A.M.A. Archives of Ophthalmology

FRANCESCHETTI, A.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050003001pmid: 13170860

Abstract AS A RULE hereditary degenerations of the cornea can be clearly distinguished from other corneal affections by their bilateral aspect, more or less typical morphology, and slow progression, with absence of vascularization. In addition, the fundamental criteria of all heredodegenerations apply equally to corneal degenerations: onset at approximately the same age in the different members of the family (homochronicity) and intrafamilial constancy of corneal alterations and of their evolution. However, their delimitation with regard to congenital malformations and certain inflammatory states is not always as simple as one would think, even when their characteristics have been quite clearly defined. In fact, certain forms of interstitial keratitis, especially Hutchinson's keratitis, may be practically avascular, a feature which explains why certain infantile forms of corneal degeneration have been mistaken for manifestations of congenital syphilis. On the other hand, secondary vascularization in familial corneal degenerations is sometimes found, owing either to a chronic References 1. Knowledge of this congenital form of hereditary dystrophy of the cornea is especially important, since there is always a risk of its being attributed to congenital syphilis, with unfortunate economic, moral, and social consequences for the patient. 2. Franceschetti, A., and Forni, S.: Acta XVI Conc. Ophth. (Britannia) , pp. 193-244, 1950. 3. Franceschetti, A., and Babel, J.: Acta XVI Cone. Ophth. (Britannia) , pp. 245-283, 1950. 4. Malbrán, J.; Panessa, J., and Vidal, T.: Ophthalmologica 126:369-378, 1953.Crossref 5. Fry, W. E.: Tr. Am. Ophth. Soc. 48:220-227, 1950. 6. Gruber: Ophthalmologica 125:380-389, 1953.Crossref 7. Cogan, D. G.; Albright, F., and Bartter, F. C.: Arch. Ophth. 40:624-638, 1948.Crossref 8. Calhoun, F. P.: Tr. Am. Acad. Ophth. 55:366-381, 1951. 9. Hogan, M. J.: Tr. Am. Ophth. Soc. 50:265-281, 1952. 10. Grant, W. M.: A. M. A. Arch. Ophth. 48:681-685, 1952.Crossref

COGAN, DAVID G.;BARROWS, LAWRENCE J.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050015002pmid: 13170861

Abstract PLATYBASIA and the Arnold-Chiari deformity are of concern to the ophthalmologist. Not only are the ocular signs and symptoms of these entities often the presenting complaints but, equally important, they simulate those of multiple sclerosis, tumor of the brain stem or cerebellum, and other lesions of the posterior fossa, which have an entirely different prognostic and therapeutic significance. Since these conditions have not received general recognition in the ophthalmological literature,* it will be the purpose of this communication to describe the abnormalities as represented in the pertinent literature and to present several cases studied by us with emphasis on the ophthalmological aspects. The abnormality variously called platybasia, flat skull, or basilar impression consists of an upward bulge or invagination of the occiput in the region of the foramen magnum.† There is usually a partial fusion of the upper cervical vertebrae to the skull and to each other, with a protrusion References 1. Walsh 1 appears to be the only one who has given a description of the abnormalities in the ophthalmic literature. 2. Strictly speaking, platybasia is an anthropological term referring to a flattening of the clivus in respect to the skull, while basilar impression refers to a protrusion of the base of the skull into the posterior fossa; but the names are used interchangeably for the clinical anomaly here described. 3. References 14, 15, and 16. 4. References 13 and 18 through 21. 5. While the sneezing would be inferred to be only incidental to the deformity, it is note-worthy that sneezing was one of the presenting complaints in another patient (362078) with the Arnold-Chiari malformation and was completely relieved by suboccipital decompression. It is also worth mentioning that this patient, who is not included in the present series for lack of an adequate ophthalmological work-up, had an exacerbation of his ataxia, headache, and blurred vision after a sneezing spell and was relieved by forceful rubbing of the back of his neck. 6. Walsh, F. B.: Clinical Neuro-Ophthalmology , Baltimore, Williams & Wilkins Company, 1947. 7. Virchow, R. L. K.: Beiträge zur physischen Anthropologie der Deutschen mit besonderer Berücksichtigung der Friesen , Abhandl. k. Akad. Wissensch. zu Berlin , 1876. 8. Homén, E. A.: Zur Kenntnis der rachitischen (?) Deformationen der Schädelbasis und der basalen Hyperostosen , Deutsche Ztschr. Nervenh. 20:3-15, 1901.Crossref 9. Schüller, A.: Zur Röntgen-Diagnose der basalen Impression des Schädels , Wien. med. Wchnschr. 61:2594-2599, 1911. 10. Chamberlain, W. E.: Basilar Impression (Platybasia): A Bizarre Developmental Anomaly of the Occipital Bone and Upper Cervical Spine with Striking and Misleading Neurologic Manifestations , Yale J. Biol. & Med. 11:487-496, 1939. 11. Bull, J. W. D., in Feiling, A.: Modern Trends in Neurology , New York, Paul B. Hoeber, Inc., 1951, p. 610. 12. Ebenius, B.: The Roentgen Appearance in Four Cases of Basilar Impression , Acta radiol. 15:652-656, 1934. 13. Arnold, J.: Myelocyste; Transposition von Gewebskeimen und Sympodie , Beitr. path. Anat. u. allg. Path. 16:1-28, 1894. 14. Chiari, H.: Über Veränderungen des Kleinhirns, des Pons, und des Medulla oblongata infolge von congenitaler Hydrocephalie des Grosshirns , Denkschr. k. Akad. Wissensch. Math.naturw. Kl. 63:71, 1895. 15. Russell, D. S., and Donald, C.: Mechanism of Internal Hydrocephalus in Spina Bifida , Brain 58:203-215, 1935. 16. Ingraham, F. D., and Scott, H. W., Jr.: Spina Bifida and Cranium Bifidum: V. The Arnold-Chiari Malformation; a Study of 20 Cases , New England J. Med. 229:108-114, 1943. 17. Penfield, W., and Coburn, D. F.: Arnold-Chiari Malformation and Its Operative Treatment , Arch. Neurol. & Psychiat. 40:328-336, 1938. 18. Lichtenstein, B. W.: Cervical Syringomyelia-like States Associated with Arnold-Chiari Deformity and Platybasia , Arch. Neurol. & Psychiat. 49:881-894, 1943. 19. McConnell, A. A., and Parker, H. L.: Deformity of Hind-Brain Associated with Internal Hydrocephalus: Its Relation to Arnold-Chiari Malformation , Brain 61:415-429, 1938. 20. Parker, H. L., and McConnell, A. A.: Internal Hydrocephalus Resulting from Peculiar Deformity of the Hindbrain , Tr. Am. Neurol. A. 63:14-16, 1937. 21. Aring, C. D.: Cerebellar Syndrome in Adult with Malformation of Cerebellum and Brain Stem (Arnold-Chiari Deformity) with Note on Occurrence of "Torpedoes" in Cerebellum , J. Neurol. & Psychiat. 1:100-109, 1938. 22. List, C. F.: Neurologic Syndromes Accompanying Developmental Anomalies of Occipital Bone, Atlas and Axis , Arch. Neurol. & Psychiat. 45:577-616, 1941. 23. Adams, R. D.; Schatzki, R., and Scoville, W. B.: Arnold-Chiari Malformation: Diagnosis, Demonstration by Intraspinal Lipiodol and Successful Surgical Treatment , New England J. Med. 225:125-131, 1941. 24. Stevens, R. H.: Platybasia: Report of a Case Treated Surgically with Improvement , Surgery 12:943, 1942. 25. O'Connell, J. E. A., and Turner, J. W. A.: Basilar Impression of Skull , Brain 73:405-426, 1950. 26. Malis, L. I.; Cohen, I., and Gross, S. W.: Arnold-Chiari Malformation , A. M. A. Arch. Surg. 63:783-798, 1951. 27. Gustafson, W. A., and Oldberg, E.: Neurologic Significance of Platybasia , Arch. Neurol. & Psychiat. 44:1184-1198, 1940. 28. Cogan, D. G.: Ocular Dysmetria, Flutter-like Oscillations of the Eyes, and Opsoclonus , A. M. A. Arch. Ophth. 51:318-335, 1954. 29. Nylén, C. O.: A Clinical Study on Positional Nystagmus in Cases of Brain Tumour , Acta oto-laryng. , (Supp. 15) , 1931.

HENKES, HAROLD E.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050032003pmid: 13170862

Abstract IN HIS MONOGRAPH Karpe1 has indicated a possible alteration in the electroretinographic response in cases of hypertensive retinopathy. In one case, showing narrowing of the arteries with retinal exudates, he found a subnormal response, whereas in another, showing slight hypertensive vascular alterations, the ERG recorded was normal. The same results have been reported by Euzière, Passouant, and Cazaban,2 who found a normal ERG in retinal sclerosis, but a pathologic ERG in more advanced stages. Regarding the ERG as a prognostic sign in cases of hypertensive retinopathy, these authors say: Mais nous ne serions pas étonnés si ce mode d'examen permettait d'apporter un nouvel élément de prognostic dans le rétinopathie hypertensive. Dollfus and Chavignac3 studied nine cases of hypertensive retinopathy. They state: On est frappé de constater que l'ERG de ces malades ne présente pas d'altérations graves et qu'au contraire l'onde b est presque toujours d'une amplitude maximale References 1. References 4 through 6. 2. References 7 through 9. 3. This instrument was supplied in part by the Netherlands Health Organisation T.N.O. 4. Karpe, G.: The Basis of Clinical Electroretinography , Acta ophth. , (Supp. 24) , 1945. 5. Euzière, J.; Passouant, P., and Cazaban, R.: Applications pratiques de l'ERG , Rev. oto-neuro-opht. 24:222, 1952. 6. Dollfus, M.-A., and Chalvignac, A.: L'électrorétinographie et ses applications à la clinique , Semaine hôp. Paris 28:1325, 1952. 7. Henkes, H. E.: The ERG in glaucoma , Nederl. tijdschr. geneesk. 94:2860, 1950. 8. Henkes, H. E.: Use of Electroretinography in Disturbances of the Retinal and Choroidal Circulation , Acta XVI Conc. Ophth. (Britannia) , 1950. 9. Henkes, H. E.: Use of Electroretinography in Measuring the Effect of Vasodilation , Angiology 2:125, 1951.Crossref 10. Henkes, H. E.: Electroretinogram in Circulatory Disturbances of the Retina: I. Electroretinogram in Cases of Occlusion of the Central Retinal Vein or One of Its Branches , A. M. A. Arch. Ophth. 49:190, 1953.Crossref 11. Henkes, H. E.: Electroretinogram in Circulatory Disturbances of the Retina: II. Electroretinogram in Cases of Occlusion of the Central Retinal Artery or of One of Its Branches , A. M. A. Arch. Ophth. 51:42, 1954.Crossref 12. Henkes, H. E.: Electroretinogram in Circulatory Disturbances of the Retina: III. Electroretinogram in Cases of Senile Degeneration of the Macular Area , A. M. A. Arch. Ophth. 51:54, 1954.Crossref 13. Karpe, G.: The Normal ERG Above 50 Years of Age , Acta opht. 28:301, 1950.Crossref

NORDMANN, J.;MANDEL, P.;IZRAELEWICZ, D.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050044004pmid: 13170863

Abstract THE PROBLEM of the respiration of the lens has been subjected to great study by Christiansen and Leinfelder. On the basis of several series of experiments, they have arrived at the conclusion that the respiration of the lens is a nonenzymatic process. The maintenance of a normal oxygen consumption in spite of boiling the lens furnishes their principal argument. We decided it would be of interest to reexamine this important problem; therefore, we ask the following questions: Does the boiled lens continue to consume oxygen? Is this oxygen consumption of the same nature as that of the fresh lens? What is the nature of oxygen consumption in the boiled lens? To answer the first question, we homogenized 10 calf lenses in 10 cc. of water in a Waring Blendor. The mixture was poured into centrifuge tubes and heated in a salt-water bath while being shaken continuously. The heating was carried References 1. Christiansen, G. S., and Leinfelder, P. J.: A Critical Study of Lens Metabolism , Am. J. Ophth. 35:21-38 (May, (Pt. 2) ) 1952.

SIGELMAN, SYLVIA;FRIEDENWALD, JONAS S.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050048005pmid: 13170864

Abstract THE CLINICAL phenomenon of so-called neuroparalytic keratitis has commonly been assumed to be the expression of some trophic disturbance in the cornea consequent upon sensory denervation of this tissue. The fact that the catastrophic events of such keratitis can be avoided by blepharoplasty and the prevention of the cornea from drying does not disprove such a trophic influence. The purpose of the present study was to see whether neuroparalytic keratitis could be produced experimentally in animals and to find out whether after sensory denervation there was any change in the mitotic or wound-healing activities of the corneal epithelium. Keratitis following injury to the trigeminal nerve has been reported by Zander and Weddell1 in experiments on rabbits and monkeys and by Kotlyarevskaya2 in cats. The latter author claims to have produced bilateral lesions following unilateral Gasserian ganglion injuries. In neither of these studies was the influence of sensory denervation References 1. Zander, E., and Weddell, G.: Brit. J. Ophth. 35:61, 1951.Crossref 2. Kotlyarevskaya, M. A.: Dokl. Akad. Nauk S.S.S.R. 80:129, 1951. 3. Friedenwald, J. S., and Buschke, W.: Am. J. Physiol. 141:689, 1944. 4. Verhoeff, F. H.: Am. J. Ophth. 8:273, 1925. 5. Buschke, W.; Friedenwald, J. S., and Fleischmann, W.: Bull. Johns Hopkins Hosp. 63:143, 1943. 6. Friedenwald, J. S., and Buschke, W.: J. Cell. & Comp. Physiol. 23:95, 1944. 7. Friedenwald, J. S., and Sigelman, S.: Exper. Cell Res. 4:1, 1953.

TROUTMAN, RICHARD C.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050060006pmid: 13170865

Abstract FOR THE past five years, since April, 1948, I have advocated and employed a magnetic implant for improving the cosmetic appearance of enucleation patients. Preliminary reports have been given before the Section of Ophthalmology of the New York Academy of Medicine,1 and the XVI. International Congress of Ophthalmology.2 A statistical survey covering the use of 1,509 implants of this and other types has been presented before the American Academy of Ophthalmology and Otolaryngology.3 I feel that after five years it is time for a definitive report on the use of the magnetic implant. This implant was devised to combine the advantages of the completely covered spherical implant and the advantages of the uncovered motility implants while eliminating, at least to some extent, the disadvantages of both the other types in use. The spherical implant, as we all know, is highly satisfactory surgically; however, postoperatively, except for the References 1. Troutman, R. C.: A Magnetic Implant for Use After Enucleation: Preliminary Report , Arch. Ophth. 43:1123-1124 ( (June) ) 1950. 2. Troutman, R. C.: An Integrated Magnetic Implant , Acta XVI Conc. Ophth., London , 1950, pp. 1228-1231. 3. Troutman, R. C.: Symposium: Orbital Implants After Enucleation: End Results of Implant Surgery , Tr. Am. Acad. Ophth. 56:30-34 ( (Jan.-Feb.) ) 1952. 4. Hughes, W. L.: Symposium: Orbital Implants After Enucleation: Classification and Mechanics Involved , Tr. Am. Acad. Ophth. 56:25-27 ( (Jan.-Feb.) ) 1952.

JACOBS, LEON;FAIR, JOHN R.;BICKERTON, JOHN H.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050065007

Abstract WITHIN recent years the question of the toxoplasmic etiology of uveitis has been the subject of various surveys and investigations. Frenkel6 (1951) found a correlation between skin test reactions and uveitis in a small group of hospital patients in California. Frenkel and Friedlander7 (1952) presented the results of the dye test of Sabin and Feldman13 on the same patients; they found most of the antibody titers to be low and postulated that the parasites could reside in the eye over long periods without stimulating antibody production. Hogan8 (1951), because of lack of correlation between serological findings and adult uveitis, considered it unlikely that many cases of adult uveitis are due to toxoplasmosis. Hogan, Thygeson, and Kimura9 (1952) later found the incidence of positive dye test reactions higher in patients of all age groups with chorioretinitis than in other groups, but in most cases the titers References 1. Feldman, H. A., in discussion on Hogan, Thygeson, and Kimura.9 2. Fair, J. R., and Jacobs, L., to be published. 3. Eyles, D. E.: Toxoplasma in the Norway Rat , J. Parasitol. 38:226-229, 1952.Crossref 4. Fair, J. R.: Uveitis—A Military Problem , A. M. A. Arch. Ophth. 51:364-368, 1954.Crossref 5. Feldman, H. A.: Clinical Manifestations and Laboratory Diagnosis of Toxoplasmosis , Am. J. Trop. Med. & Hyg. 2:420-428, 1953. 6. Franceschetti, A., and Bamatter, F.: Toxoplasmose oculaire, First Latin Ophthalmological Congress , Rome, pp. 315-437, 1953. 7. Frenkel, J. K.: Dermal Hypersensitivity to Toxoplasma Antigens (Toxoplasmosis) , Proc. Soc. Exper. Biol. & Med. 68:634-639, 1948. 8. Frenkel, J. K.: Uveitis and Toxoplasmosis Sensitivity , Am. J. Ophth. 32:127-135 (June, (Pt. 2) ) 1951. 9. Frenkel, J. K., and Friedlander, S.: Toxoplasmosis: Pathology of Neonatal Disease, Pathogenesis, Diagnosis and Treatment , Publication 141, Department of Health, Education, and Welfare, United States Public Health Service, 1952. 10. Hogan, M. J.: Ocular Toxoplasmosis , New York, Columbia University Press, 1951. 11. Hogan, M. J.; Thygeson, P., and Kimura, S.: Ocular Toxoplasmosis , Tr. Am. Acad. Ophth. 56:863-874, 1952. 12. Jacobs, L.; Melton, M. L., and Jones, F. E.: Prevalence of Toxoplasmosis in Wild Pigeons , J. Parasitol. 38:457-461, 1952. 13. Jacobs, L.; Melton, M. L., and Cook, M. K.: Experimental Toxoplasmosis in Pigeons , Exper. Parasitol. 2:403-416, 1953. 14. Jacobs, L.; Cook, M. K., and Wilder, H. C.: Serologie Data on Adults with Histologically Diagnosed Toxoplasmic Chorioretinitis , Tr. Am. Acad. Ophth. 58:193-200, 1954. 15. Sabin, A. B., and Feldman, H. A.: Dyes as Microchemical Indicators of a New Immunity Phenomenon Affecting a Protozoon Parasite (Toxoplasma) , Science 108:660-663, 1948. 16. Sabin, A. B.: Toxoplasmosis: Current Status and Unsolved Problems; Introductory Remarks , Am. J. Trop. Med. & Hyg. 2:360-364, 1953. 17. Sexton, R. C.; Eyles, D. E., and Dillman, R. E.: Adult Toxoplasmosis , Am. J. Med. 14:366-377, 1953. 18. Vivell, O.: Vergleichende Untersuchungen zwischen dem Sabin-Feldmansche Farbtest auf Toxoplasmose und dem Toxoplasminhauttest , Ztschr. Kinderh. 70:271-281, 1952. 19. Wilder, H. C.: Toxoplasma Chorioretinitis in Adults , A. M. A. Arch. Ophth. 48:127-136, 1952. 20. Woods, A. C.; Jacobs, L.; Wood, R. M., and Cook, M. K.: Study of the Role of Toxoplasmosis in Adult Chorioretinitis , Am. J. Ophth. 37:163-177, 1954.

MITSUI, YUKIHIKO;TANAKA, CHIE;YAMASHITA, KIICHI;HANABUSA, JUN

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050074008pmid: 13170867

Abstract A SERIES of trustworthy investigations indicates that distribution of trachoma virus is confined to the epithelial layer of the conjunctiva.* Nevertheless, the significant clinical change in trachoma is subepithelial inflammation, e. g., follicle formation and cellular infiltration. In addition, in the acute stage of infection there is often the association of a preauricular adenopathy. Might these changes not be incurred by a toxin or toxin-like substance produced by the trachoma virus? On the other hand, a toxin or a similar factor has been demonstrated in related viruses, namely, the viruses of psittacosis and lymphogranuloma venereum. The problem as to whether trachoma virus produces a toxin or like substance may, therefore, be worthy of investigation. DESIGN OF THE EXPERIMENT Conjunctival matter from trachoma cases with a great number of inclusion bodies no doubt contains trachoma virus in high concentration. If a soluble toxin or toxin-like substance is being produced by the References 1. References 1 to 3. 2. Supplied by Dr. S. Arakawa. Institute for Infectious Diseases, Tokyo, Japan. 3. Michail, D., and Vancea, P.: Quelques faits expérimentaux dans le trachoma , Rev. internat. trachoma 9:33-36, 1932. 4. Thygeson, P., and Richards, P.: Nature of the Filtrable Agent of Trachoma , Arch. Ophth. 20:569-582, 1938.Crossref 5. Okamura, K., and Mitsui, Y.: Contagious Trachoma Virus in Subconjunctival Tissues , Acta Soc. ophth. Jap. 43:2070-2074, 1939. 6. Meyer, K. F.: Psittacosis-Lymphogranuloma Group , in Rivers, T., and others: Viral and Rickettsial Infection of Man , J. B. Lippincott Company, Philadelphia, 1948, pp. 337-357. 7. Mitsui, Y.: Use of the New Antibiotics in the Treatment of Trachoma , J. Roy. Egyptian M. A. 35:69-77, 1952.

MICHAELSON, I. C.;GLUECKER, L.;STIEGLITZ, E.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050079009pmid: 13170868

Abstract WHEN IT is desirable to limit the amount of vascularization in the cornea, the clinician usually resorts to the use of low-voltage x-rays, cortisone, or beta radiation. Although low-voltage x-rays are used in this way rather extensively, there are few reports on experimental work which should form the basis of a procedure difficult to assess clinically. While it has been shown that large doses of x-rays produce corneal damage followed by vascularization (Rohrschneider, 1929; Martin and Reese, 1942), in a series of experimental studies using total doses as low as 1,500 r Scheie and his collaborators have concluded that the vascularization produced by intracorneal sodium hydroxide injection can be markedly inhibited by low-voltage x-rays (1950). They found that daily exposures were more effective in inhibiting corneal vascularization than exposures given at longer intervals and that small single doses, of 300 r, were as effective as larger ones, up to 1,000 References 1. Ashton, N.; Cook, C., and Langham, M.: Brit. J. Ophth. 35:718, 1951.Crossref 2. Campbell, F. W., and Michaelson, I. C.: Brit. J. Ophth. 33:248, 1949.Crossref 3. Jones, I. S., and Meyer, K.: Proc. Soc. Exper. Biol. & Med. 74:102, 1950. 4. Lister, A., and Greaves, D. P.: Brit. J. Ophth. 35:725, 1951. 5. Michaelson, I. C.: A. M. A. Arch. Ophth. 47:459, 1952. 6. Michaelson, I. C.: A. M. A. Arch. Ophth. 48:144, 1952. 7. Scheie, H. G.; Dennis, R. H.; Ripple, R. C.; Calkins, L. L., and Buessler, J. A.: Am. J. Ophth. 33:549, 1950.

DAY, ROBERT McCLELLAND;WERNER, SIDNEY C.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050087010pmid: 13170869

Abstract THE MECHANISMS responsible for the production and maintenance of the ocular complications of hyperthyroidism have not been entirely elucidated. Accordingly, the rate of removal of radioactive sodium from the orbits of healthy human subjects and of patients with the mild and severe extremes of ophthalmopathy has been observed with a view toward determining whether venous obstruction or active inflammation accounts for the phenomena. The extremes of the eye changes have been variously termed "thyrotoxic" and "thyrotropic," or "simple" and "malignant" exophthalmos, among other names, but in this paper they will be called "mild" and "severe." It has been recognized that orbital tension is increased in the severe form of thyroid ophthalmopathy. Quantitative measurements reveal an increase proportionate to the degree of exophthalmos.1 Rundle and Pochin2 have shown also that there is a significant increase in orbital bulk which tends to correlate quantitatively with the degree of exophthalmos. This References 1. Kearns, T. P.; Henderson, J. W., and Haines, S. F.: Clinical Orbitonometry in Graves' Disease , Am. J. Ophth. 36:45-55, 1953. 2. Rundle, F. F., and Pochin, E. E.: The Orbital Tissues in Thyrotoxicosis: A Quantitative Analysis Relating to Exophthalmos , Clin. Sc. 5:51-74, 1944. 3. Pochin, E. E.: Discussion on Exophthalmos and Endocrine Disturbance , Proc. Roy. Soc. Med. 38:669-670, 1945. 4. Wisham, L. H.; Yalow, R. S., and Freund, A. J.: Consistency of Clearance of Radioactive Sodium from Human Muscle , Am. Heart J. 41:810-818, 1951.Crossref 5. Whitnall, S. E.: The Anatomy of the Human Orbit and Accessory Organs of Vision , Ed. 2, London, Oxford University Press, 1932, p. 88.

HAVENER, WILLIAM H.;HENDERSON, JOHN WOODWORTH

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050093011pmid: 13170870

Abstract NINETY selected patients from the University of Michigan ophthalmology clinic have been studied with both flicker fusion and standard perimetric methods. The results obtained will be presented and analyzed to determine the comparative value of the two means of testing. The patients were chosen on the basis of known pathologic changes likely to give field defects. As is obvious from the protocols at the end of the paper, not all fields showed defects; however, the normals are included to illustrate the diversity of disease processes studied. In each patient both types of field testing were performed by the same examiner. Any positive findings by one method were very carefully tested by the other before concluding that either type of field examination was superior. The performance of both tests by the same examiner diminishes the possibility of erroneous conclusions by an enthusiastic flicker perimetrist, who may find lesions overlooked by routine References 1. References 1 and 2. 2. Miles, P. W.: Flicker Fusion Fields: Technique and Interpretation , Am. J. Ophth. 33:1069-1077 ( (July) ) 1950. 3. Miles, P. W.: Flicker Fusion Fields: Neuro-Ophthalmic Lesions , Am. J. Ophth. 34:51-56 (May, (Pt. 2) ) 1951. 4. Havener, W. H., and McReynolds, W. U.: False Scotomas Associated with High Uncorrected Refractive Errors , A. M. A. Arch. Ophth. 48:616-619 ( (Nov.) ) 1952.Crossref

GIFFORD, EDWARD S.;MAGUIRE, ELLIOTT F.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050108012pmid: 13170871

Abstract THE ASSOCIATION of abnormal serum calcium with ocular manifestations was first reported by Meesmann in 1938. His case was one in which bandshaped opacities of the cornea and opacities of the conjunctiva developed when overdosage in treatment of hypoparathyroidism following thyroidectomy caused a high serum calcium. Since then, 36 cases of disturbed calcium metabolism with calcium deposits in the cornea, or in the conjunctiva, or in both have been reported.* Such deposits appear as subconjunctival crystals or white flakes, and as diffuse, superficial, gray corneal opacities in the palpebral fissure, denser near the limbus and fading toward the center of the cornea. Usually there is a clear area of 1 or 2 mm. between the opacities and the limbus, but two of the cases reported by Ojers and Alfano3 and the present case did not have this feature. Welsh and Howard4 reported that chemical analysis of affected conjunctiva References 1. References 1 through 4. 2. Cogan, D. G.; Albright, F., and Bartter, F. C.: Hypercalcemia and Band Keratopathy , Arch. Ophth. 40:624-638, 1948.Crossref 3. Goetz, F. C.: Cases from the Medical Grand Rounds , Am. Pract. 2:976-981, 1951. 4. Ojers, G. W., and Alfano, J.: Band Keratopathy in Disturbances of Calcium Metabolism , A. M. A. Arch. Ophth. 46:531-535, 1951.Crossref 5. Welsh, F. B., and Howard, J. E.: Conjunctival and Corneal Lesions in Hypercalcemia , J. Clin. Endocrinol. 7:644-652, 1947.Crossref

GOODMAN, JOSEPH I.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050110013pmid: 13170872

Abstract ATHEROSCLEROSIS, medical sclerosis, and arteriolar sclerosis all occur more frequently in diabetic than in nondiabetic patients. The clinical features of these conditions in diabetics were reviewed in previous reports.* As a cause of morbidity and mortality, atherosclerosis is the most important form of arteriosclerosis by far. As has been pointed out elsewhere,4 it is agreed at present that the specific lesions of diabetes are in the capillaries and venules of the retina and glomerulus, i. e., retinopathy and intercapillary glomerulosclerosis (Kimmelstiel-Wilson disease). Diabetic retinopathy passes through successive stages, beginning with the microaneurysm and lesions of the venules. The exudates are small, pinpoint lesions in the early stages, coalesce to form larger, waxy exudates, but do not take on the star-shaped configuration one sees, for example, in albuminuric retinopathy. In the final stage there is hemorrhage into the vitreous and/or the fully developed picture of retinitis proliferans. Very recently, Ashton References 1. References 1, 2, and 3. 2. References 5 and 6. 3. Volk, D.: Personal communication to the author. 4. References 10 through 12. 5. References 16 and 17. 6. References 5 and 6. 7. References 16 and 17. 8. Tolstoi, E., in discussion on Root, H. F.: Complications and Sequelae of Diabetes. Relation to Control, Panel Discussion, 12th Annual Meeting of American Diabetes Association, June 8, 1952. 9. Reference 22. Rich, A. R.: John Hopkins Hospital Clinical-Pathological Conference, February, 1952. 10. References 24 and 25. 11. References 16, 17, and 28. 12. References 8 and 27, and others. 13. References 21, 24, and 39. 14. References 5 and 6. 15. References 35 and 41. 16. References 32 and 33. 17. Reference 47. Tolstoi, E., in discussion on Root, H. F.: Complications and Sequelae of Diabetes: Relation to Control, Panel Discussion, 12th Annual Meeting of the American Diabetes Association, June 8, 1952. 18. References 1 through 4. 19. Reference 22. Rich, A. R.: Johns Hopkins Hospital Clinical-Pathological Conference, February, 1952. 20. Eversole, S. L.: The Kimmelstiel-Wilson Syndrome, lecture given before the American College of Surgeons Physicians, April 25, 1952. 21. References 49 and 50. Hinkle, L. E., Jr., and Wolf. S.: Changes in Blood Glucose in Response to Stress and Their Relevance to Diabetes Mellitus, 12th Annual Meeting of the American Diabetes Association, June 8, 1952. 22. Goodman, J. I.; Wassermann, S.; Marcus, L. J., and Frankel, L.: Study of Atherosclerosis in a Group of Diabetic Patients , Am. J. M. Sc. 220:30-45 ( (July) ) 1950.Crossref 23. Goodman, J. I.: Vascular Lesions in Diabetes Mellitus: I. Pathologic and Clinical Aspects of Atherosclerosis , Ohio M. J. 48:1013-1018 ( (Nov.) ) 1952. 24. Goodman, J. I.: Specific Vascular Lesions of Diabetes Mellitus: Retinopathy and Intercapillary Glomerulosclerosis , Am. J. Ophth. 36:957-965 ( (July) ) 1953. 25. Goodman, J. I.: Specific Vascular Lesions of Diabetes Mellitus: II. Retinopathy and Intercapillary Glomerulosclerosis , Am. J. Ophth. 36:957-966 ( (July) ) 1953. 26. Ashton, N.: Vascular Changes in Diabetes, with Particular Reference to the Retinal Vessels , Brit. J. Ophth. 33:407-420 ( (July) ) 1949.Crossref 27. Ashton, N.: Retinal Micro-Aneurysms in the Non-Diabetic Subject , Brit. J. Ophth. 35:189-212 ( (April) ) 1951.Crossref 28. Becker, B., and Post, L. T., Jr.: Retinal Vein Occlusion: Clinical and Experimental Observations , Am. J. Ophth. 34:677-686 ( (May) ) 1951. 29. Givner, I.: Medical Progress: Ocular Expressions of Diabetes , New York Med. 3:15-18 ( (March 5) ) 1947. 30. Jones, D. E.: Inflammation and Repair of the Glomerulus , Am. J. Path. 27:991-1009 ( (Nov.-Dec.) ) 1951. 31. McGregor, L.: Finer Histology of the Normal Glomerulus , Am. J. Path. 5:545-558 ( (Nov.) ) 1929. 32. Zimmerman, K. W.: Über den Bau des Glomerulus der menschlichen Niere , Ztschr. mikr.-anat. Forsch. 18:520, 1929. 33. Borst, J. G. G.: Der Bau des normalen Glomerulus , Ztschr. mikr.-anat. Forsch. 23: 455-483, 1931. 34. McManus, J. F. A.: Development of Intercapillary Glomerulosclerosis , Proc. Am. Diabetes A. 9:303-306, 1949. 35. Rifkin, H.; Parker, J. G.; Polin, E. B.; Beckman, J. I., and Spiro, D.: Diabetic Glomerulosclerosis: Clinical and Pathologic Observations with Special Reference to Doubly Refractile Fatty Cells and Casts in the Urine , Medicine 27:429-457 ( (Dec.) ) 1948.Crossref 36. Allen, A. C.: So-Called Intercapillary Glomerulosclerosis—Lesion Associated with Diabetes Mellitus: Morphogenesis and Significance , Arch. Path. 32:33-51 ( (July) ) 1941. 37. Friedenwald, J. S.: Diabetic Retinopathy , Am. J. Ophth. 33:1187-1199 ( (Aug.) ) 1950. 38. Friedenwald, J. S.: Diabetic Retinopathy , J. A. M. A. 150:969-971 ( (Nov. 8) ) 1952.Crossref 39. Lewis, L. A.; Schneider, R. W., and McCullagh, E. P.: Tiselius Electrophoresis Studies of Plasma Proteins in Diabetes Mellitus , J. Clin. Endocrinol. 4:535-539 ( (Nov.) ) 1944.Crossref 40. Dolger, H.: A Clinical Evaluation of Vascular Damage in Diabetes Mellitus , Proc. Am. Diabetes A. 6:395-405, 1947. 41. Joslin, E. P.: Treatment of Diabetes Mellitus , Ed. 9, Philadelphia, Lea & Febiger, 1952. 42. Lukens, F. D. W., and Dohan, F. C.: Experimental Pituitary Diabetes of 5 Years' Duration with Glomerulosclerosis , Arch. Path. 41:19-24 ( (Jan.) ) 1946. 43. Rich, A. R.; Bethrong, M., and Bennett, I. L., Jr.: Effect of Cortisone upon the Experimental Cardiovascular and Renal Lesions Produced by Anaphylactic Hypersensitivity , Bull. Johns Hopkins Hosp. 87:549-566, 1950. 44. Wagener, H. P.; Dry, T. J., and Wilder, R. M.: Retinitis in Diabetes , New England J. Med. 211:1131-1137 ( (Dec. 20) ) 1934.Crossref 45. Newburger, R. A., and Peters, J. P.: Intercapillary Glomerulosclerosis: A Syndrome of Diabetes, Hypertension and Albuminuria , Arch. Int. Med. 64:1252-1264 ( (Dec.) ) 1939.Crossref 46. Siegal, S., and Allen, A. C.: Intercapillary Glomerulosclerosis (Kimmelstiel-Wilson) and the Nephrotic Syndrome in Diabetes Mellitus , Am. J. M. Sc. 201:516-528 ( (April) ) 1941.Crossref 47. Ballantyne, A. J., and Loewenstein, A.: Pathology of Diabetic Retinopathy , Tr. Ophth. Soc. U. Kingdom 63:95-115, 1944. 48. Wagener, H. P.: Retinopathy in Diabetes Mellitus , Proc. Am. Diabetes A. 5:203-216, 1945. 49. Kimmelstiel, P.: Intercapillary Glomerulosclerosis and Diabetes: Recent Observations and Changes of Concept , Gaz. méd. port. 4:648-656, 1951. 50. Elwyn, H.: Diabetic Retinitis , Arch. Ophth. 34:187-190 ( (Sept.) ) 1945.Crossref 51. Duke-Elder, W. S.: Diabetic Retinopathy , in Text-Book of Ophthalmology , Vol. 3, St. Louis, C. V. Mosby Company, 1941, pp. 2729-2735. 52. Beaser, S. B.; Rudy, A., and Seligman, A. M.: Capillary Fragility in Relation to Diabetes Mellitus, Hypertension and Age , Arch. Int. Med. 73:18-22 ( (Jan.) ) 1944.Crossref 53. Root, H. F.; Sinden, R. H., and Zanca, R.: Factors in the Rate of Development of Vascular Lesions in the Kidneys, Retinae and Peripheral Vessels of the Youthful Diabetic , Am. J. Digest. Dis. 17:179-186 ( (June) ) 1950.Crossref 54. Beardwood, J. T.; Roberts, E., and Trueman, R.: Observations on the Effect of Rutin and Hesperidin in Diabetic Retinitis , Proc. Am. Diabetes A. 8:243-256, 1948. 55. Levitt, L. M.; Cholst, M. R.; King, R. S., and Handelsman, M. B.: Rutin Therapy for Increased Capillary Fragility and Retinopathy Associated with Diabetes Mellitus , Am. J. M. Sc. 215:130-135 ( (Feb.) ) 1948.Crossref 56. Barnes, R. H.: Capillary Fragility Studies in Diabetes Mellitus and the Use of Rutin in Diabetic Retinitis , Am. J. M. Sc. 219:368-375 ( (April) ) 1950.Crossref 57. Peck, F. B., and Mann, M.: Effect of Hesperidin Methyl Chalcone (Vitamin P) on Diabetic Retinopathy , Am. J. M. Sc. 217:277-282 ( (March) ) 1949.Crossref 58. Frericks, C. T.; Tillotson, I. G., and Hayman, J. M., Jr.: Effect of Rutin on Capillary Fragility and Permeability , J. Lab. & Clin. Med. 35:933-939 ( (June) ) 1950. 59. Goodman, J. I.; Baumoel, S.; Frankel, L.; Marcus, L. J., and Wassermann, S.: The Diabetic Neuropathies , Springfield, Ill., Charles C Thomas, Publisher, 1953. 60. Freston, J. M., and Loughlin, W. C.: Vitamins in Diabetics , Proc. Am. Diabetes A. 2:187-195, 1942. 61. Mirsky, I. Arthur: Our Challenge for the Future , Diabetes Abst. 5:71-72 ( (July) ) 1946. 62. Post, L. T., and Stickle, A. W., Jr.: Fundus Changes in Juvenile Diabetes , Am. J. Ophth. 34:1119-1126 ( (Aug.) ) 1951. 63. Grayzel, H. G., and Warshall, H. B.: Clinical Survey of Vascular Complications in "Juvenile Diabetes Mellitus," Pediatrics 8:506-512 ( (Oct.) ) 1951. 64. Keiding, N. R.; Root, H. F., and Marble, A.: Importance of Control of Diabetes in Prevention of Vascular Complications , J. A. M. A. 150:964-969 ( (Nov. 8) ) 1952. 65. O'Brien, C. S., and Allen, J. G.: Ocular Changes in Young Diabetic Patients , J. A. M. A. 120:190-192 ( (Sept. 19) ) 1942.Crossref 66. Sherrill, J. W.: Diabetic Retinitis: Relationship Between Retinal Degenerative Changes and the Degree of Diabetic Control , Bull. Scripps Metab. Clin. 2:1-17 ( (Oct.) ) 1951. 67. Poulsen, J. E.: Recovery from Retinopathy in a Case of Diabetes with Simmonds' Disease , Diabetes 2:7-12 ( (Jan.-Feb.) ) 1953. 68. Peters, J. H.: Vascular Complications of Diabetes , Am. Pract. & Digest Treat. 2:669-672 ( (Aug.) ) 1951. 69. Heinsius, E.: Retinitis Diabetica: Role of Endocrine Function and of Vegetative Nervous System in Its Etiology , Am. J. Ophth. 35:861-862 ( (June) ) 1952. 70. Hinkle, L. E., Jr., and Wolf, S.: Importance of Life Stress in Course and Management of Diabetes Mellitus , J. A. M. A. 150:964-969 ( (Nov. 8) ) 1952. 71. Hinkle, L. E., Jr., and Wolf, S.: Effects of Stressful Life Situations on the Concentration of Blood Glucose in Diabetic and Nondiabetic Humans , Diabetes 1:383-392 ( (Sept.-Oct.) ) 1952. 72. Conway, H., and Stark, R. B.: ACTH in Plastic Surgery , Plast. & Reconstruct. Surg. 8:354-377 ( (Nov.) ) 1951.

BROCKHURST, ROBERT J.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050123014pmid: 13170873

Abstract VARIOUS types of foreign material may be introduced into the eye during intraocular surgery, for example, talc, cilias, rubber, and cotton lint fibrils. Vail1 recently reviewed this complication and reported three cases of cotton lint in the anterior chamber. In most of the cases of lint reviewed, as well as in Vail's three new cases, the foreign material was not deleterious to the eye. However, in some instances transient postoperative iritis occurred. Vail felt that the lint in his cases came from the air circulating in the operating room. He suggested several measures by which the amount of dust in the air might be reduced. It is the purpose of this paper to report four additional instances of fibrils in the anterior chamber. It is believed these fibrils were cotton threads which had broken off from the cotton sponges used during the operation. REPORT OF CASES Case 1. —A References 1. In each eye the cataract had been tumbled with an erysiphake. In each instance, there was corneal edema lasting two days. 2. Vail, D.: Lint in the Anterior Chamber Following Intraocular Surgery , Am. J. Ophth. 34:1533-1538, 1951.

CONOVER, WILLIAM G.;SPAETH, EDMUND B.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050127015pmid: 13170874

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract THIS NEW instrument was exhibited during the 1953 Session of the American Academy of Ophthalmology and Otolaryngology. The instrument was developed through the mutual efforts of one of us (E. B. S.) as a physician and the other (W. G. C.) as a patient. The instrument was worked out to obtain more complete accuracy in central field examination. At the same time, the determination can be done in much less time than is usually required for this examination with similar tangent screens. The instrument is 24 by 24 in. (60 by 60 cm.) with a fixed central fixation point. A magnet moves the test object freely upon the visible field. At the conclusion of testing for each radius the test object is withdrawn from view behind a concealment shield. At the rear, or operating, side there is a sheet of nonmagnetic metal with a circular opening which serves as a

ASKOVITZ, S. I.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050129016pmid: 13170875

Abstract THE READINGS on many types of electronic measuring and recording instruments may be significantly altered by fluctuations in the voltage of the power supply. Inadequate grounding is another frequently encountered difficulty in the use of electrical devices. That such factors must be considered, especially in work of a research nature, where accuracy is important, has been pointed out previously for the case of the electronic tonometer.* There has been developed at this laboratory a combined unit for standardizing tonography records which will maintain a stabilized voltage to within 0.5% (satisfactory for most medical purposes) and will also provide a simple test for the adequacy of an external ground connection (Figure). A voltmeter on the front panel indicates either the incoming voltage or the stabilized output, and an ammeter shows whether the current load of the attached instruments is excessive. (It may also serve to demonstrate whether the attached instrument is References 1. References 1 and 2. 2. Friedenwald, J. S.: Recent Advances in Tonometer Construction , Tr. Am. Acad. Ophth. 52:543, 1948. 3. Askovitz, S. I.: The Electronic Tonometer , Am. J. Ophth. 36:400, 1953.

LANCHNER, ABRAHAM J.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050131017pmid: 13170876

Abstract THE SUTURE which is here described is a preplaced corneoscleral suture, being inserted at the limbus before any incision is made. It can be used either with or without a conjunctival flap. One or more sutures may be used in any part of the limbal area. I prefer three sutures, at 10:30, 12, and 1:30 o'clock. The eye is prepared in the usual manner for cataract surgery, and the globe is steadied with fixation forceps. A 7 mm. Grieshaber needle attached to a 000000 nonabsorbable surgical (silk) suture is inserted near the limbus in the cornea, pene- trating about one-third of the corneal thickness. About 2 mm. of corneoscleral tissue should be included in this bite, with the needle emerging in the sclera. The needle is not pulled through but is left in the tissue, with both the tip end and the eye end protruding (Figure, I). All the needles, References 1. Baldino, S.: Sutura corneale perfezionata , Rass. ital. ottal. 4:538 ( (July-Aug.) ) 1935.

KERN, HAROLD L.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050133018pmid: 13170877

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract THE SIMPLE apparatus shown in the Figure has been found eminently satisfactory for exhaustive extraction of cornea with aqueous solutions. It was developed after we had been unable to find a suitable extractor described in the literature. It has been employed in determining cations in corneal stroma after exposure to various alkalis. The extractor should prove useful in assaying dissolved or bound ions or uncharged molecules in any small sample of firm, permeable material which is not disintegrated by the extracting medium. Rapid and near-quantitative removal of individual portions of solvent is possible with a minimum of manipulation. A 1 mm. bore capillary is sealed to the end of a 70 mm. length of 14 mm. I. D. Pyrex tubing and bent in the shape shown in the Figure. A "dimple" may be made just above the capillary to prevent plugging. In our particular application, the exposed tissue (0.1 to

Webb, Edward F.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050134019pmid: 13170878

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

WHEELER, MAYNARD C.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050136020

References 1. It was my hope to make a continuous story of the treatment of strabismus. However, so many of the articles cover several phases of the treatment that it seemed more valuable to review them singly and then to summarize them at the end of the section. Treatment, particularly orthoptics, has already been mentioned in several earlier sections of this review. 2. References 73 and 74. 3. Strabismus Symposium , Tr. Am. Acad. Ophth. 57:121-176, 1953. 4. Swan, K. C.: Introduction: The Nature of Normal Binocular Vision, pp. 121-130. 5. Burian, H. M.: Adaptive Mechanisms, pp. 131-144. 6. Adler, F. H.: The Pathologic Physiology of the Horizontal Deviations, pp. 145-156. 7. Brown, H. W.: Vertical Deviations, pp. 157-162. 8. Costenbader, F. D.: Principles of Treatment, pp. 163-169. 9. Dickey, C. A.: Surgery in the Treatment of Strabismus, pp. 170-174. 10. Swan, K. C.: Conclusions, pp. 175-176. 11. Adler, F. H.: Disturbances of Ocular Motility , in Gifford's Textbook of Ophthalmology , Ed. 5, Philadelphia, W. B. Saunders Company, 1953, pp. 56-98. 12. Asher, H.: Suppression Theory of Binocular Vision , Brit. J. Ophth. 37:37-49, 1953.Crossref 13. Winkelman, J. E.: Central and Peripheral Fusion , A. M. A. Arch. Ophth. 50:179-183, 1953.Crossref 14. Rønne, G., and Rindziunski, E.: Diagnosis and Clinical Classification of Anomalous Correspondence , Acta ophth. 31:321-345. 1953. 15. Rønne, G., and Rindziunski, E.: Pathogenesis of Anomalous Correspondence , Acta ophth. 31:347-366, 1953. 16. Jaffe, N. S.: Anomalous Projection: Its Incidence, Factors in Development, Characteristics, Tests and Treatment in 146 Surgically Treated Strabismus Cases , Am. J. Ophth. 36:829-838, 1953. 17. Castanera Pueyo, A.: Treatment of Abnormal Retinal Correspondence in Squint , Arch. Soc. oftal. hispano-am. 12:1001-1018, 1952. 18. Hamburger, F. A.: Contribution to the Bloodless Treatment of Squint in Strabismus with Anomalous Correspondence , Wien. klin. Wchnschr. 63:596, 1951 19. abstracted, Ophth. Lit. 5:1345, 1953. 20. Gittoes-Davies, R.: Examination of Cases with Small Degree Esotropia , Brit. Orthop. J. 9:113-122, 1952. 21. Dejean, C.; Viallefont, H., and Dollard: Strabismus and Left-Handedness , Bull. Soc. opht. France , pp. 563-565, 1953. 22. Alabaster, E. B.: Circumstances Leading to the Development of Squint , Brit. Orthop. J. 9:11-14, 1952. 23. Chytilová-Divišová, G.: Present Conception of the Origin and Treatment of Concomitant Squint , Prakt. lék. 32:61-63, 1952 24. abstracted, Excerpta Med. XII 7:19, 1953. 25. Nordlöw, W.: Age Distribution of the Onset of Esotropia , Brit. J. Ophth. 37:593-600, 1953.Crossref 26. Jonkers, G. H.: Origin of Squint , Ophthalmologica 126:309-311, 1953.Crossref 27. Adler, F. H.: Pathologic Physiology of Strabismus , A. M. A. Arch. Ophth. 50:19-29, 1953.Crossref 28. Urrets-Zavalía, A.: Etiology and Pathology of Concomitant Strabismus , Tr. IV Cong. Pan.-Am. oftal. 2:697-723, 1952 29. Arch. oftal. Buenos Aires 27:329-357, 1952. 30. Pesme, P., and Faure, J.: Electroencephalographic Findings in Children with Strabismus , Arch. franç. pédiat. 9:760-764, 1952 31. abstracted, Ophth. Lit. 6:713, 1953. 32. Hiroishi, M.: Electro-Oculogram in Strabismus , Acta Soc. ophth. japan. 57:607-641, 1953 33. abstracted, Am. J. Ophth. 37:145, 1954. 34. Hefel, F.: History of the Treatment of Amblyopia , Klin. Monatsbl. Augenh. 122:611-622, 1953. 35. Parsons-Smith, G.: Activity of the Cerebral Cortex in Amblyopia , Brit. J. Ophth. 37: 359-364, 1953.Crossref 36. Parsons-Smith, G.: Flicker Stimulation in Amblyopia , Brit. J. Ophth. 37:424-431, 1953.Crossref 37. Burian, H. M.: Electroretinography and Its Clinical Application , A. M. A. Arch. Ophth. 49:241-256, 1953Crossref 38. Tr. Sec. Ophth., A. M. A. , pp. 126-145, 1952. 39. Jaffe, N. S., and Brock, F. W.: Some Phenomena Associated with Amblyopia , Am. J. Ophth. 36:1075-1086, 1953. 40. Bourquin, A.: Incidence of Disease in Amblyopic Eyes , Ophthalmologica 125:405-409, 1953.Crossref 41. Bangerter, A.: Treatment of Amblyopia , Ophthalmologica , (Supp. 37) , 1953 42. Treatment of Amblyopia , Basel, S. Karger, 1953. 43. Meyer, A.: Observations on Squint Therapy in Switzerland , Brit. Orthop. J. 9:89-93, 1952. 44. Bagshaw, J.: Eccentric Fixation with Variations , Brit. Orthop. J. 9:98-102, 1952. 45. Swenson, A.: Temporal Occlusion in Concomitant Convergence Strabismus , Am. Orthop. J. 3:48-50, 1953. 46. Olmsted, K. E.: The Diffraction Lens , Tr. Am. Acad. Ophth. 56:862, 1952. 47. Ryerson, F. S., and Calahan, J. L.: Management of Squint and Amblyopia in Identical Twins , Kresge Eye Inst. Bull. 4:3-6, 1952. 48. Arruga, A.: A Screen for the Measurement of Ocular Deviations , Arch. Soc. oftal. hispano-am. 12:1344-1349, 1952. 49. Halbron, P.: Examination of Ocular Motility with the Aid of Complementary Colors , Ann. ocul. 186:202-216, 1953. 50. Halbron, P.; Paquet, C., and Correard: A Case of Hyperphoria Treated Surgically , Bull. Soc. opht. France , pp. 300-303, 1953. 51. Foster, J.: Variant of the Lancaster Diplopia Test , Brit. J. Ophth. 37:378-380, 1953.Crossref 52. Weidmann, W.: The Tropometer, a New Instrument in the Study of Ocular Motility , Ophthalmologica 125:422-424, 1953.Crossref 53. Leurent, P.: Various Methods of Examination of Ocular Paralyses: The Chéiroscope as a Supplementary Means of Diagnosis , Bull. Soc. opht. France , pp. 67-81, 1953. 54. Robinson, J.: A Survey of Intermittent Convergent Strabismus, Apparently Due to Insufficiency of the Harmonic Reflex , Brit. Orthop. J. 9:28-39, 1952. 55. Lloyd, I.: Theory of Dysfunction of Accommodation in the Convergent Squint of Childhood , Brit. Orthop. J. 9:40-45, 1952. 56. Fitton, M.: A Survey of Accommodative Squint , Brit. Orthop. J. 9:106-112, 1952. 57. Dowler, P. B.: Survey of a Series of Cases of Accommodative Strabismus , Brit. Orthop. J. 9:46-51, 1952. 58. Parsons, K. M.: Long-Term Outlook on Accommodative Squint , Brit. Orthop. J. 9:15-17, 1952. 59. Stewart, M., and Vaughton, G.: Anomalies of Fusion: Significance of Accommodation in Orthoptic Treatment , Brit. Orthop. J. 9:75-80, 1952. 60. Dobson, M.: Refraction and Treatment of Very Young Squinters , Tr. IV Cong. Pan.-Am. oftal. 3:1771-1786, 1952. 61. Fink, W. H.: Physiopathology of Convergence Insufficiency , Am. Orthop. J. 3:5-12, 1953. 62. Capobianco, N. M.: Incidence and Diagnosis of Convergence Insufficiency , Am. Orthop. J. 3:13-17, 1953. 63. Simpson, G. V.: Medical Management of Convergence Insufficiency , Am. Orthop. J. 3:18-22, 1953. 64. Healy, E.: Orthoptic Treatment of Convergence Insufficiency , Am. Orthop. J. 3:23-25, 1953. 65. Burian, H. M.: Summary of Symposium on Convergence Insufficiency , Am. Orthop. J. 3:26, 1953. 66. Knapp, P.: Intermittent Exotropia: Evaluation and Therapy , Am. Orthop. J. 3:27-33, 1953. 67. Humphriss, D.: Divergence Excess: Etiology and Treatment , Brit. J. Physiol. Optics 10:27-38, 1953. 68. Crone, R. A.: Alternating Hyperphoria , Amsterdam, Swetz & Zeitlinger, 1952. 69. Toselli, C.: Mechanism of the Dissociated Vertical Deviations , Boll. ocul. 32:305-310, 1953 70. abstracted, Am. J. Ophth. 37:146, 1953. 71. Crone, R. A.: Torticollis Ocularis , abstracted, Ophthalmologica 126:308-309, 1953.Crossref 72. Urist, M. J.: Bilateral Superior Oblique Paralysis , A. M. A. Arch. Ophth. 49:382-391, 1953.Crossref 73. Abraham, S. V.: Use of Miotics in Treatment of Nonparalytic Convergent Strabismus , Tr. IV Cong. Pan-Am. oftal. 3:2014-2021, 1952. 74. Abraham, S. V.: Special Reactions to the Miotic Floropryl , Am. J. Ophth. 36:1122-1123, 1953. 75. Lyle, T. K.: Orthoptic and Surgical Treatment of Nonparalytic Strabismus , Bull. New York Acad. Med. 29:235-248, 1953. 76. Rodriguez Barrios, R., and Martinez, E.: Strabismus: Report on 550 Cases , Tr. IV Cong. Pan-Am. oftal. 3:1567-1579, 1952. 77. Riise, P.: Results in Binocular Vision by Early Operation in Strabismus , Acta ophth. 31:117-125, 1953.Crossref 78. Ruedemann, A. D.: Foveal Co-Ordination , Am. J. Ophth. 36:1220-1224, 1953. 79. Moacyr de Aguiar, P.: An Auxiliary Method of Orthoptic Treatment , Rev. brasil. oftal. 11:43-51, 1952. 80. Barbosa da Luz, J.: Selection of Cases for Orthoptic Treatment , Rev. brasil. oftal. 11: 29-40, 1952. 81. Wareing, M. M.: Orthoptic Treatment of Strabismus , Día méd. 24:950-951, 1952. 82. Moreu Gonzáles-Pola, A., and Abraldes Puértolas, M.: Treatment in Childhood , Arch. Soc. oftal. hispano-am. 12:993-1000, 1952 83. abstracted, Ophth. Lit. 6:538, 1953. 84. Keiner, G. B., Jr.: Results of Early Strabismus Therapy , Nederl. tijdschr. geneesk. 96: 1232-1235, 1952. 85. Hugonnier, R.: Prognosis in Strabismus: Practical Note , Bull. Soc. opht. France , pp. 392-393, 1953. 86. Wehrheim, D.: Physiologic Diplopia as a Home Exercise , Am. Orthop. J. 3:62-65, 1953. 87. Robinson, J. S.: Evaluation of Home Training in Orthoptics , Am. Orthop. J. 3:51-61, 1953. 88. Smolik, H.: Demonstration of a Simple Apparatus for Orthoptic Training , Ophthalmologica 125:419-421, 1953.Crossref 89. Thomas, C.; Grimault, B., and Brocker: Orthoptic Treatment in Therapy of Paralytic Strabismus , Bull. Soc. opht. France , pp. 160-164, 1953. 90. Parfonry, J., and Polliot, L.: Surgical Treatment of Concomitant Strabismus , Bull. Soc. opht. Paris , (Supp. 4) , 1953. 91. Costenbader, F. D.: Management of Nonaccommodative Esotropia , Tr. IV Cong. Pan-Am. oftal. 1:447-454, 1952. 92. Costenbader, F. D.: Bilateral Squint Surgery: A Preliminary Report ; abstracted, Am. J. Ophth. 36:858, 1953. 93. Foroni, C.: Operation for Concomitant Squint: Personal Technique , Ann. ottal. e ocul. 78:875-880, 1952. 94. Lukić, D.: Postoperative Squint: Its Correction and Prophylaxis , Srpski arch. 81:146-151, 1953 95. abstracted, Ophth. Lit. 7:346, 1953. 96. Vila-Coro, A.: Surgery of the Obliques , Arch. Soc. oftal. hispano-am. 13:281-294, 1953 97. abstracted, Ophth. Lit. 7:346, 1953. 98. Rama, G.: Primary Congenital and Secondary Changes in the Extrinsic Muscles of the Eye in Strabismus , Folia hered. path. Pavia 1:317-334, 1952 99. abstracted, Ophth. Lit. 6:847, 1953. 100. Rama, G.: Strabismus and Nystagmus , Rass. ital. ottal. 22:245-260, 1953 101. abstracted, Am. J. Ophth. 37:146, 1954. 102. Spaeth, E. B.: Surgical Aspects of Defective Abduction , A. M. A. Arch. Ophth. 49:49-62, 1953.Crossref 103. Giardini, A.: Orthoptic and Surgical Treatment of Concomitant Squint , Boll. ocul. 31: 396-421, 1952. 104. Adelung, J. C.: Results of Measured Advancement and Recession Operation of Kuntz as Compared with Those of Simple Advancement and Tenotomy , Klin. Monatsbl. Augenh. 121:700-707, 1952. 105. Arruga, A.: The Time Factor in the Treatment of Squint in Children , Acta pediat. españ. 11: 1-22, 1953 106. abstracted, Ophth. Lit. 7:197, 1953. 107. Coppez, M. L.: Pathogenesis of Strabismus: Some Specific Ideas , Bull. Acad. roy. méd. Belgique 18:313-322, 1953. 108. Ellenberg, C.: Home-Made Apparatus for Testing Retinal Correspondence , Am. J. Ophth. 36: 1121-1122, 1953. 109. Harrison, W. J.: An Improved Muscle Tucker , Am. J. Ophth. 36:843-844, 1953. 110. Leydhecker, W.: Divergence Paralysis , Klin. Monatsbl. Augenh. 123:83-86, 1953. 111. Monjé, M.: Near Point of Accommodation and Convergence , Klin. Monatsbl. Augenh. 122:417-422, 1953. 112. Nonnenmacher, H.: Symmetrical and Equal Advancement and Recession Operation of Kunz , Klin. Monatsbl. Augenh. 121:161-168, 1952. 113. Sokolić, P.: Muscle Shortening by Torsion with Underbinding , Klin. Monatsbl. Augenh. 123: 474-476, 1953. 114. Toselli, C.: Paralysis of Divergence Associated with Paresis of an Inferior Oblique , Boll. ocul. 32:401-412, 1953.

Boyes, Truman L.;Perera, Charles A.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050165021

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

Kelly, George F. J.;Kauffman, M. Luther

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050166022

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

Adler, Francis Heed

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050172023

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.

1954 A.M.A. Archives of Ophthalmology

doi: 10.1001/archopht.1954.00920050174024

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract GENERAL NEWS Hardy Memorial Research Fund. —In recognition of the great interest of LeGrand H. Hardy in the study of physiological optics, a fund is being established for furthering research in this subject, to be known as the Hardy Memorial Research Fund. Contributions may be sent to The Hardy Memorial Research Fund, Institute of Ophthalmology, 635 W. 165th St., New York 32. PERSONAL NEWS Appointment of Dr. Fred M. Wilson. —The appointment of Dr. Fred M. Wilson as chairman of the Department of Ophthalmology in the Indiana University School of Medicine was announced today by Dean John D. Van Nuys.The appointment of Dr. Wilson was made by the University trustees upon recommendation of Dr. Robert J. Masters, who is relinquishing the chairmanship he has held for the past eleven years, to devote full time to his private practice. Active in the expansion of the eye clinic and teaching program