the conjunctiva, like those of the cornea, are 
 mostly caused by lime. The epithelial cells and the under- 
 lying tissue are infiltrated with the lime, become necrotic, 
 and then acting as foreign bodies, produce a local blen- 
 norrhoic conjunctivitis, besides the general catarrhal conjunc- 
 tivitis. Thus the burned parts are thrown off, and an ulcer 
 is formed which heals in the manner described.
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 65 
 
 If the conjunctiva of the lids has been burned at the same 
 time and the two ulcers lie close to each other, their surface 
 may heal together. This condition is called symblepharon 
 posterius. If the burn be extensive enough, it may cause 
 the formation of an anchyloblepharon. 
 
 C. Tumors of the Conjunctiva Bulbi and Episcleral 
 
 TISSUE. 
 
 In chapters I and II, I remarked that the so-called tumors 
 of the cornea and sclerotic as a rule, take their origin from 
 the limbus conjunctivae, which is so well supplied with blood- 
 vessels, and not from either cornea or sclerotic. The litera- 
 ture on this subject and the clinical experience of others as 
 well as my own numerous histological examinations have 
 thoroughly convinced me that no genuine corneal or scleral 
 tumors are observed, at least, that no tumor has so far been 
 described which undoubtedly took its origin in either the 
 cornea or the sclerotic alone. I have therefore thought it 
 proper to place the description of all these tumors here. 
 
 Metastatic tumors in these parts, resulting from intra- 
 ocular new-formations, do not of course, belong under this 
 head. 
 
 a. Lymphangiectasia and Serous Cysts. 
 
 I am not aware that the result of a histological examina- 
 tion of a lymphangiectasia of the conjunctiva has ever been 
 published before the following one which I had occasion to 
 examine and to describe in my paper on the nature and ana- 
 tomical causes of sympathetic ophthalmia. The conditions 
 were, as follows ; 
 
 In the conjunctiva bulbi I found a system of cavities and 
 canals, perfectly independant of the blood-vessels, which were 
 hyperaemic and therefore well defined. These cavities and 
 canals are in direct communication with each other, and press 
 the surrounding conjunctival tissue aside. Some of them 
 are separated from each other only by a very thin septum. 
 They contain a serous fluid, in which a small number of lym- 
 phatic cells are suspended. Their walls have an endothelial 
 lining which, however, does not seem to be continuous. The
 
 66 
 
 THE HUMAN E YE. 
 
 walls themselves are formed by the compressed fibres of the 
 conjunctival tissue (See Fig. 26). 
 
 Kio. 26. Lymphangiectasia of the bulbar conjunctiva. 
 
 If the ectasia of such lymph-canals increases still further 
 and the septa disappear altogether, all the different small 
 cavities may coalesce into one large one and form a serous 
 cyst. That serous cysts acquired after birth may be devel- 
 oped in such a way, has also been stated by clinical observers 
 {School, von Wixker). 
 
 I have had no occasion to examine congenital, uncompli- 
 cated serous and dermoid cysts of the conjunctiva. 
 
 b. Granuloma {Polypus). 
 
 Granuloma of the conjunctiva is but seldom observed 
 upon the bulbar part of this membrane. It is caused by 
 chronic inflammatory processes, or by traumatic and opera- 
 tive influences. In cases where the eye-ball is phthisical, it 
 appears sometimes, as if the granuloma had originated in the 
 corneal tissue, which is, however, not the case. According 
 to my experience, there exists no granuloma of the cornea, 
 although Pagenstecher and Geuth have described such a 
 tumor. If the eye is as yet a useful organ granulomata 
 are seldom allowed to grow to a considerable size but are re- 
 moved at an early stage. Upon phthisical (blind) eye-balls 
 these tumors sometimes grow very large. All the tumors be- 
 longing under this head and examined by me, were built up of 
 simple granulation-tissue, viz., round-cells, new-formed blood- 
 vessels and very little, if any, connective-tissue (See Fig. 27).
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 67 
 
 Fano's decription of a " fibrous " polypus in this region, may 
 be taken as a proof that this granuloma-tissue may later on 
 
 Fig. 37. Granuloma (polypus) of the bulbar conjunctiva 
 
 become transformed into dense connective-tissue. Mucoid 
 polypi {Saemisch) have never come under my observation in 
 this part of the eye. 
 
 c. Dermoid and Lipomatous Tumors. 
 
 Dermoid (Rybd) tumors of the conjunctiva are, it seems, 
 always independent new-formations. In all of the cases hith- 
 erto described the tumor was situated just upon the corneo- 
 scleral margin in such a way, that one half was adherent to the 
 cornea, while the remaining half lay upon the sclerotic. All 
 authors agree as to the benign character of these tumors, and 
 all describe them as consisting of the constituents of the normal 
 skin. In rare cases in the latter periods of life dermoid tumors 
 through some cause or other may become irritated and begin 
 to grow. They are then, of course, with regard to the useful- 
 ness of the eye of a malignant character. In a very large major- 
 ity of the cases, however, dermoid tumors remain stationary. 
 
 The histological appearance of three, such new-formations 
 which I myself had occasion to examine is described in the 
 following. (See Fig. 28). 
 
 The dermoid tumor is covered with a continuous epithe- 
 lial coat, which consists of the same layers and elements as 
 the epidermis. The most superficial layer is formed by flat- 
 tened epithelial cells, which, however, are not always horny. 
 Cells undergoing colloid metamorphosis seem to be frequent 
 in this layer. The layer under the flattened cells has well 
 marked serrated cells. Mucous-cells as they are found in the
 
 6S THE HUMAN E YE. 
 
 conjunctiva, are also found among the epithelial cells of der- 
 moid tumors. This epithelial coat has as uneven a surface 
 
 Fig. 28. — Dermoid tumor of the bulbar conjunctiva. 
 
 as that of the skin, and sends numerous offsets into the un- 
 derlying tissue surrounding the papillae of the tumor. In 
 nearly all of these indentations, we find a hair or the orifice 
 of a gland. The latter are of the acinous type and probably 
 all sudoriferous. The hairs are very thin and have very little 
 pigment. Under the epithelium lies the connective-tissue, 
 which appears very tough and dense, and contains a few elastic 
 fibrillae. At the base of the tumor the connective-tissue, be- 
 comes looser and includes a varying amount of fat cells. It 
 seems thus far only tumors, which had been removed from the 
 globe have been subjected to anatomical examination, and that 
 their basis is always found to consist chiefly of subcutaneous 
 fat-tissue. In other tumors the fat-tissue may form the bulk 
 of the tissue, and such tumors have by several authors been 
 described as lipomatous dermoid tumors. Purely lipomatous 
 tumors of this part have also been spoken of by some authors, 
 but I am inclined to think that they were actually dermoid 
 with a large amount of fat-tissue. 
 
 It has been stated by others that most of the dermoid tu- 
 mors contain only very few blood-vessels. In the three cases 
 which I examined, the blood-vessels were as numerous as in 
 the skin and the network of capillaries in the papillae was 
 especially well developed. Nerves have not been found in 
 these tumors, which, however, does not altogether prove that 
 they really do not exist. 
 
 In one of my own cases, I found the connective-tissue 
 which lay directly under the epithelium, filled with round-
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 69 
 
 cells and the blood-vessels were very hyperaemic. I think that 
 this dermoid tumor was in a state of irritation that would 
 have enabled it to grow. 
 
 The connection between these tumors and the under-lying 
 tissues has, as far as I know, not yet been described, as all 
 the published cases concerned dermoid tumors which were 
 removed from the living eye-ball. From clinical observation 
 we know, however, that while they are only loosely connected 
 with the conjunctiva (resp. sclerotic), they adhere firmly to 
 the cornea. 
 
 d. Fibroma and Osteoma. 
 
 Fibroma and osteoma of the bulbar conjunctiva have but 
 seldom been observed. 
 
 A fibroma described by Saemisch was found upon the pos- 
 terior part of the bulbar conjunctiva. It consisted of dense 
 connective-tissue with a few cells. The latter showed all the 
 stages of development of a cell into connective-tissue fibre. 
 
 Osteoma {yon Graefe, Saemisch) was found to be lying in 
 a capsule of tough connective-tissue and to be true osseous 
 tissue. Watson described an osteoma in the conjunctiva as 
 springing directly from the sclerotic. 
 
 e. Papilloma, melanoma and melanocancroid new -formations. 
 
 Among the benign tumors of the bulbar conjunctiva 
 papilloma and melanoma have been described. 
 
 Skokalsky s case of papilloma corneae is the only one 
 which has been carefully studied, and seems to allow of 
 no doubt as to the diagnosis. {Horner s case of a " fibroma 
 papillare " will be mentioned later on). The description clearly 
 shows, however, that this case, too, was not a corneal tumor, 
 but sprang from the corneo-scleral margin, that is, from the 
 conjunctival or episcleral tissue. It formed, cauliflower-like, a 
 number of cylindrical excrescences which consisted of spindle- 
 cells, containing blood-vessels, and was covered with epi- 
 thelium. 
 
 The " pure " melanoma is generally described as a benign 
 tumor. The benign character seems, however, very doubtful,
 
 70 
 
 THE HUMAN E YE. 
 
 as most of authors, including Scemisch, report that at any time 
 it may become malignant. The anatomical conditions of me- 
 lanoma of the conjunctiva generally mentioned do not ap- 
 pear to warrant its being called a distinct species of new-forma- 
 tion. Such a melanoma described by Heddaeus and taken from 
 the corneo-scleral margin, consisted of " detritus, epithelial 
 cells with and without pigment, free nuclei, free pigment, 
 numerous large round cells with large nuclei and nucleoli." 
 Probably most of these tumors belong to the sarcomata. 
 
 Once only I had myself the opportunity to examine such 
 a tumor, which had been removed from the conjunctiva as a 
 benign melanoma, and I found the following conditions. 
 
 On the whole the new-formati*on was very much like that 
 of a dermoid tumor. Under a thick layer of epithelium came 
 first connective-tissue with numerous, then one with scarcely 
 any cells, and the base of the tumors was formed by a loose 
 tissue containing fat-cells. The blood-vessels were very 
 numerous and they formed papillae like those found in the 
 skin. 
 
 The epithelium however, had several remarkable pecu- 
 liarities. (See Fig. 29.) From the epithelial layer large pa- 
 pillae spring forward like pointed condylomata, and these ep- 
 ithelial papillae contain cavities and small canals which can 
 sometimes be traced to the lymphatic vessels in the tissue 
 underneath the epithelium. The epithelial cells bordering 
 these cavities and those at the base and top of the papillae 
 are pigmented to a varying degree. The granular pigment 
 lies in the protoplasma of the cells as well as in the cement- 
 ing substance between them. The inner layers of the epithe- 
 lium consist of well defined and large serrated cells. The 
 nearer the surface the more they go over into flattened epi- 
 thelial cells and horny scales. Some of the papillae show 
 pearl-nodules. 
 
 Furthermore, the tumor contains glands and hair. The 
 hairs are very thin, only slightly pigmented and two of them 
 generally stand together. The glands are very much like the 
 Meibomian glands in the lids but I do not know their exact 
 nature. A strong nerve-branch enters the base of the tumor. 
 
 The question now is, what is the anatomical diagnosis of
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE.- 71 
 
 this " melanoma " ? In the whole of its structure the growth 
 throughout most resembles a dermoid tumor, with the differ- 
 
 FiG. 29. — Partially pigmented epithelial papilte from a dermoid tumor of the bulbar 
 conjunctiva. 
 
 ence that it has papillary and epithelial excrescences. There 
 are, however a great number of pigmented cells, among the 
 latter which may have led to the clinical diagnosis of mel- 
 anoma. Those, however, who consider pearl-nodules as a 
 sure characteristic feature of an epithelioma, will perhaps call 
 it a melano-cancroid. 
 
 I consider it to be a peculiar variety of the dermoid tumor 
 and, perhaps, some of the new-formations described as mel- 
 anomatous and melano-cancroid tumors may belong among 
 the same class. Some of them were undoubtedly cases of 
 melanosarcomatous tumors. 
 
 f. Leiicosarconia and Melanosarcoma. 
 Sarcomata of the episcleral region are comparatively rare, 
 and among them the leucosarcomata are but very seldom 
 found, therefore, the number of these new-formations de- 
 scribed in literature is but very small.
 
 J2 THE HUMAN E YE. 
 
 Only one case of leucosarcoma of the episcleral region has 
 come under my own observation. The tumor had about the 
 size of a pea and consisted of large round, mingled with a 
 few spindle-cells. A great number of these round-cells had 
 more than one nucleus. Furthermore, I found among them 
 a larger number of giant-cells. The new-formation contained 
 a great many blood-vessels, lifted the conjunctival and 
 corneal epithelium off the underlying parts and thus grew in 
 between Bowmatis layer and the corneal epithelium, without, 
 however, materially altering the tissue of the cornea. 
 
 Later on the elements of the tumor enter the sclerotic and 
 cornea proper {Pagenstecher and GentJi). Hirschberg de- 
 scribed such a case of a leucosarcoma of the conjunctiva with 
 intra-ocular metastases. In what way the tumor reaches the 
 inner membranes does not seem to be known. 
 
 Melanosarcomata of the conjunctiva have been observed 
 and histologically examined more frequently than leucosar- 
 comata. All authors agree in the prominently vascular 
 character of these new-formations. In the beginning stages 
 they were always found to be very easily separated from the 
 underlying tissue, especially from the cornea. Very fre- 
 quently an injury to the eye-ball has to be considered, as the 
 origin of the sarcoma, and it is therefore not improbable, that 
 the hemorrhage caused by the injury has something to do with 
 the formation of the pigment. 
 
 I have examined three such melanosarcomatous tumors 
 of the conjunctiva, myself, and the conditions were very 
 much alike in all of them. 
 
 The new-formation seems to always start in the vascu- 
 lar limbus conjunctivae, to gradually spread between the 
 corneal epithelium and Boivmans layer, until at a certain 
 stage, it is found to lie upon the cornea, like " pannous-tissue " 
 without as yet having changed this membrane at all. Later 
 on, however, the periphery oi Bowman s layer is destroyed and 
 the elements of the new-formation, enter the parenchyma of 
 the cornea. Bowman s layer is, however, so resistant, that 
 the elements of the tumor when they have once entered the 
 corneal parenchyma progress much quicker towards the cen- 
 tre than Bowman s layer is destroyed. It is even possible
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 73 
 
 for the new-formation to encircle the whole of the cornea, 
 before it can pierce this layer, and thus grow into the deeper 
 parts. 
 
 The elements of melanosarcomata, are round or spindle- 
 cells, which vary considerably, with regard to the amount 
 of pigment they contain. We find, therefore, in one and 
 the same tumor, parts which are nearly unpigmented, while 
 in other parts the cells, contain so much pigment, that it 
 is utterly impossible to recognize their nuclei. It seems 
 from my specimens that the highest degree of pigmenta- 
 tion is always found in the cells which lie nearest to the 
 blood-vessels. The more superficial parts are generally the 
 least pigmented ones. The cells are generally larger than 
 white blood-cells and have one or more nuclei. I have never 
 found any giant-cells in these tumors. (See Fig. 30). 
 
 Fig. 30.— Melanosarcoma of the bulbar conjunctiva. 1. Shows how the pigmented cells 
 creep along the blood-vessels of the conjunctiva and upon Bowman's layer under the 
 epithelium of the cornea. 
 
 Most of the authors on this subject, mention the scarcity 
 of an intercellular substance. In my cases, too, I could only 
 clearly demonstrate the intercellular substance, in the peri- 
 pheral parts of the tumor. The large number of capillaries 
 form a dense network. Besides them I find a number of well 
 distinguished veinous and arterial branches. The vascularity 
 of these tumors readily explains the recent and old haemor- 
 rhages usually found therein. 
 
 From my specimens it appears that in the progress of the 
 tumor, the blood-vessels play an important part. In one of
 
 74 
 
 THE HUMAN E YE. 
 
 the cases I found in the part of the episcleral tissue, which 
 lay diametrically opposite the original tumor a network of 
 pigmented stripes. Examining this part with a higher mag- 
 nifying power I found the network to be formed by blood- 
 vessels, which were not only surrounded by a sheath of pig- 
 ment but which also contained pigment molecules within their 
 lumen. The progress of the tumor into the parenchyma of 
 the cornea or sclerotic, is always preceded by the new-for- 
 mation of blood-vessels and the emigration and proliferation 
 of cells. Along these new-formed blood-vessels the pig- 
 mented elements of the tumor, are then seen to creep into 
 the corneal and sclerotic tissue and to gradually destroy the la- 
 mellae of these membranes. It does not seem to be known 
 whether such new-formations lead later on to rupture of the 
 cornea, or whether they may grow into the interior of the 
 eye-ball. 
 
 The periphery of the tumor in the tissues so involved, is 
 always formed by the well known zone of inflammation, and 
 their surface is covered with the conjunctival or corneal epi- 
 thelium. 
 
 g. Epithelioma. 
 
 Epithelioma is the most frequently observed, of all the 
 tumors of the episcleral tissue. Consequently it has already 
 often been examined and described. The authors on this 
 subject {Althoff, Classen, Horner, Knapp and others), how- 
 ever, disagree in their opinions upon important points so 
 much, that in the following I only give the results of my 
 own examinations, which up to this time embrace fourteen 
 cases. I will only mention here that a tumor described by 
 Horner as a "fibroma papillare" belongs most probably to 
 the same class of tumors, as the patient died from carcinoma. 
 Furthermore, old epitheliomata of the conjunctiva, very fre- 
 quently show the pupillary form known under the name of 
 "cauliflower ''-cancer. 
 
 Epitheliomata originate in a true hyperplasia of the epi- 
 thelial layer of the conjunctiva, whether they start directly 
 from the corneo-scleral margin or from a place somewhat re- 
 mote from it. It usually begins just where Bowman s layer
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. y^ 
 
 joins the conjunctiva, and where, as stated above, the normal 
 conjunctival epithelium dips into the underlying tissue in the 
 shape of one or two papillae. It seems that epithelioma never 
 originates from the epithelium of the cornea proper. 
 
 We find, in the beginning, the epithelial layer considerably 
 thickened, and this thickening is caused by an abnormally 
 increased number of epithelial cells. It is in this stage fur- 
 thermore, impossible to recognize the normally so distinct 
 layers of the corneal and conjunctival epithelium, since the 
 cells vary considerably in shape and size. In most cases 
 nearly the whole of this original tumor consists of serrated 
 cells, in others the cells are flat and partially horny. Every 
 cell (except the horny ones) have a large round or oval nu- 
 cleus and several nucleoli, cells with two or more nuclei are 
 very rare. If the tumor progresses, the surrounding conjunc- 
 tiva becomes hyperaemic and filled with cells, while the cornea 
 proper remains for a long time unaltered. Gradually, how- 
 ever, new blood-vessels enter the cornea or sclerotic and 
 round-cells begin to emigrate in their tissue, which process 
 is followed by the proliferation of their fixed cells. Only 
 then the elements of the tumor seem to be able to perforate 
 the peripheral parts of Bowman s layer (as in cases of sar- 
 
 FiG. 31.— Epithelioma of the bulbar conjunctiva. 
 
 coma) and grow into cornea and sclerotic, arranged in the 
 well known characteristic gland-like and cylindric way. (See 
 Fig. 31), Epithelioma enters the hard membranes of the
 
 ^6 THE HUMAX EYE. 
 
 eye-ball, without having first destroyed the peripheral parts 
 of Botvuian s layer ; the progress of the destruction of this 
 layer however, does not necessarily go pari passu with the 
 progress of the tumor in the corneal iizsw^, Descemei' s mem- 
 brane can resist much longer and may be found perfectly 
 intact, even if the whole of the corneal parenchyma is taken 
 up by the new-formation. 
 
 The following are the more minute histological details to 
 be observed in these new-formations. 
 
 If the surface of the epitheliomatous growth is ulcerated, 
 the conditions are altered accordingly. Where no such ulcer- 
 ation exists, I find the superficial layer of the tumor to con- 
 sist of flattened, often horny, epithelial elements. Under 
 these layers come the cells of the new-formation, varying in 
 size and shape and mostly serrated, and they dip into the 
 underlying parts forming the well known cylinders. These are 
 the primary epithelial cylinders. They are surrounded by a 
 tissue filled with blood-vessels and round-cells. These round- 
 cells frequently lie so close together, that their form is altered 
 by the pressure. They, too, vary in size. We find among them 
 free nuclei, cells with one or two, and larger ones with even 
 three and four nuclei. 
 
 The outlines of these primary epithelial cylinders are 
 mostly sharply defined and their periphery is formed by a 
 single layer of cylindrical or cone-shaped cells, which are also 
 frequently serrated. The centre of the cylinders, consists of 
 epithelial cells of very different size and shape ; pearl-nodules 
 are frequently found among them. 
 
 If we follow up such primary cylinders under the micro- 
 scope, we see that some of them have a blunt end, others 
 branch off into secondary and tertiary cylinders of the same 
 kind, while others again pass over into round-cell cylinders, 
 which then are gradually lost in the surrounding cellular 
 tissue. (See Fig.32). Although Knapp states distinctly that 
 all cylinders consist of epithelial cells and that he never saw 
 epithelial cell cylinders go over into round-cell cylinders, 
 my own specimens all show this condition undoubtedly. In 
 some specimens I found even large networks of such secon- 
 dary and tertiary cylinders, which consist solely of round-cells.
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. jj 
 
 Sometimes I saw a number of epitheloid cells (which are 
 similar to epithelial cells in shape, and like them, by Muel- 
 ler s hardening fluid tinted darker than the surrounding 
 
 / 
 
 Fig. 32. — Epithelioma of the bulbar conjunctiva, i. Epithelial cylinder filled with round- 
 cells. 2. Epithelial cylinders ending in round-cell cylinders. 
 
 tissue) lying just in the angle where younger cylinders 
 branched off from older ones. Although I was never able to 
 see directly the transformation of round into epithelial cells, I 
 could not explain the conditions, without assuming that such 
 a change occurs. This seems to be still more probable, as I 
 frequently found also round-cell cylinders whose periphery 
 was formed by a single layer of epithelial cells. (See Fig. 32). 
 I want to state here, furthermore, that while the round-cells 
 very distinctly show the phenomena of proliferation, the 
 number of undoubtedly proliferating epithelial cells, is but 
 very small. 
 
 The epithelial cylinders seem in the beginning to grow 
 along the corneal canals {Knapf). Later on, however, the 
 condition of the lamellae becomes changed in such a way, 
 that we can no longer speak of corneal canals. The lamellae 
 are broken up and destroyed. We then find the cylinders 
 surrounded by a tissue, consisting of very fine spindle-cells. 
 (See Fig. 33). 
 
 When the tumor has grown over the whole cornea. Bow- 
 man s layer is always wanting. During the growth of the 
 tumor, however, this layer is not as quickly destroyed, as the 
 elements of the new-formation spread in the corneal tissue. 
 Descemefs membrane, which as stated above, resists much 
 longer, may in consequence of ulceration and an increased
 
 78 
 
 THE HUMAN E YE. 
 
 intra-ocular pressure, at a later period be also perforated. 
 When this perforation takes place the capsule of the crystal- 
 line lens is often ruptured, or the lens may escape from the 
 
 
 
 Fig. 33. — Epithelioma of the bulbar conjunctiva. The tissue of the cornea is changed into 
 one consisting of long fine spindle-cells. 
 
 eye-ball in toto. When the perforation occurs, the iris prob- 
 ably always prolapses, and thus becomes adherent to the 
 new-formation. In this manner one channel is opened, by 
 which the elements of the tumor can enter the interior of 
 the eye-ball. In one case which I examined, the epithelioma 
 entered the anterior chamber by this channel and was found 
 spreading upon the surface of the iris, as well as into its par- 
 enchyma. (See Fig. 34). Doubtlessly the tumor can also 
 
 Fig. 34. — Epithelioma of the bulbar conjunctiva. The tumor has perforated the cornea, 
 and is spreading upon the surface and into the parenchyma of the iris. C. Cornea. 
 I. Iris. 
 
 enter the remaining membranes of the interior of the eye in 
 such a manner.
 
 CONJUNCTIVA BULBI AND EPISCLERAL TISSUE. 
 
 79 
 
 Another way (perhaps, a more frequent one) by which the 
 elements of the epithelioma enter the interior of the eye-ball, 
 are the lymphatic sheaths of the anterior ciliary arteries. 
 This I saw in two cases. (See Fig. 35). While in the one 
 
 Fig. 35. — Epithelioma of the bulbar conjunctiva. An anterior ciliary artery surrounded by 
 epithelial cells. Nests of epithelial cells in the tissue of the ciliary body. 
 
 case the epithelioma had only entered the ciliary body, it 
 had also invaded the choroid in the other. The alterations 
 produced in these tissues by epithelioma, resemble those 
 above described with regard to conjunctiva, cornea and scle- 
 rotic. 
 
 My examinations have thus proven, that epithelial tu- 
 mors of this region originate in a true hyperplasia of the 
 preexisting epithelial cells, and, furthermore, that the con- 
 nective-tissue, especially the round-cells, undoubtedly play 
 (not to say more) an important and active part in their pro- 
 Stress. 
 
 Gummata, lupus and tubercles, in these parts which have 
 but rarely been described, do not show any peculiar structure.
 
 8o THE HUMAN EYE. 
 
 Anglomata of the conjunctiva, do not seem to have been 
 histologically examined and they are also most probably, in 
 no way different from similar tumors in other parts. I may' 
 here mention that cysticercus and filaria medinensis have 
 been observed under the bulbar conjunctiva. |
 
 IV. 
 
 IRIS. 
 
 I. Normal Conditions. 
 
 The iris consists of the anterior unpigmented endothel- 
 ium, the parenchyma and the posterior pigmented and uveal 
 layer. 
 
 The question whether the anterior surface of the iris is 
 covered by a cellular coat, has up to a recent date been un- 
 solved, Faber, however, has lately proven that a continuous 
 endothelial layer covers the anterior surface of the iris. I 
 have never been able to see this endothelial coat in hardened 
 specimens, but only in fresh ones. I found the conditions 
 several times materially as stated by Faber. 
 
 The endothelial layer covers the whole of the anterior sur- 
 face of the iris from the ligamentum pectinatum to the pupil- 
 lary margin. Its cells are flat, varying in size, but mostly 
 oblong and quadrangular and have a large round nucleus. 
 These cells, however, do not lie in one plain next to each 
 other, but are arranged like tiles, partially, covering each 
 other as J, Arnold has stated before Faber. The endothel- 
 ium forms, as it seems, only a single layer. Faber states 
 that the nuclei of these cells are also flattened, and appear 
 rod-shaped in transverse sections, like those of connective- 
 tissue and organic muscular fibres. These cells are always 
 unpigmented. According to Faber the endothelial layer 
 ends by papillary excresences at the pupillary margin. 
 
 It appears that these endothelial cells are only loosely 
 connected with the underlying tissue or are very perishable, 
 which would explain why it is so very difficult to see them. 
 
 The parenchyma of the iris appears to be composed of 
 three layers, viz., a dense anterior, a loose middle, and a 
 dense fibrous posterior layer. They, however, do not exist in 
 reality, as distinctly separate layers, but they gradually merge 
 into each other, and the anterior and posterior layers form.
 
 82 THE HUMAN E YE. 
 
 — SO to speak — only a condensation of the middle one. The 
 chief elements of which the parenchyma of the iris consists, 
 are connective-tissue and blood-vessels. The former is in 
 different individuals, developed in a different degree ; its cel- 
 lular elements are, however, always far more numerous than 
 the fibres. The cells are partially unpigmented, partially 
 pigmented to a varying degree. Those of the anterior and 
 especially the posterior layer are mostly spindle-shaped ; 
 those of the middle layer have two or more offsets, and fre- 
 quently anastomose with each other. Moreover, we find, 
 also in the parenchyma of the iris, as in other tissues, a num- 
 ber of wandering cells. 
 
 The arteries of the iris come from the circulus iridis major 
 and run in a radiating direction towards the pupillary margin, 
 meanwhile giving off numerous smaller branches. Near the 
 pupillary margin they form the circulus iridis minor and then 
 a capillary network between the fibres of the sphincter pupillae 
 muscle, or go directly over into veins {Faber). The veins run 
 again in a radiating direction back to the ciliary bodies and 
 empty the blood into the vorticous veins. According to y. 
 ArftoM the blood-vessels of the iris have an abnormally thick 
 muscular layer. The adventitia also is more developed 
 than is commonly the case in blood-vessels of the same size. 
 
 The nerves of the iris which are hardly less numerous 
 than the blood-vessels, are on the whole arranged like these. 
 They come from the ciliary nerves and form very soon after 
 entering the iris a network with narrow meshes from which 
 branches run to the anterior and posterior surface, and into 
 the sphincter pupillae. Nothing certain is known with regard 
 to where and how they end. Faber also describes numerous 
 ganglion-cells in the iris. 
 
 The parenchyma of the iris contains, moreover, near the 
 pupillary margin the sphincter pupillae muscle. This is a 
 muscular ring which lies nearer the posterior than the ante- 
 rior surface of the iris. It consists of organic muscular fibres, 
 with a rod-like nucleus. While the existence of this muscle 
 is proven beyond a doubt, the same cannot be said of the 
 dilatator pupillae described as its antagonist. The fibres of 
 the latter are said to run in a radiating direction, from the cil-
 
 IRIS. 
 
 83 
 
 iary margin towards the sphincter and to unite with this mus- 
 cle, after being bent in an arch-like way. In the eyes of ani- 
 mals, especially of rabbits, these conditions are plainly to be 
 seen. I have, however, never yet been able to distinguish a 
 dilatator pupillae in the iris of the human eye. Iwanoff re- 
 cently tried to convince us that the spindle-cells of the pos- 
 terior layer of the iris are muscular fibres. This question can, 
 however, hardly be decided by the microscope alone, since 
 we all know, how difficult it is to distinguish by the mere 
 form and shape between organic muscular — and connective- 
 tissue cells. The effects of the different agents and staining 
 materials, upon the tissue give us more certainty, with regard 
 to this matter and even in the finest sections, I have never been 
 able to see anything which convinced me of the existence of a 
 dilatator pupillae in the human iris. 
 
 The posterior surface of the iris is covered by the very 
 darkly pigmented uveal layer. BrucJi discovered between it 
 and the posterior layer of the iris a lamina vitrea, like the 
 one upon the choroid and identical with it, {'' Bruc/is mem- 
 brane,"). Faber, too again recently maintained the existence 
 of this membrane. My own observations force me, however, 
 to agree with those authors who deny its existence in the 
 human iris. 
 
 It is very difficult to distinguish the elements which con- 
 stitute the uveal layer. With great care, it is, however, pos- 
 sible to recognize a number of round or oblong and irregu- 
 lary formed cells, which are densely crowded with pigment- 
 molecules, so that we can scarcely ever see the round nucleus. 
 These cells do not seem to possess a cell-membrane. Faber 
 describes still another kind of round cell with a cell-mem- 
 brane. It appears to me, however, that the whole of the 
 posterior part of the uveal layer is formed by a continuous 
 layer of protoplasma in which pigment-molecules are sus- 
 pended and which in transverse sections is often seen as a 
 fine light streak, forming the posterior margin of the iris. 
 
 This streak has been described as lamina pigmenti or 
 limiting membrane, and was lately by i^<3;(^^r again considered 
 to be a separate membrane. It is, however, impossible to de- 
 tach it, and pathological conditions, of which we shall speak
 
 84 I^HE HUMAN E YE. 
 
 later, do not allow us to recognize this streak as a separate 
 limiting membrane of the iris. 
 
 The uveal layer covers the whole of the posterior surface 
 of the iris and reaches somewhat farther than its pupillary 
 margin. 
 
 2. Pathological Conditions. 
 
 A . Iritis and its Results. 
 
 The different forms of iritis which are clinically distin- 
 guished can not be so separated histologically. The large 
 number of blood-vessels embedded in the parenchyma of the 
 iris must needs be the most important factors in causing the 
 symptoms of the different forms of iritis. Every inflamma- 
 tion of the iris is preceded by hyperaemia of the blood-vessels. 
 Such a hyperaemia of the iris must be considered as a dis- 
 tinct clinical affection from iritis. Histologically it does, 
 not however, appear to produce pathological alterations in 
 the tissue of the iris. The different forms of iritis are chiefly 
 characterized by the products of inflammation, the exudates 
 found upon the surfaces or in the parenchyma of the iris. 
 We consider in the following i. serous (sero-fibrinous ; hem- 
 orrhagic), 2. fibrinous (plastic) and i. purulent (parenchyma- 
 tous) forms of iritis. 
 
 a. Iritis serosa {serofibrinosa, hemorrhagica). 
 
 As in every other tissue, we find in the iris, as soon as it 
 is inflamed, a considerable degree of hyperaemia of the blood- 
 vessels and an increase of cells. In the beginning these cells 
 are exclusively emigrated, white blood-corpuscles, and no 
 signs of proliferation are to be found in the preexisting par- 
 enchymatous cells. The latter begin to proliferate at a later 
 period only. Besides these new cells, we find that the meshes 
 of the iris tissue, contain serous fluid, which makes them 
 appear distented, and renders the whole of the iris thicker 
 than normal. At the same time some serous fluid is exuded 
 upon the anterior and posterior surfaces of the iris, i. e. into 
 the posterior and anterior chambers.
 
 IRIS. 
 
 85 
 
 Serous iritis does not seem to materially alter the ante- 
 rior endothelial coat. The uveal layer, however, is mostly 
 altered in such a way, that its elements become remarkably 
 glutinous and the posterior surface of the iris thus becomes 
 adherent to the anterior capsule of the crystalline lens. I 
 have tried in vain in a large number of specimens to find cel- 
 lular elements which might unite the iris with the lens-cap- 
 sule. (I speak here only of cases of serous iritis). This may 
 explain why the posterior synechiae caused by serous iritis 
 are comparatively easier severed. If the pupillary edge of 
 the iris has thus become glued to the anterior lens-capsule, it 
 often happens that the exudate in the posterior chamber, 
 presses the periphery of the iris forward into the anterior 
 chamber, and thus causes the iris to become, what has been 
 styled " crater-shaped." (See Fig. 36). It seems that this 
 \ 
 
 Fig. 36. -Serous-iritis. The pupillary edge of the iris is adherent to the anterior lens-cap- 
 sule. The peripheral parts of the iris are protruding into the anterior chamber (crater- 
 shaped iris). 
 
 pressure from behind may produce atrophy of the blood- 
 vessels and the parenchyma of the iris, which conditions were 
 at least present in one such case which I examined. 
 
 As stated above, the endothelial cells upon the anterior 
 surface of the iris do not seem to be altered by serous iritis. 
 The latter, however, always produces pathological changes 
 in the endothelial cells lying upon Descemefs membrane. 
 These become irritated (probably by the pressure exerted 
 upon them) and begin to proliferate partially while others 
 become destroyed. In this way small deposits are formed 
 upon Descemefs membrane which consist of round-cells, free 
 nuclei and detritus. These sometimes become detached and
 
 85 THE HUMAN EYE. 
 
 then fall to the bottom of the anterior chamber. These 
 changes in the endothelial cells oi Descemef s membrane, make 
 it very probable that the endothelial cells upon the anterior 
 surface of the iris, do not remain unaltered, although I have 
 never been able to see any changes. 
 
 Serous iritis may perfectly recover and leave either no trace, 
 or only posterior synechiae behind. If this is not the case it 
 will become a chronic iritis, and will then lead to a more 
 active cell-proliferation in the parenchyma of the iris which, 
 ends in the new-formation of connective-tissue, and the grad- 
 ual atrophy and destruction of the preexisting cellular ele- 
 ments. Later on the blood vessels too, become atrophic, 
 which atrophy again produces atrophy of the whole of the 
 iris-tissue. This circulus vitiosus is materially aided in its 
 progress, by the pressure exerted upon the iris-tissue by the 
 exudation. 
 
 A variety of serous iritis is the sero-fibrinous and hsemor- 
 rhagic iritis. As far as I know, this kind of iritis has only 
 once been examined histologically, and described by myself. 
 Clinically it has been called iritis with a spongy exudation. 
 {Gunning, Knapp, Griiening). 
 
 The characteristic features of this kind of iritis are numer- 
 ous larger and smaller haemorrhages into the parenchyma of 
 the iris. While the fluid parts of the blood, are transuded 
 into the anterior chamber, its cellular elements remain lying 
 in the parenchyma of the iris, and there undergo the well 
 known changes of fatty destruction. The fibrine of the blood 
 coagulates in the anterior chamber, and is later on gradually 
 dissolved again from the cornea backwards. It happens that 
 at some time we find two different kinds of exudation in the 
 anterior chamber, viz., a gelatinous part near the cornea, and 
 a sero-fibrinous part upon the iris. (See Fig. 37). The latter 
 appears under the microscope as a network of very fine 
 fibrinous threads, not unlike those found in the alveoli in 
 croupous pneumonia, and filled with serum and a small num- 
 ber of lymphatic cells. The former is a perfectly uniform 
 transparent substance, which differs from the aqueous humor 
 only by being gelatinous. The dissolution and absorption 
 of this pecuhar exudation, always begins in the parts nearest
 
 IRIS. 
 
 87 
 
 the cornea and progress more or less concentrically. This 
 mode of absorption explains why at some time the exudation 
 is in shape and appearance very much like an opaque lens, 
 
 KiG. 37. — Hsetnorrhagic iritis (with spongy exudation). Haemorrhages in the parenchyma 
 of the iris. In the anterior chamber lies a fibrinous and a gelatinous exudation. 
 
 which before it was duly recognized, led to frequent errors 
 with regard to the treatment of this affection. 
 
 Serous inflammation of the iris may spread upon the cil- 
 iary body and choroid and thus produce more serious symp- 
 toms. It is also frequently combined with keratitis leading 
 to sclerosis of the involved part of the cornea. 
 
 b. Iritis fibrinosa {plasticd). 
 
 Fibrinous iritis shows besides hyperaemia of the blood- 
 vessels and an increase of cellular elements in the parenchyma 
 of the iris, a fibrinous exudation. This exudation generally 
 appears first at the pupillary edge and we then find besides 
 the adhesion between the posterior surface of the iris, and 
 the anterior lens-capsule (which we also found in cases of 
 serous iritis), an amorphous fibrinous coagulum upon the 
 pupillary region of the anterior lens-capsule. The exudation 
 is but seldom found upon the posterior, and yet more rarely 
 upon the anterior surface of the iris in the earlier periods of 
 the disease. The fibrinous coagulum usually contains some
 
 88 
 
 THE HUMAN EYE. 
 
 round-cells. If the process be arrested at this period the 
 fibrine may be dissolved, and totally absorbed. It is, however 
 very frequently found that the disease progresses and the 
 fibrine becomes an organized tissue. More round cells wan- 
 der into it and assume the spindle-shape, while the fibrine 
 is destroyed. We then find at some later period instead of 
 the fibrinous coagulum, a delicate membrane consisting of 
 spindle-cells, which however, later on is changed into a 
 fibrous and tough connective-tissue. This membrane, gener- 
 ally called pupillary membrane, usually spreads a short 
 distance upon the anterior and posterior surface of the iris. 
 (See Fig. 38). At a later period we frequently find that the 
 
 Fig. 38.— Plastic iritis. Pupillary membrane. 
 
 blood-vessels of the iris have grown into the pupillary mem- 
 brane. When this new-formed connective-tissue shrinks, 
 it, of course drags upon the iris, which thus is drawn towards 
 one side or towards the centre of the pupil and becomes 
 atrophic. If at the same time some fibrine has been exuded 
 upon the posterior surface of the iris, this may also be trans- 
 formed into connective-tsssue, which later on produces an 
 adhesion between iris and lens-capsule, materially different 
 from the common pupillary adhesion. 
 
 As above stated, fibrinous exudation, is but seldom de- 
 posited upon the anterior surface of the iris. It seems to 
 me that this happens only when the changes in the pupillary 
 region have taken place, and the posterior surface of the iris 
 has become adherent to the lens. In rare cases this fibrinous
 
 IRIS. 
 
 89 
 
 exudation is deposited in such a quantity, upon the anterior 
 surface of the iris that the anterior chamber is perfectly filled 
 with it. The exudation may here also become organized 
 and vascularized. Membranes thus formed, generally have a 
 lamellar structure, similar to the corneal tissue. They fre- 
 quently contain old or recent haemorrhages. (See Fig. 39). 
 
 Fig. 39. Plastic iritis.— New-formed connective-tissue upon the anterior surface of the iris. 
 This tissue is lamellar and contains blood-vessels. H. A large haemorrhage. 
 
 The alterations, caused by the above described conditions 
 in the parenchyma of the iris, produce perfect atrophy of 
 this membrane. The uveal layer frequently shows a very 
 peculiar appearance. In the beginning of the affection, it is 
 very much thickened, and when the fibrinous exudation lying 
 upon it becomes organized, it seems that the protoplasma, in 
 which the pigment-molecules are suspended is consumed. 
 The pigment molecules, thus freed, are drawn into the new- 
 formed connective-tissue, and the uveal layer appears several 
 times thicker than it does in the normal condition. 
 
 Fibrinous inflammation may, of course, also spread from 
 the iris upon the ciliary body and choroid. Furthermore, the 
 communication between the vitreous body and the anterior 
 chamber being perfectly cut off, the intra-ocular pressure, may 
 become increased and lead to results to be detailed farther on. 
 
 c. Iritis purutertta {parenchymatosd). 
 
 While in iritis serosa and fibrinosa we found the exuda- 
 tion to contain but few cells, the latter are the prevalent part 
 of the exudation of a purulent iritis. 
 
 Hyperaemia of the blood-vessels is at once followed by a 
 considerable emigration of round-cells, and proliferation of
 
 90 
 
 THE HUMAN E YE. 
 
 the parenchymatous cells of the iris. This causes the iris 
 to become rapidly swollen, and pus-cells wander into the 
 anterior chamber, at first probably through the meshes, of 
 the ligamentum pectinatum. If the changes progress, we 
 find that all the elements forming the tissue of the iris are 
 gradually destroyed. The proliferating parenchymatous cells 
 lose their pigment-molecules, which then are lying free be- 
 tween the cells, and free nuclei. Later on, the endothelial 
 cells, the muscular fibres, and lastly the blood-vessels take an 
 active part in the new-formation of round-cells. We find 
 these conditions, however, well pronounced only in cases of 
 purulent panophthalmitis, and we may then see the iris 
 replaced by a mass of round-cells and free nuclei, filling the 
 anterior chamber without showing any traces of muscles, 
 blood-vessels or even pigment, and in no way reminding one 
 of the normal conditions of the iris. We spoke of a similar 
 affection observed in the cornea, and called keratomalacia ; 
 it might be very appropriate to call this condition of the iris 
 iridomalacia. (See Fig. 40). 
 
 Fig. 40. — Purulent iritis. 
 
 Parenchymatous iritis may also appear as a merely local 
 affection, in the shape of a gumma or tubercle. In both 
 cases we find local swelling and accumulation of round-cells. 
 Colberg described a case of gumma of the iris. He found 
 free nuclei, gummy intercellular substance and new-formed 
 connective-tissue. These cell accumulations gradually under- 
 go a fatty metamorphosis, and the detritus is usually emptied 
 into the anterior chamber, after the anterior surface of the iris 
 has been ruptured. A small scar is generally the only, 
 remaining trace of such a local parenchymatous iritis. Gumma 
 as well as tubercle may, however, grow so large as to touch
 
 IRIS. 
 
 91 
 
 the posterior surface of the cornea. Anterior synechia may- 
 be thus formed with or without perforation of the cornea. 
 This is probably the only way in which anterior synechias of 
 the iris, is formed without preceding perforation of the cornea. 
 Diffuse purulent iritis, as stated above is chiefly found in 
 cases of purulent panophthalmitis. It may, however, also be 
 the primary affection, and lead to purulent panophthalmitis. 
 
 The Results of Iritis. 
 
 If iritis does not heal at an early stage, or if the in- 
 flammation, does not lead to the perfect destruction of the 
 eye-ball, by spreading over the remaining parts of this organ, 
 it leaves changes behind which always enable us to make a 
 a sure diagnosis, with the aid of the microscope. 
 
 a. Syne chics of the Iris. 
 
 The most frequent results of iritis are synechias of the 
 iris, especially posterior ones, anterior ones being only in ex- 
 ceptional cases caused by iritis. The name synechias is here 
 applied to the adhesion between the iris, (especially of its 
 pupillary edge), and the anterior capsule of the lens. 
 Synechias are caused by all the three forms of iritis. In 
 cases of simple synechias, I never could, find an organized 
 tissue, between iris and lens-capsule. In transverse sections 
 the uveal layer simply lies close upon the lens-capsule. If 
 we try to sever the synechias, the uveal layer, is torn and 
 remains partly upon the lens-capsule, partly in connection 
 with the iris. I suppose chemical processes cause these ad- 
 hesions which the microscope cannot possibly detect. The 
 conditions are very different when the whole of the posterior 
 surface of the iris is glued to the lens, in the pupillary mem- 
 branes and the new-formed tissue upon the anterior surface 
 of the iris. Here we always find anew-formed connective- 
 tissue, which at first contains a large number of cells, and 
 later on becomes tougher, denser, and loses the cellular ele- 
 ments. It is then generally vascularized by new-formed 
 blood-vessels starting from the blood-vessels of the iris. 
 (See Fig. 41.) During the period of retraction, this new-
 
 92 
 
 THE HUMAN E YE. 
 
 formed tissue drags upon the tissue of the iris and causes 
 it to atrophy. 
 
 Fi;.. 41. — New-formed connective-tissue uniting tiie posterior surface of the iris with the 
 anterior lens-capsule after plastic iritis. 
 
 b. Atrophy of the Iris. 
 
 Besides the just mentioned atrophy of the iris, caused by 
 pressure and tearing from parts outside the parenchyma of 
 the iris, atrophy of the latter may be, and is frequently the 
 result of chronic iritis. The atrophy is then the direct con- 
 sequence of the new-formation of connective-tissue, in the 
 parenchyma of the iris, or the pressure exerted upon it by the 
 exudation of serum into its meshes and interstices. It seems 
 that the first to suffer from atrophy, are the pigmented 
 parenchyma cells. They undergo fatty degeneration, become 
 granular, and are broken up. Their pigment is then found 
 scattered about in the tissue ; later on it may nearly alto- 
 gether disappear. The last to become atrophic are the uveal 
 layer and the muscular tissue of the sphincter pupillae, and 
 even in the highest degrees, of atrophy of the iris, they are 
 not totally destroyed. 
 
 In one case of very far advanced atrophy of the iris, I 
 found the anterior endothelium, in a state of colloid meta- 
 morphosis. (See Fig. 42.) With a low magnifying power it 
 appeared like a new-formed transparent lamella, covering the 
 anterior surface of the iris. (Similar vitreous lamellae, upon the 
 iris have been described by a number of authors, and declared 
 to be inflammatory new-formations ; perhaps, they ought to
 
 IRIS. 
 
 93 
 
 have been explained in the same way as the one under con- 
 sideration). With a high power it was easily seen to consist 
 of endothelial cells, filled with colloid substance. 
 
 Fig:. 42— Iritis chronica. Atrophy of the iritis and colloid metamorphosis of its anterior 
 
 endothelial coat. 
 
 Atrophy of the whole iris, of course, invoh'es also its 
 blood-vessels and nerves. 
 
 B. Injuries to the Iris and their Results, 
 Injuries to the iris are mostly combined with an injury to 
 the cornea or sclerotic or even more parts of the eye-ball. It 
 is easily understood that the histological conditions are 
 accordingly complicated. We will however, here mention 
 only those injuries which involve cornea, or sclerotic and iris, 
 and those which concern the iris alone. 
 
 Foreign bodies which enter the eye, only very seldom 
 remain lodged in the tissue of the iris. They either perforate 
 it and pass farther on, or rebound and fall into the anterior 
 chamber. If however, they remain lodged in the iris, they 
 produce at first a local, later on a diffuse iritis, which gener- 
 ally assumes a purulent character. More does not seem to 
 be known, with regard to the anatomical conditions. Foreign 
 bodies intentionally brought into the iris of animals, lead also 
 to the growth of sarcomatous new-formations. 
 
 The injury may sever the tissue of the iris to a varying 
 extent. The wound may lie at the pupillary edge, or in the 
 part between it and the ciliary margin, or at the latter, or the 
 whole of the breadth of the iris, may be rent apart in a 
 radiary direction, or it may reach from the sphincter or ciliary 
 edge, into the part between the two. If the iris tissue is thus 
 once severed, the gap generally remains a permanent one.
 
 94 
 
 THE HUMAN E YE. 
 
 The edges of such a wound heal through a small amount of 
 fibrine which becomes exuded and organized upon them. 
 The healing process after wounds caused by operations too, 
 show nothing peculiar. 
 
 Rents of the sphincter edge of the iris (coloboma) and the 
 separation of the ciliary edge of the iris from the ligamentum 
 ■ pectinatum and the ciliary body (iridodialysis) are not unfre- 
 quently caused by injuries which do not at the same time 
 rupture either of the hard membranes of the eye-ball. Rup- 
 tures of the part of the iris, between its pupillary and ciliary 
 margins, are probably always combined with wounds of one 
 or both of the hard membranes. 
 
 If the cornea or the corneo-scleral margin has been rup- 
 tured by the injury, the aqueous humor will flow out, and 
 the either wounded or normal iris, becomes entangled in the 
 wound-lips, or is thrown further into the wound-canal. This 
 causes the formation of an anterior synechia (leucoma ad- 
 haerens) or a prolapse of the iris, which may either become 
 reduced or remain stationary. If the prolapse of the iris 
 remain stationary, the prolapsed part may either decay, and 
 fall off (and thus again an anterior synechiae be the result) or 
 it may become the starting point of a granuloma of the iris, 
 of which more later on. 
 
 The histological conditions in cases of anterior synechiae, 
 of the iris have been spoken of above (See chapter I). I 
 must mention here, however, a condition resulting from 
 anterior synechiae, and involving the iris only. I mean the 
 formation of serious cysts of the iris. Von Wecker & Knapp 
 have stated (and I once had occasion to confirm their 
 statement) that serous cysts of the iris may be formed, if 
 a fold of this membrane, becomes adherent to the posterior 
 surface of the cornea (or to a wound-canal in the latter), that 
 is, that the parenchyma of the iris takes no active part in the 
 formation of these cysts. The walls of such a serous cyst of 
 the iris which I had occasion to examine were two-thirds 
 formed by the atrophic iris, and one-third by the posterior 
 surface of the cornea, and were thus perfectly lined with the 
 endothelium of the anterior chamber. (See Fig. 43.) 
 
 The cavity formed in such a way inside the anterior cham-
 
 IRIS. 
 
 95 
 
 ber, becomes larger through the pressure of the aqueous 
 humor secreted by it. Von Wecker states that such a cyst 
 
 Fig. 43 — So-called cyst of the iris, formed after an injury to the cornea. The walls of the 
 cyst are formed by Descemet's membrane, the atrophic iris and some new-formed con- 
 nective-tissue, and lined with the endothelium of the anterior chamber. 
 
 may separate itself at a later period from the cornea. This 
 appears rather improbable from the anatomical conditions, 
 and, moreover, clinical experience shows that these cysts 
 are firmly adherent to the cornea, and therefore are nearly 
 always ruptured in the attempt to remove them by an opera- 
 ration. 
 
 What we described above as crater-shaped iris, that is, 
 the bulging and atrophy of the periphery of this membrane, 
 subsequent to circular posterior synechia of the pupillary 
 margin, is by von Wecker enumerated among the cysts of 
 the iris. 
 
 Some authors described another variety of cyst, in the 
 parenchyma of the iris filled with atheromatous substance, 
 and always resulting from an injury which has been called 
 " epidermoidoma." Krause's observations leave no doubt 
 that these cysts are caused by epithelial cells, from the hair- 
 follicles of the eye-lashes, which are thrown into the pa- 
 renchyma of the iris during the infliction of an injury, arc 
 there retained, and then begin to proliferate. This is the 
 more probable, as generally in these cases one or more ciliie 
 were found in the anterior chamber or in the tissue of the 
 iris. 
 
 It follows therefore from the facts above stated, that 
 serous cysts of the iris are improperly so-called, and originate
 
 96 
 
 THE HUMAN E YE. 
 
 in an injury followed by the adhesion of a fold of the iris to 
 the cornea. Atheromatous cysts lie really in the parenchyma 
 of the iris, and are usually caused by an injury without the 
 formation of anterior synechise between this membrane and 
 the cornea. 
 
 The conditions resulting from prolapse of the iris, were 
 studied by me some time ago, experimentally on the eyes of 
 animals. The results of these examinations were published, 
 without however, applying the lessons they taught uncon- 
 ditionally to the human eye. Numerous specimens from the 
 human eye have since then, taught me, that I would have 
 been justified in doing so. 
 
 Very soon after the iris has prolapsed into a wound-canal 
 of the cornea or sclerotic, it becomes infiltrated with blood 
 in consequence of the stasis of its blood-vessels. If the pro- 
 lapse protrudes through the cornea, it may become necrotic 
 and be thrown off. The outer orifice of the wound-canal is 
 then covered by new-formed connective-tissue and epithelium, 
 and we thus find again the conditions of an anterior synechia. 
 If the prolapse is small, it may be covered in toto with scar- 
 tissue (See Fig. 44), into which a fibrinous exudation coming 
 
 Fig. ^4.~ Incarcerated iris. Small prolapse of the iris into a corneal wound, covered with 
 new-formed connective-tissue and epithelium. 
 
 from the iris is gradually transformed. This is especially the
 
 IRIS. 
 
 97 
 
 case when the iris has prolapsed at the corneo-scleral margin 
 (for instance after operations in that region). The epithe- 
 lium which finally covers such a prolapse in the corneo-scleral 
 region, takes the greater part of its origin from the conjunc- 
 tiva. The final stationary condition has received the name 
 of" incarceration " of the iris. 
 
 Injuries to the eye without inflicting wounds may some- 
 times cause a part, or the whole of the pupillary edge of the 
 iris to be tilted backwards. Such cases have, however, it 
 seems, never been microscopically examined. 
 
 • 
 C. Tumors of the Iris. 
 
 a. Granuloma Traumaticum. 
 
 Although clinicists have described a genuine (non-tran- 
 matic) granuloma of the iris, only the traumatic one has so 
 far been microscopically studied. The results of my own 
 examinations of three such cases, perfectly agree with those 
 of Hirschberg and Steinheim. 
 
 Prolapse of iris, or those parts which are exposed to the 
 air through the destruction of the cornea, often become the 
 origin of such tumors. The latter consist of round and small 
 spindle-cells, between which are found a small amount of 
 connective-tissue and new-formed blood-vessels. (See Fig. 
 45). The tumor may or may not be covered by epithelium. 
 It is probable that, like other granulomata this, also may be 
 transformed into connective-tissue and thus heal by itself. 
 
 HirscJiberg and Von Weckcr also count among the granulo- 
 mata of the iris a vascular tumor, described by Mooren, but 
 not examined anatomically. Schirmer mentioned a " cav- 
 ernous " tumor of the iris which probably belonged to the 
 same class. 
 
 b. Melanoma. 
 
 Knapp was, as far as I know, the first to describe sim- 
 ple melanoma of the iris after having seen a specimen of 
 J. Arnold's. It " consisted of circumscribed accumulations of 
 stroma-cells of the iris, the larger part of which were pig- 
 mented, had many offsets and anastomosed with each other.
 
 98 
 
 THE HUMAN EYE. 
 
 They passed without a sharp boundary into the neighboring 
 tissue, and the remainder of the iris was normal." This kind 
 
 Gr 
 
 Fig. 45. — Traumatic granuloma of the iris after this membrane has prolapsed. Gr. Gran- 
 uloma. C. Cornea. D. Descemet's membrane. Ir. Iris. Cc. Ciliary body. L.C 
 Lens-capsule. 
 
 of tumor is certainly very rare. Like all the so-called benign 
 melanomata, it is said to be able at any time to assume a 
 malignant character. 
 
 c. Leucosarcoma and Melanosarcoma. 
 
 Primary sarcomata of the iris are very rarely met with. 
 Only four such cases have so far been anatomically examined 
 and described {Dreschfeld, Knapp, Hirschberg, Kipp.) 
 
 It seems that the new-formation takes its origin from the 
 parenchyma of the iris. In Dreschfeld' s case only, it was 
 said to have started from the connective-tissue between the 
 muscular fibres. 
 
 From these different descriptions, we know of unpig- 
 mented {Kipp) pigmented {Hirschberg) spindle-cell sarcoma, 
 and pigmented round-cell sarcoma. All of the tumors were 
 very vascular. Judging from the structure of the iris, we 
 may expect (and the descriptions prove it), that the pig- 
 mented tumors have also some unpigmented parts and vice 
 versa. Dreschfeld found some small nests of organic muscu- 
 lar fibres in his case, and considered this proof, that the 
 tumor originated in the intra-muscular connective-tissue. 
 
 Sarcoma of the iris seems to grow comparatively slowly.
 
 CORPUS CI LI A RE. gg 
 
 It causes, like other intra-ocular tumors, glaucoma, and leads 
 to destruction of the eye. 
 
 Metastic tumors caused by primary sarcoma of the iris, 
 have been clinically observed. 
 
 V. Corpus Ciliare. 
 I. Normal Conditions. 
 
 The tissue of the ciliary body consists of the same ele- 
 ments as that of the iris. We find here as the outermost layer 
 (near the sclerotic) an endothelial coat, then the parenchyma 
 and inwards from this, the pigmented uveal layer which, 
 moreover, is here covered by another layer, viz., the ciliary 
 part of the retina. While the surfaces of the iris are com- 
 paratively smooth, the inner surface of the ciliary body, has a 
 large number of processes and corresponding indentations. 
 The former are called the ciliary processes. 
 
 The parenchyma of the ciliary body, like that of the iris, 
 consists in the main part of cellular elements. We here 
 again find round unpigmented cells, and cells with offsets 
 which are either pigmented or unpigmented. The pigmented 
 cells with offsets are very numerous, only in the eyes of 
 negroes. In the eyes of the white races, the tissue of the 
 ciliary body has chiefly unpigmented cells. Besides the cells, 
 we find a larger quantity of connective-tissue fibres, and elastic 
 fibres in the ciliary body, than in the iris. The connective- 
 tissue prevails in the outer parts (near the sclerotic), while the 
 cellular elements form mainly the inner layers of the ciliary 
 body. 
 
 Embedded in this tissue is the ciliary muscle. It con- 
 sists, as well known, of circular (equatorial) and longitudinal 
 (meridional) fibres. The longitudinal fibres lie in the outer, 
 the circular ones more in the inner part, of the ciliar}'' body. 
 The two kinds of fibres are, however, not perfectly dis- 
 tinct from each other, as a fibre may at first run in a longi- 
 tudinal and then in a circular direction and vice versa. The 
 elements of this muscle are organic muscular fibres. 
 
 Iwanoff was the first to point out that the proportion, 
 between the two kinds of fibres (circular and longitudinal),
 
 lOO THE HUMAN E YE. 
 
 varies in different eyes. He found that in myopic eyes, that 
 is, eyes which are very long, the longitudinal fibres prevail 
 (See Fig. 46), while in hypermetropic, that is, short eyes, the 
 
 Fig. 46. — Ciliary body from a myopic eye. 
 
 circular fibres, which are but few in an emmetropic eye, are 
 very numerous. (See Fig. 47). Rvanoff, however, has at 
 
 Fig. 47. — Ciliary body from an hypermetropic eye. 
 
 the same time to confess there are many exceptions to these 
 conditions. 
 
 To explain the mode in which accommodation takes 
 place, a number of hypotheses have been put forward and, 
 strange to say, most of them would presume just the reverse 
 condition, of the ciliary muscle from that which we frequently 
 find. This has already been pointed out by Loring. It is 
 not the place here to speak of the physiological action of this 
 muscle, but I have to state, that in eyes suffering from ciliary
 
 CORPUS CI LI A RE. lOI 
 
 or total staphyloma we find the same conditions, with regard 
 to the ciliary muscle as in myopic eyes, i. e. only longitudinal 
 fibres. This would show that any stretching of the ciliary 
 muscle, is enough to produce such conditions. 
 
 The question, how the ciliary muscle acts, when the eye 
 accommodates, can only be satisfactorily solved, by closely 
 studying the development of this muscle, and it would, be 
 very important to know, for instance, whether in a case of 
 non-progressive myopia this muscle presents the same ar- 
 rangement soon after birth, that it does in the later periods of 
 progressive myopia. The authors on the development of 
 the eye have, it seems, all neglected to study this point, 
 which is of such great importance. In the eyes of two newly 
 born children I only found longitudinal fibres, although the 
 shape of the eyes impressed me as being that of emmetropic 
 ones. 
 
 The fibres of the ciliary muscle are joined anteriorly in a 
 tendon which passes over into Descemefs membrane, and the 
 posterior lamellae of the cornea in the way, described above 
 (See Chapter I). Posteriorly the muscular fibres end in the 
 outer layers of the choroid in peculiar star-like formations 
 {leropheeff, Iwanoff), some of them pass into the sclerotic. 
 
 On equatorial sections through the ciliary body, it is seen 
 that the separation into longitudinal and circular fibres, which 
 is so well pronounced in meridional sections, is only apparent, 
 and that the fibres interlace at all sorts of angles. 
 
 The blood-vessels of the ciliary body come from the 
 arteriae ciliares posteriores longae and the arterias ciliares an- 
 teriores. Their structure shows nothing peculiar. The 
 larger part of their branches lie in the layers to the inner side 
 of the ciliary muscle. The veins of the ciliary body conduct 
 the blood either to the small veins coming from the cornea 
 (resp. conjunctiva), or to the vorticous veins {Leber). 
 
 The nerves constituting a net- work of the ciliary body, 
 come from the ciliary nerves. They lie chiefly upon the 
 outer surface of the ciliary muscle, from where smaller 
 branches enter the latter. It is not known how and where 
 they end. 
 
 If we sever the ciliary body (or choroid) from the sclero-
 
 102 THE HUMAN E YE. 
 
 tic, a number of fibres will remain in connection with the 
 latter, which have been called the lamina fusca. This 
 lamina is, however, not an independent membrane. As 
 stated above, some of the fibres of the ciliary muscles insert 
 themselves into the sclerotic, moreover, connective-tissue 
 fibres from the sclerotic enter the ciliary body, (and choroid) 
 and vice versa. It is therefore easily comprehended that in 
 separating the two layers, we tear these fibres apart. The part 
 remaining adherent to the sclerotic is the lamina fusca, the 
 part remaining connected with the ciliary body (or choroid) is 
 the so-called lamina suprachorioidea. Both of these parts are 
 formed by the fibres joining the hard membranes of the eye 
 and the uveal tract which {J. Arnold^ have one and the same 
 origin in the embryo. A structureless, homogeneous inter- 
 fibrillar substance, as described by Iwanoff, I cannot find. 
 The meshes between the fibres contain, however, a serous 
 (lymphatic) fluid which coagulates when the eye is hardened. 
 
 Between these fibres lie a large number of pigmented 
 cells. These are very irregular in shape, and have mostly 
 short, broad offsets, and are flat. Their large oval or round 
 nucleus is unpigmented. Besides these pigmented cells of 
 various shapes, {Iwanoff also described round ones), there 
 are unpigmented endothelial and lymph-cells. The latter 
 hafrve nothing peculiar. The existence of the former is proven 
 by staining with nitrate of silver. They form a continuous 
 coat upon the inner surface of the sclerotic, and the outer 
 surface of the ciliary body (and choroid), perforated only by 
 the fibres running from one of these parts to the other 
 Endothelial cells also lie upon the latter in the same way in 
 which we found them, adherent to the fibres of the ligamen- 
 tum pectinatum. 
 
 The parenchyma of the ciliary body is, on its inner sur- 
 face, covered by a thin, elastic vitreous membrane which is, 
 however, only continuous upon the so-called /^ri- non-plicata 
 Anteriorly to this it is perforated, and thus forms a net-work, 
 the meshes of which are oblong in a longitudinal direction 
 {Iwanoff). I can not, however, perfectly agree with Iwanoff, 
 who could trace this vitreous membrane even upon the ciliary 
 processes, for I never found it there.
 
 CORPUS CI LI A RE. 
 
 103 
 
 The uveal layer of the ciliary body, lies on the inner sur- 
 face of this vitreous membrane. It consists of cells which 
 vary considerably in shape and size. They are densely filled 
 with pigment-molecules, which leave only the round nucleus 
 free. The cells are united to each other by a structureless 
 cementing substance and form one, or sometimes several 
 layers. It is very difficult to distinguish the single cells 
 upon the ciliary processes and the uveal layer here greatly 
 resembles that of the iris. Where the lamina vitrea forms 
 the above described network, the pigmented cells lie in the 
 meshes. 
 
 Upon the inner surface of the uveal layer of the ciliary 
 body, lies the pars ciliaris retinae. The elements of this mem- 
 brane are according to the latest authors, to be considered as 
 the continuation of Mueller s supporting fibres of the retina. 
 
 The ciliary part of the retina, consists of one layer of more 
 or less cylindrical cells, which gradually decrease in size 
 towards the insertion of the iris. They are unpigmented and 
 have a round or oval nucleus which lies near their basis. 
 Where the vitreous body lies upon them, they are flat or 
 cone-shaped, and some of them have small offsets. We find 
 sometimes a very thin vitreous membrane lying upon them, 
 which is probably the remainder of the membrana limitans 
 interna of the retina. 
 
 2. Pathological Conditions. 
 
 A. Cyclitis and its Results. 
 
 From the similarity which exists between the structure 
 of the iris and the ciliary body, and their direct connection, we 
 may a priori expect to find the pathological processes of the 
 ciliary body analogous to those of the iris. 
 
 The three forms of cyclitis which will be spoken of pres- 
 ently, and which mostly are found at the same time with 
 similar affections in the iris or choroid, are: i. serous (sero- 
 fibrinous), 2. fibrinous (plastic) and 3. purulent cyclitis. 
 
 a. Cyclitis Serosa. 
 Serous cyclitis is hardly ever found without coexisting
 
 I04 
 
 THE HUMAN EYE. 
 
 serous iritis. The ciliary body in this disease appears very 
 hyperaemic, and the tissue around the blood-vessels contain a 
 few emigrated white blood-corpuscles. The exudation char- 
 acteristic of this kind of cyclitis is found in the posterior 
 chamber and the vitreous body, sometimes also in the tissue 
 of the ciliary body itself. If the pupillary margin of the iris 
 is at the same time adherent to the anterior capsule of the 
 crystalline lens, the exudation in the posterior chamber 
 will press the periphery of the iris forward, and give it the 
 crater-shape, above referred to. The pressure may be such 
 as to bring the peripheric parts of the iris in direct contact 
 with the posterior surface of the cornea, and if the condi- 
 tion does not soon heal, it induces atrophy of the tissue of 
 the iris. With the secretion of the serous fluid in the an- 
 terior part of the vitreous body an increased emigration of 
 cells nearly always occurs. In this way larger agregations 
 of cells are formed in the anterior part of the vitreous body, 
 and not infrequently deposited upon the posterior capsule 
 of the crystalline lens. In the latter case, the exudation is 
 mostly not of a purely serous, but of a sero-fibrinous charac- 
 ter, and the cells upon the lens-capsule are then embedded 
 in threads of fibrine. (See Fig. 48). 
 
 Fig. 48.— Sero-fibrinous cyclitis. Amorphus fibrine, containing numerous round-cells, lies 
 upon the posterior lens-capsule. 
 
 If the exudation is secreted by the tissue of the ciliary 
 body itself, it forces the fibres of the ciliary muscle apart, 
 and if this condition persists, they become atrophic. (See 
 Fig. 49). In rare cases only, we also find the inner cellular
 
 CORPUS CI LI A RE. 
 
 105 
 
 layers of the ciliary body, viz,, the uveal layer and the ciliary 
 part of the retina to take an 
 active part in the serous in- 
 flammation. They then show 
 a small degree of proliferation. 
 If the intra-ocular pressure, as 
 is not seldom the case, becomes 
 increased during the process, 
 these layers suffer accordingly. 
 Serous cyclitis like serous 
 iritis, may recover without 
 leaving a trace. More fre- 
 quently, however, it does not 
 pass off so simply. The results 
 of complications to which it 
 
 leads, will be discussed further ^"'■'*9- -serous cyclltis. The exudation lies 
 
 in the tissue of the ciliary body itself, and 
 on. presses the muscular fibres apart. 
 
 b. Cyclitis Fibrinosa {Plasticd). 
 
 The form of cyclitis most frequently met with, is the 
 fibrinous or plastic. Although this form may be found un- 
 complicated, it is in the majority of the cases combined, with 
 inflammatory processes, in other parts of the eye-ball (espec- 
 ially of the iris.) 
 
 We here again find the blood-vessels hyperaemic, and the 
 surrounding tissue more or less infiltrated with emigrated 
 white blood-corpuscles. Characteristic of this form of 
 cyclitis, is the fibrinous exudation. This is at first deposited 
 upon the inner surface of the ciliary body and zonula Zinnii. 
 In more serious cases we find it filling the whole of the pos- 
 terior chamber and traversing the eye-ball between the iris 
 and the crystalline lens, and behind the latter. 
 
 Doubtlessly this exudation may at an earlier period be 
 again absorbed, and so the serious results of plastic cyclitis 
 may be prevented. The affection is, however, more frequent- 
 ly observed to progress, and the fibrine becomes organized. 
 After it has been filled with round-cells, blood-vessels are 
 seen to grow into it, coming from the ciliary body, and 
 sometimes from the peripheral parts of the retina, and thus
 
 io6 
 
 THE HUMAN E YE. 
 
 the amorphus fibrinous substance is gradually changed into 
 a delicate connective-tissue. In this way the periphery of 
 the iris frequently becomes adherent to the ciliary processes, 
 and the posterior chamber obliterated. Moreover this new- 
 formed connective-tissue may cover the remainder of the 
 ciliary body, enclose the zonula Zinnii, and lying upon the 
 posterior capsule of the crystalline lens, traverse the whole 
 of the eye-ball. (See Fig. 50.) 
 
 Kk;. 50.— Plastic cyclitis. Cyclitic membrane upon the posterior lens-capsule. The pos- 
 terior chamber is obliterated. Lens and iris are pressed forward. 
 
 This whole process may go on without materially altering 
 the uveal and retinal layers of the ciliary body. More fre- 
 quently, however, we see that these layers take an active 
 part in the formation of the cyclitic membrane, especially 
 the retinal part of the ciliary body. The cylindrical cells of 
 this layer proliferate and begin to grow out into long spindle- 
 shaped cells, and finally into long connective-tissue fibres. 
 This alteration of the retinal layer, always begins at the 
 junction between pars plicata and pars nonplicata of the 
 ciliary body. The parts lying more anteriorly are only in- 
 volved later on and never to so great an extent. (See Fig. 51.) 
 
 Meanwhile the cells of the uveal layer have also under- 
 gone proliferation. The whole layer appears very much 
 thickened and grows into the cyclitic membrane in an irregu- 
 lar way. We also observe, however, frequently a more typ- 
 ical kind of proliferation of the cells of the uveal layer in the 
 shape of cylindrical tubes, which grow into the cyclitic mem-
 
 CORPUS CILIA RE. 
 
 107 
 
 brane and give off branches. In longitudinal and transverse 
 sections, these tubes appear like the glandulce tubulosa; or 
 
 Fig. 51. — Plastic cyclitis. Shows how the cells of the retinal layer of the ciliary body are 
 changed into spindle-cells and aid in the formation of a cyclitic membrane. 
 
 the epithelial cylinders of an epithelioma. The cells of these 
 tubes are either free of pigment or pigmented. Their shape 
 and arrangement with their branches have given some authors, 
 {Schiess-Gemuseus) the idea that they were blood-vessels, 
 whose walls were filled with pigment. Specimens in which 
 the blood-vessels have been 
 injected with a colored 
 fluid, however, plainly 
 show that they are widely 
 different from blood-ves- 
 sels. They appear, as 
 stated, just like glands or 
 epithilioma-cylinders. (See 
 Fig. 52). 
 
 Not all the cells orig- 
 inating by proliferation 
 from the uveal layer are 
 pigmented, and I am even 
 convinced that the young cells of this layer are at first always 
 unpigmented and form their pigment only later on. For this 
 
 Fig. 52.— Plastic cyclitis. Tubular excrescences 
 of the pigmented (uveal) layer of the ciliary 
 body.
 
 io8 
 
 THE HUMAN E YE. 
 
 reason we find in cycHtic membranes also the same tubular 
 formations without any pigment at all, which can nearly 
 always be traced backward to a pigmented cell-tube or the 
 uveal layer itself. (See Fig. 53). 
 
 Fig. 53. — Plastic cyclitis. 
 
 The same tubular excrescences. The younger ones as yet un- 
 pigmented. 
 
 Small and large haemorrhages are frequently found in cy- 
 clitic membranes, and later on, deposits of lime are very com- 
 mon. Such membranes may furthermore become changed 
 into osseous tissue. 
 
 Cyclitic membranes, like all new-formed connective-tissue, 
 begin at some period to shrink, and thus cause further path- 
 ological processes in the eye-ball. At first the nutrition of 
 the crystalline lens is impaired to such a degree, as to cause 
 the formation of cataract. Then the retraction, influences 
 directly the ciliary body, and the neighboring part of the cho- 
 roid. These parts become detached from the sclerotic, and 
 drawn inward — and forward. It is evident, that this detach- 
 ment could not take place if the consistency of the vitreous 
 body had not before been materially altered, and that it 
 must at the same time lead at least to the peripheral detach- 
 ment of the retina. (See Fig. 54). Plastic cyclitis may, also, 
 produce detachment of much larger parts, or even the whole
 
 CORPUS CILIA RE. IO9 
 
 of the retina, and give rise to chronic inflammatory processes 
 in all parts of the eye-ball, which finally produce phthisis 
 bulbi. 
 
 Fig. 54.— Plastic cyclitis. Cylitic membrane. Detachment of the ciliary body. 
 
 c. Cyclitis Purulenta {Parenchymatosd). 
 
 This form of cyclitis is observed especially after injuries 
 to the ciliary body itself, and as a part of purulent panoph- 
 thalmitis. Hyperaemia of the blood-vessels is always here 
 followed by the rapid formation of pus-cells. In the 
 earlier periods, the affection lies chiefly in the inner layers of 
 the ciliary body, and we find its inner surface covered with a 
 fibro-purulent substance. Gradually, however, the disease 
 spreads, and then later on we find that nearly all the layers 
 of the ciliary body, take an active part in the formation of 
 the pus-cells. The last to become involved, are the fibres of 
 the ciliary muscle which, like the nerves, seem to be very 
 resistant. When the disease has advanced so far, we find the 
 whole of the tissue of the ciliary body transformed into a 
 mass of round cells, between which lie the free pigment- 
 molecules and some muscular fibres. (See Fig. 55). 
 
 Raab at a recent date thought that in a case of purulent 
 panophthalmitis described by him, the origin of the affec- 
 tion was to be found in embolism of a ciliary blood-vessel- 
 This, I think, is for obvious reasons highly improbable, and 
 has not been observed by others.
 
 1 1 o THE H UMAN E YE. 
 
 Purulent cycHtis may as it seems, heal again at an early 
 period. If it does not, it leads to the perfect destruction of 
 the involved tissue. 
 
 Fig. 55. — Purulent cyclitis. 
 
 In most cases of purulent cyclitis, we find the anterior 
 portion of the vitreous body, also filled with threads of fibrine 
 and pus-cells. 
 
 Except after direct injuries to the ciliary body, purulent 
 cyclitis is but rarely a primary disease. If it is the primary 
 affection, the inflammation spreads very easily over the 
 remainder of the uveal tract. If the iris becomes involved, 
 we see the formation of hypopyon, if the disease spreads 
 upon the choroid, this is generally the beginning of a puru- 
 lent panophthalmitis. 
 
 This form of cyclitis, like parenchymatous iritis, may also 
 be found perfectly localized in the shape of an accumulation of 
 round cells, as gumma or tubercle. A gumma of the ciliary 
 body which I once had the occasion to examine, consisted 
 of such an accumulation of round-cells, which were so crowded 
 that they began to decay in the centre of the little tumor. 
 The muscular fibres were simply pushed aside and com- 
 pressed. No blood-vessels were found in the tumor. (See 
 Fig. 56.) 
 
 Purulent cyclitis may result from plastic cyclitis. This we
 
 CORPUS CI LI A RE. 
 
 Ill 
 
 must assume to be the case, whenever we find purulent 
 cyclitis and a cyclitic membrane, since the former never leads 
 to the formation of such membranes. 
 
 i. 
 
 Fig. 56.— Gumma of the ciliary body. I. Iiis. L. Lens. G. Gumma. Cm. Cyclitic membrane. 
 
 Results of Cyclitis. 
 Serous cyclitis usually heals without leaving a trace ; but 
 the other varieties generally cause some changes in the tissues 
 of the eye-ball, which allow of a certain diagnosis. 
 
 a. Cyclitic Mejttbranes. 
 I already have mentioned the way in which cyclitic mem- 
 branes are formed. It is certain that the retinal layer of 
 the ciliary body, when proliferating, is of great importance 
 in these new-formations, and often even their starting point. 
 The latter statement is proven, by the fact that we not in- 
 frequently find in eyes suffering from cyclitis, the beginning 
 cyclitic membrane to consist of nothing, but the proliferated 
 cells of the retinal layer. They grow towards the posterior 
 pole of the crystalline lens, and I am in the possession of 
 specimens, where this latter is as yet perfectly free. In these 
 cases the cyclitic product consequently does not form a 
 membrane, but only a ring. In other cases, the centre of 
 this ring is filled with an amorphous fibrinous substance, 
 which is deposited upon the posterior capsule of the crys- 
 talline lens.
 
 112 
 
 THE HUMAN EYE. 
 
 The cells of the uveal layer of the ciliary body, are mostly 
 destroyed during the formation of a cyclitic membrane, espe- 
 cially those of the pars non-plicata, and their pigment, being 
 freed, is with the growing membrane drawn towards the 
 centre. In other cases we find besides, partial destruction of 
 the uveal cells, a very active proliferation and new-formed 
 cells, which grow into the cyclitic membrane arranged in 
 gland-like, cylindrical and tubular formations. These start 
 chiefly from the pars non-plicata of the ciliary body. 
 
 At the same time with these changes, we find new-formed 
 blood-vessels growing into the cyclitic membrane, which in 
 consequence, is often very vascular. The new blood-vessels 
 not infrequently give rise to haemorrhages in these mem- 
 branes. I also mentioned above, that these membranes often 
 contain deposits of lime, and undergo ossification. 
 
 At a certain stage, cyclitic membranes, like all new-formed 
 connective-tissues, begin to shrink. If the cyclitis has at the 
 same time produced alterations in the posterior parts of the 
 eye, and especially in the vitreous body, this shrinking will 
 cause the ciliary body and the neighboring parts of the 
 choroid to become detached from the sclerotic. Thus we 
 may find, in a meridional section through such an eye-ball, 
 that two diametrically opposite ciliary bodies have been 
 drawn so much towards the centre, that they nearly touch 
 each other. (See Fig. 57). The same process may further 
 
 KiG. S7— Plastic cyclitis from an eye with anterior phthisis. The cyclitic membrane is very 
 considerably shrunken, and brings the ciliary bodies nearly in contact with each other. 
 
 on produce total detachment of the retina, which, however, 
 is generally preceded by an increase of intra-ocular pressure, 
 and excavation of the optic nerve entrance.
 
 CORPUS CI LI A RE. 
 
 ^3 
 
 b. Atrophy. 
 
 Although most of the cases of cyclitis, unless they heal, 
 lead to the formation of a cyclitic membrane, there are a 
 number of cases in which such a membrane is totally want- 
 ing, and yet we can judge from the conditions of the ciliary 
 body, that cyclitis must have existed during life. I had in 
 one case only, the occasion to find an undoubted hypertro- 
 phy, of the muscular tissue 
 in the ciliary body of an eye 
 which had been injured 
 (See Fig. 58). It seems 
 therefore that cyclitis may 
 cause hypertrophy of the 
 muscular tissue. Whether 
 this hypertrophy is only a 
 spurious one, and leads 
 later on to atrophy, or 
 whether it may remain per- 
 sistent, I cannot decide. 
 In most cases (without a 
 cyclitic membrane) we find 
 atrophy of the ciliary body, 
 as the result of cyclitis. ^ „ „ .. . , , 
 
 •' Fig. 58.— Hypertrophy of the cilary muscle in a 
 
 The pigmented and the caseofcyciitis. 
 
 retinal layer, as a rule, remain unaltered, while all the ele- 
 ments of the parenchyma of the ciliary body become atrophic. 
 In the most advanced cases, we find but a very thin layer of 
 connective-tissue, separating the uveal and the retinal layers 
 from the sclerotic, as the remainder of the ciliary body. In 
 the blood-vessels and nerves such cases no longer exist. 
 
 c. Staphyloma. 
 
 The mode in which chronic cyclitis may help in the forma- 
 tion of corneal and ciliary staphylomata, has been explained 
 in Chapter I. 
 
 B. Injuries to the Ciliary Body and their Results. 
 Wounds of the ciliary body but rarely happen except the
 
 114 
 
 THE HUMAN EYE. 
 
 part of the sclerotic covering it, has been pierced. The cih'ary 
 body, may however, also receive an injury from its inner 
 surface, after the foreign body has perforated other parts of 
 the eye (mostly the cornea, iris and crystalline lens). I found 
 furthermore, in several eyes which had been enucleated for 
 haemophthalmus subsequent to a contusion, a rupture of 
 the ciliary body. In one case the rupture beginning at its 
 outer surface, reached into the muscular tissue. (See Fig. 59). 
 
 Ruptures of one or more of 
 the blood-vessels of the cil- 
 iary body and subsequent 
 haemorrhagic infiltration, of 
 its tissue, are not rare in 
 eyes having received a con- 
 tusion. 
 
 If the instrument by which 
 the injury is inflicted, has 
 pierced the sclerotic and cil- 
 iary body, the latter generally 
 prolapses, and this prolapse 
 may, of course, be combined 
 with an injury to the lens. 
 
 Fig. 59.-Isolated rupture of the ciliary body. (i^'lS, COmca, choroid,) and 
 The eye was enucleated on account of prolapse of the vitrCOUS body. 
 haemophthalmus. The tissue of the cil- ^ u j T 1 u u 
 
 iary body was perfectlyfllled with blood. ->UCn WOUndS heal by the 
 
 (The latter has not been drawn, to show formation of a SCar-tisSUC, 
 the rupture better.) 
 
 preceded by the exudation of 
 fibrine into the wound-canal. The scar-formation is as a rule 
 assisted in by all of the wounded tissues (of course with the 
 exception of the crystalline lens). Later on we then find a 
 tough and frequently pigmented band of scar-tissue, uniting 
 the ciliary body firmly with the sclerotic. In a number of 
 cases the inflammation will spread, and then besides the 
 local changes we find in the wound a general plastic, or puru- 
 lent inflammatory process. 
 
 If the foreign body enters the ciliary body from the inte- 
 rior of the eye-ball, the same conditions may be found, as 
 have just been detailed. If the foreign body is very small, 
 it may remain embedded in the ciliary body, and then a
 
 CORPUS CILIA RE. 
 
 115 
 
 capsule of tough connective-tsssue is gradually formed around 
 it. In the large majority of cases, however, such a foreign 
 body will cause purulent cyclitis. 
 
 If this local inflammation gives rise to a general purulent 
 inflammation, the eye-ball may be perfectly destroyed. In- 
 juries to the ciliary body are, furthermore, among the most 
 frequent causes of sympathetic affections of the fellow-eye. 
 
 C. Tumors of the Ciliary Body. 
 
 a. Myoma. 
 
 Iwanoff has so far described the only case of myoma of 
 the ciliary body, known in literature. The tumor of the size 
 of a filbert, consisted of or- 
 ganic muscular fibres in the 
 parts nearest to the sclero- 
 tic ; the inner parts con- 
 sisted of connective-tissue. 
 It appears from this de- 
 scription rather doubtful 
 whether this tumor can be 
 really called a myoma. 
 
 b. Sarcoma. 
 
 Sarcoma, especially the 
 melanosarcoma, is the new- 
 formation most frequently 
 found to originate in the 
 ciliary body, (perhaps the 
 only one). These tumors 
 come, however, as a rule, 
 under the hands of the 
 anatomist, when their origin 
 can only be guessed at. It 
 
 , - , , , Fig. 60.— Primary melanosarcoma of the ciliary 
 
 therefore happened that body, 
 
 leucosarcomata and melanosarcomata and such sarcomata 
 which were partly pigmented, partly unpigmented, have 
 been described and said to have originated in the ciliary body 
 without a direct proof, that this was really the case. I only
 
 I 1 5 THE HUMAN E YE. 
 
 once had the occasion to examine a true case of pigmented 
 round-cell sarcoma of the ciliary body. (See Fig. 60). The 
 whole of the ciliary body in this case consisted of darkly 
 pigmented round-cells between which no longer any trace of 
 the muscular fibres could be found. 
 
 The mode in which sarcomatous tumors of the choroid 
 spread over the ciliary body, will be detailed when these 
 tumors are spoken of. Primary sarcoma of the ciliary body 
 is certainly of very rare occurrence. 
 
 VI. Choroidea. 
 
 I. Normal Condition. 
 
 The choroid consists of the vascular parenchyma, an ex- 
 terior coat of endothelium (upon its scleral surface,) and the 
 lamina vitrea. Upon the latter, lies the pigmented (uveal) 
 epithelium which was formerly considered to be part of the 
 choroid, but has recently been assigned to the retina. 
 Since it suffers always, however, when the choroid is in a 
 pathological condition, it will be spoken of after the choroid. 
 
 The parenchyma of the choroid, like that of the iris and 
 ciliary body, consists of a small amount of connective-tissue, 
 some elastic fibrillae and pigmented or unpigmented cells. 
 The cells of the parenchyma of the choroid appear to be scat- 
 tered equally over the whole of its thickness. The pig- 
 mented cells are, however, less numerous in the part which 
 lies directly outward from the lamina vitrea (the capillary 
 layer). The pigmented cells of the choroid, have mostly 
 several long offsets, and accordingly vary considerably in shape. 
 Their nucleus is round or oval, and free from pigment. The 
 pigment, filling the main body of the cell and the offsets, is 
 granular and very varying in its tint. While it can hardly 
 be called brown in albinotic eyes, it appears perfectly black 
 in the eyes of a negro, and prevents us frequently from dis- 
 cerning the nucleus of these cells. The unpigmented cells 
 are less numerous, and vary in shape, in the same way as do 
 the pigmented ones. Some of them are undoubtedly lym- 
 phatic cells, others appear as free nuclei, without being sur- 
 rounded by protoplasma. 
 
 The blood-vessels are a most important part of the paren-
 
 CHOROIDEA. 
 
 \\^ 
 
 chyma of the choroid. They form two groups, viz., the 
 capillary blood-vessels, which lie nearer the inner, and the 
 venous vessels which lie nearer the outer surface of the 
 choroid. The arteries which chiefly conduct the blood to 
 this membrane, are the short posterior ciliary arteries. After 
 having pierced the sclerotic near the optic nerve entrance 
 and entered the choroid, they branch off and these new 
 branches form the capillary network of the choroid, which 
 ends with an indented margin at the ora serrata {Leber). 
 The long posterior and the anterior ciliary arteries, send 
 small branches backwards to these vessels in the choroid. 
 The veins into which the blood passes from the capillaries, 
 collect it into from four to six larger branches, the vorticous 
 veins, which leave the eye through the sclerotic. The veins 
 as well as the arteries have perivascular sheaths. Sattler 
 has also proved the existence of such sheaths around the 
 capillaries, which, as it appears from his researches, lie free in 
 cavities which are in direct communication with the perivas- 
 cular sheaths of the larger vessels. The same author found 
 two endothelial membranes separating the capillaries from 
 the veins. I have not been able to convince myself by my 
 own observation, of the existence of these endothelial mem- 
 branes. Pathological conditions, however, especially the 
 way in which parenchymatous haemorrhages may split the 
 choroid into two layers, make it very probable, that Sattler s 
 statement is correct. 
 
 The parenchyma of the choroid furthermore, contains a 
 great many nerves. They come from the nervi ciliares breves 
 and longi, and form a net-work of pale nerve-fibres in the 
 choroid, which follows largely the arrangement of the blood- 
 vessels, and has great many ganglionic cells. The fibres of 
 this network end in the capillary layer ; the manner of their 
 termination is, however, not yet known. The ganglionic 
 cells are very large, and lie together in clusters. Several 
 authors have found organic muscular fibres in the choroid. 
 The mode in which the muscular fibres of the ciliary muscle 
 end in the choroid, has already been explained. 
 
 All that has been said in the previous chapters about the 
 laminae fuscae and suprachoroideae, holds good for the same
 
 ii8 
 
 THE HUMAN EYE. 
 
 parts of the choroid. I may only add, that the larger 
 branches of the ciliary nerves, pass through this layer of 
 fibres, and there form a network with wide meshes, before 
 entering the parenchyma of the choroid. 
 
 The choroid and sclerotic adhere more firmly to each other 
 around the optic nerve-entrance, where a larger number of 
 blood-vessels and fibres coming from the sclerotic, enter the 
 choroid. The choroid has no more a large round hole by 
 which the optic nerve enters the eye-ball in toto, than the 
 sclerotic, as we sec fibres from the so-called lamina cribosa, 
 enter the choroid and vice versa. The question whether 
 blood-vessels from the posterior parts of the choroid, pass 
 over into the optic nerve-entrance or retina, is not yet con- 
 sidered perfectly settled. Knapp has drawn such a picture 
 from a diseased eye, and Fig. 6i, taken from a normal eye, 
 
 1 
 
 Fig. 6i. — Normal entrance of the optic nerve into the eye-ball. i. A blood-vessel coming 
 from the choroid and entering the retina. 
 
 cannot leave any doubt as to the existence of such blood- 
 vessels, although they may not be found in every eye. 
 
 The inner surface of the choroid is covered by the thin 
 lamina vitrea. This is an elastic and perfectly transparent 
 membrane, upon which the (uveal) pigmented epithelium 
 lies. Recently it has been said to have a fibrous structure. 
 It is not yet known, how this membrane is united with the 
 underlying tissue. Sattler found upon its outer surface a 
 network, which he expressly says is not formed by fibres.
 
 CHOROIDEA. I 1 9 
 
 The pigmented epithelium, lying between the choroid and 
 retina, has lately, (first by Babuchin) been declared to be a 
 part of the retina. J. Arnold has, however, more recently 
 stated, that it is not yet, perfectly proven, that the lamina 
 pigmenti, (the pigmented epithelium), is formed from the 
 atrophic posterior lamella of the secondary ocular vesicle in 
 the foetus, and this conscientious author feels himself able 
 to state only, that the lamina pigmenti, "replaces" the pos- 
 terior lamella of the secondary ocular vesicle. This is the 
 more important, as the normal or pathological conditions of 
 the pigmented epithelium, are certainly found to depend 
 much more upon the conditions of the choroid, than upon 
 those of the retina. Nearly every pathological condition of 
 the choroid, exerts its influence upon the pigmented epithe- 
 lium, while the most important changes may happen in the 
 tissue of the retina, without any alteration whatsoever, in the 
 condition of the pigmented epithelial cells. Furthermore, if 
 we take the retina out of a normal eye, these cells do not ad- 
 here to it, but remain lying upon the choroid. 
 
 Most recently it has been found that this layer of epithe- 
 lial cells secretes the retinal purple, {Kuehne, Boll). It repre- 
 sents therefore a kind of gland, lying between retina and 
 choroid, as an independent organ. 
 
 The cells forming this epithelial layer are mostly hexa- 
 gonal. They are united with each other by a structureless 
 cementing substance, and form one single layer of flattened 
 epithelium. Their nuclei are round and unpigmented; their 
 protoplasm is filled with granular pigment. The pigmenta- 
 tion varies considerably in the cells of one and the same eye. 
 In the eyes of negroes, the pigment is as a rule very dark, 
 but it rarely altogether hides the nucleus. 
 
 In some eyes, especially those of old people, the cement- 
 ing substance between these cells is found to be much broader 
 and thicker, and if the cells are carefully removed, a tough 
 network remains lying upon the lamina vitrea of the choroid, 
 the meshes of which are filled by the cells. (See Fig. 62). 
 
 Nearly all of the recent authors on this subject, have de- 
 scribed and drawn very fine and long offsets which the cells 
 of the pigmented epithelium are said to send in between the
 
 1 20 THE HUMAN E YE. 
 
 rods and cones of the retina. They are said to be either pig- 
 mented or unpigmented. Schwalbe, one of these authors, 
 states, however, that in the human eye they produce only a 
 very loose union between the retina and the pigmented 
 epitheHum. I must confess, that I have searched in the hu- 
 man eye in vain for these offsets. In eyes taken from corpses 
 which have begun to decay, a condition similar to the granu- 
 ular offsets, drawn by Schwalbe, is frequently seen ; in fresh 
 eyes, however, or eyes put into Mueller s hardening fluid 
 when perfectly fresh, I cannot find them. 
 
 Cells with two or more nuclei are rare among the normal 
 pigmented epithelial cells, but there are always a number of 
 small cells, which are probably of a more recent date. 
 
 2. Pathological Conditions. 
 A. Pathological Changes of the Pigmented Epithelium. 
 It seems to me that before we go on to a description of 
 the different kinds of inflammation the choroid is subject to, 
 this is the proper place to speak of the pathological changes 
 observed in the pigmented epithelium. Nearly every patho- 
 logical process in the choroid involves this layer, and we 
 would thus be forced to frequently repeat the same ; on the 
 other hand, there are a number of pathological changes ob- 
 served in the pigmented epithelium which are peculiar to it, 
 and more or less independent of any affection of the choroid. 
 The most common pathological alteration the cells of the 
 pigmented epithelium undergo, is that they lose their regular 
 shape and uniformity in size. The new forms are very mani- 
 fold, and the pigment lies mostly in the periphery of the pro- 
 toplasma, in these cells. It seems also, as if the pigment 
 could — so to speak, be secreted by one and taken up by 
 another cell in its neighborhood. The latter then appears 
 perfectly black. Later on round or oblong, light (empty or 
 filled ?) structures are seen inside the cells, which by some 
 authors are considered to be colloid-globules, by others to be 
 vacuolae. If the cells are altered in such a way, the cement- 
 ing substance is found to be either hardened, and to remain 
 adherent to the lamina vitrea (See Fig. 62), or to have ap- 
 parently altogether disappeared.
 
 CHOROIDEA. 
 
 121 
 
 Combined with these alterations, we very frequently find 
 between the pigmented epithelial cells, round or oval, trans- 
 parent, hard bodies which ad- 
 here to the lamina vitrea. 
 These have by English au- 
 thors, received the name of 
 colloid excrescences of the 
 lamina vitrea, and have been 
 often described as such. There 
 
 U^,,,«Tr^^ ^^ ^^ C i-X^^i- Fig. 62.— Thickened and hardened intercel- 
 
 IS, however, no proof that i,,ar substance from the pigmented epi- 
 
 these bodies consist really of theliallayer, lying upon the lamlna vitrea 
 
 1, . , 1 , ,, . of the choroid; i, containing lime. 
 
 colloid substance; their per- 
 fect resistance to all chemical agents, and their hardness 
 would on the contrary tend to prove that they are not of a 
 colloid nature. In transverse sections, they resemble very 
 much the corpora arenacea of the coats of the brain. (See 
 Fig. 63). The fact, that they lie upon the lamina vitrea, 
 
 Fig. 63.— Vitreous bodies upon the lamina vitrea of the choroid; i, containing lime. 
 
 and are only found, where the pigmented epithelium is 
 altered in the manner above referred to, seems to prove that 
 their formation is caused by these, and Mayer has recently 
 tried to show that these bodies are really secreted by the 
 cells of the pigmented epithelium. I must agree with him 
 in considering this the most probable way in which they 
 are formed, although I have seen a great number of speci- 
 mens, in which it appeared as if they were the result of a 
 degenerative process of the cells themselves. While the 
 smaller sized vitreous bodies are generally covered by a
 
 122 
 
 THE HUMAN EYE. 
 
 continous layer of pigmented epithelial cells, part of which 
 are new-formed, these cells are gradually destroyed as the 
 vitreous bodies grow larger and coalesce. This may be 
 simply the consequence of the pressure, but it is possible 
 also, that the protoplasma of the cells is the material, by 
 which these vitreous bodies grow. Through these changes, 
 the pigment molecules become free, and seem to be taken 
 up by the more or less normal cells which surround the basis 
 of the vitreous bodies, and which now appear perfectly 
 dark, and sometimes in a state of proliferation. 
 
 It has often been stated that these bodies are peculiar to 
 old" age. This may in the majority of cases really be so ; 
 they are, however, found in the eyes of young individuals 
 also, for I found an immense quantity of them once in the 
 eye of a boy twelve years of age. 
 
 Later on amorphous lime is frequently deposited inside 
 these vitreous bodies and, in spite of their hardness, it cannot 
 be impossible for cells to penetrate into them, as they may 
 become organized in the form of osseous tissue. (See 
 Fig. 64). 
 
 Fig. 64. — Formation of osseous tissue in the vitreous bodies of the lamina vitrea choroidea:. 
 
 An undue and pathological new-formation of cells, is not 
 infrequent in the pigmented epithelial layer. It is seen in 
 nearly all of the cases of choroiditis and we have already 
 spoken of it, when describing the changes caused by cyclitis. 
 The new-formed cells are, (as stated already by Virchoiv) at 
 first nearly always free from pigment. They are, however, 
 as it seems, able to form their pigment at any time them- 
 selves. The new-formation of cells may produce a simple 
 thickening of the pigmented epithelium, by superposing 
 layer after layer of new cells. The formation of tubular
 
 CHOROIDEA. 
 
 123 
 
 offsets, similar to the epithelial cyHnders of an epitheliomata, 
 appears, however, to be more frequent. (See Fig. 65). 
 
 Fia. 65.— Tumor-like new-formation of pig^mented and unpigmented celUcylinders. starting 
 from the uveal layer of the ciliary body and neighboring choroid. 
 
 An affection of the retina of great clinical importance, is 
 caused by such an hyperplasia of the pigmented epithelium, 
 without any pathological change in the choroid, vis.^ pig- 
 mentary retinitis. In such cases the tubular offsets of the 
 pigmented epithelium are partly pigmented, partly unpig- 
 mented, and grow into the retina, after having first destroyed 
 its outer layers. In the retina, these foreign substances 
 cause a chronic interstitial inflammation, which leads to 
 hypertrophy of the connective-tissue, and to destruction of 
 the nervous elements. (See Fig. 66). Furthermore, new
 
 124 
 
 THE HUMAN E YE. 
 
 connective-tissue is formed in the perivascular sheaths of 
 the retinal blood-vessels (perivasculitis) and these become 
 
 Fir.. 66. — Pigmentary retinitis. Pigmented cell cylinders going over in such cylinders with- 
 out pigment. Blood-vessel changed into connective-tissue. 
 
 gradually obliterated. It seems that this process often 
 begins in the peripheral parts of the retina ; in a case which 
 I described recently, it involved only a zone of retinal tissue, 
 ten millimetres in width, and equally distant from the ora ser- 
 rata and the optic-nerve entrance. That the peripheric vision 
 is at first impaired in cases of this affection, does not depend 
 alone on the disease usually beginning in the peripheral parts 
 of the retina, but also upon the diminished quantity of 
 nutritive fluids, furnished to these parts. 
 
 We shall see later on that some forms of choroiditis, may 
 be followed by a very similar kind of pigmentation of the 
 retina. The genuine pigmentary retinitis is, however, a sec- 
 ondary affection, caused without any affection of the choroid 
 proper, by the primary pathological new-formation of cells of 
 the pigmented epithelial layer.
 
 CHOROIDEA. 125 
 
 During the process of this disease, the pigmented cells 
 may enter the perivascular sheath of a retinal blood-vessel. 
 (See Fig. 6"/). The primary disease is, however, not one of 
 the blood-vessels, as has been stated by former authors. 
 
 Fig. 67. — Pigmentary retinitis. Pigment in the perivascular sheatli of a retinal blood-vessel. 
 
 The cells of the pigmented epithelium may undergo fatty 
 degeneration. This seems to be most frequent in eyes with 
 total detachment of the retina. Such cells, are then often 
 transformed into aggregations of round fat-granules (Koern- 
 chenkugeln), which may or may not contain some pigment 
 molecules. 
 
 B. Choroiditis and its Results. 
 The large number of different forms of choroiditis which 
 the clinicists treat of, are anatomically summed up under the 
 following three heads, viz., i. serous (serous-fibrinous), 2. fibrin- 
 ous (plastic) and 3. purulent (parenchymatous choroiditis). 
 This distinction is made according to the products of the 
 inflammatory process. These are exuded either into the 
 tissue of the choroid itself, or into the parts lying to the inner 
 side of this membrane, (the pigmented epithelium, retina and 
 vitreous body), and we find therefore most cases of cho- 
 roiditis complicated with inflammatory processes in other 
 parts of the eye-ball, (especially the pigmented epithelium, 
 the retina and vitreous body). 
 
 a. Choroiditis Serosa {sero-fibrinosd). 
 
 Serous choroiditis, which is not infrequently met with, 
 has recently been perfectly identified with glaucoma. This
 
 126 THE HUMAN EYE. 
 
 Standpoint has been chiefly accepted by Schmit-Rimpler 
 and von Wecker in Gmfe and ScemiscJi s Cyclopaedia. 
 Although, as will be shown further on, it is possible 
 that glaucomatous symptoms result from serous choroiditis, 
 we do not always find serous choroiditis when there is glau- 
 coma. Whoever has had the occasion to examine a number 
 of glaucomatous eyes, will know that it is impossible in most 
 of the cases, to detect any change in the condition of the 
 choroid. 
 
 Serous choroiditis, which I therefore do not identify with 
 glaucoma, is ushered in by hyperaemia of the blood-ves- 
 sels, especially the veins of the choroid. This hyperaemia 
 may concern the whole of the choroid, or be more or less 
 localized. I found it several times to be confined to one 
 vorticous vein, or even only to a large branch of one. This 
 hyperaemia is followed by the exudation of a serous, some- 
 times a sero-fibrinous fluid. In hardened specimens, it ap- 
 pears that this fluid is but very rarely exuded into the tissue 
 of the choroid itself, which is, however, no proof that the 
 conditions are not different in life. The serous exudation is 
 mostly found inwards from the choroid, between the lamina 
 vitrea and the pigmented epithelium, or between the pig- 
 mented epithelium and the retina, or between retina and 
 vitreous body, (especially in their posterior half), or in the 
 vitreous body itself. Furthermore, I frequently found in 
 cases of serous or sero-fibrinous choroiditis, small round and 
 oval cavities in the outer granulur layer of the retipa, filled 
 with a sero-fibrinous fluid, the formation of which may be 
 caused directly by the disease of the choroid, before a sec- 
 ondary affection of the retina can be developed. 
 
 Some more recent authors have proven that chemical, not 
 histological alterations in the tissues of the eye, are the chief 
 cause of the serous exudation. If this exudation is not soon 
 absorbed, it will produce different pathological alterations, 
 in the condition of the tissues according to the place where it 
 lies. It may lead to partial or total detachment of the retina 
 (with or without the pigmented epithelium), from the choroid, 
 or to detachment of the vitreous body from the retina, or it 
 may simply produce liquefaction of the vitreous body. The
 
 CHOROIDEA. 127 
 
 consistency of the latter must, of course, have been consider- 
 ably altered, before either it or the retina can become de- 
 tached, and especially in cases of total detachment of the 
 retina, the vitreous body must either have been totally lique- 
 fied or condensed. The liquefaction of the vitreous body is, 
 however, found too, without being accompanied by detach- 
 ment. I must state here that every detachment of the 
 retina is not caused by serous choroiditis. There are quite a 
 number of factors, which may come into play in detaching 
 the retina from the choroid, which have already been partially 
 and will be more fully described further on. 
 
 The increased production of serous fluid within the eye- 
 ball, especially when the means of exit are pathologically 
 altered, or totally obliterated, may so increase the intra-ocu- 
 lar pressure, that we find later on, all the symptoms of glau- 
 coma, including excavation of the optic nerve. This is espe- 
 cially found in eyes suffering from some kind of staphyloma 
 (except posterior sclero-choroidal staphyloma). 
 
 Sometimes we find the number of wandering cells in the 
 choroid considerably increased in cases of serous choroiditis. 
 There is, however, in the choroid at least no sign of cell- 
 proliferation to be detected. The vitreous body also is 
 usually filled with a larger number of cells, and the serous 
 exudation contains them. The cells of the pigmented epithe- 
 lium are partially proliferating, partially undergoing a regres- 
 sive metamorphosis. If the exudation remains for a long 
 time lying in the same place, we frequently find crystals of 
 cholesterine formed, and lime deposited in it. The former 
 appear always in the well known tablets ; the lime is amor- 
 phous. The formation of vitreous bodies upon the lamina 
 vitrea of the choroid, is frequently met with in such cases. 
 
 h. Choroiditis Fibrinosa {plasticd). 
 
 Plastic choroiditis never attacks the whole choroid, but 
 appears in numerous small patches, which may by con- 
 fluence grow larger. Hyperaemia of the choroid in this form 
 of inflammation, is followed by a fibro-cellular exudation 
 at first into the tissue of the choroid itself. (See Fig. 68). 
 We then find in such a place, a round or oval accumulation
 
 128 
 
 THE HUMAN EYE. 
 
 of fibrinous substance involving mostly the whole thick- 
 ness of the choroid, and filled with and surrounded by round- 
 
 Fig. 68. — Plastic choroiditis. Fibro-cellular exudation in the tissue of the choroid. 
 
 cells. If the process of exudation goes on, the lamina vitrea 
 is perforated, and the fibrinous substance may remain 
 under the thus detached pigmented epithelium. In the 
 majority of cases, however, this layer, too, is perforated, and 
 the exudation enters the tissue of the retina. This fibrinous 
 substance, is later on transformed into connective-tissue, 
 which at some period will begin to shrink. If the fibrine has 
 been exuded only into the tissue of the choroid, we find, 
 later on unpigmented, round and oval patches, which are 
 very thin and consist of connective-tissue, without either 
 blood-vessels or cellular elements. In these cases, also where 
 the exudation has not directly involved the pigmented epi- 
 thelium, we find it later on changed, and the cells covering 
 the patch of exudation lose their pigment and may be totally 
 destroyed, which latter condition is caused by the pressure 
 exerted upon them, as well as by impairment in their nutri- 
 tion. Their pigment having thus been freed, is taken up by 
 the cells in the periphery of the patch of exudation, which 
 consequently appear abnormally dark. If the exudation has 
 once perforated the lamina vitrea, the retina is always sure 
 to suffer, although to a greatly varying degree. The rods 
 and cones alone may be destroyed, and the pigmented epi- 
 thelium adhere to the retina. If the pigmented epithelium 
 has been perforated by the fibrinous exudation, the latter
 
 CHOROIDEA. 
 
 129 
 
 will enter the retina and there produce a local interstitial 
 inflammation. When the fibrinous substance has been trans- 
 formed into connective-tissue and begins to shrink, retina 
 and choroid will thus become firmly adherent to each other. 
 (See Fig. 69). Moreover, the pigmented epithelium cells 
 
 Fig. 69.— Plastic choroiditis. Adhesion between retina and choroid. 
 
 may begin to proliferate and so to produce either a thick- 
 ening of this layer, or form the above described tubular ex- 
 crescences. If the latter be the case, the retina becomes 
 pigmented in the manner we have seen, in the so called pig- 
 mentary retinitis. (See Fig 70). All these processes are clin- 
 ically called chorio-retinitis. 
 
 Fig. 70. — Plastic choroiditis. Pigmentation of the retina. 
 
 In rare cases the fibrine may be exuded directly upon the 
 inner surface of the lamina vitrea, i. e. between lamina vitrea 
 and pigmented epithelium. 
 
 Retraction of the new-formed connective-tissue, uniting 
 retina and choroid in the manner above referred to, may 
 cause the neighboring parts of the retina, to become de- 
 tached from the pigmented epithelium. 
 
 The disease may in the first stages, heal by absorption ; 
 in most of the cases, however, it progresses and leads to the 
 local new-formation of connective-tissue and atrophy just
 
 I30 
 
 THE HUMAN E YE. 
 
 detailed. Vitreous bodies upon the lamina vitrea, are fre- 
 quently observed in eyes so affected. 
 
 There are a number of clinically distinct forms of cho- 
 roiditis, which anatomically all belong under this head, viz., 
 choroiditis disseminata, atrophica, exudativa, areolaris, cho- 
 rio-retinitis disseminata and chorio-retinitis centralis. The 
 latter name means that the affection is confined to the region 
 of the macula lutea. 
 
 The small patches of exudation may lie very close to each 
 other, and finally by coalescing, form very large ones. The 
 original patches are, however, always comparatively small. 
 
 c. Choroiditis Purulenta {Parenchymatosd). 
 
 The characteristic feature of purulent choroiditis, is the 
 enormous emigration and new-formation of cells, in the paren- 
 chyma of the choroid, which may lead to perfect destruction 
 of this membrane. The affection is in most of the cases a dif- 
 fuse one, and concerns the whole of the choroid. We also find, 
 however, local round-cell accumulations, like, abscesses at the 
 same time with the diffuse affection. In the very advanced 
 cases, the whole of the structure of the choroid, is simply 
 represented by an innumerable mass of round-cells. (See 
 Fig. 71). Knapp says that the formation of pus always be- 
 
 FiG. 71. — Purulent choroiditis. 
 
 gins in the capillary layer. This is not, however, without 
 exception, the case. All of the different elements constitu- 
 ting the tissue of the choroid, even the muscles, take an 
 active part in the formation of round-cells. The lamina
 
 CHOROIDEA. 
 
 131 
 
 vitrea is frequently perforated, and thus the pus enters into 
 the parts lying inwards from the choroid. The pigmented 
 epithelium begins to proliferate, and the retina becomes de- 
 tached. The vitreous body appears very soon pervaded by 
 a large number of pus-cells. The formation of pus may also 
 involve the inner layers of the sclerotic, and, when progressing, 
 lead to perforation of this membrane. The purulent inflam- 
 mation seldom remains confined to the choroid, but generally 
 spreads over the other parts of the uveal tract, or over all the 
 other membranes of the eye-ball, that is, it produces a puru- 
 lent panophthalmitis. 
 
 This form of acute purulent (diffuse) choroiditis, is either 
 of spontaneous origin, or is caused by an injury. The spon- 
 taneous form is frequently called " metastatic " choroiditis, 
 especially when found in individuals suffering from pyaemia. 
 It is, however, not yet undoubtedly proven, that in such 
 cases, the choroiditis must really be considered as a metastic 
 affection. Raab, who, as I already stated, found an embolus 
 in a ciliary artery, considered this to be proof of the metas- 
 tatic character of this variety of choroiditis. 
 
 Tubercles of the choroid, are local parenchymatous affec- 
 tions. Although such tubercles have frequently been exam- 
 ined with the microscope, the similar gummatous affection, 
 which from clinical observation may doubtless happen, does 
 not seem to have so far been examined histologically. The 
 tubercles have nothing peculiar in the choroid. They are an 
 
 Fig. 7a.— Tubercle of the choroid. 
 
 accumulation of round-cells in the parenchyma of this mem- 
 brane, and frequently contain giant-cells. (See Fig. 72). They 
 may be found in all parts of the choroid, single or coalescing.
 
 132 
 
 THE HUMAN EYE. 
 
 Acute purulent choroiditis, almost always take on a chro- 
 nic form. Secretion of pus ceases, the blood-vessels are all 
 destroyed, and formation of connective-tissue ensues. We 
 may thus have the opportunity of examining such eyes at a 
 period, when the tissue replacing the choroid, is six or more 
 times as thick as this membrane appears in the normal condi- 
 tion. This thickening is, however, not persistent, but fol- 
 lowed by shrinking of the new-formed tissue, and perfect 
 atrophy of the eye-ball. 
 
 The nerves may be found unaltered, even in the most 
 violent forms of purulent choroiditis. When the process has, 
 however, led to perfect atrophy of the choroid, we usually 
 look for them in vain. 
 
 Besides acute parenchymatous choroiditis, which goes 
 over into the chronic form, we sometimes observe a purulent 
 choroiditis, which is from the beginning of a chronic charac- 
 ter. This frequently leads to the deposition of lime, in the 
 parenchyma of the choroid, and to the formation of osseous 
 tissue. We have seen above, that the formation of osseous 
 tissue may take place in the vitreous bodies lying upon the 
 lamina vitrea of the choroid, and I am inclined to look upon 
 
 Fig. 73. — Osseous tissue, with marrow in the choroid. 
 
 these bodies as being more frequently the origin of the 
 osseous tissue, than we suspect, especially when it is found 
 lying upon the inner surface of the lamina vitrea.
 
 CHOROIDEA. 133 
 
 The formation of bone in the choroid in the beginninij, 
 usually takes place in its inner layers {Knapp). Later on, 
 the whole choroid may be found thus altered. The osseous 
 shell, formed in such a manner, never reaches farther an- 
 teriorly, than to the ciliary body. In its posterier part, it 
 is usually perforated by the optic nerve or retina. The 
 osseous tissue differs in no way from the normal osseous 
 tissue, and in rare cases may even contain cavities filled with 
 marrow. (See Fig. jt,). 
 
 Since chronic parenchymatous choroiditis usually leads 
 to chronic inflammatory processes of the eye-ball, which 
 cause the new-formation of connective-tissue, we have to look 
 upon it as the chief cause of the shrinking of the whole 
 eye-ball, known under the name of phthisis bulbi, and of con- 
 sequent sympathetic affections in the fellow-eye. 
 
 The Results of Choroiditis. 
 
 a. Detachment of the Retina and Vitreous Body. 
 
 In consequence of serous choroiditis, we may find, as 
 above stated, the retina detached from the choroid, and the 
 vitreous body from the retina. Detachment of the retina 
 may be total or only partial. We always find in these cases 
 (when the detachment has been caused by serous choroiditis) 
 more or less exudation between the retina and choroid, 
 which, in spite of the means used to harden the eye-ball, 
 remains sometimes perfectly fluid, or may become gelatinous. 
 
 It is most probable that during life, the retina too, is 
 saturated by this serous fluid, and isoedematous. Some small 
 round or oval cavities in the external granular layer, filled 
 with a sero-fibrinous fluid, were all I could find in hardened 
 eyes to prove this. The retina, too, clearly suffers from 
 some other pathological processes, which will be detailed 
 presently. With the retina, a number of cells of the pig- 
 mented epithelial layer, or even large parts of this layer may 
 be detached. Vitreous bodies from the lamina vitrea may 
 also adhere to the detached retina, and in one case, where I 
 found osseous tissue in the detached retina, this had most 
 probably originated in such detached vitreous bodies.
 
 134 THE H UMA N E YE. 
 
 The vitreous body may be found detached from the 
 retina by serous fluid, whether this membrane is removed 
 from the choroid in the manner just stated, or whether it 
 is in its normal position. The vitreous body then appears 
 condensed and pressed forward towards the ciliary body and 
 the crystalline lens. 
 
 b. Liquefaction of the Vitreous Body. 
 This condition will be detailed further on in Chapter X. 
 
 c. Glaucomatous Excavation of the Optic Papilla. 
 
 The alterations caused in the " head *' of the optic nerve, 
 and later on in the retina, in consequence of increased intra- 
 ocular pressure, will be referred to in Chapters VII and 
 VIII. 
 
 d. Atrophy ; Synechia between Retina and Choroid, and 
 Pigmentation of the former. 
 
 If atrophy of the choroid is diffuse, it has been caused by 
 a purulent (parenchymatous), if it is found in patches, by a 
 fibrinous (plastic) choroiditis. The atrophic patches caused 
 by plastic choroiditis, are round or oval, or when several have 
 coalesced, very manifold in shape. In a plain view, the pig- 
 mented epithelium is wanting upon them, and they them- 
 selves appear free from pigment and blood-vessels. The pig- 
 mented epithelium cells surrounding the patches are consid- 
 erably darker than the rest. In transverse sections, these 
 atrophic patches appear very considerably thinner than the 
 surrounding parts of the choroid. 
 
 As above stated, the retina is very frequently found to 
 adhere firmly to the atrophic patches in the choroid. In 
 such places it is very thin, and drawn towards the choroid. 
 During this process, the rods and cones become destroyed, 
 and thus the pigmented epithelium may grow into the 
 retina, and cause it to become pigmented in a manner closely 
 resembling the conditions seen in cases of pigmentary retini- 
 tis. The pigment may even enter the lymphatic sheaths of 
 the blood-vessels, as I must state contrary to vo7i Weckers 
 opinion.
 
 CHOROIDEA. 
 
 135 
 
 If atrophy of the choroid has been caused by chronic 
 parenchymatous choroiditis, it nearly always concerns the 
 whole of this membrane. We find this condition chiefly in 
 shrunken (phthisical) eye-balls. During this process, the 
 choroid may become firmly adherent to the sclerotic, and, if 
 the retina was involved, choroid and retina may also be found 
 to adhere so firmly to each other, that they can no longer 
 be separated. In some cases, if there is not pigment enough 
 left to mark the line of demarcation, it may, even with the 
 microscope, be impossible to distinguish between the re- 
 mains of the two membranes. In advanced cases, nearly all 
 the blood-vessels are perfectly destroyed, and the same is the 
 case with the nerves. 
 
 e. Ossification. 
 
 The formation of osseous tissue in the choroid, is a com- 
 paratively frequent result of chronic parenchymatous cho- 
 roiditis. Most authors consider that this ossification origi- 
 nates in a fibrino-plastic exudation {Knapf). It is true, that 
 we often find in cases of ossification of the choroid, a fibrino- 
 plastic exudation lying upon the inner surface of the choroid, 
 and partially ossified. I am, however, of the opinion that 
 the ossification, when lying upon the inner surface of the 
 choroid, very frequently has for its origin, the vitreous bodies 
 of the lamina vitrea. on the other hand I do not deny that 
 it sometimes originates in the new-formed tissue consequent 
 upon plastic choroiditis, to which we have an analogue 
 in the formation of osseous tissue in cyclitic membranes. 
 The osseous tissue within the parenchyma of the choroid, 
 however, seems to me, to be formed chiefly during a chronic 
 parenchymatous choroiditis. The whole of the choroid is 
 sometimes found to be changed into osseous tissue, so that 
 it can only be recognized by the folded lamina vitrea, which 
 is generally preserved. 
 
 It is certainly a strange fact that, in spite of the similar- 
 ity in the structure of the choroid and iris, as yet no ossifica- 
 tion has been found in the latter. The osseous formations 
 described upon the posterior surface of the iris, originated in 
 cyclitic productions in that place.
 
 136 
 
 THE HUMAN E YE. 
 
 f. Staphyloma. 
 
 The manner in which chronic choroiditis may aid in the 
 formation of a scleral staphyloma, has been sufficiently de- 
 tailed in Chapter II. 
 
 C. Injuries to the Choroid and their Results. 
 
 The peculiar fact, that a contusion of the eye-ball may 
 cause a more or less isolated rupture of the choroid, has not 
 yet been satisfactorily explained. It is greatly to be regretted, 
 that up till now no such case seems to have been histologically 
 examined and described. It appears from clinical observa- 
 tion, that the rupture chiefly concerns the inner layers of the 
 choroid. The pigmentation of the retina, frequently formed 
 in the surrounding of the rupture, is most probably the 
 result of a simultaneous rupture of the outer layers of this 
 membrane, by which the pigment is enabled to grow into it. 
 
 If the injury only leads to the rupture of some blood- 
 vessel of the choroid, a larger or smaller, parenchymatous 
 haemorrhage will, of course ensue, according to the size of 
 the blood-vessel. The blood may be so distributed in the 
 tissue, that this appears haemorrhagically infiltrated ; or it 
 may split the choroid into two layers and force them con- 
 siderably apart. (See Fig, 74). These haemorrhages later 
 
 Fig. 74.— rareuchymatous haemorrhage splitting the choroid into two layers, caused by con- 
 tusion of the eye-ball. 
 
 on undergo fatty degeneration, and become gradually ab- 
 sorbed, leaving behind them a more or less atrophic tissue, 
 filled with crystals of haematoidine.
 
 CHOROIDFA. 
 
 -^17 
 
 Foreign bodies striking the choroid must, of course, have 
 pierced the sclerotic or the retina before reaching it, and 
 such injuries therefore always produce complicated condi- 
 tions. If the sclerotic and choroid only have been injured, 
 the latter generally prolapses into the wound of the sclero- 
 tic, and the two membranes heal together by means of a local 
 plastic inflammation. The sclerotic then, as a rule, appears 
 pigmented around the wound. If the retina, choroid and 
 sclerotic, have been wounded from the interior, all the 
 wounded parts show this local plastic inflammation. Since, 
 however, the choroid has the most reproductive power of 
 the three, we frequently find a pigmented granulation-tissue 
 growing from it through the retina into the vitreous body. 
 (See Fig. 75), Later on, this granulation-tissue shrinks, and 
 
 Fig. 75. — Granulation-tissue starting from the wounded choroid. 
 
 we find pigmented scar-tissue, by which the membranes are 
 firmly united with each other. The retina surrounding the 
 scar is nearly always pigmented, and all the parts next to the 
 scar, contain crystals of haematoidine. 
 
 I have never found a foreign body to be encapsuled in 
 the choroid alone. 
 
 The inflammation caused by such injuries remains, how- 
 ever, but seldom a localized one. It generally leads to puru- 
 lent choroiditis, or even to panophthalmitis. Moreover, the 
 simple scar, as described above, may become stretched, and 
 cause the formation of a traumatic staphyloma of the scle- 
 rotic. 
 
 It appears, that injuries have in rare cases become the 
 starting point for the formation of malignant tumors in the 
 choroid.
 
 1 38 THE HUMAiY E YE. 
 
 Injuries to this membrane may also finally produce sym- 
 pathetic affections of the other eye. 
 
 D. Tumors of the Choroid. 
 
 a. Cystoid Formations. 
 
 Only once I found cystoid formations in the choroid. 
 They were situated in the peripheric part of this membrane, 
 and formed a number of large round and oval cavities, which 
 (in the hardened eye), appeared to be empty. They had a 
 membrana propria, and an endothelial coating. They proba- 
 bly originated from the lymphatic sheaths of a blood-vessel, 
 and would then be analogous to lymphangiectasia. (See Fig. 
 76). 
 
 Fig. 76.— Cystoid formation in the choroid. 
 
 b. Granuloma. 
 
 After injuries to the choroid, when abscess-like round 
 cells accumulations in this membrane have perforated the 
 lamina vitrea, we sometimes find granulation tissue starting 
 from the parenchyma of the choroid. Such a granuloma is 
 never very large, and it may either detach the retina from 
 the choroid, or if this membrane too has been perforated, it 
 may grow through it into the vitreous body. These tumors 
 seem at a later period to be always changed into tough 
 connective-tissue, and thus to form a simple scar. 
 
 Leber showed to the meeting of oculists at Heidelberg, in 
 1878, specimens of granuloma of the choroid, from an individ- 
 ual who had suffered from granulated eye-lids (trachoma). 
 
 c. Sarcoma. 
 The most frequent new-formations of the choroid, are the
 
 CHOROIDEA. 139 
 
 sarcomata. Knapp has written a very extensive book on this 
 subject, and to him belongs the merit of having placed our 
 knowledge with regard to choroidal tumors, on a more exact 
 basis. Since its appearance, only very little has been added 
 to this chapter. There are pigmented and unpigmented sar- 
 comata of the choroid. The unpigmented ones are, however 
 rarely altogether free from pigment. The cells of these tu- 
 mors are either round or spindle-shaped. The pigmented 
 sarcomata consist mostly of large cells, and the latter show a 
 varying degree of pigmentation. Sometimes the cells are so 
 crowded with pigment molecules, that it is impossible to see a 
 nucleus. While the unpigmented round-cell sarcomata consist 
 chiefly of small cells, and are frequently very vascular, the 
 unpigmented spindle-cell sarcomata are tougher, less vascular, 
 and of a more fibromatous character. 
 
 According to Knapp, the unpigmented sarcomata take 
 their origin from the outer layers of the choroid, which are 
 more fibrous, while the pigmented ones spring chiefly from 
 the inner, especially the capillary layer. It is as yet not 
 known whether and, if so, in what way, the pigmented 
 epithelium may help in the formation of these tumors. 
 
 The sarcomata of the choroid may be very vascular, and 
 contain cavernous spaces of varying size. The latter, the 
 so-called teleangiectatic form of sarcoma, seems to be more 
 frequently found in unpigmented than in pigmented tumors, 
 and is often combined with haemorrhages in the surrounding 
 tissue. In the small-celled sarcoma more so than in. any 
 other variety, fatty degeneration of the cells is often seen. 
 Also chalky deposits have been described in sarcomatous 
 tumors. Knapp, however, has never seen them, and mine is 
 the same experience. It is therefore likely that the tumors 
 in which they were seen, were retinal and not choroidal new- 
 formations. 
 
 Intra-ocular enchondroma of the eye has been described 
 by Knapp. I had occasion to describe two cases of choroidal 
 sarcoma with formation of cartilage tissue, and having exam- 
 ined the tumor described by Knapp, I am strongly inclined to 
 believe that it belonged to the same class. Hyaline cartilage 
 appears in the choroidal sarcoma in shape of islets which
 
 I40 
 
 THE HUMAN EYE. 
 
 generally lie in the neighborhood of larger blood-vessels. 
 These islets are surrounded by a capsule of connective-tissue. 
 Although it is certainly not impossible that the cartilage is 
 formed by the transformation of the formative cells of a sar- 
 coma, my opinion, based upon anatomical facts, is, that the 
 remains of the vitreous body inclosed in the sarcoma, are its 
 real starting point. (See Fig. 77, 
 
 Fig. 77. — From a chondrosarcoma of the choroid, i. Sarcoma-cells. 2. Cartilage-tissue ; in 
 its centre, (3) remains of the vitreous body changed into delicate, myxomatous tissue. 
 4. Connective-tissue surrounding the cartilage-tissue. 
 
 The formation of osseous tissue in intra-ocular sarcomata, 
 is but rarely observed. I have only once come across such 
 a specimen. (See Fig. 78). 
 
 Cowell described a cysto-sarcoma of the choroid. The 
 cysts were filled with a transparent fluid, and were probably 
 formed by the incarcerated exudation, or parts of the vitreous 
 body. 
 
 Besides these forms of choroidal tumors, a great many 
 others have been described by other writers, analogues of 
 which the more modern authors have not seen. I consider 
 it therefore better not to mention them at all, as their ex- 
 istence must be proven by more exact anatomical observa- 
 tions. 
 
 During its growth the retina may for a long time remain 
 adherent to the choroidal sarcoma. In most cases this mem-
 
 CHOROIDEA. 141 
 
 brane is, however, detached by exudation. In the later stages 
 the retina may altogether disappear. 
 
 Fig. 78. — Osseous tissue formed in a sarcomatous tumor of the choroid. 
 
 The new-formation later on spreads upon the ciliary body 
 and iris, either simply by continuous growth or by infection. 
 The elements of the tumor may furthermore invade the 
 sclerotic and optic nerve. If the sclerotic becomes perforated 
 by the tumor, or the optic nerve is destroyed, extra-ocular 
 tumors are formed. 
 
 During the growth of the new-formation the nutrition of 
 the anterior parts of the eye must needs become greatly im- 
 paired, and the intra-ocular pressure increased. This pro- 
 duces the formation of abscesses in the cornea, and some- 
 times perfect destruction of this membrane. This is another 
 way, in which the tumor may grow out of the eye-ball. 
 
 Finally, the new-formation leads to metastases, which are 
 of the same structure as the primary tumor in other organs. 
 Such metastatic tumors are found chiefly in the liver ; they 
 may appear also in the lungs, pleura, intestines, kidneys, 
 spleen, brain and other organs.
 
 VII. 
 
 NERVUS OPTICUS. 
 I. Normal Condition. 
 
 Although this book is meant to deal only with the tis- 
 sues of the eye-ball itself, it would be impossible to speak of 
 the intra-scleral part of the optic nerve, and to utterly disre- 
 gard the parts of the nerve which lie farther back. In thus 
 transgressing my programme, I do so in order to aid in a bet- 
 ter understanding of the relations of the intra-ocular part 
 of the optic nerve. We will speak in the following pages of 
 the optic nerve near and within the sclerotic and choroid, 
 and of the papilla nervi optici, or the so-called " head " of 
 the optic nerve. The latter I do not consider as Schwalbe 
 does, to constitute a part of the retina, although it lies in- 
 wards from the choroid. 
 
 When speaking of the optic nerve, we have to make a 
 distinction between its outer and its inner sheath, and the 
 nerve itself. 
 
 The outer sheath of the optic nerve consists of two parts, 
 viz., the dura mater and the arachnoid. The inner sheath, 
 which lies close to the optic nerve, is analogous to the pia 
 mater. 
 
 The dura mater sheath is by far the thickest of the three. 
 It passes directly over into the sclerotic, and its structure is 
 essentially the same as that of the latter membrane. It con- 
 sists of tough connective-tissue fibrillae, which, according to 
 Schwalbe, in its outer layers run mostly in a longitudinal, in 
 its inner layers in a circular direction. Near the junction 
 with the sclerotic we find only longitudinal fibres. Elastic 
 fibrillae are also frequently found in the dura mater sheath. 
 Between these fibres lie a number of flat cells (Schwalbe) 
 which are very thin, have an oval nucleus and an nucleolus. 
 If not isolated, they appear like spindle-cells. The inner 
 surface of this sheath is lined with a single layer of delicate
 
 NERVUS OPTICUS. 
 
 143 
 
 endothelial cells. It contains, moreover, numerous blood- 
 vessels and nerves. 
 
 The arachnoid sheath which lies comparatively close to 
 the dura mater sheath, is a very thin membrane. It consists 
 chiefly of a network of fine connective-tissue fibres, in the 
 meshes of which lie endothelial cells. Thin connective- 
 tissue trabeculae unite these two sheaths, while we find much 
 thicker ones connecting the arachnoid sheath with the pia 
 mater sheath. 
 
 The pia mater sheath which closely surrounds the optic 
 nerve itself, has a tough outer and a delicate, loose inner 
 layer. It also contains a number of elastic fibres, and is lined 
 on its outer surface with a single layer of delicate endothelial 
 cells. Such cells are furthermore found to adhere to the 
 trabeculae uniting the outer and inner sheaths with each 
 other. The numerous blood-vessels found in the pia mater 
 come from those of the dura mater, and returning branches 
 of the short ciliary arteries. 
 
 The peculiar network of connective-tissue which en- 
 sheathes the nerve fibre bundles of the optic nerve, takes its 
 origin from the pia mater sheath. 
 
 The trabeculae of this network form comparatively small 
 meshes in which the numerous nerve fibre bundles appear 
 embedded. In transverse sections the connective-tissue is 
 seen to form rings (alveoli) of different size. In longitudinal 
 sections we see the trabeculae regularly arranged in longitu- 
 dinal and transverse directions and intersecting each other. 
 The fibrillae of this connective-tissue are closely attached to 
 each other, and it has therefore the sclerotic appearance, 
 which we mentioned in connection with the fibres of the 
 ligamentum pectinatum iSchwalbe). 
 
 The optic nerve is pierced near or just at its axis by a 
 small amount of delicate, loose connective-tissue, in which 
 the central retinal artery and vein are embedded. 
 
 The nerve itself is by the connective-tissue divided into 
 a very large number of small bundles of varying size and 
 shape. 
 
 The nerve fibre bundles of the optic nerve consist of 
 double contoured nerve fibres, which vary in thickness, and
 
 144 ^^^ HUMAN E YE. 
 
 lack a Schwann s sheath {Schwalbe). These fibres are united 
 with each other by neuroglia, which consists of a homogen- 
 eous matrix and numerous cells. The oval short nuclei of 
 the latter in hardened and stained specimens are readily dis- 
 tinguished from those of the connective-tissue. In longitu- 
 dinal sections they appear arranged in rows in a longitudinal 
 direction. The cells are of a varying shape, but are mostly 
 flat and must be considered as endothelial cells. 
 
 At the optic nerve entrance, the dura mater sheath and 
 the arachnoid sheath, now firmly united into one, pass 
 directly over into the sclerotic and make part of its outer 
 layers. The pia mater sheath enters the eye with the optic 
 nerve until it has reached the choroid. It then is united with 
 the inner layers of the sclerotic, and helps in the formation 
 of the lamina cribrosa. 
 
 While the space between the pia mater and arachnoid thus 
 becomes obliterated behind the sclerotic, the wider space be- 
 tween the arachnoid and pia mater (subarachnoidal, subvagi- 
 nal, intervaginal space) can be traced into the sclerotic. 
 Sometimes it even appears to be enlarged within this mem- 
 brane, and in certain (chiefly myopic) eyes, it is seen to bend 
 at right angles and thus (in transverse sections) to divide the 
 sclerotic into two, generally unequal parts. 
 
 The optic nerve itself becomes much thinner after having 
 entered the sclerotic. The cause of this is found in the fact 
 that the double-contoured nerve fibres are changed into non- 
 medullated ones. I would here like to point out a difference 
 in the manner in which this change of the nerve fibres takes 
 place in very short (hypermetropic) and in very long (myopic) 
 eye-balls, which as far as I know has not yet been mentioned 
 elsewhere. While in short eyes the nerve becomes only 
 very gradually thinner, and this attenuation begins already 
 somewhat behind the sclerotic, it takes place in a very abrupt 
 manner in long eyes, and just where the thin sclerotic and 
 choroid surround the nerve. This is caused by the different 
 manner in which the double-contoured nerve fibres go over 
 into non-medullated ones. In the short eyes the boundary 
 line between the two appears in a longitudinal section through 
 the axis of the nerve in the shape of a funnel, the basis of
 
 NERVUS OPTICUS. 
 
 H5 
 
 Fic. 79 — Shows how the double-contoured nerve- 
 fibres of the optic nerve changed into non. 
 medulatedones in an hypermetropic eye. 
 
 which lies within the outer lamellae of the sclerotic, while its 
 apex lies considerably farther backward. (See Fig. 79). In 
 long eyes the transforma- 
 tion of the nerve fibres 
 takes place in such a way, ^^B 
 that the boundary line is 
 straight or convex towards 
 the front of the eye-ball, 
 and lies just where sclerotic 
 and choroid surround the 
 nerve, that is, within the 
 lamina cribrosa. (See Fig. 
 80). I am at a loss to explain this fact ; it is, however, also 
 in macroscopical specimens so evident, that it invites further 
 investigations. 
 
 After the pia mater has joined the sclerotic, the latter 
 surrounds the nerve directly, and we see numerous thick 
 trabeculae of connective-tissue spring from it, traverse the 
 optic nerve and thus form, what is called, the lamina 
 cribrosa. In the formation of the latter the choroid also 
 aids. In longitudinal sections of these parts, we see the 
 longitudinal connective-tissue trabeculse become gradually 
 thinner ; at the same time the number and thickness of 
 the transverse ones is so considerably increased, that while 
 
 Fig. 80. — Shows how the double-contoured nerve-fibres ot the optic nerve are changed into 
 non-medulated ones in a myopic eye. 
 
 we find in a part of the optic nerve lying farther backward, 
 but of the same size, perhaps, half a dozen transverse trabe- 
 culae, we find here twenty, thirty and more. In transverse 
 sections of this region we see furthermore, that the meshes 
 between the connective-tissue trabeculae are much smaller
 
 146 THE HUMAN EYE. 
 
 and more numerous, than in those parts of the nerve which 
 lie farther back. 
 
 The blood-vessels of the optic nerve come from those of 
 its sheaths and from the central retinal vessels. They form 
 a capillary network between the nerve fibre bundles to which 
 small branches are added within the lamina cribrosa, which 
 come from Hallers " vascular ring " formed by the short 
 ciliary arteries. 
 
 The subdural and the subarachnoidal spaces are continua- 
 tions of the intra-cranial spaces of the same name, and must 
 be considered as lymphatic spaces. Through minute fissures 
 in the sclerotic, they are in communication with the supra- 
 choroidal space ; they furthermore communicate with fissures 
 in the nerve itself, and through these with the perivascular 
 spaces in the retina, which we will describe later on. 
 
 When the optic nerve has passed through the lamina 
 cribrosa, its fibres are bent nearly at right angles, and before 
 entering the retina, f^rm the so-called papilla nervi optici. 
 Most of these nerve fibres take a radiary direction, and ac- 
 cording to Liebreich, a larger number run upward and down- 
 wards than towards the sides of the eye-ball. The fibres bend 
 gradually, and in the papilla are accompanied by a great many 
 connective-tissue elements, which later on partly disappear 
 and partly enter the retina. The manner in which the nerve 
 fibres enter this membrane, causes the papilla to have a more 
 or less central depression, which is surrounded by walls differ- 
 ing in height according to the distribution of the nerve bun- 
 dles entering the retina. 
 
 The papilla contains a large number of capillary blood- 
 vessels and within it both the central retinal artery and vein 
 are divided into branches. Injections into the lymphatic 
 sheaths show in the papilla a number of fissures radiating 
 from its centre towards the retina. 
 
 2. Pathological Conditions. 
 
 We shall speak only of the pathological conditions of 
 that part of the optic nerve which lies close to the eye-ball 
 and within it. We shall also find here that the affections
 
 NERVUS OPTICUS. 
 
 H7 
 
 called by numerous clinical names become but few, when 
 anatomically considered. The nerve-tissue proper is no 
 more prone to independent inflammation here than else- 
 where and in many forms of the affections, clinically de- 
 scribed as neuritis optica, the nerve-tissue as such, takes but 
 little or no part at all in the inflammatory process. 
 
 Anatomical researches have proven beyond doubt, that 
 every affection causing an increase of intra-cranial pressure 
 (especially tumors of the brain) may exert a direct influence 
 upon the optic nerve, especially its intra-ocular part by caus- 
 ing dropsical enlargement of the intervaginal space, and 
 serous exudation into the nerve, consequent upon the former. 
 Furthermore, we may observe an inflammatory process of the 
 sheaths which leads to obliteration of the intervaginal space 
 and consequent inflammatory processes in the connective- 
 tissue of the optic nerve. Nearly as frequent as dropsical 
 enlargement of the sheaths we meet with primary inflamma- 
 tory processes in the connective-tissue of the nerve, especially 
 the papilla. The rarest affection is certainly an independent 
 inflammation of the nervous fibres themselves. 
 
 We shall describe in the following pages, i. oedema of 
 the optic nerve and papilla ; 2. inflammation of the sheaths 
 of the optic nerve ; 3. interstitial and 4. parenchymatous 
 neuritis. 
 
 a. CEdema of the Optic Nerve and Papilla. 
 
 As stated above, various causes, producing an increase of 
 intra-cranial pressure, may lead to the filling of the inter- 
 vaginal space with an abnormal quantity of serous fluid, and 
 thus gradually distent it. The increase of pressure in the 
 intervaginal space, of course, can not exist for any length of 
 time without influencing the condition of the optic nerve. 
 As described, the intervaginal space communicates with the 
 lymphatic canals within the optic nerve, and we must there- 
 fore soon also find an increased pressure within these. They 
 appear sometimes very considerably enlarged, and are seen 
 as fissures and small cavities within the connective-tissue 
 trabeculae. The connective-tissue fibres, by which the sheaths
 
 148 
 
 THE HUMAN EYE. 
 
 of the optic nerve are united, and which run through the in- 
 tervaginal space become atrophied, in rare cases hypertro- 
 phied. 
 
 These changes in and around the optic nerve cause com- 
 pression of its blood-vessels, thus leading again to serous 
 transudation from that source, and to oedema of the papilla 
 optici. The latter is characterized by hyperaemia, especially 
 of the veinous blood-vessels, and later on we find serous fluid 
 between the swollen fibres. Wide canals and cavities sever 
 the fibres, which, in hardened specimens, appear empty. It 
 seems that neither the serous fluid in the intervaginal space 
 nor within the papilla, contains a large quantity of cellular 
 elements. (See Fig. 8i). 
 
 y 1 ''"- ^ 
 
 Fig. 8i.— CEdema of the intervaginal space and optic papilla, i. The enlarged mtervagma- 
 space. 3. Spaces in the optic papilla filled with serum. 
 
 This oedema of the optic nerve and papilla may again 
 disappear as soon as the increased pressure becomes reduced, 
 and the normal conditions may be reestablished. During the 
 existence of the oedema, haemorrhages into the optic nerve 
 and papilla frequently occur. If the disease progresses, 
 atrophy of the optic nerve fibres, and hypertrophy of the 
 connective-tissue will be the result. The affection evidently 
 must also influence the retina. At a later period we find 
 this membrane also in a state of serous imbibition, and its 
 nerve fibres swollen ; furthermore, we meet with hypertrophy 
 of the connective-tissue, haemorrhages and fatty metamor- 
 phosis, especially of the ganglionic cells.
 
 NEK V us OPTICUS. 
 
 149 
 
 An active inflammation of the parts thus affected, seems 
 to be of rare occurrence. 
 
 b. Vaginitis Nervi Optici. 
 
 As we may find each of the meninges of the brain sepa- 
 rately inflamed (pachymeningitis and leptomeningitis), there 
 are probably also separate inflammatory processes in the outer 
 and inner sheath of the optic nerve. Since, however, the 
 earliest stages of vaginitis optici have as yet not been satis- 
 factorily examined, this is not proven. But there is, no 
 doubt left, that a fibrinous or purulent inflammation of the 
 meninges may cause the same affection in the sheaths of 
 the optic nerve, and influence the conditions of the latter ac- 
 cordingly. 
 
 Fibrinous vaginitis is combined with a high degree of 
 hyperaemia in the sheaths. The intervaginal space at first 
 contains a large amount of amorphous fibrine mixed with 
 lymphatic cells. Later on, it is found to be altogether filled 
 with fibrine and cells, and the latter begin to proliferate. 
 Thus the exudation is gradually organized, the proliferation 
 of the endothelial cells of the intervaginal space aids mate- 
 rially in this process. Blood-vessels are seen to spread into 
 this fibro-cellular substance, and soon we find it transformed 
 into connective-tissue. The intervaginal space in this way 
 becomes perfectly obliterated. (See Fig. 82). During the 
 
 Fig. 8j.— Fibrinous vaginitis of the optic nerve, i. Intervaginal space obliterated by new- 
 formed connective-tissue. Optic nerve atrophic. 
 
 progress of this transformation, haemorrhages frequently 
 occur. 
 
 While these changes take place in the intervaginal space.
 
 I50 
 
 THE HUMAN E YE. 
 
 the optic nerve and papilla cannot remain unaltered. Their 
 connective-tissue is more and more infiltrated with round- 
 cells, and numerous new blood-vessels are formed. Then the 
 connective-tissue becomes hypertrophied, the nervous ele- 
 ments atrophy and simply fade away. During these changes 
 haemorrhages frequently take place within the optic nerve 
 and papilla. 
 
 Besides the fibrinous vaginitis optici, there is a purulent 
 form, which is, however rare, and probably only observed in 
 consequence of purulent meningitis. In such cases we find 
 the sheaths, as well as the intervaginal space filled with 
 round-cells, and later on also the optic nerve and papilla. 
 It seems that in consequence of an early death in these affec- 
 tions, further changes have not been observed. 
 
 c. Interstitial Neuritis. 
 
 Probably the most frequent, certainly the most important 
 affection of the optic nerve, is inflammation of the inter- 
 stitial connective-tissue. Although such an interstitial neu- 
 ritis may, as we have seen, arise from oedema of the nerve 
 and inflammation of its sheaths, it is very frequently a pri- 
 mary disease. The inflammatory process involves the neu- 
 roglia as well as the connective-tissue trabeculae, which sever 
 the nerve fibre bundles. 
 
 A high degree of hyperaemia of the optic nerve and papilla 
 is followed by an enormous cell-infiltration and proliferation 
 in the connective-tissue. (See Fig. 83). The connective- 
 tissue trabeculae appear thicker, and in consequence of the 
 large number of new cells in them and the neuroglia, the 
 whole of the nerve appears in fine sections infiltrated with 
 round-cells. (See Fig. 84). The infiltration, however, con- 
 cerns the nerve fibres themselves but very slightly, if at all. 
 Later on, a large number of new-formed blood-vessels fill the 
 papilla, which in consequence of these changes is sometimes 
 enormously swollen. The blood-vessels of the nerve as well 
 as those of the papilla are frequently found to be surrounded 
 by a mantle of round-cells. 
 
 These new-formed cells are gradually changed into connec-
 
 NERVUS OPTICUS. 
 
 151 
 
 tive-tissue. When the trabeculae become thus hypertrophied, 
 the nerve fibres and blood-vessels are accordingly compressed, 
 
 Fig. 83.— Interstitial inflammation of the optic nerve. Longitudinal section. 
 
 and the thus impaired nutrition, leads to atrophy of the 
 nerve fibres, of which latter we have two different forms. In 
 one of them the nerve fibres become simply thinner, and we 
 find lying between them a number of fatty cells, probably 
 aeuroglia cells undergoing a regresssive metamorphosis ; in the 
 
 Fig. 84.— Interstitial inflammation of the optic nerve. Transverse section. 
 
 other form the whole of the nervous elements is represented 
 by a grumous substance, formed of molecular fat drops, that
 
 1 5 2 THE HUM A N E YE. 
 
 is, detritus. The connective-tissue grows thicker and thicker 
 and this fatty substance or the simply atrophying nerve fibres 
 disappear more and more. The process as a rule attacks 
 some part of the optic nerve more than the other, and 
 thus the periphery of the nerve or a sector (in a transverse 
 section) may appear perfectly atrophied, while the remainder 
 may as yet be little altered. 
 
 At the same time the optic papilla is filled with round- 
 cells, and its connective-tissue also becomes gradually hyper- 
 trophied, while the nervous elements become atrophic. 
 Among the latter we frequently find nerve fibres having a 
 spindle-shaped swelling of varying size, which has been called 
 " sclerotic hypertrophy " of the nerve fibres. I have never 
 been able to see nuclei in these swellings. Cells undergo- 
 ing fatty metamorphosis are also found, and are probably 
 cells of the neuroglia. 
 
 When the new-formed connective-tissue gradually shrinks 
 the optic nerve, which had before been greatly thickened, 
 becomes thinner, and its blood-vessels, which are thus com- 
 pressed become atrophied. The formerly much swollen 
 papilla decreases in height and shows a gradually deepening 
 flat excavation, the so-called atrophic excavation of the optic 
 papilla. 
 
 Such an atrophy of the optic nerve and papilla must, of 
 course, influence the condition of the retina. We find its nerve 
 fibre layer always thinner than normal. In later stages of the 
 affection, perivasculitis and interstitial retinitis are observed. 
 
 Interstitial neuritis may remain stationary at any period, 
 but it is generally progressive. Nerves in which nervous 
 elements can no longer be detected, and which are totally 
 changed into connective-tissue, are, however, but rarely seen. 
 
 Haemorrhages occurring in the optic nerve during the 
 progress of the disease, leave their traces behind in the shape 
 of crystals of haematoidine. 
 
 The sheaths of the optic nerve also generally become in- 
 flamed and hypertrophied. 
 
 d. Medullary Neuritis. 
 Although the possibility of a primary medullary neuritis
 
 NERVUS OPTICUS. 
 
 153 
 
 cannot a priori be denied, it is certain that the nervous ele- 
 ments are not prone to active inflamation. I have never seen 
 a case of neuritis in which I thought myself justified in con- 
 sidering the nerve fibres as the seat of the primary inflamma- 
 tion. The description of this form of neuritis given by Leber 
 agrees essentially with mine, of the changes in the nerve and 
 papilla in cases of interstitial neuritis, but I cannot consider 
 it as evidence of the existence of such a primary medullary 
 neuritis optici. 
 
 Results. 
 
 Besides the dropsical enlargement of the intervaginal 
 space combined with stretching of the outer sheath of the 
 optic nerve, and its obliteration by new-formed connective- 
 tissue, the most important and frequent results of the affec- 
 tions just described, are atrophy of the optic nerve and 
 papilla, and consequent alterations in the retina. 
 
 Even when the nervous elements of the optic nerve 
 have been totally destroyed, we find the connective-tissue 
 arranged in a manner resembling the normal condition (at 
 least in the longitudinal direction). Such nerves, however, 
 but rarely come under observation. In most cases we find 
 only the connective-tissue trabeculae very considerably thick- 
 ened at the expense of the nerve fibres. Their sclerotic ap- 
 pearance is still more striking than in the normal and the 
 blood-vessels are greatly reduced in number. The remaining 
 nerve fibres have either lost their medulla, grown very thin 
 and lie as indifferent fibres, which can be stained with car- 
 mine, between the connective-tissue fibres, or they appear 
 changed into a yellowish, grumous substance, which cannot 
 be stained by any staining material, and consists of drops of 
 fat and myeline of varying size. 
 
 Inward from the hypertrophied lamina cribrosa, the con- 
 nective-tissue of the papillae is also hypertrophic, and the 
 nervous elements are destroyed or thin and atrophic. In the 
 latter case they may still be distinguished from the connec- 
 tive-tissue. Some nerve fibres may be found in a state of 
 sclerotic hypertrophy, as described above. In later stages
 
 154 
 
 THE HUMAN EYE. 
 
 we find that the papilla consists chiefly of a network of areo- 
 lar connective-tissue, the meshes of which appear empty. 
 
 In the farther progress of the affection, the new-formed 
 connective-tissue shrinks, and from this shrinkage the so- 
 called atrophic excavation of the papilla nervi optici ensues ; 
 and the gradually flattened papilla may finally be nearly or 
 entirely reduced to the lamina cribrosa, which in this afifec- 
 
 FiG. 85.— Atrophic excavation of the optic papilla filled with a delicate connective-tissue 
 formed in the neighboring vitreous body. 
 
 tion always remains in its normal position. (See Fig, 85). 
 The walls of the remaining blood-vessels are thickened and 
 sclerosed. Atrophy of the optic nerve and papilla leaves in 
 its wake atrophy of the nerve fibre layer of the retina, and 
 regressive metamorphosis of the ganglionic cells. 
 
 During the inflammatory affections of the papilla nervi 
 optici, the adjacent part of the vitreous body also seem fre- 
 quently to become inflamed. As a result of this inflamma- 
 tion (circumscribed plastic hyalitis) we see a small amount 
 of connective-tissue formed in the posterior parts of the 
 vitreous body, into which blood-vessels starting from the 
 papilla are seen to enter. If in such cases an atrophic excava- 
 tion of the papilla is formed, we may find the latter filled with 
 delicate connective-tissue, which anteriorly is lost in the 
 vitreous body. (See Fig. 85). The granuloma of the optic 
 nerve to be described later on, is not to be confounded with 
 this affection.
 
 NERVUS OPTICUS. 
 
 Appendix. 
 
 155 
 
 Glaucomatous Atrophy and Excavation, and Embolic Atrophy 
 of the Optic Nerve. 
 
 In the foregoing, we have had occasion several times to 
 state that, in spite of a large number of very careful inves- 
 tigations, we are not yet in the possession of an anato- 
 mical explanation of the cause of the array of symptoms 
 to which we apply the clinical name of glaucoma. Knies, 
 too, who thought to have found this cause in the obliteration 
 of Fontana's spaces, has certainly gone beyond the mark, 
 since, as many have already proven, this obliteration is often 
 found without having caused glaucoma, and on the other 
 hand, is frequently wanting in glaucomatous eyes. My own 
 investigations concerning a large number of glaucomatous 
 eyes, have not taught me any anatomical fact, which can 
 be considered as the common cause of this disease. Its most 
 important symptom is certainly atrophy of the optic nerve, 
 and glaucomatous excavation of the optic papilla. The 
 anatomical conditions of a glaucomatous excavation are so 
 characteristic that they always enable us to make a positive 
 diagnosis. 
 
 While simple atrophic excavation is flat, and only reaches 
 to the lamina cribrosa, which, as stated, remains in its normal 
 position, we find in a case of glaucomatous excavation that 
 the fibres of the lamina cribrosa are compressed and forced 
 backward, often behind the outer surface of the sclerotic. 
 The nerve fibres of the papilla which are pressed aside are 
 atrophied, and the optic nerve behind the lamina cribrosa 
 shows the conditions of atrophy after interstitial neuritis. 
 (See Fig. 86). 
 
 Led by clinical observation, Schnabel sought the cause of 
 glaucoma in an inflammatory process of the tissues surround- 
 ing the optic nerve entrance, especially of the choroid. This 
 idea seemed to be rather plausible, and I tried hard to find 
 anatomical facts to prove it. I could not, however, find them. 
 In most of the cases of glaucoma, I had the opportunity to 
 examine, I found the choroid normal ; in one case it appeared
 
 156 
 
 THE HUMAN E YE. 
 
 inflamed on the nasal side of the papilla, and was infiltrated 
 with round-cells ; in a number of cases the choroid was atro- 
 phied. 
 
 Fig. 86.— Very deep glaucomatous excavation. Atrophy of the optic nerve. 
 
 To sum up, the essential difference between an atrophic 
 and a glaucomatous excavation of the papilla nervi optici, is 
 the following, viz., in the former affection the papilla and 
 optic nerve are affected, while the lamina cribrosa retains its 
 normal position, in the latter the lamina cribrosa is pressed 
 outward, while atrophy of the papilla and optic nerve takes 
 place. 
 
 According to Schweigger, a small secondary excavation 
 may be found in the larger one, if in consequence of the glau- 
 coma the tissue surrounding the central retinal blood-vessels 
 is also distended. 
 
 We frequently find also in glaucomatous excavations, a 
 delicate connective-tissue, which is formed in the adjacent 
 part of the vitreous body. 
 
 Atrophy of the optic nerve is, moreover, observed after 
 embolism of the central retinal artery. Anatomically, it in 
 no way differs from the atrophy consequent upon glaucoma 
 or inflammatory processes within the optic nerve or its sur- 
 roundings. Neither has atrophy caused by retinal affections 
 anything peculiar. 
 
 Hcemorrhage in the Optic Nerve. Hoematogeneous Pigment. 
 
 Haemorrhages of a varying size are not rare in the tissue 
 of the optic nerve. They may be caused by injuries or ope-
 
 NERVUS OPTICUS. 
 
 157 
 
 rations, or may occur during inflammatory processes. In 
 recent cases we find the optic nerve or papilla filled with red 
 blood corpuscles, which press the nerve fibre bundles aside. 
 These blood-corpuscles later on are gradually destroyed, and 
 the amorphous or crystallized hsematoidine remains lying 
 within the connective-tissue of the nerve. (See Fig. 87). It 
 
 Fig. 87. — From an atrophic optic nerve. Hypertrophy of the connective-tissue, which con- 
 tains some pigment. The nerve-fibres are broken up into a grumous substance. 
 
 is very probable, as Knapp conjectured, that the abnormal 
 pigmentation, sometimes seen with the ophthalmoscope in 
 the papilla nervi optici, is caused by such haemorrhages. 
 Whether haemorrhages in the intervaginal space {Leber) may 
 cause a similar ophthalmoscopic picture, seems to me 
 doubtful. 
 
 In transverse sections of such pigmented optic nerves, we 
 frequently find that the nerve fibre bundles surrounded by 
 pigmented connective-tissue are atrophied. This atrophy is 
 probably due to the pressure exerted upon them by the 
 haemorrhage. The connective-tissue in which the pigment 
 lies embedded, is always hypertrophied. (See Fig. 87). 
 
 Tumors of the Intra-Ocular part of the Optic Nerve. 
 
 Tumors of the " head " of the optic nerve have, it seems, 
 never been observed. The tumors of the optic nerve re-
 
 158 
 
 THE HUMAN E YE. 
 
 ported in literature, all originated in the intra-cranial or 
 intra-orbital part of this nerve, and do not here come under 
 consideration. 
 
 It seems that a direct injury to the optic papilla may lead 
 to the formation of a granuloma ; I had, at least once, the 
 opportunity of examining such a tumor. It consisted of 
 round-cells and small spindle-cells, which lay between a fine 
 network of connective-tissue and blood-vessels. The con- 
 nective-tissue and the blood-vessels of the tumor were con- 
 tinuations of those parts in the papilla nervi optici. (^See 
 Fig. 88). 
 
 Fig. 88.— Granuloma of the optic papilla. 
 
 The similiarity between such an anatomical condition and 
 the one clinically observed by Manz, and called retinitis 
 proliferans, and the affections drawn and described by JcBger 
 and Becker as new-formation of connective-tissue and blood- 
 vessels in the vitreous body, is very striking. In the cases 
 reported by these authors, the eyes however, were, not in- 
 jured.
 
 VIII. 
 
 RETINA. 
 
 I. Normal Condition. 
 
 The retina consists of ten distinct layers, if we count the 
 pigmented epithelium as part of this membrane. We have 
 treated of this layer already, and considered it as a sepa- 
 rate one, in which I think we are the more justified, since a 
 direct proof of the genetic connection between the retina and 
 the pigmented epithelium has yet to be found. 
 
 The layers of the retina are therefore the following : 
 
 1. Internal limiting membrane. 
 
 2. Nerve fibre layer. 
 
 3. Ganglionic layer. 
 
 4. Inner molecular layer. 
 
 5. Inner granular layer. 
 
 6. Outer molecular layer. 
 
 7. Outer granular layer. 
 
 8. External limiting membrane (?) 
 
 9. Rods and cones. 
 
 The first six of these layers have by Schwalbe been called 
 the brain layer of the retina, the remaining three the neuro- 
 epithelial layer. 
 
 The different elements of the retina are held in position 
 by a common, easily distinguished substance (supporting- 
 tissue) which forms the so-called supporting or radiary fibres 
 of the retina. Schwalbe says that this substance is not true 
 connective-tissue. Pathological processes, however, prove it 
 to be in no way different from it. 
 
 The radiary fibres traverse the retinal tissue at right 
 angles to its surfaces. They are flat cylindrical structures 
 having on their sides wing-like offsets of varying shape which 
 anastomose with each other. Every radiary fibre has within 
 the inner granular layer an oval nucleus which is either en- 
 closed in a spindle-shaped enlargement, or, as it seems fre-
 
 l6o THE HUMAN EYE. 
 
 quently, only adheres to the fibre. By the site of this nucleus 
 the radiary fibres are divided into an inner and an outer part. 
 Their inner part ends with a cone-like swelling within the 
 nerve fibre layer at the internal limiting membrane. Their 
 outer part reaches the limitans externa. According to 
 Schwalbe, the cone-like swelling of the inner part of the 
 radiary fibres also contains a nucleus. I have never been 
 able to see it. 
 
 Merkel states that the supporting tissue forms a tube-like 
 sheath for every cone-fibre and every cone-granule, and he 
 draws a similar sheath around the rods. In teased specimens 
 the former may without doubt frequently be seen. 
 
 The limitans interna and externa enclose, so to speak, the 
 retina. In transverse sections the former always appears as 
 a double-contoured, vitreous membrane. Recent authors 
 have denied the existence of an internal limiting membrane, 
 and stated that, what appeared to be such, was formed by the 
 coalescence of the cone-like enlargements of the inner part 
 of the radiary fibres. This they declare to be proven, since 
 in a plain view of the inner surface of the retina, we can see 
 the basis of these cone-shaped ends, and when they are 
 stained with nitrate of silver, their Outlines are very similar 
 to those of endothelial cells. I am not prepared to agree with 
 these authors, and must insist upon the existence of a separate 
 internal limiting membrane, which is not formed by the coales- 
 cence of the basis of the cone-shaped terminus of the support- 
 ing fibres, but which covers these and can become detached by 
 itself, as we frequently find it in pathological eyes. Besides 
 I once had an opportunity to observe vitreous bodies lying 
 upon it, similar in appearance and nature to those of the 
 lamina vitrea of the choroid. I consider this to be a further 
 proof of the existence of a separate internal limiting mem- 
 brane, similar to the lamina vitrea of the choroid, and the 
 membrana Descemetii. This membrane is, however, not to 
 be confounded with what has been called the hyaloid mem- 
 brane, and which will be spoken of in Chapter X. 
 
 While I thus unite in the opinion of those authors who 
 acknowledge the existence of an internal limiting membrane, 
 I do not consider that, what has been called the external
 
 RETINA. 16 1 
 
 limiting membrane, is really a membrane. In the outer 
 granular layer, all the parts of the supporting tissue coalesce 
 in such a way that they fill all the spaces between the fibres 
 of the rods and cones and their granules. The free ends of 
 the rods and cones reach beyond this, — sit venia verbo — 
 cementing substance, and the outer surface of the latter rep- 
 resents in transverse sections a single line, which is sharply 
 defined, but is not a membrane. If the latter were the case, 
 we would see a double contour. 
 
 The sheaths of the outer parts of the rods and cones 
 reach with them beyond this surface, and are, as Mcrkel 
 states, probably open towards the choroid. 
 
 The nerve fibre layer of the retina consists, as its name 
 implies, chiefly of the nerve fibres which radiate from the 
 optic nerve, as soon as it has entered the eye-ball. The ma- 
 jority of fibres continue to run in a radiating direction 
 towards the periphery of the retina. Only those fibres which 
 go to the macula lutea deviate from this direction, and 
 are concentrically bent into arches, by which arrangement 
 a larger number of nerve fibres are enabled to reach the 
 yellow spot, than would be possible, if they approached it in 
 a radiating direction. The fibres are axis-cylinders of vary- 
 ing thickness, and are united into bundles. Near the optic 
 nerve entrance there are several layers of such bundles, 
 which at a short distance from it are spread into one. To- 
 wards the periphery of the retina the thickness of the nerve 
 fibre layer continually decreases, and the fibres end at the so- 
 called ora serrata in a terminal plexus {Merkel). Schwalbe 
 described flat endothelial-like cells with an oval nucleus in 
 this layer. They are neuroglia-cells, and can be easily recog- 
 nized as such. 
 
 The nerve fibres are said to branch off at acute angles 
 while on their way to the ora serrata, and to anastomose with 
 each other. The varicose appearance which they often have, 
 is probably a post mortem symptom, or is caused by chemical 
 agents. 
 
 Outwards from the nerve fibre layer lies the ganglionic 
 cell layer. These ganglionic cells form, only in the region of 
 the macula lutea, several layers. They lie very near each
 
 l62 THE HUMAN EYE. 
 
 other in the neighborhood of the optic nerve entrance, and 
 are found farther apart the nearer the ora serrata. It must 
 be mentioned here that the ganglionic cell layer is not well 
 defined, and many of its cells lie in the nerve fibre or in the 
 inner molecular layer. 
 
 The cells themselves vary in size. They are round or 
 oval, and have a large round or ellipsoid nucleus with several 
 nucleoli. A nerve fibre coming from the opticus enters into 
 every such ganglionic cell, and we see springing from the 
 cells one or more offsets which go into the inner molecular 
 layer. In the region of the macula lutea, the ganglionic cells 
 are said by all authors to be oval and to have only one per- 
 ipheral offset, that is, to be bipolar. The ganglionic cells lie 
 embedded in notches on the wing-like offsets of the support- 
 ing fibres. Schwalbe found a homogeneous, lustrous cement- 
 ing substance between them. The offsets, after entering the 
 inner molecular layer, give off numerous branches in a radia- 
 ting or oblique direction. According to Mcrkel, these branches 
 then enter the inner granular-layer and anastomose with the 
 central fibres of the inner granules. 
 
 The inner molecular layer consists of these fine fibres 
 just mentioned, and the so-called granular (molecular) sub- 
 stance. Merkel and others describe the latter as a homo- 
 geneous substance containing numerous small cavities. These 
 cavities are said to be filled with fluid which refracts the light 
 in a different manner, or to contain solid granules. {^Merkel, 
 Henle, Retzius). The inner molecular layer is comparatively 
 thick, and remains of about the same thickness all over the 
 retina, except in the region of the macula lutea. The sup- 
 porting fibres simply pass through it. Retzius states that 
 the offsets from the ganglionic cells have a radiating direc- 
 tion in this layer, others found them to branch off at right or 
 acute angles before entering the inner granular layer. 
 
 The inner granular layer is mainly formed of nuclei. 
 We stated above that the supporting fibres have a nucleus in 
 this layer, and besides these we find another kind of delicate 
 oval nuclei with a nucleolus, and surrounded by a small 
 amount of protoplasm. These have a central and a periphe- 
 ral (inner and outer) offset, the former of which is thinner
 
 RETINA. 
 
 163 
 
 than the latter. According to Merkel and others, the central 
 offsets of these nuclei of the inner granular layer, anastomose 
 with the peripheral offsets of the ganglionic cells in the inner 
 molecular layer. Their peripheral offsets pass through the 
 outer molecular layer in a radiating direction or are bent like 
 a bayonet, and give off several smaller branches. Merkel 
 undoubtedly found an anastomosis between these peripheral 
 offsets of the nuclei of the inner granular layer and the central 
 fibres of the cones in the outer molecular layer. Such an 
 anastomosis with the rod-fibres, although it is very probable, 
 has as yet not been found. 
 
 The outer molecular layer is very thin. Besides the 
 fibres just mentioned, we find in it a small quantity of the 
 same granular (molecular) substance, with which we already 
 met in the inner molecular layer. I can confirm the statement 
 oi Merkel, that in transverse sections of this layer, nearly with- 
 out exception, we see a broken line (Huelfslinie). This is 
 formed by the broader end of the central fibres of the cones 
 and their sheaths, and will be spoken of again later on. 
 Schwalbe also found flat cells in the outer molecular layer, 
 the offsets of which took part in the formation of the network 
 of fibres of which this layer partly consists. These cells are 
 said to be of a ganglionic nature. 
 
 Rods and cones and the outer granular layer, are accord- 
 ing to Schwalbe the " neuro-epithelium " of the retina. 
 
 Let us first examine the cones. The cone-fibre originates 
 with a cone-shaped swelling in the outer molecular layer, and 
 is there, as proven by Merkel, in direct connection with the 
 fibres coming from the inner granular layer. The cone-fibre 
 then becomes a little thinner, until just under the limitans 
 externa, it again swells rapidly, and there forms the cone 
 itself. This part of the cone, inwards from the limitans ex- 
 terna, contains a large oval nucleus with a nucleolus (the so- 
 called cone-granule). Besides these cone-fibres, the rod-fibres 
 originate in the outer molecular layer. A direct connection 
 between the rod-fibre and the fibres coming from the inner 
 granular layer has, as stated above, not yet been found. As 
 soon as the rod-fibre has left the outer molecular layer, it has 
 a small swelling, and somewhat farther on, near the limitans
 
 164 
 
 THE HUMAN E YE. 
 
 externa, it encloses in a larger swelling the " rod-granule." 
 This swelling has in fresh specimens a peculiar transverse 
 striation, which disappears soon after death. Only then the 
 nucleus is distinctly recognizable. While the cone-granule 
 always lies (except in the region of the macula lutea and the 
 ora serrata) just inwards from the limitans interna, the rod- 
 granules which are much more numerous, form several layers, 
 that is, their distance from the limitans externa is varying. 
 We find therefore the rod-fibres generally thinner again to 
 the outside of the swelling which encloses the granule, until 
 they pass over into the rods themselves. 
 
 The rods and cones lie outwards from the limitans externa, 
 as we stated before. The cones are bottle-shaped structures 
 which spring from the part of the cone-fibre containing the 
 nucleus ; they consist of the inner conical and the outer 
 thinner cylindrical part. The inner part appears granulated, 
 and encloses in its outer half, the so-called ellipsoid body, a 
 structure the nature of which is as yet not understood. The 
 outer part of the cones consist of a homogeneous substance 
 which refracts the light strongly, and cannot be stained with 
 carmine. After death, or under the influence of several 
 chemical agents, it splits into fine lamellae. 
 
 The rods, too, may be divided into an inner and an outer 
 part. The inner part is generally thicker than the outer, and 
 both are, as a rule, cylindrical. The inner part, moreover, 
 appears granulated. Their outer part, too, is broken up 
 into fine lamellae when dying or under the influence of chemi- 
 cal agents. Some authors describe it as having a number of 
 longitudinal stripes on its surface. 
 
 As stated above, the rods and cones with their fibres and 
 granules, have a sheath {Merket). The sheaths of the cone- 
 fibres end in the outer molecular layer, and their bases there 
 form the broken line, above referred to. The longitudinal 
 stripes often seen on the surface of the inner parts of the rods 
 and cones, is explained by folds in these sheaths. According 
 to Kraiise and Schultze, small fibrillae start from the limitans 
 externa, and surround the basis of the inner parts of the rods 
 and cones, forming the so-called fibre-baskets (Faserkoerbe). 
 
 In plain views of the external surface of the retina, the
 
 RETINA 
 
 ■i6s 
 
 optical transverse sections of the rods and cones, form a regu- 
 lar mosaic. This shows, however, a different arrangement 
 according to the region from which the specimen is taken. 
 While in the region of the macula lutea every cone appears 
 to be surrounded by a single ring of rods, the latter are more 
 and more numerous and the cones farther apart from each 
 other, the nearer they approach the periphery of the retina. 
 
 Kuehne, Boll ^.nA others have recently found that during 
 life the outer part of the rods has a purple hue, being satura- 
 ted with the so-called retinal purple which is secreted from 
 the pigmented epithelial layer. 
 
 From the description given in the foregoing, the way 
 in which the connection between the optic nerve and 
 the rods and cones is established, is the following: The opti- 
 cus fibres enter the ganglionic cells which send one or two 
 peripheral offsets into the inner molecular layer, where they 
 anastomose with the central offsets of the nuclei of the inner 
 granular layer. The peripheral offsets of these enter the 
 outer molecular layer from which the central offsets of the 
 rods and cones (the rod-fibres and cone-fibres) are seen to 
 emerge. As Merkel has proven, the peripheral fibres of the 
 inner granules are in direct connection with the central off- 
 sets of the cone-granules ; the same has not yet been proven 
 for the rods. We know therefore of a direct communication 
 between the cones and the central organ, while the same is 
 not yet established for the rods. 
 
 It is certainly a very remarkable fact, that the so-called 
 " visual purple " which by recent investigations has been ac- 
 corded so important an influence in the act of vision, does 
 not tint the cones, which are undoubtedly percipient organs, 
 but renders the rods, which appear to be at least less im- 
 portant for direct vision, purple. It would therefore appear 
 that the physiological value of the visual purple has been 
 overrated. 
 
 The structure of the retina, as we have described it, is 
 very materially altered in its peripheral parts, and in the 
 region of the macula lutea. 
 
 Near the ora serrata the nerve fibres, rods and cones 
 gradually disappear, while the supporting tissue becomes
 
 1 66 
 
 THE HUMAN EYE. 
 
 more and more prevalent. The rapid attenuation observed 
 in the periphery of the retina is, however, due in a great 
 measure to the abrupt, not gradual disappearance of the inner 
 molecular layer. The granular layers become gradually thin- 
 ner, and the outer one sooner so than the inner, and finally 
 the one cell layer of the retina, which lies upon the ciliary 
 body is formed. In the parts nearest to the ora serrata, we 
 sometimes find (especially in the eyes of old people) an alter- 
 ation which Iwanoff called, as it seems to me very inap- 
 propriately, " oedema " of the retina. In plain views of such 
 a retina, when stained, we see an irregular network of light 
 bands, varying in breadth, and surrounding islets of a darker 
 tint. In transverse sections we see, that these lighter bands 
 are caused by a system of cavities varying in size, which lie 
 in the inner and outer granular layer. These cavities are 
 round or oval, and coalesce with each other, or are separated 
 by pillars, the capitals of which form the darker islets above 
 referred to and seen in the plain views. These pillars consist 
 of fibres with a nucleus and long spindle-shaped cells. Some- 
 times their transverse septa are formed by trabeculae running 
 in a transverse direction from one pillar to another. Proba, 
 bly these cavities are filled with a serous fluid during life. 
 (See Fig. 89). This condition of the retina I never found 
 
 Fig. 89.— Cystoid degeneration of the retina near the ora serrata. 
 
 combined with the symptoms of retinal oedema, which are 
 to be detailed farther on, and I therefore think it much more 
 appropriate to call this condition cystoid degeneration of the 
 ora serrata retinae {Nettleshif). 
 
 The greatest changes in the structure of the retina are
 
 RETINA. 
 
 167 
 
 found in the region of the macula lutea, and in the fovea 
 centralis. The macula lutea according to Koelliker lies, from 
 forty-two to forty-five mm. distant from the optic nerve 
 entrance, and has a small depression somewhat eccentrically 
 situated, viz., the fovea centralis. The examinations as to 
 the cause of the yellow tint of this part of the retina are not 
 yet concluded. The macula lutea usually forms an oval, the 
 longitudinal axis of which lies in a horizontal direction. 
 
 In the fovea centralis, the limitans interna forms a line 
 which is convex towards the choroid. While the whole of 
 the retina must therefore be thinner in this place, its layers 
 (except the nerve fibre layer) are considerably thickened in 
 the parts surrounding the fovea centralis. All of the layers, 
 however, are not of equal thickness, and the nerve fibre 
 layer becomes gradually thinner, so much so that we find the 
 ganglionic cells near the fovea centralis lying directly under 
 the limitans interna. The ganglionic cell layer is here found 
 to be six or eight times thicker, than in other parts of the 
 retina, and its cells in this region are said always to be of an 
 oval shape and bipolar. 
 
 The inner granular and inner molecular layer are compara- 
 tively but little thickened. The molecular substance of the 
 outer molecular layer is totally wanting in the fovea centralis. 
 Its fibres are, however, strongly developed, and while in other 
 parts of the retina they run mainly in a vertical direction, 
 they are here all bent like a bayonet, so, that the horizontal 
 part is longer than the others, and grows more so the nearer 
 the fovea centralis. The outer granular layer in this re- 
 gion is also somewhat thinner. The rods are as already 
 stated, very much less numerous, and the number of the 
 cones is considerably increased, the latter are thinner and 
 considerably longer, than in other regions of the retina. 
 Right in the fovea centralis all the layers of the retina are so 
 close to each other and so much thinner, that it is very diffi- 
 cult to distinguish them from each other. It seems, however, 
 that none of the cellular layers disappear entirely. The 
 supporting fibres are very much thinner in the region of the 
 mucula lutea, and in the fovea centralis itself, they are alto- 
 gether wanting. The fovea centralis has, furthermore, no
 
 1 68 THE HUM A N E YE. 
 
 rods. Schzvalbe states that the basis of the cells of the pig- 
 mented epithelial layer is much smaller in this region, but 
 that they are much higher. 
 
 At the papilla the retina (except its nerve fibre layer) ter- 
 minates, as Schwalbe first stated, on the lateral side in a 
 vertical line ; on the opposite side the end forms an oblique 
 line, and the outer layers reach farther towards the optic 
 nerve than the inner ones. The rod-fibres and cone-fibres 
 must therefore also here, as in the region of the macula lutea, 
 run in an oblique direction, 
 
 2. Pathological Conditions. 
 
 A. CEdema Retince. 
 
 OEdema of the retina may be a purely passive infiltra- 
 tion of this membrane with serous fluid caused by an affec- 
 tion of the choroid, or it may be more or less the result of 
 an inflammatory process in the retina itself. 
 
 In the latter case, the affection is always accompanied by 
 hypersemia of the retinal blood-vessels, while in the former, 
 hyperaemiais usually wanting. In oedema of the retina we find 
 all the elements constituting this membrane saturated with 
 a serous fluid. They consequently appear swollen and some- 
 what dim. Moreover, there are a small quantity of lymph- 
 cells to be seen in the nerve fibre layer. In consequence of 
 these changes, the whole of the retina is thicker than normal, 
 which is, however, most pronounced in the neighborhood 
 of the optic papilla. Later on small cavities filled with serum 
 may be found in the connective supporting tissue and in the 
 molecular substance, especially in the outer molecular layer. 
 These press the cellular elements aside, and the latter may 
 at a remote period be destroyed in consequence of fatty de- 
 generation, resulting from the undue pressure exerted upon 
 them. In this way the cavities may grow larger, and the 
 serum which fills them wjll then contain some detritus besides 
 the lymph-cells. The cavities have mostly an oval shape. 
 Capillary haemorrhages are but rarely observed in the course 
 of such an oedema. 
 
 CEdema may be found in all parts of the retina, and is
 
 RETINA. i6q 
 
 not, like the cystoid degeneration of the parts near the ora 
 serrata, confined to one region. In the latter affection, 
 moreover, the hyperaemia of the blood-vessels and the serous 
 imbibition of the cellular elements which surround the cavi- 
 ties, are wanting. 
 
 A number of larger serous cysts have been described in 
 detached retina. Whether they have originated in such an 
 oedema, I cannot tell. 
 
 I have not been able to ascertain what the final changes 
 in retinal oedema are ; but it seems that it may exist as a 
 chronic affection for a very long time, without changing 
 the retinal tissue in any other way than in the manner above 
 described. 
 
 B. Inflammatory Processes in the Retina, and their Results. 
 
 Retinitis like choroiditis, has been clinically divided into 
 a large number of varieties. The histological conditions do 
 not however warrant these clinical distinctions. The nervous 
 elements of the retina, like those of the opticus, are not apt to 
 become independently inflamed. The inflammatory process 
 seems always to originate in the connective-tissue of the 
 retina, and its nervous elements become only secondarily 
 affected. We will speak, i. of retinitis as we find it as a pecu- 
 liar symptom in albuminuria, 2. of diffuse atrophic retinitis, 
 and 3. of purulent retinitis. 
 
 a. Retinitis Albuminurica. 
 
 The peculiar form of interstitial retinitis found especially 
 during an inflammatory process in the kidneys, concerns pre- 
 eminently those regions of the retina in the neighborhood of 
 the optic papilla and the macula lutea. Within these regions 
 all the parts of the retina gradually suffer from the affection 
 and in advanced cases we find not only the blood-vessels and 
 connective-tissue, but also the nerve elements (these only 
 secondarily) altered. 
 
 The most visible, microscopical symptom of this affection 
 is the considerable swelling of the involved parts, especially 
 of the optic papilla and its surroundings. Furthermore, the 
 thickened retina around the optic papilla is usually wrinkled
 
 I/O 
 
 THE HUMAN E YE. 
 
 and partially detached. The considerable swelling is chiefly 
 due to an inflammatory infiltration and hyperplasia of the 
 connective-tissue and oedema. The connective-tissue fibres 
 are longer and thicker, and have that sclerotic appearance 
 caused by a strong refraction of the light, which we found 
 to be normal to the fibres of the ligamentum pectinatum. 
 The hyperplasia and swelling are most pronounced in the 
 nerve fibre-layer, especially in the papilla. The hyper- 
 semic blood-vessels are usually surrounded by white blood- 
 corpuscles, which lie in the neighboring connective-tissue. 
 The fluid with which all elements of the nerve fibre layer 
 seem to be sodden, is homogenous, in some cases it appears 
 somewhat granular. The swelling of the nerve fibre layer is, 
 furthermore, due to the peculiar club-like swelling of the 
 nerve fibres, already above described, as sclerotic atrophy of 
 these elements. We not unfrequently see such nerve fibres 
 in teased specimens. They are either thickened at one or 
 both ends or altogether, and refract the light strongly. The 
 thickened part is very darkly tinted when carmine has been 
 used. As stated already, I have never found nuclei in these 
 swellings. Nerve-fibres which have been altered in such 
 a way are not only found lying indiscriminately among the 
 others, but sometimes they are seen crowded together in 
 larger quantities. Where this is the case, the nerve fibre 
 layer appears to be more especially swollen, it projects more 
 or less into the vitreous body above the surrounding parts, 
 and crowds the outer layers of the retina close together. (See 
 Fig. 90). Former authors have also mentioned a sclerotic 
 swelling of the ganglionic cells, which by more recent authors 
 is declared to be erroneous. I must, however, state again 
 that besides the sclerotic swelling of the nerve fibres, which 
 as I said contain no nucleus, I frequently found large round 
 and sometimes star-shaped bodies, undoubtedly containing 
 a nucleus, and which I consider to be such sclerosed gang- 
 lionic cells. 
 
 We find, furthermore, in the nerve fibre layer, and espe- 
 cially in the region of the macula lutea, cells which contain 
 numerous fat-granules. They appear round or semi-lunar, 
 have one or more offsets, and a shining round nucleus. I
 
 RETINA. Y-ji 
 
 think, these cells, too, may be considered as ganglionic ones 
 undergoing a regressive metamorphosis. I must state, 
 
 Fig. 90. — Albuminuric retinitis, i. Nerve fibre layer, considerably thickened through 
 sclerosed hypertrophic nerve fibres. 2. Haemorrhage. 
 
 however, that the majority of the ganglionic cells appear un- 
 altered, so does the inner molecular layer. 
 
 Besides the round-cells which lie around the blood-vessels 
 and those scattered among the elements of the nerve fibre 
 layer, I not unfrequently found tubercle-like aggregations of 
 round-cells in this layer. 
 
 The swelling of the nerve fibre layer may, moreover, be 
 increased by a granular exudation, found under the limitans 
 interna. This exudation sometimes detaches the inner limi- 
 ting membrane to some extent, and thus makes it protrude 
 into the vitreous body. 
 
 Further changes characteristic of albuminuric retinitis, 
 are found in the outer layers of the retina. In these, also, 
 we find the connective-tissue in a state of hypertrophy 
 and partly sclerosed, or in a state of fatty infiltration. A 
 more striking change is, however, the formation of cavities 
 in the inner and outer granular, and in the outer mole- 
 cular layer. These cavities are round or oval, and in the 
 latter case, their longitudinal diameter usually lies at right 
 angles to the surface of the retina. The cavities found in 
 the region of the macula lutea generally make an exception 
 to this rule, and lie parallel with the surface of the retina. 
 If the cavities are small, they lie either in one of the three 
 named layers or in two neighboring ones (the inner granular 
 and outer molecular, or the latter and outer granular layers). 
 The larger cavities may reach from the inner granular layer
 
 172 
 
 THE HUMAN E YE. 
 
 even to the rods and cones. We found similiar cavities in 
 cases of oedema of the retina. While these, however, are 
 filled with a serous fluid, the cavities found in albuminuric 
 retinitis contain threads of fibrine or cellular elements. (See 
 91). The latter are large round cells, filled with fat- 
 3 4 
 
 Fig 
 
 Fig. Qi. — Albtcinniicric retinitis. 1. Outer granular layer. 2. Inner granular layer. 3. 
 Cavity filled with fibrine. 4. Cavity tilled with cells containing fat-granules. Both 
 cavities containing, moreover, peculiar structures of varying size, which coalesce and 
 refract the light very strongly. Some fat granule cells lie in the outer granular layer. 
 
 granules and they have a small shining round nucleus, often 
 one or more offsets, and are of slightly brownish tint. Be- 
 tween these cells drop-like yellow-brown bodies frequently 
 lie, varying in size, which may be seen to coalesce. The 
 hardening fluids seem to cause a shrinking of these bodies, 
 and their surface consequently may appear wrinkled. Some 
 of them have a notch, into which one of the fatty cells would 
 fit. The substance which forms these bodies is too darkly 
 tinted, and too hard to be considered beyond doubt as a col- 
 loid substance, it appears to be more like amyloid substance. 
 It lacks, however, the concentric structure, and with iodine 
 does not show the reaction so characteristic of the amyloid 
 substance. Perhaps, these bodies are the result of a further 
 regressive metamorphosis of the above-named cells filled with 
 fat-granules, or they may be simply an exudation coagulated 
 under the influence of the hardening fluid. 
 
 The fibrine seen in such cavities always forms a net- 
 work of fine threads, similar to those found in the alveoli 
 of the lungs in croupous pneumonia. Cells and fibrine 
 are but rarely found together in the same cavity. These
 
 RETINA. 
 
 "^71 
 
 cavities contain either cells or fibrine and seem never to be 
 empty. 
 
 A fibrinous exudation frequently lies between the retina 
 and the pigmented epithelial layer, and this seems to be found 
 most frequently in the region of the macula lutea. Where- 
 cver it is found, the rods and cones are changed into short 
 club-shaped structures. This change in the shape of the 
 rods and cones is, however, not at all characteristic of albu- 
 minuric retinitis. These sometimes may be altered in 
 another manner which I never met with in other diseases of 
 the retina. I am in the possession of specimens where the 
 rods and cones in the neighborhood of the papilla, are two 
 and three times longer than in the normal state. Such 
 elongated (hypertrophied) rods and cones are somewhat 
 granular, and in appearance are similar to the sclerosed nerve 
 fibres and ganglionic cells, that is, they refract the light very 
 strongly and are stained very dark with carmine. It is, 
 furthermore, impossible to distinguish between their outer 
 and inner part, and they are firmly adherent to each other. 
 
 The rods and cones may also be broken up into fine 
 lamellae and myeline-like drops. 
 
 Cells containing fat-granules, like those in the cavities, are 
 also seen scattered about in the granular layers. 
 
 The blood-vessels show pathological changes which, how- 
 ever, are not characteristic of albuminuric retinitis. We 
 hardly ever examine a retina suffering from the affection 
 under consideration, without finding in it a large number of 
 haemorrhages. These are either found only in the nerve fibre 
 layer and in the neighborhood of blood-vessels, or they reach 
 through the whole thickness of the retina to the limitans ex- 
 terna, or they may even perforate the outer or inner surface 
 of the retina. Crowded red blood-corpuscles are seen between 
 the elements of the retina in all stages of destruction. They 
 usually undergo fatty degeneration before being absorbed. 
 [Virchotv). It is a strange fact that we never find either 
 crystals of haematoidine or any abnormal pigmentation after 
 such haemorrhages in a retina suffering from albuminuric 
 retinitis. 
 
 These haemorrhages are undoubtedly caused by some
 
 174 
 
 THE HUMAN EYE. 
 
 pathological changes in the walls of the blood-vessels and 
 cannot be explained by the simple process of diapedesis. 
 The existence of such changes is, however, very difficult to 
 prove. I have sometimes found a fatty infiltration of the 
 endothelial cells of blood-vessels. Other changes, found in 
 the walls of the blood-vessels can hardly be the cause of 
 these haemorrhages, as they are found in other diseases with- 
 out causing them. I mean the sclerosis of the blood-vessels 
 and a slight degree of perivasculitis. The characteristic fea- 
 tures of sclerosis of the blood-vessels are, that their walls be- 
 come very thick, (and the lumen consequently very narrow), 
 appear hyaline and refract the light strongly. Sometimes 
 the thickening of the walls leads to perfect obliteration of the 
 blood-vessels. This process, which seems to chiefly attack 
 the smaller branches, may, moreover, cause the formation of 
 a thrombus in the blood-vessels. 
 
 In cases of perivasculitis, we find the adventitia of the 
 blood-vessels filled with round-cells. This affection is, how- 
 ever, of rare occurrence in albuminuric retinitis. 
 
 During this disease of the retina, the optic nerve often 
 shows the symptoms of interstitial neuritis. 
 
 b. Retinitis Inter stitialis Diffusa {Atrophica). 
 
 Diffuse interstitial retinitis is very frequently observed in 
 phthisical eye-balls. It is, moreover, caused by compound 
 injuries to the eye, which do not lead to phthisis, and by such 
 injuries as are inflicted directly upon the retina itself. De- 
 tached retinae also usually show the symptoms of this variety 
 of retinitis, especially when the folds of the detached retina 
 are glued together into one cord. In the so-called pigmenta- 
 ry retinitis, diffuse interstitial retinitis is only a secondary 
 symptom. 
 
 The cases which so far have been submitted to anatomi- 
 cal examination, it seems all showed the disease in a too far 
 advanced stage, to allow of determining the original seat of 
 this affection. Diffuse interstitial retinitis, unlike albuminu- 
 ric retinitis, is not confined to certain regions of the retina, 
 except in staphylomatous and glaucomatous eyes. In the 
 former the process is confined to the staphylomatous por-
 
 RETINA. 
 
 175 
 
 tions, in the latter (at least at the beginning of the disease) to 
 the neighborhood of the optic papilla. 
 
 In whatever region of the retina the affection begins, it 
 always attacks at first the inner layers of this membrane and, 
 even where the disease is far advanced, the outer layers may 
 yet be found in a comparatively normal condition. The rods 
 and cones make an exception to this rule, especially in cases 
 of detachment of the retina. 
 
 According to Leber, we find in the first stage of the affec- 
 tion under consideration, the nerve fibre layer thickened in 
 consequence of a round-cell infiltration which is most pro- 
 nounced along the blood-vessels. This cell-infiltration leads 
 to the new-formation of connective-tissue in the nerve fibre 
 layer and the ganglionic cell layer. We find accordingly at 
 this period in transverse sections, connective-tissue hyper- 
 trophy, some of the nerve fibres and ganglionic cells under- 
 going a regressive metamorphosis, and the remainder of them 
 crowded aside by the connective-tissue. Soon also the sup- 
 porting (radiating) fibres become thicker, and they frequently 
 assume the sclerosed appearance above referred to. The ad- 
 ventitia of the blood-vessels, which in the beginning appears 
 infiltrated with round-cells, is also thickened by the transfor- 
 mation of these cells into connective-tissue and the lumen of 
 the blood-vessels is accordingly narrow. 
 
 When the new-formed connective-tissue begins to shrink, 
 the nerve fibres and ganglionic cells gradually disappear 
 through fatty degeneration. Sometimes we also find gang- 
 lionic cells undergoing a colloid metamorphosis. In conse- 
 quence of these changes, the nerve fibre layer (and by this 
 means the whole of the retina) becomes very much thinner. 
 
 The hypertrophy of the radiating fibres is sometimes so 
 considerable, that they perforate the internal limiting mem- 
 brane, and form little connective-tissue tumors on its inner 
 surface, which may either be flat and have a broad basis, or 
 have a thin pedicle. Moreover, this form of retinitis is very 
 frequently combined with the new-formation of connective- 
 tissue in the peripheral layers of the vitreous body (those 
 touching the inner surface of. the retina). This new-formed 
 connective-tissue, which always firmly adheres to the retina,
 
 i;r6 THE HUMAN E YE. 
 
 has generally a lamellar structure, and is often thicker than 
 the retina itself. In other cases we find the connective-tissue 
 of the nerve fibre layer arranged in an arcade-like manner, 
 enclosing smaller and larger spaces and canals, which are 
 usually empty or sometimes contain a few remains of the 
 nerve fibres. These spaces during life are probably filled with 
 serum. The arcade-like arrangement of the connective-tis- 
 sue seems to be most frequent in the neighborhood of the 
 optic papilla. 
 
 While the nerve fibre layer undergoes the changes above 
 detailed, usually the outer layers too, begin to suffer, although 
 in rare cases, as stated, they may reimain intact for a much 
 longer period. The inner and outer molecular layers disap- 
 pear at first, and the two granular layers are thus united into 
 one. Later on also, the cells of these two layers can no 
 longer resist the pressure exerted upon them by the retrac- 
 tion of the new-formed connective-tissue. They become 
 granular and undergo fatty degeneration, and soon the retina 
 consists of almost nothing but connective-tissue and blood- 
 vessels, the walls of which are often enormously thickened. 
 The arrangement of the connective-tissue may, however, 
 for a long time still imitate the normal structure of the 
 retina, and only in the very last stage of this affection, we 
 find the retina replaced by a thin layer of tough connective- 
 tissue containing some blood-pigment, and in no way resem- 
 bling this membrane. This I saw in a case of traumatic 
 retinitis twelve years after the beginning of the disease. 
 
 The rods and cones, as already stated, are usually altered 
 at an early period. They mostly appear as club-shaped 
 structures, as we found them in cases of albuminuric retinitis. 
 According to several authors, hypertrophy of the rods and 
 cones as described above, is also found in diffuse interstitial 
 retinitis {Leber). 
 
 The blood-vessels of the retina gradually become quite 
 obliterated and transformed into bands of connective-tissue, 
 which at first are easily distinguishable from the surrounding 
 tissue. Later on this distinction becomes impossible, unless 
 their former site can be recognized by some blood pigment 
 embedded in the tissue.
 
 Sometimes also, in this form of retinitis, the pigmented epi- 
 thelial cells proliferate into the retina. Diffuse retinitis which 
 is, however, consequent upon the immigration of pigmented 
 epithelial cells into the retina, and above referred to as pig- 
 mentary retinitis, is totally different because a secondary 
 affection, although histologically the same, changes are ob- 
 served as in the disease now under consideration. 
 
 c. Retinitis Puriilenta. 
 
 Purulent retinitis is in most cases a part of purulent 
 panophthalmitis. We furthermore observe it after injuries 
 which involve the retina directly or in cases of metastatic 
 choroiditis, which latter disease usually leads to purulent 
 panophthalmitis. 
 
 The first symptom characteristic of this affection, is a very 
 considerable infiltration of round-cells into the nerve fibre 
 layer consequent upon hyperaemia of the blood-vessels. On 
 account of the infiltration, this layer appears much swollen. 
 Its normal elements are gradually destroyed, and at a later 
 period it seems to consist solely of round-cells, separated from 
 the vitreous body, by the internal limiting membrane, which 
 generally appears wrinkled. Gradually this membrane, too, 
 is destroyed and the neighboring parts of the vitreous body 
 which have for some time also been filled with round-cells, 
 come into direct contact with the altered nerve fibre layer 
 of the retina. During this process, very numerous haemor- 
 rhages of varying size are observed in the retina. According 
 to Leber and others, th'ese are caused by capillary embolism, 
 which opinion is as yet not to be considered proven. It is 
 certain, however, that the walls of the blood-vessels take an 
 active part in the formation of round-cells, and it appears to 
 me, that the changes in the structure of the blood-vessels 
 necessarily caused by this process, very easily explain the 
 occurrence of the haemorrhages. 
 
 The remainder of the retina is generally invaded by the 
 disease at a much later period than the nerve fibre layer, and 
 it is very difficult to distinguish, when the formation of 
 round-cells in the granular layer really begins, on account of 
 the similarity of their cellular elements to the round-cells.
 
 178 
 
 THE HUMAN E YE. 
 
 It seems, however, that the radiating fibres are the first to 
 suffer, and that the process only later on spreads upon the 
 cellular elements. 
 
 In advanced cases, the whole of the retina is replaced by 
 a mass of round-cells leaving no trace whatever of its original 
 structure. Purulent retinitis is generally combined with 
 purulent hyalitis, and it is then impossible to discern which 
 part of the round-cells has taken the place of the retina. 
 The rods and cones are usually changed at an early period. 
 They at first take the club-shaped form above mentioned, 
 and later on are totally destroyed. Frequently we find in 
 their stead a layer of round-cells, (which probably come from 
 the choroid) even before the outer layers of the retina are 
 materially altered. 
 
 Circumscribed accumulations of round-cells in the retina 
 have recently been described as tubercles by Weiss. 
 
 C. Changes in the Structure of the Retinal Blood-vessels, 
 Hcemorrhages and Detachment of the Retina. 
 
 Besides the alterations which the retinal blood-vessels 
 undergo when this membrane is inflamed, and which have been 
 described above as general ecstasia, fatty degeneration, nar- 
 rowing of the lumen consequent upon swelling and hyaline 
 degeneration of the walls, thrombosis and perivasculitis, there 
 are a few such alterations which, as it seems, are not neces- 
 sarily combined with an inflammatory process in the retinal 
 tissue. 
 
 Small aneurysms of the retinal arteries are but rarely ob- 
 served. They appear either as spindle-shaped or diverticlum- 
 like enlargements of the blood-vessels. 
 
 In one single case I found an amyloid degeneration of 
 the walls of the retinal blood-vessels in a case of detachment 
 of the retina, caused by a choroidal sarcoma. The walls of 
 some of the blood-vessels appeared perfectly hyaline, the 
 walls of others contained only a number of aggregations of 
 a hyaline substance. The chemical reaction, produced by 
 iodine, was that characteristic of amyloid degeneration. 
 
 Haemorrhages in the tissue of the retina are of very fre- 
 quent occurrence. We had already several times occasion
 
 RETnVA. 
 
 179 
 
 to mention them. They are found without any inflammatory 
 process in the retinal tissue in the cases which have chnically 
 very inappropriately been called retinitis apoplectica and 
 haemorrhagica. They result from disease of the heart, throm- 
 bosis of the arteria or vena centralis retinae, from injuries to 
 the eye-ball, haemorrhagic glaucoma and several constitu- 
 tional diseases. They are, of course, in no way different'from 
 those caused by the different varieties of retinitis above de- 
 tailed, and we may frequently find the rupture in the blood- 
 vessel which has caused them. They disappear after having 
 undergone a fatty degeneration by being absorbed. 
 
 Sometimes the haemorrhage destroys the elements of the 
 part of the retina in which it occurs. In these cases, usually 
 a circumscribed retinitis is found to follow, which leads to 
 the formation of a scar, sometimes containing crystals of 
 blood-pigment. 
 
 Deposits of lime are but very rarely found in the walls 
 of retinal blood-vessels and chiefly in phthisical eye-balls and 
 detached retinae. In the earliest period of this pathological 
 process, the walls of the blood-vessels appear infiltrated with 
 minute granules. Later on, larger bodies of amorphous lime 
 are found, and finally entire blood-vessels may be seen 
 changed into cylinders of lime. (See Fig. 92). 
 
 The various methods by which the retina may become 
 detached, are not yet definitely ascertained, and it is not the 
 place here to speak more extensively about this subject than 
 has already been done in the foregoing chapters, as we are 
 here only interested in the pathological changes found in the 
 tissue of the detached retina. 
 
 As we stated above, the retina can only become detached 
 when the structure of the vitreous body has been materially 
 altered. When detachment has taken place, the blood-ves- 
 sels of the retina are twisted and bent in many ways so that 
 we may a priori assume that the nutrition of the detached 
 membrane must be considerably impaired, even if there are 
 no pathological changes present in the uveal tract. The 
 latter is, however, usually the case. 
 
 The result of this impairment of nutrition also undoubt- 
 edly of the loss of function, is a regressive metamorphosis of
 
 i8o 
 
 THE HUMAN E YE. 
 
 the nervous elements of the retina. The elements undergo 
 a fatty degeneration, sometimes also a colloid metamorpho- 
 sis, which may give rise to the formation of larger cystoid 
 structures. Meanwhile the connective-tissue has become 
 
 Fig. 9a. -Detached and perfectly atrophied retina. Capillaries changed into cylinders of 
 
 amorphous lime. 
 
 hyperplastic, and later on we find all the symptoms of diffuse 
 interstitial (atrophic) retinitis. The blood-vessels are tran.s- 
 formed into bands of connective-tissue, or sometimes, as 
 stated above, into cylinders of amorphous lime, and often we 
 can recognize their former site, only by the remains of the 
 blood pigment. 
 
 While the whole of the structure of the retina is thus per- 
 fectly destroyed and replaced by connective-tissue, the limi- 
 tans interna is always found intact between the folds of this 
 new tissue. This fact, combined with all the reasons already 
 mentioned, proves the limitans interna to be undoubtedly a 
 separate and independent membrane. 
 
 Sometimes we find detached with the retina and lying 
 within this membrane, vitreous bodies from the lamina vitrea 
 of the choroid. They may contain lime, and lead to ossifi- 
 cation in the atrophic retina. 
 
 The Results of Retinitis. 
 In rare cases we may clinically observe that all the symp-
 
 RETINA. l8l 
 
 toms of albuminuric retinitis disappear. It appears doubtful 
 also whether histologically, a perfect restitutio ad integrum, 
 especially when the disease has reached an advanced state, is 
 possible. The final changes caused by albuminuric retinitis 
 are, it seems not known. This is easily explained by the 
 fact that death nearly always results from the primary disease, 
 while the retinitis is as yet progressing. If we find in a retina 
 sclerotic hypertrophy of the nerve fibres, fatty degeneration, 
 oval cavities filled with fibrine, or the cells containing fat- 
 granules and above described, sclerosis of the walls of the 
 blood-vessels and numerous haemorrhages, we are justified in 
 making the diagnosis of albuminuric retinitis. We shall, how- 
 ever, always find that the inflammatory process is not yet at 
 an end. 
 
 The changes which occur after diffuse interstitial retinitis, 
 are different. The chief symptom of this disease is the 
 transformation of the retina into connective-tissue, and par- 
 tial or total destruction of the nervous elements. 
 
 If the process had come to an end during life, we find the 
 retina replaced by a very thin membrane, consisting of tough 
 connective-tissue which usually contains some haematoidine 
 crystals and uveal pigment. This membrane can only be 
 recognized as the former retina by its position in the eye- 
 ball. 
 
 I frequently found in phthisical eye-balls or eyes which 
 had been blind for a long period before death occurred, the 
 nerve fibre layer of the retina abnormally thin, and some 
 new-formation of connective-tissue going on within it ; 
 furthermore, some ganglionic cells undergoing fatty or colloid 
 metamorphosis, and the cells of the granular layers in a state 
 of molecular infiltration. I think these alterations are due 
 to the loss of function, and cannot be considered as the symp- 
 toms of a diffuse interstitial retinitis. 
 
 In consequence of purulent retinitis, the retina is also 
 usually entirely destroyed, and we are often unable to find a 
 trace of it in eyes which have been lost from purulent pan- 
 ophthalmitis. This is more particularly the case, if the 
 vitreous body too has been altered into a mass of round- 
 cells.
 
 1 82 THE HUMAN EYE. 
 
 D. Injuries to the Retina and their Results. 
 
 The position of the retina inside the eye-ball, of course, 
 does not allow of any direct injuries being inflicted upon 
 it, unless other parts have first been perforated. The most 
 frequent and most important combination, is simultaneous 
 injury of retina, choroid and vitreous body. We had 
 already occasion to speak of these injuries when treating upon 
 the conditions found after injuries to the choroid. 
 
 Injuries to the retina mostly produce a circumscribed in- 
 terstitial retinitis. The tissue of the lips of the wound is at 
 first found to be infiltrated with red and white blood-corpus- 
 cles, and the wound-canal is filled with a fibrinous coagulum, 
 especially, if the choroid, too, has been wounded. The white 
 blood-corpuscles then increase in number, invade the fibrinous 
 coagulum and gradually lead to the formation of connective- 
 tissue. Such scars seems afterwards always to contain some 
 blood pigment. Sometimes we also find that the pigmented 
 epithelial cells have proliferated into the scar. This is espe- 
 cially the case, when the choroid is injured also. In the 
 neighborhood of the scar the rods and cones are destroyed, 
 and retina and choroid are as a rule firmly adherent to each 
 other. Berlin also found sclerosed hypertrophic nerve fibres, 
 like those described above, near such retinal wounds. 
 
 We stated already, that granulation tissue may start from 
 the wounded choroid, and grow through the wound canal of 
 the retina into the vitreous body. If the vitreous body has 
 been injured, connective-tissue is formed in it, also near the 
 retinal wound, and thus we find retina and vitreous body 
 firmly united at the site of the wound at a later period. 
 
 In rare cases, injuries inflicted upon the retina will cause 
 purulent retinitis, which, as we have stated, may lead to the 
 perfect destruction of this membrane. It is usually accom- 
 panied by purulent choroiditis, which finally leads to pan- 
 ophthalmitis. 
 
 Although foreign bodies may be retained in the retina, 
 they are but seldom seen to become encapsuled in this mem- 
 brane, as they mostly cause a purulent retinitis. If, however, 
 they become encapsulated, they are surrounded by a dense
 
 RETINA. 
 
 183 
 
 connective-tissue, in the formation of which the choroid and 
 vitreous body usually take an active part. 
 
 E. TUMORS OF THE RETINA. 
 
 a. Fibroma. 
 
 Some authors described small new-formations upon the 
 inner surface of this membrane as fibromatous tumors. 
 These are, however, probably not what we would call a real 
 tumor of the retina, but new-formations of connective-tissue 
 in the outer layers of the vitreous body or hypertrophic 
 radiary jfibres which have perforated the inner limiting mem- 
 brane in the way above referred to and observed in cases of 
 diffuse interstitial retinitis. 
 
 The conditions seem to be different, however, in the 
 cases of teleangiectatic fibromatous tumors, which we find 
 drawn in PagenstecJier s and GentJi s atlas. They are small 
 tumors with a broad base or a thin pedicle, and are very vas- 
 cular. 
 
 b. Small-celled Medullary Sarcoma {Glioma^. 
 
 During the infantile age, the retina is often the seat of a 
 new-formation, which was formerly described as fungus 
 haematodes, by Virchow and his followers, as glioma. Vir- 
 chow called this new-formation glioma, because it originates 
 in the soft connective-tissue of the retina, which is analogous 
 to the neuroglia of the brain, and because it appears to be 
 identical with the brain tumors described as gliomata. Virchow 
 himself stated that it is very difficult to distinguish between 
 glioma and sarcoma, and overcame the difficulty by calling 
 some of these tumors glio-sarcomata. Most of the recent 
 authors have adopted this name for the tumors under con- 
 sideration. Delafield has recently called them sarcomata of 
 the retina, being forced to do so by the result of a number 
 of examinations of such retinal tumors both in a fresh con- 
 dition, and after being hardened. I too, am convinced that, 
 if we want to call them gliomata still, we cannot consider 
 them as anything else than sarcomata. Leber, too, seems to 
 be of this opinion.
 
 1 84 ^'^-^ HUMAN EYE. 
 
 All the different authors {Virchozu, Schweigger, Knapp, 
 Hirschberg, Delafield, Leber, etc.) agree in the description of 
 the structure and elements of these new-formations, and I can 
 add nothing new to their observations. They consist of 
 round-cells, which are sometimes smaller, sometimes larger 
 than white blood-corpuscles, or in other cases are perfectly 
 identical with them. When hardened, they have a large 
 round nucleus. Sometimes these cells have one or more off- 
 sets. It has been stated by some authors, that they are iden- 
 tical with, and derived from the nuclei of the granular layers, 
 which however, is not the case. Between these round-cells 
 we find free nuclei and sometimes very much larger round 
 and even spindle-cells. The tumors in which these spindle- 
 cells have been found, have more especially been called glio- 
 sarcomata. 
 
 The cells of the tumor are embedded in a very small 
 quantity of intercellular substance, which when fresh is gran- 
 ular. Knapp states that this granular appearance is caused 
 by the hardening fluid. 
 
 The tumors under consideration are sometimes very vas- 
 cular. The blood-vessels (mostly of a capillary character), 
 are unusually wide. They take their origin from the retinal 
 blood-vessels. 
 
 Sarcomata of the retina are said to originate sometimes 
 from the inner, sometimes from the outer granular layer, 
 in a few cases, also from the nerve fibre layer. Leber found 
 primary tumors at the same time in different layers, and 
 Livajioffxs of the opinion, in which I concur, that the tumor, 
 being a connective-tissue growth, may spring from the con- 
 nective-tissue elements of all the layers of the retina. It 
 seems, however, that it most frequently starts from the outer 
 layers, and we may sometimes find the inner layer as yet 
 perfectly intact, when the outer ones have already been per- 
 fectly destroyed by the new-formation. In these cases, the 
 retina seems to be always detached, and lying nearer the axis 
 of the eye-ball. There are however, cases in which the retina 
 may remain in contact with the choroid, and the tumor 
 spread inwardly. Delafield has, moreover, described a case, 
 in which the tumor originated from the inner granular layer.
 
 RETINA. 
 
 185 
 
 and had protruded into the vitreous chamber, while the rods 
 and cones were as yet found to be perfectly intact. 
 
 During the growth of the tumor, haemorrhages fre- 
 quently take place, and as their results, we find smaller 
 and larger patches of blood-pigment. This pigment is 
 either enclosed in cells, or hes between them in the shape 
 of crystals or as an amorphous substance. Fatty infiltration, 
 a complete fatty softening, and the formation of cheesy mat- 
 ter, is not infrequently found in some parts of these tumors, 
 and generally is accompanied by the formation of deposits 
 of lime. We find either minute granules of lime enclosed in 
 the cells, or free larger roundish bodies which may coalesce, 
 and so grow to a considerable size. 
 
 The tumor, like all sarcomata, may spread continuously, 
 or produce secondary nodules by infection at some distance 
 from the primary ones. The former seems to be the preva- 
 lent manner of their growth in the retina, and the tumor may 
 thus grow all over the retina, spread to the optic nerve and 
 even to the choroid, after an adhesion between retina and 
 choroid has taken place (Knapp). The second mode of 
 growth is generally the origin of isolated secondary tumors 
 found in the choroid, the sclerotic and the episcleral tissue. 
 Furthermore, metastatic tumors have been observed in the 
 bones, the lymphatic glands, the liver and other organs. 
 
 While the eye-ball is gradually being filled by the new- 
 formation, the intra-ocular pressure becomes increased. 
 This together with the impairment in nutrition of the anterior 
 portions of the eye-ball, causes the formation of abscesses in 
 the cornea, and leads to the total destruction of this mem- 
 brane, thus opening a channel by which the tumor can spread 
 upon the outer surface of the eye. The tumor but seldom 
 perforates the sclerotic. 
 
 When the eye-ball is perfectly filled by the new-formation, 
 the whole of the uveal tract may be destroyed and entirely 
 disappear, leaving only small quantities of pigment behind. 
 
 From this description it seems evident, that the so-called 
 glioma of the retina in no way differs histologically from the 
 medullary small-cell sarcomata. I therefore see no reason 
 why we should not call these new-formations by that name.
 
 1 86 THE HUMAN EYE. 
 
 Some few cases have been described, in which glioma is 
 said to have disappeared by a general shrinking of the eye- 
 ball. From these observations, the new-formation has been 
 thought to be of a fibromatous character. The observations 
 are, however doubtful on the one hand, and on the other a 
 very considerable number of so-called glioma of the retina 
 have up to this date been examined without proving this 
 opinion to be the correct one.
 
 IX. 
 
 LENS CRYSTALLINEA. 
 
 I. Normal Conditions. 
 
 The crystalline lens is fastened to the ciliary body by 
 means of the zonula of Zimi, which encloses the canalis 
 Petilii, consists of the lens-capsule, the capsular epithelium 
 and the lens-fibres. 
 
 The lens-capsule forms a sac in which the remainder of 
 the elements constituting the crystalline lens are enclosed. 
 The clinical distinction between an anterior and a posterior 
 lens-capsule is not histologically justifiable. 
 
 The lens-capsule is a perfectly transparent membrane, 
 which is not equal in thickness in all its parts. It is thickest 
 at and around the anterior pole of the crystalline lens, and 
 thinnest upon its posterior surface, especially at the posterior 
 pole. The lens-capsule is generally thicker in advanced age 
 than in youth. 
 
 In plain views it appears perfectly homogeneous. A 
 number of authors have seen a fine striation upon its trans- 
 verse section, which I have never been able to recognize. 
 Such a lamellar structure would, however, be sure proof of 
 the connective-tissue character of the lens-capsule, of which 
 I have no doubt, as it is analogous in every way to Dcscemefs 
 membrane and the lamina vitrea choroideae. 
 
 As has been stated by a great many authors, the lens- 
 capsule is an elastic membrane. If ruptured or partially de- 
 tached from the lens substance, it will roll itself up. From 
 experiments on the eyes of animals, I had formed the opinion 
 that the lens-capsule would always roll itself up in a centri- 
 fugal direction, I have, however, since then seen the human 
 lens-capsule to be rolled up in a centrifugal as well as a cen- 
 tripetal manner. The lens-capsule may furthermore simply 
 retract and thus become wrinkled. 
 
 The capsular epithelium is a single layer of epithelial
 
 1 8 8 THE H UMA N E YE. 
 
 cells, lying on the inner surface of the anterior lens-capsule, 
 which appear hexagonal in a plain view, similar to the 
 endothelium oi Descetnet's membrane. Each cell has a large 
 round or oval nucleus. IVed/ and HoscJi have also described 
 cells with hyaline offsets. These cells are united by a small 
 quantity of cementing substance, which is easily seen when 
 stained with nitrate of silver. At the equator of the lens 
 these epithelial cells grow longer and appear like cylinder 
 cells, and gradually form the so-called lens fibres. The pos- 
 terior lens-capsule, that is, the portion of the lens-capsule 
 which, beginning at the equator, covers the posterior surface 
 of the lens substance, has no epithelium. Some authors have 
 been misled into the description of such an epithelium by 
 hardened cementing substance, or by the ends of lens fibres 
 attached to it. 
 
 The cells of the capsular epithelium are all somewhat 
 granular. According to y. Arnold, this granular appearance 
 is more pronounced near the equator, while the outlines of 
 the cells there grow less distinct. 
 
 I have never seen any new-formation of cells in the nor- 
 mal capsular epithelium. 
 
 The bulk of the crystalline lens is formed of the lens- 
 fibres or lens-bands (y. Arnold^. Isolated lens-fibres when 
 lying flat, appear as broad bands, and are striated in a longi- 
 tudinal direction. The transverse striation which has been 
 described by a number of authors, I never found in normal, 
 but sometimes in pathological lenses. When the lens-fibres 
 lie on their edge, they appear much narrower. Their real 
 shape is best seen in transverse sections, and we then find 
 them to be hexagonal prisms. They vary in size, and those 
 taken from the centre of the crystalline lens are usually 
 smaller than those taken from its periphery. The lens- 
 fibres taken from the centre have, moreover, especially at an 
 advanced age, no nucleus, while those from the periphery 
 always have an oval nucleus lying with its long axis in the 
 direction of the lens-fibre. Every such lens-fibre contains 
 only one nucleus, and the statements with regard to fibres 
 with two and more nuclei, do not seem to be correct. 
 
 The body of the peripheral lens-fibres seems to consist
 
 LEA'S CRYSTALLIKEA. i8q 
 
 of two parts ; a tough peripheral and a softer central part. 
 The latter is formed of myeline, and called liquor Morgagni 
 The nearer the centre of the lens-fibres, the more of the 
 harder, tougher substance, and the less liquor Morgagni is 
 found. On their narrow sides, the margins of the lens-fibres 
 are indented. This indentation is according to J. Arnold's 
 statement, more pronounced in the central fibres,.-and grad- 
 ually disappears towards the periphery. The little offsets of 
 the neighboring lens-fibres interlace like those of the bones of 
 the skull. All the fibres are united with each other by a 
 cementing substance, which when fresh is homogeneous or 
 slightly granular, and can be well recognized when stained 
 with nitrate of silver. I never saw as beautiful regular hexag- 
 onal figures in a transverse section of the lens-fibres as 
 J. Arnold has drawn. The lines produced by the stained 
 cementing substance have always appeared wavy in my speci- 
 mens. Where the ends of the lens-fibres touch each other 
 upon the anterior and posterior surface of the crystalline 
 lens, they form the so-called lens-stars. In the newly-born, 
 these stars each consist of three lines which lie at angles of 
 about one hundred and twenty degrees to each other, and are 
 united in the anterior and posterior pole. While two of 
 these lines on the anterior surface run upwards and one 
 downwards, the condition is the reverse one upon the poste- 
 rior surface. These lines never reach the equator, and end in 
 what has been called the " fibre-vortex." In the adult, they 
 branch off into secondary ones. In very old lenses we find 
 these lines changed into fissures filled with liquor Morgagni. 
 The lens fibres as they approach these lines, are a little 
 broader and bent. 
 
 According to J. Arnold, the lens-fibres in a meridional 
 direction, have the shape of a Roman S, from the back 
 towards the front, but they never entirely reach from one pole 
 to the other. 
 
 If we divide the lens by cutting through both its poles, 
 and vertically upon the equator, we see that the most peri- 
 pheral lens-fibres are convex towards the centre ; this convex- 
 ity is gradually changed into the opposite direction, as the 
 fibres come nearer the centre. The nuclei of the lens-fibres
 
 J 90 
 
 THE HUMAN E YE. 
 
 appear in such a section arranged in such a way, as to form 
 a line which is convex towards the anterior surface of the 
 crystalh'ne lens and lies near it. 
 
 2. Pathological Conditions. 
 
 The tissue of the crystalline lens does' not become in- 
 flamed like other tissues. Although Iwanoff and Becker 
 have described a hyperplastic process in the capsular epithe- 
 lium as taking place within the perfectly intact lens-capsule, 
 and called it phakitis, I have never been able to see it. 
 According to Rvanoff, the " new-formed cells are much larger 
 and the nucleus easily divides itself into two and more.'' 
 Furthermore, these cells are said " to be very prone to under- 
 go a colloid or mucoid metamorphosis, and then to form large 
 vesicles, filled with colloid substance, which crowd the nucleus 
 to one side." These vesicles, which Becker calls giant-cells, 
 seem to me to be identical with the myeline globules of which 
 we shall speak farther on, and which never contain a nucleus. 
 The pathological changes of the crystalline lens when the 
 capsule is intact, and which are called cataract, are simply 
 regressive metamorphoses of the elements constituting the 
 crystalline lens. We find frequently the anterior capsule of 
 such pathological crystalline lenses very much thickened. 
 Transverse sections of such thickened capsules, show it to be 
 either perfectly homogeneous, or to possess a longitudinal 
 striation {Babuchin, Becker). 
 
 Atrophy of the lens-capsule, which H. Mueller and Becker 
 have described, has never come under my own observation, 
 and the thickness of the lens-capsule varies so much in differ- 
 ent individuals, that such an atrophy must be very difficult 
 to diagnose. 
 
 The deposits upon the outer surface of the anterior and 
 posterior lens-capsule, caused by iritis and cyclitis, do not 
 belong among the pathological changes of the crystalline 
 lens. 
 
 A. Cataract formed within an Intact Lens-capsule. 
 
 It is possible to distinguish both clinically and anatomi- 
 cally between a large number of cataracts, since the dimness
 
 LE.VS CRYSTALLINEA. Igi 
 
 caused by regressive metamorphosis of the lens fibres, may 
 have a varying shape, and lie in very different regions. The 
 histological conditions are the same in nearly all of these cases 
 and we can only distinguish between cataract caused by 
 physiological progressive sclerosis of the lens fibres, and 
 that caused by a pathological regressive metamorphosis of 
 these elements. 
 
 As above stated, the central lens fibres when in a normal 
 condition are harder than the peripheral ones, and have no 
 nucleus. This central sclerosis, like the formation of horny 
 scales on the surface of the epithelium of the skin, is pro- 
 gressive, and gradually spreads towards the periphery in such 
 a way, that more and more lens fibres become sclerosed, until 
 finally all, or nearly all of them are thus altered. At the 
 same time, small quantities of liquor Morgagni are found to 
 lie outside the lens fibres. They form round and oval drops 
 of a varying size, and lie chiefly between the ends of the 
 lens fibres. The latter elements appear very brittle, no longer 
 have any nucleus, and in transverse sections we see, that they 
 have lost their comparatively regular hexagonal shape, are 
 sometimes perfectly cylindrical, and no longer indented at 
 their margins. When all the fibres have been thus altered, 
 we call the condition clinically a mature senile cataract 
 (cataracta nigra). Frequently, however, we find in these 
 cataracts a larger quantity of free myeline globules (liquor 
 Morgagni ) and a part of the lens is accordingly more fluid 
 (especially the peripheral layers). 
 
 This hard cataract caused by the physiological progressive 
 sclerosis is seldom, if ever stationary, and the fibres usually 
 undergo a further regressive metamorphosis, that is, the catar- 
 act becomes what we clinically call hypermature. These 
 regressive metamorphoses are, however, also found without 
 preceding sclerosis, and are the histological factors causing 
 all other kinds of cataract, especially those found congenitally 
 or in young people. 
 
 In such cataracts we find beside the globules of liquor 
 Morgagni, that the lens fibres are at first granular, which is 
 the beginning stage of fatty degeneration. Later on, the 
 molecular granules are changed into larger drops which coa-
 
 192 
 
 THE HUMAN EYE. 
 
 lesce. In this way the whole of the lens substance may be- 
 come fluid, and then consists of liquor Morgagni and fat- 
 globules. The existence of the latter is especially proven 
 by the formation of cholestearine crystals, which may be found 
 in such cataracts. Sometimes we also see myeline drops 
 filled with crystals of margaric acid. In other cases, a num- 
 ber of lens fibres which are not yet perfectly broken up, are 
 found to have spindle-shaped enlargements which phenome- 
 non is probably caused by imbibition. 
 
 In rare cases (according to Iwanoff always) lens fibres, 
 before being broken up, may be found to have a transverse 
 striation. This striation resembles that of the muscular 
 fibres, from which it is, however, distinct, since the striae do 
 not lie at regular intervals, and do not cross the longitudinal 
 direction of the fibres at right angles. 
 
 In most of the cases of soft cataract, we find lens fibres in 
 all stages of destruction. Even where the clinical appear- 
 ance would seem to justify the idea that all of the lens fibres 
 must be destroyed, we may yet find normal ones and others 
 which, although they are granular, have not yet lost their 
 normal shape. 
 
 During the destruction of the lens fibres, lime may be de- 
 posited in the lens. Becker s statement, however, that lime 
 is only deposited in a place where the lens fibres have been 
 altogether destroyed, is not correct. I have in my possession 
 some specimens of a lens which show only the symptoms 
 of senile sclerosis with a quantity of deposits of lime. 
 
 The lime is found in small granules which coalesce and 
 thus form larger bodies. These may also again coalesce, but 
 even very large accumulations of lime retain the granular 
 structure. 
 
 During all these changes, the capsular epithelium may 
 either remain unaltered, or it is gradually destroyed by fatty 
 degeneration. 
 
 As mentioned above, Iwajioff, H. Mueller and Becker de- 
 scribed a new-formation of cells in the capsular epithelium. 
 Becker says that this new-formation may appear later on as 
 a tissue consisting of spindle-shaped cells, and more than ten 
 times as thick as the normal capsular epitheliiiiii. I have
 
 LENS CR YSTALLINEA. 
 
 193 
 
 never seen this tissue or any new-formation of the cells of the 
 capsular epithelium where the lens-capsule was perfectly 
 intact ; I shall however, later on have to describe a perfectly 
 similar cell new-formation found when the lens-capsule has 
 been ruptured. Perhaps, this was also the case with the 
 lenses in which Becker saw these changes. 
 
 Furthermore, he mentions the formation of " giant-cells," 
 and states expressly that they could not possibly be myeline 
 globules, since they have a nucleus. He found them, espe- 
 cially in cases of cortical cataract, in dislocated lenses, in 
 traumatic and secondary cataracts. I must state that I have 
 never seen these cell formations. I have, however, very fre- 
 quently thought I saw a nucleus in such large myeline-globules 
 and convinced myself only by further examination, that I was 
 deceived by another smaller globule lying above or under-' 
 neath the larger one. Sometimes the myeline-globules have 
 also a double contour, and it may thus appear as if we had to 
 do with a cell membrane. 
 
 The formation of pus-cells in the lens substance, while the 
 capsule was unruptured, has only once been seen by Knapp. 
 Becker has never seen it, and I have looked for it in vain, 
 even, in cases of purulent panophthalmitis, and when the lens- 
 capsule was ruptured. 
 
 Two varieties of cataract formed inside of a perfectly intact 
 capsule are yet to be mentioned, as showing some peculiar 
 histological conditions ; I mean, cataracta polaris anterior 
 (pyramidalis) and cataracta haemorrhagica. 
 
 Cataracta polaris anterior (pyramidalis) is formed by a cone 
 which lies upon the normal lens substance in the region of the 
 anterior pole. This cone is always covered with lens-capsule, 
 and the latter accordingly has a diverticalum in which 
 the cone lies. The normal capsular epithelium reaches up 
 to the base of this cone. According to Becker, the apex of 
 the cone is filled with coagulated fluid, while nearer the base 
 he found a tissue consisting of spindle-shaped cells, very simi- 
 lar to the tissue of the cornea. H. Mueller and Schweigger 
 found the cone to consist of a fatty cretaceous substance, in 
 which H. Mueller could not find any cellular elements. 
 Hiilke also states that cells are found in this substance. I
 
 194 
 
 THE HUMAN EYE. 
 
 had occasion to examine one such cataract. The cone was 
 also in this case enclosed in the wrinkled lens-capsule, and 
 two-thirds of it consisted of a lamellar substance without any 
 cellular elements. Its basis was formed by fat-drops and 
 lime granules, and reached below the level of the surrounding 
 normal capsular epithelium. (See Fig. 93). 
 
 Fjg. 93. — Anterior polar cataract. The apex of the cone is formed by a lamellar, dim 
 tissue, without any cellular elements. The basis consists of lime and fat. 
 
 Haemorrhagic cataract has been once examined and de- 
 scribed by von Groefe. He found the lens fibres brown, 
 which color was caused by granular and crystallized blood- 
 pigment within them, while their shape was unaltered. The 
 capsular epithelial cells too, were filled with the pigment. 
 It could not be ascertained in this case whether the lens-cap- 
 sule was intact or ruptured. 
 
 Wagner and Lohmayer have described the formation of 
 osseous tissue within the lens-capsule. Whether the capsule 
 was ruptured or not, is not stated. More recently Voorhies 
 again described such an ossification of the lens substance, but 
 omitted to state anything regarding the state of the lens-cap- 
 sule. ^^^>^iT draws attention to the fact, that ossification in a 
 cyclitic membrane might easily lead to deception, and be taken 
 for ossification of the crystalline lens. I shall later on also have 
 to refer to the formation of osseous tissue within the lens- 
 capsule, which I found, however, always to be ruptured. A 
 direct change of epithelial tissue, like the lens fibres, into 
 osseous tissue has not yet been definitely observed. 
 
 B. Injuries to the Lens-capsule a?id the Lens-substance and 
 their Results. 
 
 Single small wounds of the lens-capsule can, as it appears 
 from Ritters experimental observations, heal by simple repo- 
 sition of the lips of the wound. Becker states, that by seeing
 
 LENS CRYSTALLINEA, 
 
 195 
 
 specimens oi Leber s, he came to the conclusion that such small 
 wounds of the capsule may heal with the new-formation of a 
 small amount of vitreous substance, analogous to the capsular 
 substance, and that the capsular epithelial cells do 7iot take 
 part in the production of this new-formation. This is a 
 remarkable observation, as we know that similar wounds of 
 Desceinefs membrane never heal. I am however, not in the 
 position to criticise Becker s statement, as I do not possess 
 any similar specimens. 
 
 (At the last meeting of oculists at Heidelberg, 1878, 
 Leber showed such specimens from the crystalline lens of 
 rabbits. He came to the conclusion, however, that the 
 capsular epithelial cells produced the newly formed glass sub- 
 stance. He stated that these cells proliferate into the wound- 
 canal. Gradually, at first thinner, later thicker layers of an 
 inter-cellular homogeneous substance are formed, and the 
 surrounding lens-capsule grows thicker by the new-formation 
 of vitreous substance on its inner surface). 
 
 Larger wounds of the lens-capsule remain permanently 
 open, and this is due to the folds in the capsule which accord- 
 ing to Becker are observed, or to the rolling up of the lens- 
 capsule, as Raab and myself have described. This rolling up, 
 as stated above, takes place mostly in a centrifugal, sometimes 
 in a centripetal direction. 
 
 In consequence of these larger wounds of the lens-capsule 
 the lens substance becomes exposed to the influence of the 
 aqueous humor or vitreous body, and the result of this 
 exposure is the formation of a traumatic cataract. In the 
 simplest form of these cataracts, we find the lens fibres near 
 the capsular wound swollen (by imbibition) and granular. 
 Gradually these lens fibres are broken up, and the myeline 
 becomes free and can be absorbed. The capsular epithelial 
 cells may by imbibition swell too, and appear as large vesi- 
 cle-like cells. Becker speaks also in these cases of an inflam- 
 matory new formation of cells and " giant-cells." My own 
 examinations have not enabled me to agree with this state- 
 ment. 
 
 In this way the whole of the lens substance may be broken 
 up and absorbed, and the anterior and posterior halves of
 
 196 
 
 THE HUMAN EYE. 
 
 the inner surfaces of the lens-capsule may become adherent 
 to each other. 
 
 Ruptures of the posterior lens capsule cause the same 
 conditions, although the progress seems to be a slower one, 
 and we frequently then find particles of the broken lens fibres 
 suspended in the vitreous body. 
 
 If, in consequence of the injury, the iris and ciliary body, 
 or the whole of the uveal tract become inflamed, the conditions 
 inside the ruptured lens-capsule may appear very different. 
 The fibrino-plastic exudation, caused by these inflammations, 
 can enter the wound in the lens-capsule, and here also be 
 transformed into connective-tissue, which gradually leads to 
 destruction of the lens fibres. The new formed tissue con- 
 sisting of round-cells and spindle-cells lies close to the lens- 
 capsule, and fills all its folds and wrinkles. Frequently it is 
 seen to contain new formed blood-vessels which are some- 
 
 FiG. 94.— Connective-tissue within the ruptured lens-capsule. 
 
 times of comparatively large calibre. (See Fig. 94). This 
 tissue is exactly the same which Becker has described as 
 formed within the intact lens-capsule. How far the capsular 
 epithelial cells help to form this tissue, I have not been able 
 to ascertain, as they were always wanting in my specimens. 
 
 I once found the same tissue inside the ruptured capsule 
 of a crystalline lens, which had been dislocated under the 
 conjunctiva. 
 
 The remainder of the lens fibres in these cases were 
 always granular or broken up. 
 
 This new-formed tissue sometimes glues the crystalline- 
 lens to the cornea, and probably always to the iris, except 
 where it is found in dislocated lenses, and the conditions are 
 changed accordingly. Synechiae between the usually cata-
 
 LENS CR YSTALLINEA. 
 
 197 
 
 ractous crystalline lens and the cornea may, as we have seen, 
 also happen when the capsule is perfectly intact. 
 
 The osseous tissue sometimes found within the lens-cap- 
 sule probably always takes its origin from such new-formed 
 connective-tissue. Possibly the deposits of lime, usually 
 found in such lenses, have a direct influence upon the forma- 
 tion of osseous tissue. I am in the possession of an eye with 
 general ossification of the choroid, in which the folded lens- 
 capsule, which lies embedded in a cyclitic membrane, is 
 perfectly filled with osseous tissue. The origin of the affec- 
 tion was an injury. (See Fig. 95.) I have, however, not yet 
 
 Fig. 95. — Osseous-tissue formed within the ruptured lens-capsule. 
 
 seen a specimen, where the whole of the lens substance was 
 changed into the spindle cell tissue, above described. 
 
 Foreign bodies are sometimes retained in the lens sub- 
 stance. Iwanoff states that they are then found to be 
 surrounded with pus cells, and Becker adds that these pus 
 cells come from tissues outside the lens-capsule.
 
 X. 
 
 VITREOUS BODY AND ZONULA ZINNII. 
 
 I. Normal Conditions of the Vitreous Body. 
 
 The vitreous humour consists of a jelly-like substance, 
 in which cells are suspended. 
 
 A number of authors are of the opinion that the vitreous 
 body is inclosed in a membrane, the so-called membrana 
 hyaloidea, and Schwalbe has recently joined in this view. I 
 cannot, however, agree with this opinion. According to 
 my examinations, no such limiting membrane belongs to the 
 vitreous body, and it is separated from the retina only by the 
 limitans interna of that membrane. The jelly-like substance 
 of the vitreous body is, however, somewhat tougher and 
 denser in its periphery. The endothelial and epithelial cells 
 described upon the membrana hyaloidea, I am convinced, do 
 not exist. 
 
 The jelly-like substance consists of a denser mucoid and 
 a thinner fluid part. Most authors speak of concentric 
 layers in the denser peripheral part, while the inner part, the 
 nucleus, is said to be more homogeneous. Schwalbe, more- 
 over, found septa in the vitreous body running in a radiary 
 direction, and one septum running concentrically with the 
 surface of the vitreous body. After having hardened the 
 vitreous body in a dilute solution of chromic acid, I have seen 
 similar conditions, and it seems therefore that we have 
 concentric layers in the periphery, and radius-like septa 
 between which the thin fluid part of the vitreous body is 
 lying. 
 
 A canal is found beginning at the optic papilla and run- 
 ning through the vitreous body to the fossa patellaris (into 
 which latter the crystalline lens fits), which is filled with 
 fluid, the so-called canalis hyaloideus. During foetal life this 
 canal encloses the arteria hyaloidea. By injecting a stained 
 fluid into the intervaginal space of the optic nerve, this canal
 
 VITREOUS BODY AND ZONULA ZINNIl. jgg 
 
 may be filled, and we must therefore consider it to be a 
 lymphatic channel, in direct communication with those of the 
 optic nerve and retina. According to Schwalbe, this canal is 
 surrounded by a vitreous membrane to which some cells are 
 often attached. They form, however, no endothelial coating 
 of this canal, but are the cells of the vitreous body, to be 
 spoken of directly. 
 
 A number of authors have found fibrillae in the vitreous 
 body. I have never been able to find them in the normal 
 condition. 
 
 The vitreous body always, however, contains cellular ele- 
 ments. They appear to be more numerous in its outer than 
 its central parts, and ScJnvalbe calls some of them directly 
 subhyaloid cells. The same cells are, however, found in other 
 parts of the vitreous body, and this name appears therefore 
 inappropriate. 
 
 Iwanoff makes a distinction between three separate kinds 
 of cells in the vitreous body. Although they may be here 
 referred to as different types, I must state that these cells are 
 very variable in shape, and the different kinds are seen to 
 merge into each other. We find round-cells with one or more 
 nuclei, some of which are seen to contain smaller and larger 
 vacuolae, by which the nucleus is crowded to one side, and 
 which appear like seal rings. Then we find cells with one or 
 more offsets, and of an accordingly varying aspect. The 
 third kind of cells described by Iwano^ contain light vesicles, 
 which are said to be filled with a fluid, and are perhaps, 
 identical with those containing vacuolae. Liebcr and Ktiehn 
 saw minute granules taken up by these cells, in molecular 
 motion. These cells, furthermore, have been considered as 
 producing the mucoid tissue of the vitreous body, and have 
 accordingly been called physaliphora. 
 
 With regard to the nature of all these cell forms, I must 
 agree with Schwalbe, who declares them to be lymph cells, 
 that is, wandering cells coming from the membranes sur- 
 rounding the vitreous body. 
 
 2. Pathological Conditions. 
 The question whether the vitreous body can become in-
 
 200 ^^^ HUMAN E YE. 
 
 flamed, independent of an inflammatory process in any of 
 the surrounding membranes, has of late been frequently 
 discussed. Since the vitreous body has neither blood-vessels 
 nor cells of its own, we are justified, it seems, in denying a 
 priori, the possibility of such an independent inflammation. 
 Experiments made in order to solve the question, have led 
 to the same result, since it is simply impossible to bring a 
 foreign substance into the vitreous body with the intention 
 of there creating an inflammation, without piercing other mem- 
 branes of the eye ball, which can thus become inflamed. The 
 best conditions for such experiments would be found in an 
 eye, from which the crystalline lens had been removed, while 
 the posterior lens-capsule remained intact, by bringing the 
 foreign substance into the eye ball through cornea and lens- 
 capsule. Schmitt-Rimpler has used such eyes for his experi- 
 ments. But even in these eyes the hyalitis, caused by the 
 experiment, does not prove the possibility of an independent 
 inflammation of the vitreous body. Pagenstecher has, further- 
 more, directly observed by experiments, that the cells found 
 in the vitreous body thus artificially irritated, come from the 
 surrounding membranes. 
 
 I agree therefore with those authors, who deny the possibil- 
 ity of an independent inflammation of the vitreous body, and 
 can only acknowledge the existence of secondary hyalitis. As 
 we find in the contents of the synovia of a joint the results of 
 a serous, fibrinous or purulent inflammation of this membrane, 
 so we find in the vitreous body the products of the inflam- 
 matory processes of the surrounding membranes. These 
 latter may, hov^^ever, show a different form of inflammation 
 from the one found in the vitreous body, as the cells when 
 once exuded into the latter have ample space for further 
 changes. 
 
 A, Liquefaction of the Vitreous Body {Sync hisis). 
 
 Chronic affections of the uveal tract may produce a change 
 in the consistency of the vitreous body, which finally leads to 
 its complete liquefaction. 
 
 Von Wccker states that this liquefaction is caused by a 
 large number of cells which immigrate into the vitreous
 
 VITREOUS BODY AND ZONULA ZINNII. 20I 
 
 body. This appears, however, not to be the case, as the 
 immense number of cells found in the vitreous body in a 
 case of purulent hyalitis do not cause synchisis. Moreover, 
 he explains the opacities, clinically observed in such a lique- 
 fied vitreous body, by these cells. 
 
 We sometimes find in the liquefied vitreous crystals of 
 cholesterine, and then the disease is clinically styled synechisis 
 scintillans. Recently Poncet also found crystals of tyrosine 
 and phosphates in a case of synchisis scintillans. 
 
 B. Plastic Hyalitis, 
 
 When describing the conditions which exist during the 
 inflammation of the ciliary body and especially the formation 
 of cyclitic membranes, we had to mention plastic hyalitis in 
 the fossa patellaris which helps considerably in the formation 
 of these structures. 
 
 We jind at first a larger number of round-cells immigrating 
 into the vitreous body which then appear to lie chiefly behind 
 the lens, often embedded in a fibrinous coagulum, which grad- 
 ually go over into spindle-cells and lead to the formation of 
 a tough connective-tissue with new-formed blood-vessels. 
 
 The same process is observed, if a foreign body has 
 pierced the vitreous. The immigrated cells then chiefly 
 lie along the wound canal, and again are transformed into 
 connective-tissue. I possess a specim.en of an eye, injured by 
 a piece of a gun cap which perforated the cornea, iris, lens and 
 vitreous body before becoming retained in the sclerotic, 
 choroid and retina at the opposite side of the eye ball. In 
 spite of the ensuing purulent iritis and cyclitis, the inflamma- 
 tion in the vitreous body remained confined to the wound 
 canal, and led to the formation of a band of tough connective- 
 tissue running from the place of its entrance to the place 
 where the foreign body became embedded in the sclerotic. 
 
 Such a new-formation of connective-tisspe in the vitreous 
 body is also seen after haemorrhages into its structure. We 
 then generally find a small amount of fibrine filled with round- 
 cells and surrounded by the red blood-corpuscles. Gradually 
 this fibrine is changed into connective-tissue, in the formation
 
 202 THE HUMAN EYE. 
 
 of which the red blood-corpuscles also seem to take an active 
 part as they entirely disappear. 
 
 We had, furthermore, occasion to mention plastic hya- 
 litis, occasioned by affections of the retina and optic nerve. I 
 mean here the new-formation of connective-tissue in the 
 excavated optic papilla, and the membrane like new-formations 
 upon the inner surface of the inflamed retina. In these cases 
 the plastic hyalitis only concerns the outer layers of the 
 vitreous body. 
 
 If such membranous new-formations do not adhere to the 
 retina, they may by their retraction lead to detachment 
 of the vitreous body, in which the substance of the latter 
 becomes naturally condensed. We find this detachment, as 
 has first been made known by Iwanoff, in a number of 
 pathological, especially injured eye balls, and most frequently 
 when a foreign body has become encapsuled in the vitreous. 
 
 Von Wecker mentions an observation made by Poncet, 
 which proves that the connective-tissue in the posterior parts 
 of the vitreous body too, can be ossified. The formation 
 of osseous tissue in cyclitic membranes has been mentioned 
 above. 
 
 The blood-vessels found in the connective-tissue which is 
 formed in the vitreous body, come from the ciliary body, the 
 retina or the optic nerve. 
 
 The vitreous body may also become detached by fluids 
 which are found to lie between it and the retina, and this 
 mode of detachment seems to be caused more by chemical 
 than by mechanical influences. If this were not the case, the 
 fluid would certainly be taken up by the vitreous body, and 
 the detachment thus heal. 
 
 C. Purulent Hyalitis. 
 
 After injuries, and in the course of a purulent inflamma- 
 tion of the uveal tract or during purulent panophthalmitis 
 we may find purulent hyalitis, which is characterized by the 
 presence of an immense number of cells in the vitreous body. 
 Their number may be so large that it is hardly possible to see 
 anything but cells. The latter have all sorts of shapes, and
 
 VITREOUS BODY AND ZONULA ZINNII. 203 
 
 frequently two or more nuclei. They have sometimes very 
 long thin offsets, which appear like a network of fibrillae. 
 
 This condition may lead to perforation of the eye ball or 
 it may become chronic and lead to the formation of connec- 
 tive-tissue, which is one of the chief factors from which the 
 shrinking of the eye ball, clinically called phthisis bulbi 
 results. 
 
 In rare cases this formation of connective-tissue is very 
 quickly accomplished, and concerns the whole of the vitreous 
 body and may lead to the incorrect diagnosis of introcular 
 tumor. It may furthermore make the eye ball as hard as in 
 glaucoma, and when shrinking produce again phthisis bulbi. 
 
 Anatomically we can speak of phthisis bulbi only, when the 
 vitreous body has thus been changed, and we must make a 
 more distinct separation between anterior phthisis and 
 phthisis bulbi, than this is usually done by clinicists. 
 
 The Zonula Zinnii. 
 
 I. Normal Conditions. 
 
 In the region of the ora serrata, a number of well con- 
 toured, light and tough fibres are seen to spring from the 
 vitreous body, of which they are a part, as J. Arnold has 
 proven. They lie at first upon the retinal layer of the ciliary 
 body, and follow all its windings up to the most anterior 
 portion of that body. From there they are bent inward and 
 pass on to the anterior and posterior lens-capsule ; some of 
 them return to the vitreous body. They have therefore like 
 the ciliary body a pars plicata and a pars non-plicata. These 
 fibres which hold the crystalline-lens in position are called 
 zonula zinnii (ligamentum suspensorium lentis, zonula ciliaris). 
 They are arranged in bundles by a very fine and easily de- 
 stroyed homogeneous substance, after they have bent inward 
 from the ciliary body. According to J. Arnold, we find be- 
 sides these fibres, which run in a meridional direction, a num- 
 ber which after having run a short time in this direction, go 
 over into an equatorial one. 
 
 Some authors have seen a transverse striation on these 
 fibres, and therefore considered them to be of a character mus-
 
 204 THE HUMAN EYE. 
 
 cular Cells sometimes found between them, are wandering 
 (lymphatic) cells. 
 
 Where the zonula fibres are merged into the lens-capsule, 
 this latter appears thickened. 
 
 2. Pathological Conditions. 
 
 Pathological changes in the tissue of the vitreous body 
 must needs influence the condition of the fibres of the zonula 
 Zinnii. There have, however, but few pathological changes 
 of these fibres been observed. Becker states that they may 
 become thin and atrophic, or thickened and granular. 
 
 When the fibres of the zonula have been severed, they 
 appear wavy like elastic fibres. 
 
 THE END.
 
 1 1^ D E X. 
 
 Abscess of the cornea, i6. 
 
 Arachnoidal sheath of the optic nerve, 
 
 142. 
 A reus senilis cornea, 39. 
 Argyrosis conjunctival, 63. 
 Atrophy of choroid, 134. 
 iris, 92, 
 
 lens capsule, 190. 
 optic nerve, 153. 
 retina, 187. 
 Bowman's layer, 2. 
 
 Bruch's membrane, 83. 
 Burns with lime of conjunctiva, 64. 
 of cornea, 37. 
 Canalis hyaloideus. 
 Capsule of lens, 187. 
 Capsular epithelium of lens, 188. 
 Cataracta, 190. 
 
 hemorrhagic, 194, 
 nigra, 191. 
 polar anterior, 193. 
 pyramidal, 193. 
 soft, [92. 
 traumatic, 194. 
 Choroidea, 116. 
 
 atrophy of, 134. 
 blood-vessels of, 116. 
 cystoid formations in, 138. 
 granuloma of, 138. 
 nerves of, 117. 
 ossification, 135. 
 pigmented epithelium, 119. 
 sarcoma of, 138. 
 tubercles of, 131. 
 Choroiditis, 135. 
 Choroiditis atrophic, 127. 
 
 disseminate, 130. 
 exudative areolar, 130. 
 parenchymatous, 130. 
 plastic, 127. 
 purulent, 130. 
 serous, 135. 
 Chorio-retinitis centralis, 130. 
 
 disseminate, 130. 
 Ciliary staphyloma, 48. 
 Circulus iridis major, 82. 
 minor, 82. 
 Cone-fibres of retina, 164. 
 Conjunctiva bulbi, 55. 
 
 blood-vessels of, 57. 
 inflammation of, 58. 
 injuries to, 63. 
 lymph-vessels of, 57. 
 nerves of, 57. 
 tumors of, 65. 
 Conjunctival oedema, 57. 
 
 haemorrhage, 57. 
 Conjunctivitis, 58. 
 
 blennorrhoic, 59. 
 catarrhal, 58. 
 croupous, 61. 
 diptheritic, 61. 
 gonorrhoic, 57. 
 phlyctsenular, 58. 
 purulent, 59. 
 trachomatous, 61. 
 Cornea, i. 
 
 abscess of, 16. 
 blood-vessels of, 10. 
 cysts of, 35. 
 fistule of, 34. 
 infiltration of, 11. 
 inflammation of, 13. 
 injuries to, 31. 
 lymphatic canals of, 3. 
 necrosis of, 32. 
 nerves of, 10. 
 ossification of, 24. 
 scars of, 23. 
 ectatic of, 35. 
 sclerosis of, 16. 
 synechiae with iris, 25. 
 lens, 37. 
 
 vitreous body, 37. 
 tumors of, 38. 
 ulcer of, 19. 
 xerosis of, 39. 
 Cornea-scleral margin, 8. 
 
 staphyloma, 47. 
 Corpus ciliare, 99. 
 
 atrophy of, 113. 
 blood-vessels of, loi. 
 gumma of, no. 
 hypertrophy of, 113. 
 injuries to, 113. 
 muscles of, 99. 
 nerves of, loi. 
 retinal layer of, 103.
 
 2o6 
 
 INDEX. 
 
 rupture of, 114. 
 tumors of, 115. 
 uveal layer of, 103. 
 Cyclitic membranes, iii. 
 Dermoid Tumors, see tumors. 
 Descemet's membrane, 6. 
 Detachment of ciliary body, 112. 
 retina, 179. 
 vitreous body, 143. 
 Dislocation of lens under conjunctiva 64. 
 Dura mater sheath of optic nerve, 142. 
 Episcleral tissue, 56. 
 Episcleritis, 58. 
 Epithelioma, see tumors 
 Excavation of optic papilla, 155. 
 Fibrinous choroiditis, 127. 
 iritis, 87. 
 Fibromatous tumors, see tumors. 
 Fontona's spaces, 9. 
 Foreign bodies in choroid, 136. 
 
 conjunctiva, 64. 
 cornea, 31. 
 corpus ciliare, 113. 
 iris, 93. 
 lens. 197. 
 retina, i8j. 
 sclerotic, 53. 
 vitreous body, 301. 
 Fovea centralis, 167. 
 Glaucoma, 155. 
 
 Glaucomatous excavation ofpapilla, 155 
 Granulomata, see tumors. 
 Haller's vascular ring, 146 
 
 Haemorrhage in choroid, 136. 
 
 conjunctiva, 57. 
 iris, 86. 
 
 optic nerve, 156. 
 retina, 178. 
 vitreous body, 201 
 Haemorrhagic cataract, 194. 
 Hyalitis, 201. 
 
 plastic, 201. 
 purulent, 202. 
 Hyaloid artery, 198. 
 canal, 198. 
 Hypopyon, 17. 
 iDflammation of choroid, 135. 
 
 ciliary body, 103. 
 conjunctiva, 58. 
 cornea, n. 
 iris, 84. 
 
 optic nerve, 150. 
 retina, 169. 
 sclerotic, 43. 
 vitreous body, 301. 
 Injuries to choroid, 136. 
 
 ciliary body, 113. 
 conjunctiva, 61. 
 
 cornea, 31. 
 
 iris, 93. 
 lens, 194. 
 optic nerve, 157. 
 retina, 183. 
 sclerotic, 53. 
 Interfascicular canals, 4. 
 Interfibrillar canals, 3. 
 Interlamellar canals, 4. 
 Interstitial neuritis, 150. 
 retinitis, 174. 
 Intervaginal space, 144. 
 Iris, 81. 
 
 atrophy of, 92. 
 blood-vessels of, 83. 
 cysts of, 94. 
 endothelium of, 81. 
 incatceration ot, 37. 
 injuries to, 93. 
 muscles of, 83. 
 nerves of, S3, 
 prolapse of, 39. 
 synechiae anteriores of, 36. 
 
 posteriores of, 91. 
 uveal layer, 83. 
 Iritis, 84. 
 
 fibrinous, 87. 
 haemorrhagic, 86. 
 parenchymatous, 89. 
 plastic, 87. 
 purulent, 89. 
 serous, 84. 
 Keratitis, 11. 
 
 parenchymatous, 15. 
 phyctaenular, 15. 
 purulent, 16. 
 striped, 15. 
 Keratoconus, 39. 
 Keratomalacia, 32. 
 Lamina cribrosa, 40. 
 fusca, 103. 
 
 vitrea choroideae, ii8. 
 Lens, 1S7. 
 Lens-capsule, 187. 
 
 epithelium, 18S. 
 fibres, 188. 
 Leucosarcoma, see tumors 
 Ligamentum pectinatum, 9. 
 Limitans externa, 161. 
 Limitans interna, 160. 
 Lipomatous tumors, see tumors. 
 Lymphangiectasia, 65. 
 Macula lutea, 167. 
 
 Medullary neuritis, 153. 
 Melanocancroid tumors, see tumors. 
 Melanoma, see tumors. 
 Melanosarcoma, see tumors.
 
 INDEX. 
 
 207 
 
 Myocephalon, 32. 
 Nervi ciliares breves, 117. 
 longi, 117. 
 Nervous opticus, 142. 
 
 blood-vessels of, 146. 
 sheaths of, 142. 
 Neuritis, 150. 
 
 interstitial, 150. 
 medullary, 152. 
 Neuro- epithelial layer of retina, 163. 
 Normal conditions of choroid, ti6. 
 ciliary body, yg. 
 conjunctiva, 55. 
 cornea, i. 
 iris, 81. 
 lens, 187. 
 optic nerve, i42. 
 retina, 159. 
 sclerotic, 39. 
 vitreous body, 198, 
 zonula zinnii, 203, 
 CEdema of conjunctiva, 57. 
 optic nerve, 147. 
 retina, 16S. 
 Opticus, 142. 
 
 Ora serrata of retina, 165. 
 Ossification of choroid, 132. 
 
 choroidal sarcoma, 141. 
 cornea, 24. 
 vitreous body, loi. 
 Osteoma, see tumors. 
 Pannus., 23. 
 
 Papillioraa, see tumors, 
 Pathological conditions of choroid, 120. 
 ciliary body, 103, 
 conjunctiva, 58. 
 cornea, 11. 
 iris, 84. 
 lens, 190. 
 optic nerve, 146. 
 retina, 168. 
 sclerotic, 43. 
 vitreous body, 199 
 zonula zinnii, 204. 
 Phlyctenula of conjunctiva, 59. 
 
 cornea, 15. 
 Phthisis anterior, 24. 
 
 bulbi totalis, 203. 
 Physaliphora, 199. 
 Pia mater sheath, 143. 
 Pigmented cells of choroid, 116. 
 cornea, 6. 
 iris, 82. 
 sclerotic, 39. 
 Pigmented epithelium, 119. 
 Pinguecula, 56. 
 Polypoid tumors, see tumors. 
 
 Prolapse of iris, 36. 
 Pterygium, 30. 
 Pupillary, membrane, 88. 
 Recklinghausen's canals, 3. 
 Reichert's layer, a. 
 Results of choroiditis, 133. 
 cyclitis, III. 
 iritis, 91. 
 keratitis, 33. 
 neuritis optica, 153. 
 retinitis, 180. 
 scleritis, 44. 
 Retina, 159. 
 
 ciliary part of, 103. 
 detachment of, 112, 
 external limiting membrane of, 161. 
 ganglionic layer of, 161. 
 inner granular layer of, 162. 
 inner molecular layer of, 163. 
 internal limiting membrane of, 160. 
 nerve fibre layer of, i6i. 
 outer granular layer of, 163. 
 outer molecular of, 163. 
 rods and cones, 163. 
 tumors of, 183. 
 Retinitis, 169. 
 
 albuminuric, 169. 
 apoplectic, 179. 
 atrophic, 174. 
 pigmentary, 133. 
 purulent, 177. 
 Rod-fibres, 163. 
 Rod-granules, 164. 
 Sarcomatous tumors, see tumors 
 Schlemm's canal. 41. 
 Scleral staphyloma, 47. 
 ciliary, 48. 
 equatorial, 49. 
 posterior, 49. 
 partial, 47. 
 total, 47. 
 Scleritis, 42. 
 
 infiltration, 42. 
 purulent, 43. 
 Sclerotic, 39- 
 
 atrophy of, 46. 
 blood-vessels of, 41. 
 ectasy of, 46. 
 hypertrophy of, 45. 
 nerves of, 41. 
 scars of, 44. 
 tumors of, 54. 
 Serous cysts, see tumors. 
 Subarachnoidal space, 144. 
 Subhyaloid cells, 199. 
 Subvaginal space, 144. 
 Synchisis simplex, 300. 
 scintillans, 301.
 
 2o8 
 
 INDEX. 
 
 Trachoma, 6i. 
 
 Tumors of the choroid, 138. 
 
 cysts, 138. 
 
 enchondroma, 139. 
 
 granuloma, 138. 
 
 sarcoma, 138. 
 Tumors of the ciliary body, 115. 
 
 myoma, 115. 
 
 sarcoma, 115. 
 
 Tumors of the conjunctiva, 65. 
 
 cysts, serous, 65. 
 
 dermoid tumors, 67. 
 
 epithelioma, 74. 
 
 fibroma, 69. 
 
 granuloma, td. 
 
 leucosarcoma, 71. 
 
 lipoma, 67. 
 
 lymphangiectasia, 65. 
 
 melanocancroid tumors, 
 
 melanosarcoma, 71. 
 
 osteoma, 69. 
 
 papilloma, 69. 
 
 polypoid tumors, 66. 
 Tumors of the cornea, 38. 
 Tumors of the iris, 97. 
 
 cysts, 94. 
 
 epidermoidoma, 9$. 
 granuloma traumaticum, 97- 
 leucosarcoma, 98. 
 melanoma, 97. 
 melanosarcoma, 98. 
 Tumor of the optic papilla, 157. 
 Tumors of the retina, 182. 
 fibroma, 183. 
 glioma, 182. 
 sarcoma, 182. 
 Tumors of the sclerotic, 54. 
 Ulcer of the cornea, 19. 
 Vaginitis nervi optic, 149. 
 Venae vorticosse, 117. 
 Viterous body, 198. 
 
 detachment of, 133. 
 inflammation of, igg. 
 liquefaction of, 200. 
 synechia with cornea, 27. 
 Vitreous bodies of the lamina vitrea 
 choroidese, 121. 
 Xerosis of conjunctiva, 63. 
 
 cornea, 39. 
 Zonula of Zinn, 203.
 
 UNIVERSITY OF CALIFORNIA UBRARY 
 
 Los Angeles 
 This book is DUE on the last date stamped below. 
 
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 SEP 
 
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 SEP ^0 1960 
 
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