NECROSIS OF INTRAOCULAR TISSUESSAMUELS, BERNARD
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030106001pmid: 18106936
Abstract IN TEXTBOOKS on general pathology, considerable space is devoted to the study of the death of tissues. However, in the teaching of the special pathology of the eye, disease from this standpoint fails to receive the attention that its frequency and extent warrant. In accordance with the nomenclature of general pathology, the term necrosis means the local death of cells or of tissues in an organ, notwithstanding the loss of which the organ as a whole continues to live. Intimately associated with necrosis are the conditions of degeneration, atrophy and gangrene. Degeneration signifies an alteration in the metabolism of the cells that compose a tissue, but not to such an extent as actually to cause the death of the cells. Atrophy means acquired diminution in the size of cells or of tissues after maturity has been attained. Degenerated or atrophic tissue may be converted into necrotic tissue. Gangrene signifies necrosis References 1. Samuels, B.: Necrosis of the Iris , Tr. Ophth. Soc. U. Kingdom 49:421-436, 1929 2. A Study of the Anatomic and Clinical Manifestations of Necrosis in Eighty-Four Cases of Choroidal Sarcomas , Samuels Tr. Ophth. Soc. U. Kingdom 53:520-570, 1933.
INCIDENCE OF DEFECTIVE COLOR VISION AMONG PSYCHOTIC PATIENTSHARDY, LeGRAND H.;RAND, GERTRUDE;RITTLER, M. CATHERINE
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030126002pmid: 18106937
Abstract INTEREST in the incidence of color blindness among psychotic patients has recently been aroused by the report in 1945 of Kaplan and Lynch1 from the Hudson County Hospital of Mental Diseases, Secaucus, N. J. These authors concluded that psychotic patients, both male and female, show a high incidence of defective color vision. Of a group of 223 male schizophrenic patients, for example, they claimed to find evidence of defective color vision in 32.8 per cent, and of a group of 148 female schizophrenic patients, in 4.8 per cent. The generally accepted values for incidence of anomalies in color vision among male and female persons of the white race are, in round numbers, respectively, 8 and 0.5 per cent. The incidence claimed by Kaplan and Lynch is, then, approximately four times as great in male and nine to ten times as great in female psychotic subjects as that among subjects References 1. Kaplan, H. M., and Lynch, R. J.: Color Blindness in the Psychoses , Am. J. Psychiat. 101:675-676 ( (March) ) 1945. 2. Millard, M. S., and Shakow, D.: A Note on Color-Blindness in Some Psychotic Groups , J. Social Psychol. 6:252-256 ( (May) ) 1935.Crossref 3. A personal communication from Dr. Shakow indicates that the fifth edition of the Ishihara test was used. 4. Miles, W.: One Hundred Cases of Color-Blindness Detected with the Ishihara Test , J. Gen. Psychol. 2:535-543 ( (Oct.) ) 1929.Crossref 5. Gallagher, J. R.; Gallagher, C. D., and Sloane, A. E.: A Critical Evaluation of Pseudo-Isochromatic Plates and Suggestions for Testing Color Vision , Yale J. Biol. & Med. 15:79-98 ( (Oct.) ) 1942. 6. Hardy, L. H.; Rand, G., and Rittler, M. C.: A Screening Test for Defective Red-Green Vision , J. Optic. Soc. America 36:610-614 ( (Oct.) ) 1946 7. Arch. Ophth. 38:442-449 ( (Oct.) ) 1947. 8. Hardy, L. H.: Standard Illuminants in Relation to Color Testing Procedures , Arch. Ophth. 34:278-282 ( (Oct.) ) 1945. 9. Smith, T., and Guild, J.: The C.I.E. Colorimetric Standards and Their Use , Tr. Optic. Soc. 33:73-134, 1931-1932. 10. Ishihara, S.: Tests for Colour-Blindness , ed. 5, Tokyo, Kanehara, 1925. 11. Pseudo-Isochromatic Plates for Testing Color Perception , Philadelphia, Beck Engraving Co., 1940. 12. Hardy, L. H.; Rand, G., and Rittler, M. C.: Color Vision and Recent Developments in Color Vision Testing , Arch. Ophth. 35:603-614 ( (June) ) 1946. 13. Hardy, L. H.; Rand, G., and Rittler, M. C.: Tests for Detection and Analysis of Color Blindness: I. An Evaluation of the Ishihara Test , Arch. Ophth. 34:295-302 ( (Oct.) ) 1945. 14. It may be of interest to note that the criterion of Miles and the Worcester III criterion of Millard and Shakow were also applied to the test records of our psychotic and nonpsychotic subjects of both the groups with normal and the groups with defective color vision. The criterion of Millard and Shakow gave a diagnosis as to color vision that was consistent in every case with our own. On the Miles criterion, however, 4 additional members (6 per cent) of the nonpsychotic group, 3 male and 1 female subjects, and 6 additional members (3 per cent) of the psychotic group, 3 of each sex, would have been rated as having defective color vision.
PREPLACEMENT OF AIR IN CYCLODIALYSISROME, SOL;KOFF, RAPHAEL
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030139003pmid: 18106938
Abstract THE ADVANTAGES of the use of air after cyclodialysis have been fully discussed by Barkan1 and several other writers in recent articles.2 These advantages were summarized by Barkan as follows: The injection of air (1) controls hemorrhage, (2) widens the cyclodialysis cleft, (3) makes the cleft visible and (4) deepens the anterior chamber. He stated: Cyclodialysis combined with air injection is indicated in primary glaucoma of the wide angle type. It is especially indicated, to the exclusion of trephination, iridencleisis and iridectomy in the late stage of the narrow angle type after peripheral adhesions have closed the angle in large part, irrespective of whether there is congestion or not. It is indicated in those varieties of secondary glaucoma in which cyclodialysis is commonly accepted as being indicated, [e. g., aphakia].... A high degree of pressure has not contraindicated its use. In all the methods described in the literature References 1. Barkan, O.: Cyclodialysis, Multiple or Single with Air Injection: An Operative Technique for Chronic Glaucoma , California Med. 67:78 ( (Aug.) ) 1947. 2. (a) Randolph, M. E.: A New Cyclodialysis Instrument , Am. J. Ophth. 26:187 ( (Feb.) ) 1943. 3. (b) Shaffer, R. N.: Inverse Cyclodialysis , Am. J. Ophth. 30:860 ( (July) ) 1947. 4. (c) Sugar, H. S.: Cyclodialysis: A Follow-Up Study , Am. J. Ophth. 30:843 ( (July) ) 1947. 5. Hughes, W., and Cole, J.: Technical Uses of Air in Ophthalmology , Arch. Ophth. 35:525 ( (March) ) 1946.Crossref
DEEP KERATITIS ASSOCIATED WITH ATYPICAL LICHEN PLANUS: Report of a CaseGOLDSMITH, J.
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030143004pmid: 18106939
Abstract RECENT studies1 have shown that there is a close relation between prolonged quinacrine ("atabrine") medication and the development of cutaneous lesions bearing a striking resemblance to classic lichen planus. Because of this resemblance, the name "atypical lichen planus" was designated as the most appropriate term for the disease. It is my opinion that both the quinacrine medication and the subsequent cutaneous lesions played an important role in the production of the keratitis. This belief will be elaborated on later. In all the literature dealing with this disease and in a personal observation of over 250 cases, only 1 case was encountered in which the deeper layers of the cornea were affected. This ocular involvement was particularly, interesting not only because of its rarity but because of its close relation to the course of the cutaneous disease. It appeared during the height of the cutaneous disturbance and subsided in a References 1. Bazemore, J. M.; Johnson, H. H.; Swanson, E. R., and Hayman, J.: Relation of Quinacrine Hydrochloride to Lichenoid Dermatitis (Atypical Lichen Planus) , Arch. Dermat. & Syph. 54:308-324 ( (Sept.) ) 1946. 2. Rosenthal, J.: Atypical Lichen Planus (Southwest Pacific) , Am. J. Path. 22:473-491 ( (May) ) 1946. 3. Dantzig, L., and Marshall, L. E.: Tropical Lichen Planus (New Guinea Variety): Clinical Report on Twenty-Four Cases (Possible Role of Quinacrine) , New York State J. Med. 46:991-995 ( (May 1) ) 1946. 4. Berliner, M. L.: Biomicroscopy of the Eye , New York, Paul B. Hoeber, Inc., 1943, vol. 1, p. 519. 5. Chamberlain, W. P., Jr., and Boles, D. J.: Edema of Cornea Precipitated by Quinacrine , Arch. Ophth. 35:120-134 ( (Feb.) ) 1946. 6. Sugar, H. S., and Waddell, W. W.: Ochronosis-Like Pigmentation Associated with Use of Atabrine (Quinacrine) , Illinois M. J. 89:234-239 ( (May) ) 1946.
AN AID IN DETECTING TRACHOMA-LIKE INCLUSION BODIES IN THE CONJUNCTIVABODIAN, MARTIN
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030152005pmid: 18122926
Abstract IN 1907, while in Java to investigate the immunology of syphilis, Halberstädter and von Prowazek1 discovered the inclusion bodies associated with trachoma. This observation was the first demonstration of such bodies in the eye. A few investigators have expressed the belief that the infectious agent of trachoma is a rickettsial body.2 In support of this view, Cuénod and Nataf2b claimed the passage of the agent through the louse onto a normal conjunctiva, with the production of clinical trachoma. Halberstädter-Prowazek inclusion bodies are observed in the conjunctival scrapings in cases of certain ocular infections. Although trachoma is the most important of these, similar bodies are also seen in cases of inclusion conjunctivitis, psittacosis and lymphogranuloma venereum.3 Whether, as Lindner4 stated, these bodies constitute the agent causing trachoma or whether they are the by-products of a tissue reaction to this agent is not clear. What does seem References 1. Duke-Elder, W. S.: Textbook of Ophthalmology , St. Louis, C. V. Mosby Company, 1940, vol. 2, p. 1599. 2. (a) Busacca, A.: Is Trachoma a Rickettsial Disease? Arch. Ophth. 17: 117 ( (Jan.) ) 1937.Crossref 3. (b) Cuénod, A., and Nataf, R.: Researches on the Aetiology of Trachoma , Brit. J. Ophth. 21:309, 1937Crossref 4. (c) Deuxiéme note sur la présence d'éléments infra-microbiens dans la follicules trachomateux , Arch. d'opht. 52:573, 1935 5. (d) Sur la présence d'éléments rickettsoïdes très abondants et très constants dans les follicules trachomateux , Rev. internat. du trachome 12:110, 1935. 6. Thygeson, P.: Viruses and Virus Diseases of Eye , Arch. Ophth. 29:635 ( (April) ) 1943.Crossref 7. Lindner, K., in Berens, C.: The Eye and Its Diseases , Philadelphia, W. B. Saunders Company, 1936, p. 439. 8. Bodian, M.: Trachoma: A Possible Carrier State , Arch. Ophth. 38:450 ( (Oct.) ) 1947.Crossref 9. Duke-Elder,1 1939, vol. 1, p. 938. 10. Caries, R.: Rapid Diagnosis of Malaria by the Use of a Wratten Light Filter , J. Lab. & Clin. Med. 28:1150, 1943.
OCCLUSION OF THE CILIORETINAL ARTERYLEVITT, JESSE M.
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030157006pmid: 18106940
Abstract IN CLOSURE of the central retinal artery, sparing of the macula with preservation of central vision due to the presence of a cilioretinal artery is a well recognized entity. The converse, closure of the cilioretinal artery with a normal functioning central retinal artery, has seldom been observed. Only 6 cases have been reported in the literature, and none within recent years. The main data in the reported cases are given in the accompanying table. Closure of the cilioretinal artery is usually manifested by sudden loss of central vision. Young people are affected. The fundus presents a large band of retinal opacity extending from near the temporal margin of the optic nerve to or beyond the macula. A cherry red spot in the macula is a frequent finding. The margins of the optic nerve are slightly hazed, especially temporally. A cilioretinal artery is observed coursing through the affected portion of the References 1. Knapp, H.: Ueber Verstopfung der Blutgefasse des Auges: Embolie der Ciliararterien , Arch. f. Ophth. 14:237, 1868. 2. Goldstein, I., and Wexler, D.: Embolism of the Central Retinal and Ciliary Arteries, in a Case of Chronic Lipoid Nephrosis with Thrombosis of the Innominate Artery , Arch. Ophth. 10:70 ( (July) ) 1933.Crossref
SILENT DACRYOCYSTITISTHEODORE, FREDERICK H.
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030162007pmid: 18106941
Abstract THE PURPOSE of this paper is to call attention to a mild type of dacryocystitis, usually mucoid in character, which is often the unsuspected cause of persistent conjunctivitis, or of unexplained tearing. This clinical entity may be called the "silent" type of dacryocystitis. For the most part, the patients comprising the present series had been treated for long periods by conventional methods, without improvement. In almost every case the lacrimal sac had been declared normal because irrigation had revealed its patency. Yet when irrigation of the lacrimal passages was performed with the purpose of collecting and examining the washings, certain clinical and bacteriologic evidence was obtained indicating inflammation of the lacrimal sac. The clinical evidence consisted in mucus, mucopus or small amounts of frank pus in the collected fluid washed through the lacrimal passages. Bacteriologically, cultures of both the conjunctiva and the material in the washings usually revealed the same References 1. Knapp, H., in Norris, W. F., and Oliver, C. A.: System of Diseases of the Eye , Philadelphia, J. B. Lippincott Company, 1898, vol. 3, p. 897. 2. Fuchs, E.: Text-Book of Ophthalmology , translated by A. Duane, ed. 8, Philadelphia, J. B. Lippincott Company, 1924, p. 515.
THE HISTORY OF THE DARTMOUTH EYE INSTITUTEBURIAN, HERMANN M.
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030168008
Abstract THE DARTMOUTH Eye Institute, of Hanover, N. H., has closed its doors. A unique institution has passed from the scene of American ophthalmology. It is worth while looking at its history. The origin of what in 1937 became the Dartmouth Eye Institute dates back to 1919. In that year Adelbert Ames Jr. came to Hanover, N. H., to join with Prof. Charles Proctor, of the department of physics of Dartmouth College, in carrying out research on the optical properties of the human eye. Ames is neither an ophthalmologist nor a physicist. Trained as a lawyer, he abandoned law to become an artist. Being of an analytic as well as artistic temperament, he soon became interested in the question of the relation of what one sees to what is represented on the canvas. The pursuit of this problem led to the question how the organ of sight reproduces the environment. In References 1. Ames, A., Jr., and Proctor, C. A.: Dioptrics of the Eye , J. Optic. Soc. America 5:22-84 ( (Jan.) ) 1921.Crossref 2. Gliddon, G. H.: An Optical Replica of the Human Eye for the Study of the Retinal Image , Arch. Ophth. 2:138-163 ( (Aug.) ) 1929.Crossref 3. Ames, A., Jr.: Cyclophoria , Am. J. Physiol. Optics 7:3-38 ( (Jan.) ) 1926. 4. Lancaster, W. B.: The Ames Spectacle Device for the Treatment of Cyclophoria with a Report of a Successful Case , Arch. Ophth. 57:332-338 ( (April) ) 1928. 5. Ames, A., Jr., and Gliddon, G. H.: Ocular Measurements , Tr. Sect. Ophth., A. M. A. , 1928, pp. 1-68. 6. Ames, A., Jr.; Ogle, K. N., and Gliddon, G. H.: Corresponding Retinal Points, the Horopter and Size and Shape of Ocular Images , J. Optic. Soc. America 22:538-578 ( (Oct.) )Crossref 7. 575-632 (Nov.) 1932. 8. Ogle, K. N.: An Analytical Treatment of the Longitudinal Horopter: Its Measurement and Application to Related Phenomena, Especially to the Relative Size of the Ocular Images , J. Optic. Soc. America 22:665-728 ( (Dec.) ) 1932.Crossref 9. Ames, A., Jr.: Sensations, Their Nature and Origin: Brief Statement of the Findings of the Dartmouth Eye Institute , Hanover, N. H., Dartmouth Eye Institute, 1945.
DI-ISOPROPYL FLUOROPHOSPHATE (D F P) IN TREATMENT OF GLAUCOMA: Further ObservationsLEOPOLD, IRVING H.;McDONALD, P. ROBB
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030181009pmid: 18122927
Abstract DI-ISOPROPYL fluorophosphate (DFP) has been shown to have a marked and prolonged miotic effect in normal1 and in glaucomatous eyes.1b It has been shown to lower intraocular tension in these eyes. Furthermore, there is evidence that these effects are brought about entirely by inactivation of cholinesterase, and not by direct action on the iris and ciliary muscle.2 Although in this respect the pharmacologic effects of DFP resemble those of physostigmine and neostigmine, the DFP—cholinesterase combination is an irreversible one.3 None of the methods successfully employed to split physostigmine and cholinesterase will break down this combination. Because of these properties of DFP and, more especially, because of the prolonged effect of very dilute preparations when locally applied to the normal eye, this drug was tested for its efficacy in the therapy of glaucoma.1b The initial studies indicated that DFP in 0.05 and 0.1 per cent concentrations References 1. (a) Scholz, R., and Wallen, L. J.: The Effect of Di-Isopropyl Fluorophosphate on Normal Human Eyes , J. Pharmacol. & Exper. Therap. 88:238, 1946. 2. (b) Leopold, I. H., and Comroe, J. H., Jr.: Use of Di-Isopropyl Fluorophosphate in Treatment of Glaucoma , Arch. Ophth. 36:1 ( (July) ) 1946. 3. (a) Leopold, I. H., and Comroe, J. H., Jr.: Effect of Di-Isopropyl Fluorophosphate on the Normal Eye , Arch. Ophth. 36:17 ( (July) ) 1946. 4. (b) Comroe, J. H., Jr.; Todd, J., and Koelle, G. B.: The Pharmacology of Di-Isopropyl Fluorophosphate in Man , J. Pharmacol. & Exper. Therap. 87:281, 1946. 5. (a) Koelle, G. B., and Gilman, A.: The Relationship Between Cholinesterase Inhibition and the Pharmacological Action of Di-Isopropyl Fluorophosphate , J. Pharmacol. & Exper. Therap. 87:421, 1946. 6. (b) Gilman, A., and Cattell, M.: Systemic Agents: Action and Treatment , in Andrus, E. C., and others: Advances in Military Medicine , Boston, Little, Brown & Company, 1948, vol. 2, chap. 36, p. 561. 7. McDonald, P. R.: The Treatment of Glaucoma with Di-Isopropyl Fluorophosphate , Am. J. Ophth. 29:1071, 1946. 8. Lebensohn, J. E.: Di-Isopropyl Fluorophosphate ("D F P") in Treatment of Glaucoma, Correspondence , Arch. Ophth. 36:621 ( (Nov.) ) 1946. 9. Haas, J. S.: Response to D F P , Am. J. Ophth. 31:227, 1948. 10. Dunphy, E.: Observations on the Use of Miotics, read before Section on Ophthalmology, College of Physicians, Philadelphia, March 1948. 11. von Sallmann, L.: Medical Treatment in Ophthalmology, Panel Discussion, New York Society of Clinical Ophthalmology, New York, April 1948. 12. Marr, W. G.: Clinical Use of D F P in Chronic Glaucoma , Am. J. Ophth. 30:1423, 1947. 13. (b) Scholz, R.: Studies on the Ocular Reactions of Rabbits to Di-Isopropyl Fluorophosphate , J. Pharmacol. & Exper. Therap. 88:23, 1946. 14. (c) von Sallmann, L., and Dillon, B.: Effect of D F P on Rabbit Eyes , Am. J. Ophth. 30:1244, 1947. 15. (d) Aldrege, W. H.; Davson, H.; Dunphy, E. B., and Uhde, G. I.: Effect of D F P Vapor on the Eye , Am. J. Ophth. 30:1405, 1947. 16. Sugar, S. H.: Acute Glaucoma , Am. J. Ophth. 30:451, 1947. 17. Macrae, H. M.: Personal communication to the authors. 18. Gradle, H. S., and Snydacker, D.; Retinal Detachment Occurring in Primary Compensated Glaucoma , Am. J. Ophth. 23:52, 1940. 19. Chandler, P. A., and Johnson, C. C.: A Neglected Cause of Secondary Glaucoma in Eyes in Which the Lens Is Absent or Subluxated , Arch. Ophth. 37:740 ( (June) ) 1947. 20. Comroe, J. H., Jr.; Todd, J.; Leopold, I. H.; Koelle, G. B.; Bodansky, O., and Gilman, A.: The Effect of Di-Isopropyl Fluorophosphate (D F P) upon Patients with Myasthenia Gravis , Am. J. M. Sc. 212:641, 1946.
LATTICE TYPE OF HEREDITARY CORNEAL DEGENERATION: Report of Five Cases, Including One of a Child of Two YearsSTANSBURY, FREDERICK C.
1948 Archives of Ophthalmology
doi: 10.1001/archopht.1948.00900030194010
Abstract THE LATTICE type of familial corneal dystrophy was first described in 1890 by Hugo Biber,1 a pupil of Haab, as gitterige Keratitis. He called it a chronic disease of the cornea, producing a bilateral opacity which at first looked like the residue of interstitial keratitis. The margin of the cornea was spared. Close examination revealed that the opacity was due to a lattice-like system of lines and to fine, rounded dots, which together resembled a spider's web. In regard to the lines, Biber said: They run in various directions and sometimes cross each other. They remind one of a birch twig, branching here and there. Ledgelike projections on the surface of the cornea appear to correspond to these lines.1 Symptoms of inflammation were insignificant, and at most included slight congestion and photophobia. The disease ran a long and painless course, eventually resulting in serious impairment of vision. Biber References 1. Biber, H.: Ueber einige seltenere Hornhauterkrankungen (Ulcus rodens, Keratomalacie Neugeborener, recidivierevale Keratitis bullosa nach Trauma, gitterige Keratitis), Inaug. Dissert., Zurich, A. Diggelmann, 1890, pp. 35-42. 2. Haab, O.: Die gitterige Keratitis , Ztschr. f. Augenh. 2:235-246, 1899. 3. Dimmer, F.: Ueber oberflachliche gittrige Hornhauttrübung , Ztschr. f. Augenh. 2:353-361, 1899. 4. Hauenschild, W.: Ein Fall von gittriger Keratitis , Ztschr. f. Augenh. 6:139-141, 1901. 5. Collins, T.: A Case Presenting an Unusual Form of Opacity in the Central Part of Each Cornea , Tr. Ophth. Soc. U. Kingdom 22:148-150, 1902. 6. Caspar, L.: Gitterförmige Hornhauttrübung nach Augenverletzungen , Klin Monatsbl. f. Augenh. 41:289-293, 1903. 7. Freund, H.: Die gittrige Hornhauttrübung , Arch. f. Ophth. 57:377-399, 1903. 8. Fehr, I.: Ein Fall von gittriger Hornhauttrübung , Centralbl. f. Augenh. 28:173-176, 1904. 9. Spicer, W. T. H.: Nodular Opacities of the Cornea in Father and Daughter, with a History of the Same in the Father's Brother and Sister , Tr. Ophth. Soc. U. Kingdom 24:42-45, 1904. 10. Patterson, J. V.: A Case of Reticular Opacity of the Cornea (gittrige Keratitis, Haab) , Ophth. Rev. 26:223-226, 1907. 11. Kipp, C.: A Case of Grill-Like Keratitis , Tr. Am. Ophth. Soc. 11:537-540, 1908. 12. Jacqueau, L.: Une forme de kératite héréditaire et familiale , Clin. opht. 15:434-439, 1909 13. abstracted, Jahresb. u. Ophth. , 1909, p. 649. 14. Groenouw, A.: Knötchenformige Hornhauttrübungen , Arch. f. Augenh. 21:281-289, 1890 15. translated, Arch. Ophth. 19:245-254, 1890. 16. Groenouw, A.: Knötchenförmige Hornhauttrübungen , Arch. f. Ophth. 46: 85-102, 1898. 17. Groenouw, A.: Knötchenförmige Hornhauttrübungen, vererbt durch drei Generationen , Klin. Monatsbl. f. Augenh. 58:411-420, 1917. 18. Groenouw, A.: Knötchenförmige Hornhauttrübungen, vererbt durch vier Generationen , Klin. Monatsbl. f. Augenh. 90:577-592, 1933. 19. Fleischer, B.: Ueber familiäre Hornhautentartung , Arch. f. Ophth. 53:263-344, 1905. 20. Doyne, R. W., and Stephenson, S.: Upon Five Cases of Family Degeneration of the Cornea , Ophthalmologica 3:213-221, 1905. 21. Folker, H.: Nodular Opacity of the Cornea in Three Generations , Tr. Ophth. Soc. U. Kingdom 23:42-52, 1909. 22. Roy, D.: Report of Six Cases of Degeneration of the Cornea in the Same Family (Nodular Keratitis) , Tr. Am. Ophth. Soc. 13 ( (pt. 1) ):101-108, 1912. 23. Weeks, J.: Family Nodular Keratitis , Arch. Ophth. 42:179-180, 1913. 24. Neame, H., in discussion on Hine,23 p. 45. 25. Hine, M. L.: Familial Nodular and Reticular Keratitis , Proc. Roy. Soc. Med. (Sect. Ophth.) 16:43-45, 1923. 26. Gutzeit, R.: Ueber familiäre knöchenförmige Hornhauttrübung , Ztschr. f. Augenh. 68:349-353, 1929. 27. Ladekarl, P. M.: Two Atypical Cases of Keratitis Nodosa Groenouw, with Histological Examinations , Acta ophth. 8:213-232, 1930.Crossref 28. Srivinasan, E. V.: A Family of Groenouw's Dystrophy , Brit. J. Ophth. 16:296-297, 1933.Crossref 29. Judd, J. H.: Nodular Degeneration of the Cornea , Am. J. Ophth. 16:310-318, 1933. 30. Frykholm, R.: Familiäre Hornhautentartung, vererbt durch sechs Generationen: Klinisch nachgewiesen bei dreizehn Mitglieden der dreizehn Letzen , Klin. Monatsbl. f. Augenh. 94:76-106, 1935. 31. Freiberger, M.: Corneal Dystrophy in Three Generations , Arch. Ophth. 16:257-270 ( (Aug.) ) 1936.Crossref 32. Somerset, E. J.: Three Cases of Corneal Dystrophy , Proc. Roy. Soc. Med. 30:389-394, 1937. 33. Bücklers, M.: Die erblichen Hornhautdystrophien , Klin. Monatsbl. f. Augenh. 99:676-681, 1937 34. The Three Forms of Familial Corneal Degeneration and Their Hereditary Transmission , Arch. Ophth. 18:331-332 ( (Aug.) ) 1937. 35. Berliner, M. L.: Biomicroscopy of the Eye , New York, Paul B. Hoeber, Inc., 1943, vol. 1, pp. 324-339. 36. Franceschetti, A., and Babel, J.: Essai de classification anatomique des dégénérescences familiales de la cornée , Ophthalmologica 109:169-202, 1945.Crossref 37. von der Heydt, R.: Corneal Dystrophies: Types , Am. J. Ophth. 20:738-740, 1937. 38. Mutch, J. R.: Hereditary Corneal Dystrophy , Brit. J. Ophth. 28:49-86, 1944.Crossref 39. Goulden, C.: Reticular Opacity of the Cornea , Tr. Ophth. Soc. U. Kingdom 41:193-194, 1921. 40. Zaun, W.: Ueber die gitterige Hornhauttrübung , Klin. Monatsbl. f. Augenh. 72:151-154, 1924. 41. Adrogué, E.: Lattice-Like Degeneration of the Cornea , Rev. Soc. argent. de oftal. 1:32-39, 1925 42. Semana méd. 32 ( (pt. 2) ):1657-1659, 1925. 43. Jeandelize, P., and Bretagne, P.: Un cas de kératite héréditaire et familiale vu en microscopie oculaire , Ann. d'ocul. 163:608-613, 1926. 44. Koby, F. E.: Sur la dégénérescence réticulaire superficielle de la cornée , Arch. d'opht. 44:149-166, 1927. 45. Caddy, A.: Reticular Opacity of the Cornea , Proc. Roy. Soc. Med. (Sect. Op hth.) 21:412 and 826, 1928. 46. Löwenstein, A.: Zur Klinik, Histologie und Therapie der gitterförmige Hornhautdegeneration , Klin. Monatsbl. f. Augenh. 82:752-762, 1929. 47. Greenwood, A.: Lattice Keratitis: Studies of Four Cases Observed in One Family , Tr. Am. Acad. Ophth. 35:248-258, 1930. 48. Nemeth, L.: Ueber die gitterige Entartung der Hornhaut , Klin. Monatsbl. f. Augenh. 95:73-76, 1935. 49. Shapira, T. M.: Lattice Type of Corneal Dystrophy , Arch. Ophth. 14: 387-391 ( (Sept.) ) 1935.Crossref 50. von der Heydt, R., and Gradle, H. S., cited by Shapira.45 51. Aurand, D.: Trosis cas de kératite en grillage observes dans la même famille , Arch. d'opht. 52:684-685, 1935. 52. Maury, F. H.: The Pathology of Lattice and Nodular Dystrophy of the Cornea , Am. J. Ophth. 19:866-872, 1936. 53. Hruby, K.: Gitterige Hornhautdystrophie , Klin. Monatsbl. f. Augenh. 103:342-343, 1939. 54. Lloyd, R.: A Family with Lattice Dystrophy of the Cornea , Tr. Am. Ophth. Soc. 37:120-126, 1939. 55. Hesse, E.: Beitrag zum Beginn und sur Erblichkeit der gittrigen Hornhautdystrophie , Arch. f. Ophth. 141:1-19, 1940. 56. Cavka, V.: Beitrag zur familiären Hornhautdegeneration , Klin. Monatsbl. f. Augenh. 106:348-352, 1941. 57. Streiff, E. B., cited by Franceschetti and Babel.33 58. Fuchs, E.: Ueber knöchenförmige Hornhauttrübung , Arch. f. Ophth. 53: 423-438, 1901-1902 59. Ophth. Rev. 21:187-190, 1902. 60. Byers, W.: Reticular Keratitis , Am. J. Ophth. 3:717-721, 1920. 61. Pillat, A.: Ueber gitterige und andere Formen degenerativer Hornhauterkrankungen , Klin. Monatsbl. f. Augenh. 69:681-682, 1922. 62. Hermann, C.: La dystrophie grillage de la cornée , Ophthalmologia 112: 350-363, 1946.Crossref 63. Wehrli, E.: Die knötchenförmige Hornhauttrübung Groenouw13) eine primäre isolierte, chronische, tuberkulose Erkrankung der norderen Schichten der Cornea: Lupus Cornea , Ztchr. f. Augenh. 13:322-334, 1910 64. Weitere klinische und histologische Untersuchungen über den unter dem Bilde der knötchenförmige Hornhauttrübung (Groenouw13) verlaufenden chronischen Lupus der Hornhaut , Arch. f. Ophth. 55:126-184, 1906. 65. Green, J.: Nodular Opacity of the Cornea, with Special Reference to Its Etiology , J. A. M. A. 53:920-924 ( (Sept. 18) ) 1909.Crossref 66. Schieck, F.: Die Degenerationen der Cornea ; in Schieck, F., and Bruckner, A.: Kurzes Handbuch der Ophthalmologie , Berlin, Julius Springer, 1931, vol. 4, pp. 398-403. 67. Fuchs, A.: Zur Kenntnis der gitterigen Hornhautentartung: HaabDimmer , Ztschr. f. Augenh. 57:159-186, 1925. 68. Collins, T.: Hereditary Ocular Degenerations: Ophthalmic Abiotrophies , Tr. Internat. Cong. Ophth. 1:103-143, 1922. 69. Kraupa, E.: Die familiär degenerativen Hornhautveränderungen im System des sogenannten Dystrophien der Hornhaut , Klin. Monatsbl. f. Augenh. 70:397-398, 1923. 70. Koby, F.: Slit Lamp Microscopy of the Living Eye , Philadelphia, P. Blakiston's Son & Co., 1925, p. 103. 71. Footnote deleted. 72. Stanka, R.: Ueber familiäre gitterige Hornhautdegeneration , Klin. Monatsbl. f. Augenh. 7:357-360, 1925. 73. Fuchs, E.: Ueber knötchenförmige Hornhauttrübungen , Arch. f. Ophth. 89:336-349, 1915. 74. Löwenstein, A.: Glass Membranes in the Eye , Am. J. Ophth. 23:1229-1242, 1940. 75. Paderstein, R.: Bemerkungen zu Wehrli's Kritik meines Falles von knotchenförmiger Hornhautdegeneration , Klin. Monatsbl. f. Augenh. 47:156-167, 1909. 76. Puscarin, E.: Deux observations d'opacité nodulaires de la cornée (Maladie de Groenow) , Arch. d'opht. 33:362-373, 1913. 77. Uhthoff, W.: Weitere klinische und anatomische Beiträge zu den degenerativen Erkrankungen der Hornhaut , Klin. Monatsbl..fAugenh. 55:290-299, 1915. 78. Wirth, M.: Zur Histologie der knötchenförmigen Hornhauttrübung , Ztschr. f. Augenh. 58:106-114, 1926. 79. Verhoeff, F. H., discussion on Lloyd,50 p. 125. 80. Franceschetti, A., and Streiff, E. B.: Hereditary and Constitutional Dystrophies of the Cornea , in Ridley, F., and Sorsby, A.: Modern Trends in Ophthalmology , London, Butterworth & Co., Ltd., 1940, pp. 419-420.