Archives of Ophthalmology

KOCH, FERDINAND L. P.;PAUL, ST.;WOLF, ABNER;COWEN, DAVID;PAIGE, BERYL H.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130015001

Abstract Human toxoplasmosis, a protozoan infection, was first encountered in infants as a severe disseminated encephalomyelitis,1 after which it was observed in older children as a milder form of encephalitis2 and in adults as a generalized infection with pulmonary involvement.3 The large reservoir of spontaneous toxoplasmic infection in rodents and in birds is the most likely source of the human infection ; however, no definite evidence of the mode of transmission from the lower animals to man is available. The prominence and the regular occurrence of lesions in the eyes were stressed in previous papers of this series and in related publications in which the infantile form of the disease was first described.4 These lesions, together with the symptoms and signs of widespread involvement of the central nervous system, frequently including internal hydrocephalus, convulsions which appeared at birth or soon thereafter and cerebral calcification detected by roentgenographic methods, References 1. Wolf, A.; Cowen, D., and Paige, B. H.: (a) Human Toxoplasmosis: Occurrence in Infants as an Encephalomyelitis; Verification by Transmission to Animals , Science 89:226-227 ( (March 10) ) 1939Crossref 2. (b) Toxoplasmic Encephalomyelitis : III. A New Case of Granulomatous Encephalomyelitis Due to a Protozoon , Am. J. Path. 15:657-694 ( (Nov.) ) 1939 3. (c) Toxoplasmic Encephalomyelitis: IV. Experimental Transmission of the Infection to Animals from a Human Infant , J. Exper. Med. 71:187-214 ( (Feb.) ) 1940.Crossref 4. Sabin, A. B.: Toxoplasmic Encephalitis in Children , J. A. M. A. 116:801-807 ( (March 1) ) 1941.Crossref 5. Pinkerton, H., and Weinman, D.: Toxoplasma Infection in Man , Arch. Path. 30:374-392 ( (July) ) 1940. 6. Pinkerton, H., and Henderson, R. G.: Adult Toxoplasmosis: A Previously Unrecognized Disease Entity Simulating the Typhus-Spotted Fever Group , J. A. M. A. 116:807-814 ( (March 1) ) 1941.Crossref 7. (a) Wolf, A., and Cowen, D.: Granulomatous Encephalomyelitis Due to an Encephalitozoon (Encephalitozoic Encephalomyelitis) , Bull. Neurol. Inst. New York 6:306-371 ( (July) ) 1937. 8. (b) Paige, B. H.; Cowen, D., and Wolf, A.: Toxoplasmic Encephalomyelitis : V. Further Observations of Infantile Toxoplasmosis; Intra-Uterine Inception of the Disease; Visceral Manifestations , Am. J. Dis. Child. 63:474-514 ( (March) ) 1942.Crossref 9. (c) Cowen, D.; Wolf, A., and Paige, B. H.: Toxoplasmic Encephalomyelitis: VI. Clinical Diagnosis of Infantile or Congenital Toxoplasmosis; Survival Beyond Infancy , Arch. Neurol. & Psychiat. 48:689-739 ( (Nov.) ) 1942. 10. Wolf, Cowen and Paige.1b Wolf and Cowen.4a Paige, Cowen and Wolf.4b 11. Wolf, Cowen and Paige (footnote 1a and c). Paige, Cowen and Wolf.4b 12. Jankû, J.: Parasites in Coloboma of the Macula , Časop. lék. česk. 62:1021-1027, 1054-1059, 1081-1085, 1111-1115 and 1138-1143, 1923. 13. Wolf, Cowen and Paige (footnote 1a and b). Wolf and Cowen.4a 14. Levaditi, C.; Schoen, R., and Sanchis-Bayarri, V.: L'infection toxoplasmique expérimentale de l'œil , Compt. rend. Soc. de biol. 98:1414-1419 ( (May 21) ) 1928. 15. Hepding, L.: Ueber Toxoplasmen (Toxoplasma gallinarum n. sp.) in der Retina eines Hühnes und über deren Beziehung zur Hühnerlähmung , Ztschr. f. Infektionskr. 54-55:109-116, 1938-1939. 16. Wolf, A.; Cowen, D., and Paige, B. H.: Fetal Encephalomyelitis: Prenatal Inception of Infantile Toxoplasmosis , Science 93:548-549 ( (June 6) ) 1941. 17. Pfeiffer, R. L.: Roentgenographic Diagnosis of Retinoblastoma , Arch. Ophth. 15:811-821 ( (May) ) 1936. 18. McKeown, H. S.: Retinal Hemorrhages in the Newborn , Arch. Ophth. 26:25-37 ( (July) ) 1941.

PIERSOL, GEORGE MORRIS

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130044002

Abstract It is no mere accident that during the past decade increasing attention has been paid to the aging process in its varying aspects. The interest is due to two definite factors that have been exerting a far reaching influence on the nation for many years. They are, first, the noteworthy increase in life expectancy that has occurred and, second, the changing trend in the age composition of the population. It is unnecessary to dwell at length on the frequently quoted statistics that show the steady increase in life expectancy from antiquity to the present. It is sufficient to emphasize that, whereas from the outbreak of the Revolutionary War until the turn of the nineteenth century, expectancy of life in this country increased only from thirty-five and one-half to fifty years, since 1900 it has shown an increase little short of dramatic. In 1930 the expectancy for the white population was References 1. United States Life Tables (Preliminary) : Estimated Future Population by Age and Sex, 1945-1980, Bureau of the Census, United States Department of Commerce, 1941. 2. Piersol, G. M., and Bortz, E. L.: Ann. Int. Med. 12:964, 1939.Crossref 3. Christian, H. A.: Ann. Int. Med. 12:1499, 1939.Crossref 4. Stieglitz, E. J.: New England J. Med. 225:247, 1941.Crossref 5. Sherman, H. C.: Bull. New York Acad. Med. 13:311, 1937. 6. Minot, G. R.: New England J. Med. 215:1147, 1936.Crossref 7. McCay, C. M.: Tr. & Stud. Coll. Physicians Philadelphia 10:1, 1942. 8. Pepper, O. H. P.: M. Clin. North America 20:1, 1936. 9. Cowdry, E. V.: Scient. Monthly 50:51-58, 1940.

TERRY, T. L.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130054003

Abstract So-called persistent tunica vasculosa lentis, or a fibroblastic sheath behind the crystalline lens, is known to occur sporadically. Usually the condition is discovered a few days after birth in an infant born at full term, but the correct diagnosis is often not established until the eyes are examined pathologically after removal because of a clinical diagnosis of retinoblastoma. Almost invariably this lesion is unilateral. That it is infrequent is borne out by the paucity of the literature on the subject and the scarcity of pathologic specimens.1 Within the last year a similar condition has been found in both eyes of a number of infants born about eight weeks prematurely. This bilateral fibroplasia2 at first appeared to be a new disease entity related to prematurity. Only after study of cases 5 and 7, reported hereafter, was it apparent that the condition observed sporadically at birth was a different phase References 1. (a) Fleming, P., and Parsons, J. H.: Tr. Ophth. Soc. U. Kingdom 23: 242, 1903. 2. (b) Collins, E. T. : Developmental Deformities of the Crystalline Lens , J. A. M. A. 51:1051 ( (Sept. 26) ) 1908Crossref 3. Tr. Sect. Ophth., A. M. A. , 1908, p. 452. 4. (c) Howard, H.: Tr. Am. Ophth. Soc. 15:244, 1917. 5. (d) Lane, F.: Arch. Ophth. 48:572, 1919. 6. (e) Lent, E. J., and Lyon, M. B.: Am. J. Ophth. 5:706, 1922. 7. Considerable thought has been given to the selection of an appropriate term for this disease condition. Early in the study, when the condition was thought to be represented fully by a massive growth of embryonic connective tissue behind the lens, the term "retrolental fibroplasia" was formulated by Dr. Harry K. Messenger. As the study progressed, it was proved that many other conditions also belonged to the disease entity, but so far no all-inclusive name has been devised. Perhaps the term "fibroplasia" might be as satisfactory as any, because all the changes appear to be related to a mesodermal overgrowth or to a persistence of embryonic mesodermal tissue, and so far as I know this term has not been used for any other condition. 8. Terry, T. L.: Tr. A. Research Ophth., 1942, to be published. 9. Terry, T. L.: Am. J. Ophth. 25:203, 1942. 10. This will be discussed further in a later publication. 11. The diagnosis of bilateral persistent fibrovascular sheath was made by Dr. E. B. Dunphy four months previous to the date when patient 1 was first seen. 12. The low body temperature of the premature infant in the incubator as an etiologic factor will be discussed in a later publication. 13. Mann, I.: Developmental Anomalies of the Eye , London, Cambridge University Press, 1937, p. 223. 14. Personal communication to the author. 15. Howard, 1c p. 254, figure 7. 16. Cowan, A., and English, B. C.: Causes of Blindness in Pennsylvania: Analysis of Blindness in over Thirty Thousand Eyes , Arch. Ophth. 26:797 ( (Nov.) ) 1941.Crossref 17. Terry.3 This will also be discussed further in a later paper. 18. Thompson, G. W., cited by Collins.1b

TERRY, T. L.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130074004

Abstract A new syndrome of ocular maldevelopments in infants born prematurely has been reported previously.1 No conclusive statement can be made at this time as to the exact cause or causes of this entity. However, a discussion of the various etiologic factors, stressing the theory that now appears most logical, is of value in bringing the problem to the attention of many observers. By this means the solution may be arrived at more quickly, with regard not only to the most satisfactory preventive measures but to the best treatment, perhaps soon enough to be of practical value for infants now under observation. This syndrome, consisting primarily in bilateral fibroplasia, is based on : (1) persistence of some part of the tunica vasculosa lentis system, (2) growth of embryonic connective tissue behind the crystalline lens and/or (3) persistence of the fibrillar structure of the vitreous humor. It has been pointed out1c References 1. Terry, T. L.: (a) Am. J. Ophth. 25:203, 1942 2. Hess, J. H.; Mohr, G. J., and Bartelme, P. F.: The Physical and Mental Growth of Prematurely Born Children , Chicago, University of Chicago Press, 1934. 3. Hac, L. R. ; Adair, F. L., and Hesseltine, H. C. : Am. J. Obst. & Gynec. 38:57, 1939. 4. Ross, S. G., and Mallory, H. T.: Canad. M. A. J. 45:417, 1941. 5. Goldberg, H.: Personal communication to the author. Goldberg has observed 5 infants with fibroplasia, concerning whom he wrote after seeing my preliminary report of the condition.1a 6. Clifford, S.: Personal communication to the author. 7. Needham, J.: Chemical Embryology , London, Cambridge University Press, 1931, vol. 3. 8. Blackfan, K. D., and Yaglou, C. P.: Premature Infant , Am. J. Dis. Child. 46:1175 ( (Nov.) , pt. 2) 1933. 9. McCrady, E.: Embryology of the Opossum , Philadelphia, Wistar Institute of Anatomy and Biology, 1938. 10. To evaluate some of the factors which might be involved, experiments are being carried out with (1) variations in temperature, (2) variations in light, (3) vitamin deficiency, (4) decrease in the oxygen-carrying powers of the blood by exposure to carbon monoxide and by feeding of sulfanilamide, (5) intraocular injection of blood, (6) graded constriction of the neck and (7) injection of pressor and depressor substances to vary the blood pressure. As a therapeutic measure of possible value, the sulfuric acid ester of hyaluronic acid was injected into eyes of opossum pouch young in which the hyaloid arterial system was still present, to determine whether this would stimulate a precocious closure of the arterial system. This ester was supplied by Dr. Karl Meyer, of the Eye Institute, New York. Animals were chosen for the experiments whose young had a patent hyaloid arterial system at birth. The opossum has been used in many experiments, because, since it is a marsupial, the young are born in a very immature stage. Pregnant and newborn rats, cats and pigs have also been used. To date none of the experiments has gone far enough to enable me to report scientifically significant results. However, several trends of interest, one of possible therapeutic value, have been noted. 11. Held, R.: Arch. f. Anat. u. Entwcklungsgesch. , 1896, p. 222. 12. Salzmann, M.: Anatomy and Development of the Human Eyeball , translated by E. V. L. Brown, Chicago, University of Chicago Press, 1912, p. 208. 13. J. Exper. Med. 76:1, 1942 14. Bessey, O., and Wolbach, B.: J. Exper. Med. 69:1, 1939. 15. From the Blood Grouping Laboratory of the Children's Hospital. 16. Woodbury, R. A.; Robinson, M., and Hamilton, W. F.: Am. J. Physiol. 122:472, 1938. 17. Hess,2 figures 66 and 67, p. 284. 18. Patten, B. M.: Anat. Rec. 35:129, 1931. 19. Christie, A.: Normal Closing Time of Foramen Ovale and Ductus Arteriosus , Am. J. Dis. Child. 40:323 ( (Aug.) ) 1930. 20. Eppinger, E. C.; Burwell, C. S., and Gross, R. E.: J. Clin. Investigation 20:127, 1941. 21. Wislocki, G. B.: Personal communication to the author. 22. Graybiel, A.; Allen, A. W., and White, P. D.: J. Clin. Investigation 14:52, 1935. 23. Reid, M. R.: Abnormal Arteriovenous Communications , Arch. Surg. 11:25 ( (July) ) 1925. 24. Haden, H. C. : Personal communication to the author.

PATCH, ESTHER M.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130089005

Abstract Cataracts in the tiger salamander, Amblystoma tigrinum, were first observed by me1 in the summer of 1933 in larvae raised from Illinois eggs and used in a study of the nutritional needs of this rapidly growing larval form for the formation of bone and blood. Cortical opacities (fig. 1 A) with a thin subcapsular space developed in larvae fed for a month or more a semisynthetic ration containing a high level of purified casein and a smaller amount of powdered milk. The disease did not appear in animals of the same lot fed the same ration with added cystine or in those (fig. 1 B) fed pulverized beef muscle as a source of protein in a semisynthetic diet with different combinations of the calcifying vitamin and minerals. An early stage of the opacities was seen rarely (fig. 1 C) as striations from the equator to the anterior pole. The References 1. Patch, E. M.: Cataract as a Result of Dietary Deficiency in Larval Amblystoma Tigrinum , Science 79:57-58, 1934.Crossref 2. May, C. H.: Manual of the Diseases of the Eye for Students and General Practitioners, revised with the assistance of C. A. Perera , ed. 17, Baltimore, William Wood & Company, 1941. 3. Patch, E. M.: (a) Cataracts in Amblystoma Tigrinum Larvae Fed Experimental Diets , Proc. Soc. Exper. Biol. & Med. 46:205-207, 1941 4. (b) Dietary Production of Cataracts in Larval Amblystoma Tigrinum , J. Nutrition 22:365-382, 1941. 5. Franz, V.: Vergleichende Anatomie des Wirbeltierauges , in Bolk, L.; Göppert, E.; Kallius, E., and Lubosch, W.: Handbuch der vergleichenden Anatomie der Wirbeltiere , Berlin, Urban & Schwarzenberg, 1934, vol. 2, pt. 2, pp. 989-1292. 6. Mann, I. C. : The Development of the Human Eye , London, Cambridge University Press, 1928. 7. Spemann, H.: The Development of the Vertebrate Eye as an Example of a Composite Organ , in Embryonic Development and Induction , New Haven, Conn., Yale University Press, 1938, chap. 3. 8. (b) Calcifying Factors in the Diet of Salamander Larvae , Science 81:494-495, 1935 9. (c) Dietary Production and Prevention of Anemia in Larval Amblystoma , Science 83:560-561, 1936. 10. (a) Clapp, C. A.: Cataract : Its Etiology and Treatment , Philadelphia, Lea & Febiger, 1934. 11. (b) Krause, A. C. : The Chemistry of the Lens, in The Biochemistry of the Eye , Baltimore, Johns Hopkins Press, 1934, chap. 8. 12. (c) Bourne, M. C. : Metabolic Factors in Cataract Production , Physiol. Rev. 17: 1-27, 1937. 13. Fuchs, E.: Diseases of the Eye , 15th German edition translated by E. V. L. Brown, English ed. 10, Philadelphia, J. B. Lippincott Company, 1933. 14. Kirby, D. B.: Diseases of the Crystalline Lens , in Berens, C.: The Eye and Its Diseases, Philadelphia, W. B. Saunders Company, 1936, chap. 37. 15. Patch (footnote 7 a and b). 16. Kunde, F.: Ueber Wasserentziehung und Bildung vorübergehende Katarakte , Ztschr. f. wissensch. Zool. 8:466-486, 1857. 17. Mitchell, S. W.: On the Production of Cataracts in Frogs by the Administration of Sugar , Am. J. M. Sc. 39:106-110, 1860. 18. Lebensohn, J. E.: Biochemistry of the Lens: A Résumé , Am. J. Ophth. 23:784-792, 1940. 19. Bellows, J. G., and Chinn, H.: Biochemistry of the Lens: XIII. Production of Lens Opacities by Injection of Hypertonic Solutions , Arch. Ophth. 25: 796-810 ( (May) ) 1941. 20. Sherman, H. C.: Chemistry of Food and Nutrition , ed. 6, New York, The Macmillan Company, 1941. 21. Bourne, M. C., and Young, L.: The Metabolism of Naphthalene in Rabbits , Biochem. J. 28:803-808, 1934. 22. Bourne, M. C., and Pyke, M. A.: The Occurrence of Cataract in Rats Fed on Diets Deficient in Vitamin B2 , Biochem. J. 29:1865-1871, 1935. 23. Bellows, J. G.: Biochemistry of the Lens : IX. Influence of Vitamin C and Sulfhydryls on the Production of Galactose Cataract , Arch. Ophth. 16:762-769 ( (Nov.) ) 1936. 24. Yudkin, A. M., and Geer, H. A.: An Investigation of Experimental Cataracts in the Albino Rat: Clinical Implications , Arch. Ophth. 23:28-40 ( (Jan.) ) 1940. 25. Bellows, J. G., and Chinn, H.: Theories of Cataract , Arch. Ophth. 26: 1066-1093 ( (Dec.) ) 1941.

COHEN, MARTIN

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130105006

Abstract During the past years many investigations and clinical studies have been made for the purpose of determining the primary causative factor of hypertensive vascular disease, or essential hypertension, but this factor has not as yet been established. Hypertensive vascular disease is considered a clinical entity. It is extremely prevalent and in its terminal stages is liable to produce disastrous involvement of the vital organs. Its cardinal symptom is persistent high blood pressure. Two forms of hypertensive disease are considered in this paper : essential benign hypertension and malignant hypertension. This classification is not accepted by all internists, but since it is in general use it will be employed here. Essential benign hypertension (benign nephrosclerosis) occurs generally in middle-aged persons with persistent high blood pressure. The subjective symptoms are of a mild and chronic nature. The patient is apparently in good health and may live for many years. The vision frequently is

McDONALD, P. ROBB

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130112007

Abstract Vascular accidents affecting the eye and the visual pathways are not uncommon, and the sequelae vary according to the extent and the site of the lesion. The ocular changes may be but a small part of an extensive lesion causing gross disturbances of motor and of sensory function. One may have paralysis of conjugate deviation, oculomotor palsies or complete or incomplete homonymous defects in the visual fields. Frequently the lesion can be located with anatomic precision but without much benefit to the patient. Hemianopsia of vascular origin is usually sudden in onset and is caused by an embolus, thrombosis or rupture of a vessel supplying the optic pathways or the visual cortex. Such defects are fairly common and unless complete frequently pass unnoticed and are only discovered on a routine examination of the visual fields. The occurrence of bilateral hemianopsia with sparing of the macular field is, however, rather rare. References 1. Pallarès, J.: Un cas d'hémianopsie double avec conservation de la vision maculaire après la naissance , Ann. d'ocul. 168:45, 1931. 2. Traquair, H. M.: Clinical Perimetry , St. Louis, C. V. Mosby Company, 1940. 3. Dunn, T. D.: Double Hemiplegia with Double Hemianopsia and Loss of Geographical Centre , University M. Mag. 7:578, 1895. 4. Cords, R.: Optisch-motorisches Feld und optisch-motorische Bahn. Ein Beitrag zur Physiologie und Pathologie der Rindeninnervation der Augenmuskeln , Arch. f. Ophth. 117:58, 1926. 5. Holmes, G., and Horrax, G.: Disturbances of Spatial Orientation and Visual Attention with Loss of Stereoscopic Vision , Arch. Neurol. & Psychiat. 1:385 ( (April) ) 1919. 6. Riddoch, G.: Dissociation of Visual Perception Due to Occipital Injuries with Especial Reference to Appreciation of Movement , Brain 40:15, 1917. 7. Duke-Elder, W. S.: Text-Book of Ophthalmology , St. Louis, C. V. Mosby Company, 1932, vol. 1. 8. Holmes, G.: The Cerebral Integration of the Ocular Movements , Brit. M. J. 2:4045, 1938. 9. Holmes, G.: A Contribution to the Cortical Representation of Vision , Brain 54:470, 1931. 10. Shellshear, J. L.: A Contribution to Our Knowledge of the Arterial Supply of the Cerebral Cortex in Man , Brain 50:236, 1927. 11. Förster: Ueber Rindenblindheit , Arch. f. Ophth. ( (pt. 1) ) 36:94, 1890. 12. Whitnall, S. E.: The Anatomy of the Human Orbit , New York, Oxford University Press, 1932. 13. Bramwell, B.; Bolton, J. S., and Robinson, W.: Bilateral Lesion of the Occipital Lobes with Retention of Macular as Distinct from Panoramic Vision , Brain 38:447, 1915.

SMOLEROFF, JULES W.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130118008

Abstract Inflammation of the sclera and of the episclera, the latter first called subconjunctivitis by von Graefe, have long been known to be associated with diseases of the articular structures of the body. Hutchinson1 in 1885, Fuchs2 in 1895 and Wagenmann3 in 1897 reported cases of gout in which episcleritis was a notable complication. Wood4 in 1936 found crystalline deposits in the sclera of a gouty patient who manifested active scleritis. As recently as 1924, Rateau5 reported an interesting case in which sclerotenonitis was the prodromal symptom of an attack of rheumatic fever. In 1938 Verhoeff and King6 presented a case of rheumatoid arthritis in which an eye was removed because of an inflammatory perforating scleral lesion. This eye was histologically examined in great detail. These authors analyzed 14 previously recorded cases of a similar nature in which the lesion was designated by the name References 1. Hutchinson, J.: Tr. Ophth. Soc. U. Kingdom 5:1, 1885. 2. Fuchs, E.: Arch. f. Ophth. ( (pt. 4) ) 41:229, 1895. 3. Wagenmann, A.: Arch. f. Ophth. ( (pt. 1) ) 43:83, 1897. 4. Wood, C.: Brit. J. Ophth. 20:510, 1936.Crossref 5. Rateau, J.: Arch. d'opht. 41:226, 1924. 6. Verhoeff, F. H., and King, M. J.: Scleromalacia Perforans: Report of Case in Which Eye Was Examined Microscopically , Arch. Ophth. 20:907 ( (Dec.) ) 1938.Crossref 7. Van der Hoeve, J.: Scleromalacia Perforans , Arch. Ophth. 11:111 ( (Jan.) ) 1934.Crossref 8. Holthouse, E. H.: Roy. London Ophth. Hosp. Rep. 13:415, 1893.

MUNSON, EDWIN S.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130129009

Abstract Before the middle of the nineteenth century, there was a vague understanding of some of the refractive states of the eye. Myopia, with its obvious symptom of poor distant vision, had been recognized since ancient times and was accurately defined by Kepler in 1611. Presbyopia, with the inability to see near objects in old age, had long been noted but was confused with hypermetropia. What is now known to be hypermetropia was suggested by Kästner in 1755 but was not well understood until about a century later. The accepted conception of accommodation was presented by Thomas Young in 1801, and, to complete the dioptric faults, the presence of astigmatism was demonstrated by George Airy in 1827. The conditions present to constitute a normal refractive state received but scant attention by the older writers, owing to a lack of knowledge of the exact ocular structure and manner of functioning. Progress was References 1. Mackenzie, W.: Diseases of the Eye , ed. 3, London, Longman, Orme, Brown, Green & Longmans, 1840, p. 778. 2. Donders, F. C.: On the Anomalies of Accommodation and Refraction of the Eye , translated by W. D. Moore, London, New Sydenham Society, 1864, pp. 81 and 173. 3. Duke-Elder, W. S.: The Practice of Refraction , ed. 2, Philadelphia, P. Blakiston's Son & Co., 1935, p. 68. 4. Cowan, A.: Refraction of the Eye , Philadelphia, Lea & Febiger, 1938, p. 136. 5. Thorington, J.: Methods of Refraction , ed. 3, Philadelphia, P. Blakiston's Son & Co., 1939, p. 146. 6. May, C. H.: Diseases of the Eye , ed. 16, Baltimore, William Wood & Company, 1939, p. 362. 7. Gifford, S. R.: A Textbook of Ophthalmology , ed. 2, Philadelphia, W. B. Saunders Company, 1941, p. 48. 8. Juler, H. E.: Ophthalmic Science and Practice , ed. 3, Philadelphia, Lea Brothers & Co., 1904, p. 476. 9. Gould, G. M.: Biographic Clinics , Philadelphia, P. Blakiston's Son & Co., 1909, vol. 6, p. 420. 10. Gould,9 1907, vol. 5, p. 15. 11. Smith, H. E.: Applied Refraction , New York, William Wood & Company, 1927, p. 45. 12. Norris, W. F., and Oliver, C. A.: A Text-Book of Ophthalmology , Philadelphia, Lea Brothers & Co., 1893, p. 382. 13. Ball, J. M.: Modern Ophthalmology , ed. 5, Philadelphia, F. A. Davis Company, 1926, vol. 2, p. 1181.

BURIAN, HERMANN M.

1943 Archives of Ophthalmology

doi: 10.1001/archopht.1943.00880130136010

Abstract I. INTRODUCTION AND DEFINITIONS The two eyes are never identical. Between them there are always numerous discrepancies in the neuromuscular apparatus, the dioptric system and the sensorial apparatus. The discrepancies of the neuromuscular apparatus, the heterophorias, cause a faulty relative position of the eyes when fusion is suspended. The aberrations and other irregularities of the dioptric system cause faulty dioptric images, which in some cases may differ considerably in the two eyes. Furthermore, the differences in the relative position of objects in space and in their distance from the two eyes cause geometrically different images to be formed in the two eyes. The discrepancies of the sensorial apparatus are caused by a special distribution of the receptor elements.As a result of all these discrepancies and incongruities, the two ocular images1 of the visual system are different even under normal conditions. The incongruities as a rule are overcome by References 1. Ocular image is used to describe the impression which reaches consciousness through the vision of one eye. It is determined not only by the properties of the dioptric image that is formed on the retina of the eye but by the modifications imposed on that image by the anatomic and physiologic properties of the structures by which it is carried to the higher brain centers. 2. In the case of axial ametropia (and anisometropia) the lenses correcting the refraction do not cause a change in the size of the dioptric images if their second principal points coincide with the anterior focal points of the eyes. 3. Carleton, E. H., and Madigan, L. F. : Relationship Between Aniseikonia and Anisometropia , Arch. Ophth. 18:237 ( (Aug.) ) 1937.Crossref 4. Highly interesting experimental and clinical material on these incongruities will be published in the near future by Prof. Adelbert Ames, Jr., Prof. Kenneth N. Ogle and Dr. Walter B. Lancaster. 5. Hughes, W. L.: Some Clinical Observations in Aniseikonia , Am. J. Ophth. 18:715 [ (Aug.) ] 1935 6. E. H. Carleton and L. F. Madigan ( Size and Shape of Ocular Images: II. Clinical Significance , Arch. Ophth. 7:720 [ (May) ] 1932).Crossref 7. Hughes, W. L.: Clinical Aspects of Aniseikonia , Proc. Post-Grad. Course in Ophth., George Washington Univ. M. School 5:116-145, 1940. 8. Carleton and Madigan,5 noted general symptoms in 80 out of 96 cases and trouble in viewing moving objects in 64 out of 96 cases. 9. Hughes, W. L.: Aniseikonia in Emmetropia , Am. J. Ophth. 20:887 ( (Sept.) ) 1937. 10. R. E. Bannon ( Headaches and Aniseikonia , Am. J. Optom. 17:448 [ (Oct.) ] 1940)Crossref 11. Hughes 8 reported that 29 out of 43 patients with emmetropia measured for aniseikonia showed a clinically significant amount ; 14 of these patients received complete relief by wearing aniseikonic corrections. 12. Hughes, W. L.: Aniseikonia , Am. J. Ophth. 19:686 ( (Aug.) ) 1936. 13. Adams, F. D.: Personal communications to the author. 14. (a) Ames, A., Jr.; Ogle, K. N., and Gliddon, G. H.: Corresponding Retinal Points, the Horopter and Size and Shape of the Ocular Images , J. Optic. Soc. America 22:538 ( (Oct.-Nov.) ) 1932.Crossref 15. (b) Ogle, K. N.: Induced Size Effect: I. A New Phenomenon in Binocular Space Perception Associated with the Relative Sizes of the Images of the Two Eyes , Arch. Ophth. 20:604 ( (Oct.) ) 1938.Crossref 16. Bannon, R. E., cited in footnote 9. 17. Footnote deleted. 18. Burian, H. M., in discussion on the papers of Lancaster, Berens and Loutfallah , Am. J. Ophth. 22:639 ( (June) ) 1939. 19. (a) Ames, A., Jr.; Gliddon, G. H., and Ogle, K. N.: Size and Shape of Ocular Images: I. Methods of Determination and Physiologic Significance , Arch. Ophth. 7:576 ( (April) ) 1932.Crossref 20. (b) Ogle, K. N., and others: Repeatability of Eikonometer Measurements , Arch. Ophth. 24:1179 ( (Dec.) ) 1940.Crossref 21. Ames, A., Jr., and Gliddon, G. H.: Ocular Measurements , Tr. Sect. Ophth., A. M. A. , 1928, pp. 102-176. 22. Lancaster, W. B.: Stigmatoscopy , Tr. Am. Ophth. Soc. 32:130, 1934. 23. Ogle, K. N.: An Optical Unit for Obtaining Variable Magnification in Ophthalmic Use , J. Optic. Soc. America 32:143 ( (March) ) 1942.Crossref 24. The meridians and axes in aniseikonia are designated analogously to the meridians and axes of astigmatism : A size lens at axis 90 magnifies the ocular image in the horizontal meridian. 25. Footnote deleted. 26. Ogle and others.17b 27. Ogle, K. N.: The Correction of Aniseikonia with Ophthalmic Lenses , J. Optic. Soc. America 26:323 ( (Aug.) ) 1936.Crossref