1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030702001
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Wilson, Roy;Walker, Alexander M.;Dueker, David K.;Crick, R. Pitts
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030741002pmid: 6979327
Abstract • Factors affecting the progression of visual field loss were examined in 57 patients with bilateral open angle glaucoma. Patients who already had marked visual field loss experienced further field loss at a greatly accelerated rate. Family history of glaucoma, sex, and initial registration intraocular pressure were also important prognostic factors for progressive visual field loss, whereas age and systemic blood pressure were not found to affect rate of visual field loss. Followup data from these patients were drawn from a computer-based clinic record system that may serve as a prototype for the collection of information on the natural history of ophthalmic diseases. References 1. Crick RP: Chronic glaucoma: A preventable cause of blindness . Lancet 1974;1:205-207.Crossref 2. Crick RP: Prevention of blindness from glaucoma using the King's College Hospital computerized problem oriented medical record . Br J Ophthalmol 1975;59:236-248.Crossref 3. Cowan EC, Linton D, Bryars JH: Design and planning of a specialized glaucoma unit . Trans Ophthalmol Soc UK 1974;94:1055-1057. 4. Greenfield R, Kass M, Livingston J: A computerized glaucoma data base . Arch Ophthalmol 1977;95:1365-1367.Crossref 5. Metz HS, Madden EE, Williams VR, et al: Use of a computer in a glaucoma clinic . Arch Ophthalmol 1969;81:155-158.Crossref 6. Stockdill PC, Coulthard WJ, Drance SM: A computer-based method for the storage and retrieval of glaucoma records . Can J Ophthalmol 1974;9:106-112. 7. Gross AJ, Clark VA: Survival Distributions: Reliability Applications in the Biomedical Sciences . New York, John Wiley & Sons Inc, 1975. 8. Cox DR: Regression models and life tables . J R Statist Soc B 1972;34:187-220. 9. Armaly MF: Ocular pressure and visual fields: A ten-year follow-up study . Arch Ophthalmol 1969;81:25-40.Crossref 10. Becker B, Kolker A, Roth D: Glaucoma family study . Am J Ophthalmol 1960;50:557-567. 11. Perkins ES: The Bedford glaucoma survey: I. Long-term follow-up of borderline cases . Br J Ophthalmol 1973;57:179-185.Crossref 12. Wilensky JT, Podos SM, Becker B: Prognostic indicators in ocular hypertension . Arch Ophthalmol 1974;91:200-202.Crossref 13. Wilensky JT, Podos SM: Prognostic parameters in primary open-angle glaucoma , in Anderson DR, Drance SM, Galin MA (eds): Symposium on Glaucoma: New Orleans Academy of Ophthalmology . St Louis, CV Mosby Co, 1975, pp 7-30. 14. Hayreh SS: Pathogenesis of optic nerve damage and visual field defects , in Heilmann K, Richardson KT (eds): Glaucoma: Conceptions of a Disease . Philadelphia, WB Saunders Co, 1978, pp 105-137. 15. Armaly MF: The heritable nature of dexamethasone induced ocular hypertension . Arch Ophthalmol 1966;75:32-35.Crossref 16. Becker B: Intraocular pressure response to topical corticosteroids . Invest Ophthalmol Vis Sci 1965;4:198-205. 17. Becker B, Hahn KA: Topical corticosteroids and heredity in primary open-angle glaucoma . Am J Ophthalmol 1964;57:543-551. 18. Phelps CD, Podos SM: Glaucoma , in Goldberg MF (ed): Genetic and Metabolic Eye Disease . Boston, Little Brown & Co, 1974, pp 237-259. 19. Armaly MF: On the distribution of applanation pressure: I. Statistical features and the effect of age, sex, and family history of glaucoma . Arch Ophthalmol 1965;73:11-18.Crossref 20. Miller SJH, Paterson GD: Studies on glaucoma relatives . Br J Ophthalmol 1962;46:513-522.Crossref 21. Becker B, Ross M: Phenlythiourea taste testing and glaucoma . Arch Ophthalmol 1964;72:323-326.Crossref 22. Kass MA, Kolker AE, Becker B: Prognostic factors in glaucomatous visual field loss . Arch Ophthalmol 1976;94:1274-1276.Crossref 23. Schwartz B: Primary open-angle glaucoma , in Duane T (ed): Clinical Ophthalmology . Hagerstown, Md, Harper & Row Publishers Inc, 1976, vol 3, p 145. 24. Hollows FC, Graham PA: Intraocular pressure, glaucoma, and glaucoma suspects in a defined population . Br J Ophthalmol 1966;50:570-586.Crossref 25. Graham PA: Epidemiology of simple glaucoma and ocular hypertension . Br J Ophthalmol 1972;56:223-229.Crossref 26. Armaly MF, Krueger D, Maundes L: Biostatistical Analysis of the Collaborative Glaucoma Study: Final Report on Contract 1-EY-4-2167 , report PB 80-135502. Washington, DC, National Technical Information Service, US Dept of Commerce, 1977. 27. Drance SM, Morgan RW, Sweeney VP: Shock-induced optic neuropathy: A cause of nonprogressive glaucoma . N Engl J Med 1973;288:392-395.Crossref 28. Harrington DO: The pathogenesis of the glaucoma field . Am J Ophthalmol 1959;47:177-185. 29. Lobstein A, Herr FS: L'ophtalmodynamometre dans le glaucome . Ann Oculist 1966;199:38-69. 30. Dobree JH: Calibre changes in retinal vessels occurring in raised ocular tension: Circulatory compensation in chronic glaucoma . Br J Ophthalmol 1956;40:1-13.Crossref
Korey, Michael S.;Hodapp, Elizabeth;Kass, Michael A.;Goldberg, Ivan;Gordon, Mae;Becker, Bernard
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030746003pmid: 7044351
Abstract • Thirty-two ocular hypertensive subjects were treated for 90 days with either 0.5% timolol maleate or 2% epinephrine hydrochloride twice daily to one eye and both drugs to the fellow eye. The ocular hypotensive effects of timolol and epinephrine were partially additive throughout the course of this study. On the 91st day, eyes treated with epinephrine had a 25.8% mean reduction of intraocular pressure from baseline, whereas their fellow eyes treated with epinephrine and timolol had a 33.9% reduction. Eyes treated with timolol had a 27.2% mean reduction of IOP, whereas fellow eyes treated with timolol and epinephrine had a 29% reduction. These results suggest that the majority of patients being treated with either drug are unlikely to have a substantial long-term reduction in IOP when the other drug is added to their therapeutic regimen. References 1. Goldmann H: L'origine de l'hypertension oculaire dans le glaucome primitif . Ann Oculist 1951;184:1086-1105. 2. Weekers R, Prijot E, Gustin J: Recent advances and future prospects in the medical treatment of ocular hypertension . Br J Ophthalmol 1952;38:742-746.Crossref 3. Becker B, Ley AP: Epinephrine and acetazolamide in the therapy of the chronic glaucomas . Am J Ophthalmol 1958;45:639-643. 4. Garner LC, Johnstone WW, Ballintine EJ, et al: Effect of 2% levo-rotary epinephrine on the intraocular pressure of the glaucomatous eye . Arch Ophthalmol 1959;62:230-238.Crossref 5. Sears ML: Catecholamines in relation to the eye , in section 7, Endocrinology: Adrenal Glands, in Geiger SR (ed): Handbook of Physiology-Endocrinology . Washington, DC, American Physiological Society, 1975, vol 6, pp 553-590. 6. Richards JSF, Drance SM: The effect of 2% epinephrine on aqueous dynamics in the human eye . Can J Ophthalmol 1976;2:259-265. 7. Becker B, Pettit TH, Gay AJ: Topical epinephrine therapy of open-angle glaucoma . Arch Ophthalmol 1961;66:219-225.Crossref 8. Katz IM, Hubbard WA, Getson AJ, et al: Intraocular pressure decrease in normal volunteers following timolol ophthalmic solution . Invest Ophthalmol Vis Sci 1976;15:489-492. 9. Zimmerman TJ, Kaufman HE: Timolol, a β-adrenergic blocking agent for the treatment of glaucoma . Arch Ophthalmol 1977;95:601-604.Crossref 10. Zimmerman TJ, Kaufman HE: Timolol: Dose response and duration of action . Arch Ophthalmol 1977;95:605-607. 11. Zimmerman TJ, Kass MA, Yablonski ME, et al: Timolol maleate: efficacy and safety . Arch Ophthalmol 1979;97:656-658. 12. Nielsen NV: Timolol: Hypotensive effect, used alone or in combination for treatment of increased intraocular pressure . Acta Ophthalmol 1978;56:504-509. 13. Obstbaum SA, Galin MA, Katz IM: Timolol: Effect on intraocular pressure in chronic open-angle glaucoma . Ann Ophthalmol 1978;10:1347-1351. 14. Keates EU: Evaluation of timolol maleate combination therapy in chronic open angle glaucoma . Am J Ophthalmol 1979;88:565-571. 15. Thomas JV, Epstein DL: Timolol and epinephrine in primary open-angle glaucoma: Transient additive effect . Arch Ophthalmol 1981;99:91-95. 16. Boger WP III, Puliafito CA, Steinert RF, et al: Long-term experience with timolol ophthalmic solution in patients with open angle glaucoma . Ophthalmology 1978;85:259-267. 17. Goldberg I, Ashburn FS, Palmberg PF, et al: Timolol and epinephrine: A clinical study of ocular interactions . Arch Ophthalmol 1980;98:484-486. 18. Higgins RG, Brubaker RF: Acute effect of epinephrine on aqueous humor formation in the timolol-treated normal eye as measured by fluorophotometry . Invest Ophthalmol Vis Sci 1980;19:420-423. 19. Helwig JT, Council KA: Statistical Analysis System Users Guide . Cary, NC, SAS Institute Inc, 1979. 20. Yablonski ME, Zimmerman TJ, Waltman SR, et al: A fluorophotometric study of topical timolol on aqueous humor dynamics . Exp Eye Res 1978;27:135-142. 21. Radius R, Diamond GR, Pollack IP, et al: Timolol: A new drug for the management of chronic simple glaucoma . Arch Ophthalmol 1978;96:1003-1008. 22. Neufeld AH, Zawistowski KA, Page ED, et al: Influences on the density of the β-adrenergic receptors in cornea and iris ciliary body of the rabbit . Invest Ophthalmol Vis Sci 1978;17:1069-1075. 23. Neufeld AH: Experimental studies on the mechanism of action of timolol . Surv Ophthalmol 1979;23:363-370.Crossref 24. Townsend DJ, Brubaker RF: Acute effect of epinephrine on aqueous humor formation in the normal eye as measured by fluorophotometry . Invest Ophthalmol Vis Sci 1980;19:420-423. 25. Lee PF: The influence of epinephrine and phenylephrine on intraocular pressure . Arch Ophthalmol 1958;60:863-867.Crossref 26. Leydhecker W: Sympathikomimetika und sympathikolytika in der glaucomtherapie . Klin Monatsbl Augenheilkd 1977;171:538-546.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030749004
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 In a recent article by Rudy et al (Arch Ophthalmol 1981;99:2030-2033), an error occurred in the reported dose fed to the mice. The dose of allopurinol fed was 0.05 mg per mouse per day (or 2.5 mg/kg/day).
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030750005pmid: 7082204
Abstract • Twenty-seven children and infants underwent surgery for bilateral infantile cataracts. In each infant, the lens in one eye was removed by discission and aspiration, and the other lens was removed by lensectomy and anterior vitrectomy. Ten of 27 eyes undergoing lensectomy and vitrectomy developed aphakic cystoid macular edema; in only one eye that underwent discission and aspiration did macular edema develop. Six of the eyes of the first group developed persistent cystoid macular edema, of which four seem to be visually important. Further long-term studies of the prevalence and functional importance of cystoid macular edema after lensectomy and anterior vitrectomy in children are needed. We do not presently advocate this technique except in the treatment of complicated infantile cataracts. References 1. Tolentino FI, Schepens CL: Edema of posterior pole after cataract extraction: A biomicroscopic study . Arch Ophthalmol 1965;74:781-786.Crossref 2. Gehring JR: Macular edema following cataract extraction . Arch Ophthalmol 1968;80:626-631.Crossref 3. Gass JD, Norton EWD: Follow-up study of cystoid macular edema following cataract extraction . Trans Am Acad Ophthalmol Otolaryngol 1969;73:665-669. 4. Jacobson DR, Dellaporta A: Natural history of cystoid macula edema after cataract extraction . Am J Ophthalmol 1974;77:445-447. 5. Hitchings RA, Chisholm IH, Bird AC: Aphakic macular edema: Incidence and pathogenesis . Invest Ophthalmol Vis Sci 1975;14:68-72. 6. Poer DV, Helveston EN, Ellis FD: Aphakic cystoid macular edema in children . Arch Ophthalmol 1981;99:249-252.Crossref 7. Peyman GA, Sanders DR, Rose M, et al: Vitrophage in management of congenital cataracts . Albrecht Von Graefes Arch Klin Exp Ophthalmol 1977;202:305-308.Crossref 8. Offret H, Saraux H, Limon S, et al: Vitréophagie par la pars-plana de deux cas de persistance du vitré primitif . Arch Ophthalmol 1977;37:473-478. 9. Malbran E, Dodds R, Hulsbus R: The influence of new surgical procedures on retinal pathology in aphakia after congenital cataract surgery . Mod Probl Ophthalmol 1977;18:511-517. 10. Benson WE, Blankenship GW, Machemer R: Pars plana lens removal with vitrectomy . Am J Ophthalmol 1977:84:150-152. 11. Girard LJ: Lensectomy through the pars plana by ultrasonic fragmentation . Ophthalmology 1979;86:1985-1989.Crossref 12. Odom JV, Hoyt CS, Marg E: Effect of natural deprivation and unilateral eye patching on visual acuity of infants and children . Arch Ophthalmol 1981;99:1412-1416.Crossref 13. Beller R, Hoyt CS, Marg E, Odom JV: Good visual function in monocular congenital cataracts with neonatal surgery . Am J Ophthalmol 1981;91:559. 14. Trese MT, Foos RY: Infantile cystoid maculopathy . Br J Ophthalmol 1980;64:206-209.Crossref 15. Hiles DA, Chotiner B: Vitreous loss following infantile cataract surgery . Int Ophthalmol Clin 1977;17:167-171. 16. Irvine AR: Review cystoid maculopathy . Surv Ophthalmol 1976;21:1-17.Crossref 17. Maumenee AE: Clinical entities in uveitis: An approach to the study of intraocular inflammation: XXIV. Edward Jackson Memorial Lecture . Am J Ophthalmol 1970;69:1-27. 18. Ryan SI: Cystoid maculopathy in phakic retinal detachment procedures . Am J Ophthalmol 1973;76:519-521. 19. Michels RG, Maumenee AE: Cystoid macular edema associated with topically applied epinephrine in aphakic eyes . Am J Ophthalmol 1975;80:379-385. 20. Brownstein S, Orton R, Jackson B: Cystoid macular edema with equatorial choroidal melanoma . Arch Ophthalmol 1978;96:2105-2107.Crossref 21. Fishman GA, Goldberg MF, Troutman JC: Dominantly inherited cystoid macular edema . Ann Ophthalmol 1979;11:21-27. 22. Aaberg TM: Pars plana vitrectomy for persistent aphakic cystoid macular edema secondary to vitreous incarceration in the cataract wound , in McPherson A (ed): New and Controversial Aspects of Vitreoretinal Surgery . St Louis, CV Mosby Co, 1977, pp, 230-239. 23. Federman JL, Annesley WH, Sarkin LK, et al: Vitrectomy and cystoid macular edema . Ophthalmology 1980;87:622-627.Crossref 24. Kramer SG: Cystoid macular edema after aphakic penetrating keratoplasty. Ophthalmology, to be published. 25. Gass JDM, Norton EWD: Cystoid macular edema and papilledema following cataract extraction: A fluorescein fundoscopic and angiographic study . Arch Ophthalmol 1966;76:646-661.Crossref 26. Martin NF, Green WR, Martin LW: Retinal phlebitis in the Irvine-Gass syndrome . Am J Ophthalmol 1977;83:377-386. 27. Tso MOM, Shih CY: Experimental macular edema after lens extraction . Invest Ophthalmol Vis Sci 1977;16:381-392.
Felder, Kenneth S.;Brockhurst, Robert J.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030754006pmid: 6177305
Abstract • Neovascular fundus abnormalities are an unusual complication of peripheral uveitis. Peripheral retinal neovascularization was seen in 11 patients, six of whom had retinal angioma-like lesions. Most of the patients had loss of vision caused by vitreous hemorrhage. In four additional patients with peripheral uveitis, neovascularization developed either at the disc or elsewhere in the posterior pole. References 1. Schepens CL: L'inflammation de la region de l'ora serrata et ses sesqueles . Bull Soc Ophtalmol Fr 1950;63:113-124. 2. Schlaegel TF: Ocular Toxoplasmosis and Pars Planitis . New York, Grune & Stratton Inc, 1978, pp 263-360. 3. Brockhurst RJ, Schepens CL, Okamura ID: Uveitis: II. Peripheral uveitis: Clinical description, complications and differential diagnosis . Am J Ophthalmol 1960;49:1257-1266. 4. Brockhurst RJ, Schepens CL, Okamura ID: Uveitis: III. Peripheral uveitis: Pathogenesis, etiology and treatment . Am J Ophthalmol 1961;51:19-26. 5. Shorb SR, Irvine AR, Kimura SJ: Optic disc neovascularization associated with chronic uveitis . Am J Ophthalmol 1976;82:175-178. 6. Cardosa RD, Brockhurst RJ: Perforating diathermy coagulation for retinal angiomas . Arch Ophthalmol 1976;94:1702-1715.Crossref 7. Pruett RC, Brockhurst RJ, Letts N: Fluorescein angiography of peripheral uveitis . Am J Ophthalmol 1974;77:448-453. 8. Auerbach R, Kubai L, Sidky Y: Angiogenesis induction by tumors embryonic tissues and lymphocytes . Cancer Res 1976;36:3435-3440. 9. Doxanas MT, Kelley JS, Prout TE: Sarcoidosis with neovascularization of the optic nerve head . Am J Ophthalmol 1980;90:347-351. 10. Aaberg TM, Cesarz TJ, Flickinger RR: Treatment of peripheral uveo-retinitis by cryotherapy . Am J Ophthalmol 1973;75:685-688.
Cogan, David G.;Chu, Fred C.;Reingold, Douglas B.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030759007pmid: 7082205
Abstract • Ocular signs of cerebellar disease have been increasingly appreciated with the advent of means for quantitative recording of eye movements. The graphs in this article illustrate ocular flutter, dysmetria, abnormal (nonsmooth) pursuit, instability of fixation, faulty vestibular suppression, impaired optokinetic response, end-position nystagmus, and rebound nystagmus. The signs may be categorized as follows: (1) proprioceptive abnormalities manifest by flutter, dysmetria, and instability of gaze and (2) defects of vision-dependent functions manifest by abnormalities of pursuit, vestibular suppression, optokinetic response, and nystagmus. References 1. Robinson DA: How the oculomotor system repairs itself . Invest Ophthalmol Vis Sci 1975; 14:413-415. 2. Gauthier GM: Bio-engineering Studies of Cerebellar Influences on Oculomotor Control, thesis. University of Illinois, Chicago, 1970. 3. Holmes G: Clinical symptoms of cerebellar disease and their interpretation . Lancet 1922; 2:59-65. 4. Whitteridge D: Central control of eye movements , in Neurophysiology, vol 2, in Handbook of Physiology . Baltimore, Waverly Press Inc, 1960, pp 1089-1109. 5. Ocular deviations , in Neuro-ophthalmology, vol 12, in Duke-Elder S, Scott GI (eds): System of Ophthalmology . St Louis, CV Mosby Co, 1966, pp 848-849. 6. Robinson DA: A method of measuring eye movements using a scleral search coil in a magnetic field . IEEE Trans Biomed Eng 1963;10:137-145. 7. Reingold DB, Chu FC, Cogan DG, et al: A computerized testing facility for clinical study of versional eye movement control , in Greenfield RH (ed): Computers in Ophthalmology . Silver Spring, Md, IEEE Computer Society, 1979, pp 220-222. 8. Goldberg RT, Jampel RS: Flutterlike oscillations of the eyes in cerebellar disease . Am J Ophthalmol 1963;55:1229-1233. 9. Cogan DG: Ocular dysmetria; flutter-like oscillations of the eyes, and opsoclonus . Arch Ophthalmol 1954;51:318-335.Crossref 10. Higgins DC, Daroff RN: Overshoot and oscillation in ocular dysmetria . Arch Ophthalmol 1966;75:742-745.Crossref 11. Solingen LD, Baloh RW, Myers L, et al: Subclinical eye movement disorders in patients with multiple sclerosis . Neurology 1977;27:614-619.Crossref 12. Monday LA, Lemieux B, St Vincent H, et al: Clinical and electronystagmographic findings in Friedreich's ataxia . Can J Neurol Sci 1978; 5:71-73. 13. Kirkham TH, Guitton D, Katsarkas A, et al: Oculomotor abnormalities in Friedreich's ataxia . Can J Neurol Sci 1979;6:167-172. 14. Jung R, Kornhuber HH: Results of electronystagmography in man: The value of optokinetic, vestibular, and spontaneous nystagmus for neurologic diagnosis and research , in Bender MB (ed): The Oculomotor System . New York, Harper & Row Publishers Inc, 1964, p 440. 15. Dell'Osso LF, Troost BT, Daroff RB: Macro square wave jerks . Neurology 1975;25:975-979.Crossref 16. Daroff RB, Hoyt WF: Supranuclear disorders of the ocular control systems in man , in Bach-y-Rita P, Collins CC, Hyde JE (eds): The Control of Eye Movements . New York, Academic Press Inc, 1971, pp 175-235. 17. Selhorst JB, Stark L, Ochs AL, et al: Disorders in cerebellar ocular motor control: I. Saccadic overshoot dysmetria: An oculographic control system and clinico-anatomical analysis . Brain 1976;99:497-508.Crossref 18. Dale RT, Kirby AW, Jampel RS: Square wave jerks in Friedreich's ataxia . Am J Ophthalmol 1978;85:400-406. 19. Takemori S, Cohen B: Loss of visual suppression of vestibular nystagmus after flocculus lesions . Brain Res 1974;72:213-224.Crossref 20. Hassul M, Daniels PD, Kimm J: Effects of bilateral flocculectomy on the vestibulo-ocular reflex in the chinchilla . Brain Res 1976;118:339-343.Crossref 21. Takemori S: Visual suppression test . Ann Otol Rhinol Laryngol 1977;86:80-85. 22. Zee DS: Suppression of vestibular nystagmus . Ann Neurol 1977;1:207.Crossref 23. Baloh RW, Konrad HR, Honrubia V: Vestibulo-ocular function in patients with cerebellar atrophy . Neurology 1975;25:160-168.Crossref 24. Zee DS, Yee RD, Cogan DG, et al: Ocular motor abnormalities in hereditary cerebellar ataxia . Brain 1976;99:207-234.Crossref 25. Baloh RW, Jenkins HA, Honrubia V, et al: Visual-vestibular interaction and cerebellar atrophy . Neurology 1979;29:116-119.Crossref 26. Leech J, Gresty M, Hess K, et al: Gaze failure, drifting eye movements and centripetal nystagmus in cerebellar disease . Br J Ophthalmol 1977;61:774-781.Crossref 27. Hood JD, Kayan A, Leech J: Rebound nystagmus . Brain 1973;96:507-526.Crossref 28. Westheimer G, Blair SM: Functional organization of primate oculomotor system revealed by cerebellectomy . Exp Brain Res 1974;21:463-472.Crossref 29. Daroff RB, Dell'Osso LF, Abel LA: Pursuit defect nystagmus . Ann Neurol 1979;6:458-459.Crossref 30. Mauritz KH, Dichgans J, Hufschmidt A: Quantitative analysis of stance in late cortical cerebellar atrophy of the anterior lobe and other forms of cerebellar ataxia . Brain 1979;102:461-482.Crossref 31. Ron S, Robinson DA: Eye movements evoked by cerebellar stimulation in the alert monkey . J Neurophysiol 1973;36:1004-1022. 32. Raybourn MS, Keller EL: Colliculoreticular organization in primate oculomotor system . J Neurophysiol 1977;40:861-878. 33. Richie L: Effects of cerebellar lesions on saccadic eye movements . J Neurophysiol 1976; 39:1246-1256. 34. Fuchs AF, Kornhuber HH: Extraocular muscle afferents to the cerebellum of the cat . J Physiol 1969;200:713-722. 35. Baker R, Precht W, Llinas R: Mossy and climbing fiber projections of extraocular muscle afferents to the cerebellum . Brain Res 1972; 38:440-445.Crossref 36. Berthoz A, Llinas R: Afferent neck projection to the cat cerebellar cortex . Exp Brain Res 1974;20:385-401.Crossref 37. Aschoff JC, Cohen B: Changes in saccadic eye movements produced by cerebellar cortical lesions . Exp Neurol 1971;32:123-133.Crossref 38. Llinas R, Wolfe JW: Functional linkage between the electrical activity in the vermal cerebellar cortex and saccadic eye movements . Exp Brain Res 1977;29:1-14.Crossref 39. Burde RM, Stroud MH, Roper-Hall G, et al: Ocular motor dysfunction in total hemicerebellectomized monkeys . Br J Ophthalmol 1975; 59:560-565.Crossref 40. Yamazaki A, Zee DS: Rebound nystagmus: EOG analysis of a case with floccular tumour . Br J Ophthalmol 1979;63;782-786.Crossref 41. Lisberger SG, Fuchs AF: Response of flocculus Purkinje cells to adequate vestibular stimulation in the alert monkey: Fixation vs compensatory eye movements . Brain Res 1974;69:347-353.Crossref 42. Miles FA, Fuller JH: Visual tracking and the primate flocculus . Science 1975;189:1000-1002.Crossref 43. Dow RS: Effect of lesions in the vestibular part of the cerebellum in primates . J Neurol Neurosurg Psychiatry 1938;47:500-520. 44. Carrea RME, Mettler FA: Physiologic consequences following extensive removals of the cerebellar cortex and deep cerebellar nuclei and effect of secondary cerebral ablations in the primate . J Comp Neurol 1947;87:169-288.Crossref 45. Maekawa K, Natsui T: Climbing fiber activation of Purkinje cells in rabbit's flocculus during light stimulation of the retina . Brain Res 1973;59:417-420.Crossref 46. Lisberger SG, Fuchs AF: Role of primate flocculus during rapid behavioral modification of vestibulo-ocular reflex: I. Purkinje cell activity during visually guided horizontal smooth-pursuit eye movements and passive head rotation . J Neurophysiol 1978;41:733-763. 47. Zee DS, Namazaki A, Butler PH, et al: Effects of ablation of flocculus and paraflocculus on eye movements in primates . J Neurophysiol 1981;46:878-899. 48. Gonshor A, Jones GM: Extreme vestibuloocular adaptation induced by prolonged optical reversion of vision . J Physiol 1976;256:381-414. 49. Robinson DA: The effect of cerebellectomy on the cat's vestibulo-ocular integrator . Brain Res 1974;71:195-207.Crossref
Miller, Neil R.;Morris, Jacqueline E.;Maquire, Maureen
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030765008pmid: 7082206
Abstract • Forty-four patients with diplopia caused by myasthenia gravis, ocular myopathies, and ocular motor nerve palsies underwent complete orthoptic evaluations before and after intramuscular injection of neostigmine (Prostigmin) methylsulfate. A test score combining the results of binocular and uniocular measurements was developed that allowed correct classification of 70% (31) of patients studied. References 1. Drachman DB: Myasthenia gravis . N Engl J Med 1978;298:136-142.Crossref 2. Osserman KE: Ocular myasthenia gravis . Invest Ophthalmol Vis Sci 1967;6:277-279. 3. Miller NR: Myasthenia gravis: Systemic and ocular considerations . Trans Am Acad Ophthalmol Otolaryngol 1979;86:2165-2174. 4. Fambrough DM, Drachman DB, Satyamurti S: Neuromuscular junction in myasthenia gravis: Decreased acetylcholine receptors . Science 1973;182:293-295.Crossref 5. Drachman DB, Kao L, Pestronk A, et al: Myasthenia gravis as a receptor disorder . Ann NY Acad Sci 1976;274:226-234.Crossref 6. Pestronk A, Drachman DB, Josifek LF: Measurement of junctional ACh receptors in myasthenia gravis: Diagnostic value and clinical correlates . Neurology 1981;31:83.Crossref
Blair, Norman P.;Feke, Gilbert T.;Morales-Stoppello, Julian;Riva, Charles E.;Goger, Douglas G.;Collas, Gail;McMeel, J. Wallace
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030768009pmid: 7044352
Abstract • Retinal mean circulation time (MCT) and vascular sizes were measured in 21 normal individuals and 32 individuals with diabetes, and segmental blood flow (SBF) was calculated. The MCT was similar in the normal individuals (4.0 ± 1.1 s) and the individuals with diabetes (4.2 ± 1.9 s) when seven individuals with diabetes with prolonged but not quantifiable MCT were excluded. Including them by nonparametric statistics revealed that MCT was significantly longer in individuals with diabetes with proliferative retinopathy than in normal individuals or in individuals with diabetes with nonproliferative retinopathy. The prolonged MCT correlated significantly with advanced retinopathy as judged by leakage, neovascularization, and the need for photocoagulation therapy. Reduced SBF may account for the prolonged MCT, since the increase in vascular sizes observed failed to do so. However, pathologic vascular changes may alter the relation between SBF and MCT. Irrespective of implications about SBF, prolonged MCT, which indicates marked circulatory disturbance, represents an important new observation in diabetic retinopathy. References 1. Hickam JB, Frayser R: A photographic method for measuring the mean retinal circulation time using fluorescein . Invest Ophthalmol Vis Sci 1965;4:876-884. 2. Bulpitt CJ, Dollery CT: Estimation of retinal blood flow by measurement of the mean circulation time . Cardiovasc Res 1971;5:406-412.Crossref 3. Kohner E: Retinal blood flow in diabetes mellitus , in Lynn JR, Snyder WB, Vaiser A (eds): Diabetic Retinopathy . New York, Grune & Stratton Inc, 1974, pp 71-79. 4. Kohner EM, Hamilton AM, Saunders SJ, et al: The retinal blood flow in diabetes . Diabetologia 1975;11:27-33.Crossref 5. Kohner EM: The problems of retinal blood flow in diabetes . Diabetes 1976;25( (suppl 2) ):839-844.Crossref 6. Soeldner JS, Christacopoulos PD, Gleason RE: Mean retinal circulation time as determined by fluorescein angiography in normal, prediabetic, and chemical-diabetic subjects . Diabetes 1976; 25( (suppl 2) ):903-908. 7. Van Heuven WAJ, Malik AB, Schaffer CA, et al: Retinal blood flow derived from dye dilution curves: Televised fluorescein angiography . Arch Ophthalmol 1977;95:297-301.Crossref 8. Eberli B, Riva CE, Feke GT: Mean circulation time of fluorescein in retinal vascular segments . Arch Ophthalmol 1979;97:145-148.Crossref 9. Cunha-Vaz JG, Lima JJP: Studies on retinal blood flow: I. Estimation of human retinal blood flow by slit-lamp fluorophotometry . Arch Ophthalmol 1978;96:893-897.Crossref 10. Cunha-Vaz JG, Fonesca JR, de Abreu JRF, et al: Studies on retinal blood flow: II. Diabetic retinopathy . Arch Ophthalmol 1978;96:809-811.Crossref 11. Riva CE: Retinal blood flow . Arch Ophthalmol 1979;97:173-174.Crossref 12. Cunha-Vaz JG: Reply to Riva CE: Retinal blood flow . Arch Ophthalmol 1979;97:174-175.Crossref 13. Van Heuven WAJ: Comment on Riva CE: Retinal blood flow and Cunha-Vaz JG: Reply . Arch Ophthalmol 1979;97:175.Crossref 14. Kohner EM, Shilling JS, Hamilton AM: The role of avascular retina in new vessel formation . Metab Ophthalmol 1976;1:15-23. 15. Merin S, Ber I, Ivry M: Retinal ischemia (capillary non-perfusion) and retinal neovascularization in patients with diabetic retinopathy . Ophthalmologica 1978;177:140-145.Crossref 16. Cogan DG, Toussaint D, Kuwabara T: Retinal vascular patterns: IV. Diabetic retinopathy . Arch Ophthalmol 1961:66:366-378.Crossref 17. Goldberg MF: The role of ischemia in the production of vascular retinopathies , in Lynn JR, Snyder WB, Vaiser A (eds): Diabetic Retinopathy . New York, Grune & Stratton Inc, 1974, pp 47-63. 18. Bresnick GH, De Venecia G, Myers FL, et al: Retinal ischemia in diabetic retinopathy . Arch Ophthalmol 1975;93:1300-1310.Crossref 19. Riva CE, Feke GT, Ben-Sira I: Fluorescein dye-dilution technique and retinal circulation . Am J Physiol 1978;234:H315-H322. 20. Lee PF, McMeel JW, Schepens CL, et al: A new classification of diabetic retinopathy . Am J Ophthalmol 1966;62:207-219. 21. Skovborg F, Nielsen AV, Lauritzen E, et al: Diameters of the retinal vessels in diabetic and normal subjects . Diabetes 1969;18:292-298. 22. McMillan DE, Utterback NG, La Puma J: Reduced erythrocyte deformability in diabetes . Diabetes 1978;27:895-901.Crossref 23. Little HL: The role of abnormal hemorrheodynamics in the pathogenesis of diabetic retinopathy . Trans Am Ophthalmol Soc 1976;74:573-636. 24. Colwell JA, Halushka PV, Sarji K, et al: Altered platelet function in diabetes mellitus . Diabetes 1976;25( (suppl 2) ):826-831. 25. McMillan DE: Disturbance of serum viscosity in diabetes mellitus . J Clin Invest 1974; 53:1071-1079.Crossref 26. Almér L-O, Pandolfi M: Fibrinolysis and diabetic retinopathy . Diabetes 1976;25( (suppl 2) ):807-810. 27. Zierler KL: Circulation times and the theory of indicator-dilution methods for determining blood flow and volume , in Hamilton WF (ed): Handbook of Physiology . Washington, DC, American Physiological Society, 1962, vol 1, §2, pp 585-615. 28. Cunha-Vaz J, de Abreu JRF, Campos AJ, et al: Early breakdown of the blood-retinal barrier in diabetes . Br J Ophthalmol 1975;59:649-656.Crossref 29. Ishibashi T, Tanaka K, Taniguchi Y: Disruption of blood-retinal barrier in experimental diabetic rats: An electron microscopic study . Exp Eye Res 1980;30:401-410.Crossref 30. Goresky CA, Ziegler WH, Bach GG: Capillary exchange modeling: Barrier-limited and flow-limited distribution . Circ Res 1970;27:739-764.Crossref 31. Törnquist P: Capillary permeability in cat choroid, studied with the single injection technique (II) . Acta Physiol Scand 1979;106:425-430.Crossref 32. Henkind P, Wise GN: Retinal neovascularization, collaterals, and vascular shunts . Br J Ophthalmol 1974;58:413-422.Crossref
Gass, J. Donald;Oyakawa, Ray T.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030773010pmid: 7082207
Abstract • Twenty-seven healthy adult patients had visual loss in one or both eyes because of exudation from juxtafoveolar retinal capillary telangiectasis of uncertain cause. These patients were subdivided as follows: group 1, men with uniocular involvement, intraretinal lipid exudation, and telangiectasis largely confined to the temporal half of the juxtafoveolar area; group 2, mostly men with symmetric areas of telangiectasis affecting the temporal half of the juxtafoveolar areas and minimal intraretinal exudation; group 3, both sexes with symmetric involvement of all of the parafoveolar capillary bed and minimal exudation; and group 4, one case of telangiectasis with occlusive perifoveolar capillary changes and familial optic disc pallor. The visual acuity prognosis in groups 1 through 3 is relatively good. Photocoagulation may be of some value in the treatment of patients in group 1. References 1. Gass JDM: A fluorescein angiographic study of macular dysfunction secondary to retinal vascular disease: V. Retinal telangiectasis . Arch Ophthalmol 1968;80:592-605.Crossref 2. Gass JDM: Macular distinction caused by retinal vascular disease , in Stereoscopic Atlas of Macular Diseases , ed 2. St Louis, CV Mosby Co, 1977, pp 234-292. 3. Gass JDM: Photocoagulation of macular lesions . Trans Am Acad Ophthalmol Otolaryngol 1971;75:580-608. 4. Gass JDM: Retinal telangiectasis , in Differential Diagnosis of Intraocular Tumors: A Stereoscopic Presentation . St Louis, CV Mosby Co, 1974, pp 248-310. 5. Gass JDM: Treatment of retinal vascular anomalies . Trans Am Acad Ophthalmol Otolaryngol 1977;83:432-442. 6. Gass JDM: Macular dysfunction caused by retinal vascular diseases , in Stereoscopic Atlas of Macular Diseases , ed 2. St Louis, CV Mosby Co, 1977, pp 262-271. 7. Chopdar A: Retinal telangiectasis in adults: Fluorescein angiographic findings and treatment by argon laser . Br J Ophthalmol 1978;63:243-250.Crossref 8. Yannuzzi LA, Gitter KA, Schatz H: The Macula: A Comprehensive Text and Atlas . Baltimore, Williams & Wilkins Co, 1979, pp 118-126. 9. Reese AB: Telangiectasia of the retina and Coats' disease . Am J Ophthalmol 1956;42:1-8. 10. Leber T: Üeber eine durch VorKommen multipler Milaraneurysmen charakterizierte Form von Retinal degeneration . Arch Ophthalmol 1912;81:14. 11. Gass JDM: Cavernous hemangioma of the retina: A neuro-oculo-cutaneous syndrome . Am J Ophthalmol 1971;71:799-814. 12. Hutton WL, Snyder WF, Fuller D, et al: Focal parafoveal telangiectasis . Arch Ophthalmol 1978;96:1362-1367.Crossref 13. Fishman GA, Trimble S, Rabb MF, et al: Pseudovitelliform macular degeneration . Arch Ophthalmol 1977;95:73-76.Crossref 14. Gass JDM: Macular dysfunction secondary to diseases of the pigment epithelium , in Stereoscopic Atlas of Macular Diseases , ed 2. St Louis, CV Mosby Co, 1977, pp 170-175. 15. Gass JDM: A clinicopathologic study of a peculiar foveomacular dystrophy . Trans Am Ophthalmol Soc 1974;72:139-156. 16. Ehlers N, Jensen VA: Hereditary central retinal angiopathy . Acta Ophthalmol 1973;51:171-178.Crossref 17. Gass JDM: Macular dysfunction caused by retinal vascular diseases , in Stereoscopic Atlas of Macular Diseases , ed 2. St Louis, CV Mosby Co, 1977, p 285.
Mark, David B.;McCulley, James B.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030785011pmid: 7082208
Abstract • A distinctive keratitis occurs commonly in Reiter's syndrome. In three patients with Reiter's keratitis, two demonstrated the typical features of prodromal conjunctivitis, subepithelial and anterior stromal infiltrates, ragged epithelial erosions, and spontaneous resolution. A third case of rare, severe keratitis in addition had an associated finding of disciform keratitis. To our knowledge, this last finding has not previously been reported. Chlamydia has been implicated as an etiologic agent in Reiter's syndrome. Giemsa's stain of corneal epithelial cells in one of our patients disclosed intracytoplasmic inclusions that resembled those seen in Chlamydia-caused conjunctivitis. The patient also exhibited a rising serum titer to Chlamydia antigen. References 1. Reiter H: Ueber eine bisher unerkannte Spirochäteninfektion . Dtsch Med Wochenschr 1916;42:1535-1536.Crossref 2. Ostler HB, Dawson C, Schachter J, et al: Reiter's syndrome . Am J Ophthalmol 1970;71:986-991. 3. Csonka GW: Clinical aspects of Reiter's syndrome . Ann Rheum Dis , (suppl 1) , 1979, pp 4-7. 4. Mills RP, Kalina RE: Reiter's keratitis . Arch Ophthalmol 1972;87:447-449.Crossref 5. Csonka GW: Long-term follow up and prognosis of Reiter's syndrome . Ann Rheum Dis , (suppl 1) , 1979, pp 24-28. 6. Dunlop EMC, Freedman A, Garland JA, et al: Infection by Bedsoniae and the possibility of spurious isolation: II. Genital infection, disease of the eye, Reiter's disease . Am J Ophthalmol 1967;63:1073-1081. 7. Dawson CR, Schachter J, Ostler HB, et al: Inclusion conjunctivitis and Reiter's syndrome in a married couple: Chlamydia infections in a series of both diseases . Arch Ophthalmol 1970;83:300-306.Crossref 8. Schachter J, Barnes MG, Jones JP, et al: Isolation of Bedsoniae from the joints of patients with Reiter's syndrome . Proc Soc Exp Biol Med 1966;122:283-285.Crossref 9. Ostler H, Schachter J, Dawson CR: Ocular infection of rabbits with a Bedsonia isolated from a patient with Reiter's syndrome . Invest Ophthalmol Vis Sci 1970;9:256-262. 10. Smith DE, James P, Schachter J, et al: Experimental bedsonial arthritis . Arthritis Rheum 1973;16:21-29.Crossref 11. Amor B, Kahan A, Orfila J, et al: Immunological evidence of chlamydial infection in Reiter's syndrome . Ann Rheum Dis , (suppl 1) , 1979, pp 116-118. 12. Noer HR: An 'experimental' epidemic of Reiter's syndrome . JAMA 1966;198:693-698.Crossref 13. Warren CPW: Arthritis associated with Salmonella infections . Ann Rheum Dis 1970;29:483-487.Crossref 14. Solem JH, Lasen J: Reiter's disease following Yersinia enterocolitica infection . Scand J Infect Dis 1971;3:83-85. 15. Ford DK: Non-gonococcal urethritis and Reiter's syndrome . Can Med Assoc J 1968;99:900-910. 16. Wright V: Arthritis associated with veneral disease: A comparative study of gonococcal arthritis and Reiter's syndrome . Ann Rheum Dis 1963;22:77-90.Crossref 17. Thaubaut A, Laverdant C, Bertein J, et al: Contributions to the study of adenovirus infections: Adenoviruses and the Fiessinger-Leroy-Reiter syndrome . Rev Immunol 1962;26:335-343. 18. Calin A: Management of Reiter's syndrome . Ann Rheum Dis , (suppl 1) , 1979, pp 96-97. 19. Ford DK: Antibiotic treatment in Reiter's syndrome . Ann Rheum Dis , (suppl 1) , 1979, pp 98-99.
Sommer, Alfred;Muhilal, ;Tarwotjo, Ignatius
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030789012pmid: 6805451
Abstract • In a controlled clinical trial of massive-dose vitamin A therapy for xerophthalmia, holo-retinol-binding protein (holo-RBP) response was related to baseline protein status. Corneal healing was more commonly delayed or transient in children with protein-energy malnutrition (PEM), despite the vast majority achieving holo-RBP levels incompatible with severe corneal destruction. Correction of PEM is essential to ensuring a sustained clinical cure, and repeated massive vitamin A therapy is advisable until that occurs. References 1. Sommer A: Nutritional Blindness: Xerophthalmia and Keratomalacia. Oxford, England, Oxford University Press, to be published. 2. Sommer A, Muhilal, Tarwotjo I, et al: Oral versus intramuscular vitamin A in the treatment of xerophthalmia . Lancet 1980;1:557-559.Crossref 3. Sommer A: Vitamin A, xerophthalmia and diarrhea . Lancet 1980;1:1411-1412. 4. Sommer A, Emran N, Tjakrasudjatma S: Clinical characteristics of vitamin A responsive and nonresponsive Bitot's spots . Am J Ophthalmol 1980;90:160-171. 5. Sommer A: The xerophthalmic cornea , in Trevor-Roper P (ed): The Cornea in Health and Disease . London, Academic Press Inc and the Royal Society of Medicine, 1981, pp 1107-1112. 6. Neeld JR, Pearson WN: Macro- and micromethods for the determination of serum vitamin A using trifluoroacetic acid . J Nutr 1963;97:454-462. 7. Glover J, Moxley L, Muhilal H, et al: Micromethods for fluorometric assay of retinol-binding protein in blood plasma . Clin Chim Acta 1974;50:371-380.Crossref 8. Mancini G, Carbonara AD, Heremans JF: Immunochemical quantitation of antigens by single radial immunodiffusion . Immunochemistry 1965;2:235-254.Crossref 9. Sommer A, Emran N, Tamba T: Vitamin A responsive punctate keratopathy in xerophthalmia . Am J Ophthalmol 1979;87:330-333. 10. Muto Y, Smith JE, Milch PO, et al: Regulation of retinol-binding protein metabolism by vitamin A status in the rat . J Biol Chem 1972;247:2542-2550. 11. Muhilal H, Glover J: Effects of dietary deficiencies of protein and retinol on the plasma level of retinol-binding protein in the rat . Br J Nutr 1974;32:549-558.Crossref 12. Arroyave G, Wilson D, Mendez J, et al: Serum and lines vitamin A and lipids in children with severe protein malnutrition . Am J Clin Nutr 1961;9:180-185. 13. Ingenbleek Y, van den Schriek HG, de Nayer P, et al: Albumin, transferrin and the thyroxine-binding prealbumin/retinol-binding protein complex in assessment of malnutrition . Clin Chim Acta 1975;63:61-67.Crossref 14. Peterson A, Nilsson SF, Ostberg L, et al: Aspects of the metabolism of retinol-binding protein and retinol . Vitam Horm 1974;32:181-214.
Dubord, Paul J.;Krachmer, Jay H.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030792013pmid: 6979328
Abstract • Seven children from two unrelated families had lattice corneal dystrophy. Their ages ranged from 3 to 13 years at initial examination. The children were observed for an average of 35 months. Three distinct early slitlamp characteristics were found. The first characteristic was subepithelial white opacities that were discrete, round or ovoid, nonrefractile, nonstaining, variably sized (estimated at 0.1 to 0.5 mm), and larger than the previously reported minute refractile dots. The second finding was a diffuse axial anterior stromal haze that was either the initial sign or developed in conjunction with the other two characteristics. The third finding was anterior stromal dots and filamentary lines that were refractile on indirect slitlamp illumination and white on direct illumination. Knowledge of these three slitlamp characteristics in conjunction with examination of older family members will facilitate the early diagnosis of lattice corneal dystrophy. References 1. Biber H: Über einige seltenere Hornhauterkrankungen: Die oberflächliche gittrige Keratitis, dissertation, Zurich, 1890. 2. Haab O: Die gittrige keratitis . Z Augenheilkd 1899;2:235-246. 3. Dimmer F: Ueber oberflächliche gittrige Hornhauttrübung . Z Augenheilkd 1899;2:354-361. 4. Stansbury FC: Lattice type of hereditary corneal degeneration . Arch Ophthalmol 1948; 40:189-217.Crossref 5. Dark AJ, Thomson DS: Lattice dystrophy of the cornea . Br J Ophthalmol 1960;44:257-279.Crossref 6. Malbran ES: Corneal dystrophies: A clinical, pathological and surgical approach . Am J Ophthalmol 1972;74:771-809. 7. Bücklers M: Die bisherige Auffassung vom Wesen der Hornhautdegenerationen . Klin Monatsbl Augenheilkd , (suppl 3) , 1938, pp 5-143. 8. Waring GO, Rodrigues MM, Laibson PR: Corneal dystrophies: I. Dystrophies of the epithelium, Bowman's layer and stroma . Surv Ophthalmol 1978;23:71-122.Crossref 9. Mutch JR: Hereditary corneal dystrophy . Br J Ophthalmol 1944;28:49-86.Crossref 10. Franceschetti A: Classification and treatment of hereditary corneal dystrophies . Arch Ophthalmol 1954;52:1-12.Crossref 11. Rabb MF, Blodi FC, Boniuk M: Unilateral lattice dystrophy of the cornea . Trans Am Acad Ophthalmol Otolaryngol 1974;78:440-444. 12. Francois J, Hanssens M, Teuchy H: Ultrastructural changes in lattice dystrophy of the cornea . Ophthalmic Res 1975;7:321-344.Crossref 13. Duke-Elders: Lattice Dystrophy, in vol 8, The Ocular Adnexa , in System of Ophthalmology . St Louis, CV Mosby Co, 1965, pt 2, pp 933-939. 14. Németh L: Ueber die gittrige Entartung der Hornhaut . Klin Monatsbl Augenheilkd 1936;95:73-76. 15. Yanoff M, Fine BS, Colosi NJ, et al: Lattice corneal dystrophy . Arch Ophthalmol 1977;95:651-655.Crossref 16. Grayson M: Degenerations, dystrophies and edema of the cornea , in Duane TD (ed): Clinical Ophthalmology . Hagerstown, Md, Harper & Row Publishers Inc, vol 4, pp 12-13. 17. Mannis MJ, Krachmer JH, Rodrigues MM, et al: Polymorphic amyloid degeneration of the cornea . Arch Ophthalmol 1981;99:1217-1223.Crossref
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030795014pmid: 6979329
Abstract • A comparison of surgical techniques with phacoemulsification showed that changing from anterior to posterior chamber emulsification afforded a drop in endothelial cell loss from 24.6% to 12.5%. Implantation of a Shearing posterior chamber lens instead of a Binkhorst two-loop iridocapsular lens did not decrease the cell loss using anterior chamber emulsification. Cell loss was approximately 25% in both groups. The addition of sodium hyaluronate (Healon) to the procedure of posterior chamber emulsification and implantation of a Shearing lens did not raise or lower the cell loss noted when using air alone. However, with the technique described whereby most of the sodium hyaluronate is irrigated from the eye at the end of the procedure, there was no increase in intraocular pressure postoperatively and no untoward effects. Posterior chamber emulsification seems mandatory, and though sodium hyaluronate did not improve cell loss, its use as a precaution seems to be completely safe when correct procedures are followed. References 1. Miller D, O'Conner P, Williams J: Use of Na-hyaluronate during intraocular lens implantation . Ophthalmic Surg 1977;8:58. 2. Hoffer KJ: Vertical endothelial cell disparity . Am J Ophthalmol 1979;87:344-349.
Conn, Howard;Green, W. Richard;de la Cruz, Zenaida C.;Hillis, Argye
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030797015pmid: 6177306
Abstract • To our knowledge, this is the first clinicopathologic report of a previously unrecognized maculopathy in which there is thickening and mucopolysaccharide deposition in the sclera subjacent to the macula. A healthy 50-year-old man had bilateral mottling of the retinal pigment epithelium (RPE) in the macular region. The left eye was enucleated because of a choroidal melanoma. Histopathologic examination disclosed a thickened sclera with abnormal collagen fibrils with diameters up to 5,800 A and compressed choroid. The overlying RPE had areas of hypopigmentation, hyperpigmentation, and hyperplasia and contained intracytoplasmic lipofuscin. References 1. Spicer SS, Horn RG, Leppi TJ: Histochemistry of connective tissue mucopolysaccharides , in Wagner BM, Smith DE (eds): The Connective Tissue . Baltimore, Williams & Wilkins Co, 1967, pp 251-303. 2. McKusick VA: Heritable Disorders of Connective Tissue , ed 4. St Louis, CV Mosby Co, 1972, pp 629-630. 3. Brunning RD: Morphologic alterations in nucleated blood and marrow cells in genetic disorders . Hum Pathol 1970;1:99-124.Crossref 4. Scott JE, Quintarelli G, Dellovo MC: The chemical and histochemical properties of Alcian blue: I. The mechanism of Alcian blue staining . Histochemistry 1964;4:73-85.Crossref 5. Garner A: Histochemistry of corneal macular dystrophy . Invest Ophthalmol Vis Sci 1969;8:475-483. 6. Sero N, Meyer K, Anderson B, et al: Variations in keratosulfate . J Biochem 1965;240:1005-1010. 7. Okada S, O'Brien JS: Generalized gangliosidosis: β-Galactosidase deficiency . Science 1968;160:1002-1004.Crossref 8. MacBrinn MC, Okada S, Ho MW, et al: Generalized gangliosidosis: Impaired cleavage of galactose from a mucopolysaccharide and a glycoprotein . Science 1969;163:946-947.Crossref 9. Hoffman P, Meyer K, Linker A: Transglycosilation during the mixed digestion of hyaluronic acid and chondroitin sulfate by testicular hyaluronidase . J Biol Chem 1956;219:653-663. 10. Howard GM: Obscure scleral thickening. Read before the Eastern Ophthalmic Pathology Society Meeting, Philadelphia, April 12, 1971. 11. Virgilio LA, Williams RJ, Klintworth GK: An unusually large human eye with abnormal scleral collagen . Arch Ophthalmol 1976;94:101-105.Crossref 12. Mann I: The Development of the Human Eye , ed 3. New York, Grune & Stratton Inc, 1969, pp 254-255. 13. Duke-Elder S: System of Ophthalmology . St Louis, CV Mosby Co, pt 1, 1913, vol 3, pp 162-163.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030804016pmid: 7082209
Abstract • A Fasanella-Servat upper-eyelid tarsal excision was coupled with reimplantation of the excised specimen into the lower lid between its antitarsal margin and the retractor muscles of the lower lid. The reimplantation of tissues preserved secretory elements in four dry-eyed patients whose upper-lid blepharoptosis and lower-lid retraction were both surgically corrected by this procedure. References 1. Jones LT, Wobig JJ: Surgery of the lower eyelid , in Surgery of the Eyelids and Lacrimal System . Birmingham, Ala, Aesculapius Publishing Co, 1976, chap 10, pp 133-136. 2. Fasanella RM, Servat J: Levator resection for minimal ptosis: Another simplified operation . Arch Ophthalmol 1961;65:493-496.Crossref 3. Sisler HA: Injected mixture for hemostasis in dacryocystorhinostomy . Ann Ophthalmol 1976;8:502-505. 4. Lauring L: Blepharoptosis correction with the sutureless Fasanella-Servat operation . Arch Ophthalmol 1977;95:671-674.Crossref
Binder, Perry S.;Akers, Patti H.;Deg, Janet K.;Zavala, Edward Y.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030806017pmid: 7044353
Abstract • We performed routine microkeratome and freehand lamellar keratectomies in 65 canine eyes and 24 human eye-bank eyes. The microkeratome technique produced more predictable resections compared with the freehand technique and at the same time produced a wound that would allow for better wound coaptation. Neither technique damaged the corneal endothelium. We conclude that one of the reasons for the success of the refractive keratoplasty procedures is the refined microkeratome technique. References 1. Binder PS, Woodward C: Extended wear hydrocurve and Sauflon contact lenses . Am J Ophthalmol 1980;90:309-316. 2. Worthen D, Boucher JA, Buxton JN: Interim FDA report on intraocular lenses . Ophthalmology 1980;87:267-271.Crossref 3. Binder PS, May CH, Grant SC: An evaluation of orthokeratology . Ophthalmology 1980;87:729-744.Crossref 4. Barraquer JI: Queratomileusis Y Queratofaquia . Bogota, Colombia, Instituto Barraquer de America, 1980. 5. Bourne WM: Refractive keratoplasty . Surv Ophthalmol 1972;16:375-381. 6. Barraquer JI: Keratomileusis for the correction of aphakia , in Symposium on Medical and Surgical Diseases of the Cornea . St Louis, CV Mosby Co, 1980, pp 450-479. 7. Troutman TC, Swinger CA, Kelly RJ: Keratophakia: A preliminary evaluation . Ophthalmology 1979;86:523-530.Crossref 8. Troutman TC, Gaster RN, Swinger C: Refractive keratoplasty , in Symposium on Medical and Surgical Diseases of the Cornea . St Louis, CV Mosby Co, 1980, pp 428-449. 9. Friedlander MH, Rich LF, Werblin TP, et al: Keratophakia using preserved lenticules . Ophthalmology 1980;87:687-692.Crossref 10. Kaufman HE: The correction of aphakia . Am J Ophthalmol 1980;89:1-10. 11. Rich LF: A technique for preparing corneal lamellar donor tissue using simplified keratomileusis . Ophthalmic Surg 1980;11:606-608. 12. Richard JM, Paton D, Gesset AR: A comparison of penetrating keratoplasty and lamellar keratoplasty in the surgical management of keratoconus . Am J Ophthalmol 1978;86:807-811. 13. Zavala EY, Binder PS: The pathologic findings of epithelial ingrowth . Arch Ophthalmol 1980;98:2007-2014.Crossref 14. Wickham MG, Binder PS: Evaluation of corneal endothelial damage using correlated microscopy techniques . Ophthalmic Res 1976;8:407-413.Crossref 15. Binder PS, Beale JP, Zavala EY: The histopathology of a case of keratophakia . Arch Ophthalmol 1982;100:101-105.Crossref 16. Binder PS, Akers PH, Zavala EY, et al: Refractive keratoplasty: Microkeratome and tissue stains . Invest Ophthalmol Vis Sci 1980;19(April (suppl) ):261.
Quigley, Harry A.;Addicks, Earl M.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030811018pmid: 7082210
Abstract • We compared the clinical appearance of the retinal nerve fiber layer (NFL) and its histology in primate eyes. In 12 eyes with NFL lesions induced by orbital optic nerve trauma, clinical detection of NFL atrophy was possible after loss of 50% of the neural tissue in a given area. Some retinal areas with no visible NFL striations had remaining nerve fibers. The detectability of NFL atrophy was directly affected both by the pattern of nerve fiber loss as well as by the zone of the retina in which the loss occurred. While each nerve bundle gives rise to a single light striation nasal and temporal to the nerve head, this one-to-one correspondence is not true above and below the disc, where bundles are thicker and incompletely divided by glial septa. References 1. Hoyt WF, Frisen L, Newman N: Funduscopy of the nerve fiber layer in glaucoma . Invest Ophthalmol Vis Sci 1973;12:814-829. 2. Hoyt WF: Ophthalmoscopy of the retinal nerve fiber layer in neuro-ophthalmologic diagnosis . Aust J Ophthalmol 1976;4:14-36.Crossref 3. Quigley HA, Addicks EM, Green WR: Optic nerve damage in human glaucoma: III. Quantitative correlation of nerve fiber loss and visual field defect in glaucoma, ischemic neuropathy, papilledema, and toxic neuropathy . Arch Ophthalmol 1982;100:135-146.Crossref 4. Sommer A, Miller NR, Pollack I, et al: The nerve fiber layer in the diagnosis of glaucoma . Arch Ophthalmol 1977;95:2149-2156.Crossref 5. Quigley HA, Miller NR, George T: Clinical evaluation of nerve fiber layer atrophy as an indicator of glaucomatous optic nerve damage . Arch Ophthalmol 1980;98:1564-1571.Crossref 6. Miller NR, George T: Monochromatic (redfree) photography and ophthalmoscopy of the peripapillary retinal nerve fiber layer . Invest Ophthalmol Vis Sci 1978;17:1121-1124. 7. Quigley HA, Davis EB, Anderson ER: Descending optic nerve degeneration in primates . Invest Ophthalmol Vis Sci 1977;16:841-849. 8. Hoyt WF, Luis O: Visual fiber anatomy in the infrageniculate pathway of the primate: Uncrossed and crossed retinal quadrant fiber projections studied with Nauta silver stain . Arch Ophthalmol 1962;68:94-106.Crossref 9. Vrabec F: The temporal raphe of the human retina . Am J Ophthalmol 1966;62:926-938. 10. Minckler DS: The organization of nerve fiber bundles in the primate optic nerve head . Arch Ophthalmol 1980;98:1630-1636.Crossref 11. Radius RL, Anderson DR: The histology of retinal nerve fiber layer bundles and bundle defects . Arch Ophthalmol 1979;97:948-950.Crossref 12. Radius RL, Anderson DR: The course of axons through the retina and optic nerve head . Arch Ophthalmol 1979;97:1154-1158.Crossref 13. Radius RL: Thickness of the retinal nerve fiber layer in primate eyes . Arch Ophthalmol 1980;98:1625-1629.Crossref 14. Quigley HA, Anderson DR: The histologic basis of optic disc pallor in experimental optic atrophy . Am J Ophthalmol 1977;83:709-717.
Pederson, Jonathan E.;MacLellan, Helen M.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030819019pmid: 7044354
Abstract • Experimental hypotony was induced in rhesus monkeys by the following procedures: ciliochoroidal detachment, retinal detachment, or cyclodialysis. Two days later, at the time of greatest hypotony, 10% methacholine chloride was deposited in the cornea by iontophoresis, and 0.25% physostigmine salicylate ointment was applied topically to each eye. The intraocular pressure rose to normal levels in all eyes for eight to 24 hours. The peak rise in IOP occurred one to four hours after drug administration and was 7.2, 6.8, and 11.3 mm Hg higher than the pretreatment levels in eyes with ciliochoroidal detachment, retinal detachment, and cyclodialysis, respectively. In a group of normal eyes, this drug combination caused a transient 5.7 mm Hg fall in IOP. The mechanism of pressure elevation by methacholine and physostigmine probably is caused by stimulation of aqueous humor formation or reduced uveoscleral outflow, or both. References 1. Chandler PA, Maumenee AE: A major cause of hypotony . Am J Ophthalmol 1961;52:609-618. 2. Waitzman MB, King CD: Prostaglandin influences on intraocular pressure and pupil size . Am J Physiol 1967;212:329-334. 3. Krupin T, Weiss A, Becker B, et al: Increased intraocular pressure following topical azide or nitroprusside . Invest Ophthalmol Vis Sci 1977;16:1002-1007. 4. Podos SM: The effect of cation ionophores on intraocular pressure . Invest Ophthalmol Vis Sci 1976:15:851-854. 5. Heilmann K: Special pharmacology , in Heilmann K, Richardson KT (eds): Glaucoma: Conceptions of a Disease . Philadelphia, WB Saunders Co, 1978, p 270. 6. Hupsel O, Henkes HE: The treatment of ocular hypotonia with phosphorylcholine chloride: Report on preliminary experimental and clinical results , in Acta XVII International Congress of Ophthalmology . Toronto, University of Toronto Press, 1955, vol 1, pp 143-150. 7. Boet DJ: Clinical results with phosphorylcholine calcium . Ophthalmologica 1956;132:150-152.Crossref 8. Macri FJ, Cevario SJ: The induction of aqueous humor formation by the use of ACh+ eserine . Invest Ophthalmol Vis Sci 1973;12:910-916. 9. Pederson JE, Gaasterland DE, MacLellan HM: Experimental ciliochoroidal detachment: Effect on intraocular pressure and aqueous humor flow . Arch Ophthalmol 1979;97:536-541.Crossref 10. Pederson JE, MacLellan HM: Experimental retinal detachment: I. Effect of subretinal fluid composition on reabsorption rate and intraocular pressure. Arch Ophthalmol, to be published. 11. Vannas M, Bjorkenheim B: On hypotony following cyclodialysis and its treatment . Acta Ophthalmol 1952;30:63-64. 12. Shaffer RN, Weiss DI: Concerning cyclodialysis and hypotony . Arch Ophthalmol 1962; 68:25-31.Crossref 13. Miller SJH; Hypotony following cyclodialysis . Br J Ophthalmol 1963;47:211-214.Crossref 14. Barasch K, Galin MA, Baris I: Postcyclodialysis hypotony . Am J Ophthalmol 1969;68:644-645. 15. Portney GL, Purcell TW: Surgical repair of cyclodialysis induced hypotony . Ophthalmic Surg 1974;5:30-32. 16. Maumenee AE, Stark WJ: Management of persistent hypotony after planned or inadvertent cyclodialysis . Am J Ophthalmol 1971;71:320-327. 17. Mackensen G, Corydon L: Verbesserter Eingriff gegen das Hypotonie-Syndrom mit Kammerwinkelspalt nach drucksenkender Operation . Klin Monatsbl Augenheilkd 1974;165:696-704. 18. Norris JL, Cleasby GW: Prolonged hypotony following cataract extraction . Ann Ophthalmol 1978;10:525-528. 19. Shea M, Mednick EB: Ciliary body reattachment in ocular hypotony . Arch Ophthalmol 1981;99:278-281.Crossref 20. Camras CB, Bito LZ, Eakins KE: Reduction of intraocular pressure by prostaglandin applied topically to the eyes of conscious rabbits . Invest Ophthalmol Vis Sci 1977;16:1125-1134. 21. Koelle GB: Parasympathomimetic agents , in Goodman LS, Gilman A (eds): The Pharmacological Basis of Therapeutics . New York, MacMillan Publishing Co Inc, 1970, p 467. 22. Guyton AC, Scheel K, Murpree D: Interstitial fluid pressure: III. Its effect on resistance to tissue fluid mobility . Circ Res 1966;19:412-419.Crossref 23. Bill A, Wahlinder PE: The effects of pilocarpine on the dynamics of aqueous humor in a primate (Macaca irus) . Invest Ophthalmol Vis Sci 1966;5:170-175.
Nagataki, Shigetoshi;Brubaker, Richard F.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030822020pmid: 7082211
Abstract • The effect of pilocarpine on aqueous humor flow in the human eye was studied using fluorophotometry. Methods of measuring fluorescent intensity and of calculating aqueous humor flow were used that reduced the problem of uneven mixing of fluorescein, which is observed in the presence of miosis. The rate of aqueous humor flow through the anterior chamber of the placebo-treated eyes was 2.2 ± 0.35 μL/min and of the pilocarpinetreated eyes was 2.5 ± 0.47 μL/min. This increase in flow (14%) was statistically significant but too small to be clinically important. Pilocarpine was observed to reduce the anterior chamber volume of these subjects from 204 ± 26 to 188 ± 32 μL. References 1. Van Buskirk EM, Grant WM: Lens depression and aqueous outflow in enucleated primate eyes . Am J Ophthalmol 1973;76:632-640. 2. Kaufman PL, Barany EH: Loss of acute pilocarpine effect on outflow facility following surgical disinsertion and retrodisplacement of the ciliary muscle from the scleral spur in the cynomolgus monkey . Invest Ophthalmol Vis Sci 1976;15:793-807. 3. Bill A, Wålinder P-E: The effects of pilocarpine on the dynamics of aqueous humor in a primate (Macaca irus) . Invest Ophthalmol Vis Sci 1966;5:170-175. 4. Barsam PC: Comparison of the effect of pilocarpine and echthiophate on intraocular pressure and outflow facility . Am J Ophthalmol 1972;73:742-749. 5. Chandler MR: Aqueous flow measurements in man by the perilimbal suction cup technique . Br J Ophthalmol 1964;48:432-438.Crossref 6. Rosenthal AR: Pressure cup and tonography: In chronic simple glaucoma before and during pilocarpine therapy . Am J Ophthalmol 1969;67:713-723. 7. Edwards J, Hallman VL, Perkins ES: Perfusion studies on the monkey eye . Exp Eye Res 1967;6:316-326.Crossref 8. Wålinder P-E, Bill A: Influence of intraocular pressure and some drugs on aqueous flow and entry of cycloleucine into the aqueous humor of vervet monkeys (Cercopithecus ethiops) . Invest Ophthalmol Vis Sci 1969;8:446-458. 9. Gaasterland D, Kupfer C, Ross K: Studies of aqueous humor dynamics in man: IV. Effects of pilocarpine upon measurements in young normal volunteers . Invest Ophthalmol Vis Sci 1975; 14:848-853. 10. Anselmi P, Bron AJ, Maurice DM: Action of drugs on the aqueous flow in man measured by fluorophotometry . Exp Eye Res 1968;7:487-496.Crossref 11. Jones RF, Maurice DM: New methods of measuring the rate of aqueous flow in man with fluorescein . Exp Eye Res 1966;5:208-220.Crossref 12. Coakes RL, Brubaker RF: Method of measuring aqueous humor flow and corneal endothelial permeability using a fluorophotometry nomogram . Invest Ophthalmol Vis Sci 1979; 18:288-302. 13. Dixon LCW: Nonlinear Optimization . London, Universities Press Ltd, 1972, pp 41-43. 14. Sawa M, Araie M, Nagataki S, et al: Permeability of the human corneal endothelium as determined by oral fluorescein . Jpn J Ophthalmol 1981;25:60-68.
Stulting, R. Doyle;Leif, Robert C.;Clarkson, John G.;Bobbitt, Dorothy
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030826021pmid: 6177307
Abstract • Centrifugal cytology is a new technique for the preparation of ocular fluids for cytologic examination. It differs from conventional cytocentrifuge techniques, since fixation is carried out simultaneously with centrifugation. It avoids air-drying artifacts and can be applied to small (50 μL) or large (200 mL or more) sample volumes and dilute cell suspensions, such as might be obtained by anterior chamber paracentesis, vitreous aspiration, or vitrectomy. The resultant preparation is a permanent, stained, well-preserved, flattened, homogeneous cell dispersion suitable for detailed cytologic evaluation. References 1. Thelmo W, Csordas J, Davis P, et al: The cytology of acute bacterial and follicular conjunctivitis . Acta Cytol 1972;16:172-177. 2. Gelender H, Forster RK: Papanicolaou cytology in the diagnosis and management of external ocular tumors . Arch Ophthalmol 1980;98:909-912.Crossref 3. Leif RC, Gall S, Dunlap LA, et al: Centrifugal cytology: IV. The preparation of fixed stained dispersions of gynecological cells . Acta Cytol 1975;19:159-168. 4. Leif RC, Silverman MA, Bobbitt D et al: Centrifugal cytology: A new technique for cytodiagnosis . Lab Management 1979;17:38-41. 5. Barrett DL, King EB: Comparison of cellular recovery rates and morphologic detail obtained using membrane filter and cytocentrifuge techniques . Acta Cytol 1976;20:174-180. 6. Watson P: A slide centrifuge: An apparatus for concentrating cells in suspension onto a microscope slide . J Lab Clin Med 1966;68:494-501. 7. Goldberg M: Cytologic diagnosis of phacolytic glaucoma utilizing Millipore filtration of the aqueous . Br J Ophthalmol 1967;51:847-853.Crossref 8. Fowler JH, Basu PK: Cytology of the anterior chamber fluid in eyes with corneal xenografts . Can J Ophthalmol 1971;6:68-71. 9. Naib ZM: Cytology of ocular lesions . Acta Cytol 1972;16:178-185. 10. Hogan MJ, Wood IS, Godfrey WA: Aqueous humor cytology in uveitis . Arch Ophthalmol 1973;89:217-220.Crossref 11. Michels RG, Knox DL, Erozan YS, et al: Intraocular reticulum cell sarcoma: Diagnosis by pars plana vitrectomy . Arch Ophthalmol 1975;93:1331-1335.Crossref 12. Koss LG: Cytologic techniques , in Bates CE, Durfee GR (eds): Diagnostic Cytology and Its Histopathologic Basis , ed 3. Philadelphia, JB Lippincott Co, 1979, pp 1205-1206. 13. Leif RC, Easter HN, Warters RL, et al: Centrifugal cytology: I. A quantitative technique for the preparation of glutaraldehyde-fixed cells for the light and scanning electron microscope . J Histochem Cytochem 1971;19:203-215.Crossref 14. Thornwaite JT, Thornwaite BN, Cayer ML, et al: A new method for preparing cells for critical point drying , in Scanning Electron Microscopy/1975 (Part I), proceedings of the Eighth Annual Scanning Electron Microscope Symposium . Chicago, Illinois Institute of Technology, 1975, pp 387-402.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030830022
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030830023
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 Meeting. —The Canadian Implant Association will hold its annual meeting at the Hotel Bonaventure in Montreal on May 29, 1982. For further information, contact Dr Marvin L. Kwitko, 5591 Cote des Neiges, Suite 1, Montreal, Quebec, Canada H3T 1Y8. Congress Meeting. —The Fifth International Orthoptic Congress will be held in Cannes, France, Oct 11-13, 1982. For further information, contact Michele Marsot, General Secretary, 119, Cours Gambetta, 69003 Lyons, France. Annual Meeting. —The next annual meeting of the Pennsylvania Academy of Ophthalmology and Otolaryngology will be held May 25-28,1982, at the Hotel Hershey & Country Club in Hershey, Pa. For further information, contact Dr Edward A. Jaeger, 240 E Rose Tree Rd, Media, PA 19063. Posthumous Awards Given. —The Joint Commission on Allied Health Personnel in Ophthalmology (JCAHPO) presented Dr Robert Hugh Monahan, Jr, its special distinguished service award entitled "Man of the Decade for the 1970s" and its "Statesmanship Award."
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030845026
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 To the Editor. —I read with interest the article by Dodd et al that described a 4-year-old girl with suspected malignant hyperthermia who underwent surgery for esotropia.In the description of the case, there is a most grievious error mentioned that needs to be strongly stressed to all ophthalmologists and anesthesiologists. This patient had been given succinylcholine chloride before tracheal intubation. Almost immediately, the patient experienced tachycardia. The administration of halothane, which was used as an inducing agent, was discontinued, and enflurane therapy was started. The tachycardia persisted. The patient was then given a second dose of succinylcholine. This is strictly contraindicated.Although this patient actually did not experience any true hypetthermia, ie, a temperature higher than 37.2 °C (99 °F), it is true that the first sign of malignant hyperthermia is not a rise in temperature but tachycardia. Therefore, with that persistent tachycardia, a second dose of succinylcholine was
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030845024pmid: 7082212
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 To the Editor. —The article by Tobin et al published in the January Archives (1982;100:81-83) on the safety of hydroxychloroquine sulfate recalls my experience with this drug in rheumatic diseases. During the past 15 years, I have followed up approximately 100 patients with rheumatoid arthritis and lupus erythematosus who were given hydroxychloroquine sulfate in doses of 200 to 400 mg/day. The average length of drug use was 36 months, with 12 patients using the drug up to eight years. In this whole group, no functional visual or anatomic ocular defects were noted on ocular examination.Since central vision tends to be most affected by this drug, it is my recommendation to use Amsler's charts, principally the red chart, to pick up the smallest and earliest central or paracentral defects.
Sedwick, Lyn A.;Romano, Paul E.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030845025
Abstract To the Editor. —We would like to congratulate Dodd et al on their article entitled "Suspected Malignant Hyperthermia in a Strabismus Patient: A Case Report," which was published in the July Archives (1981;99:1247-1250). As authors of a recent review of this subject as it pertains to ophthalmology,1 we recognized many of the same historical, diagnostic, and predictive concerns that were cogently discussed in the Archives article. However, we would differ with Dodd et al concerning the presumed capability of lidocaine hydrochloride for causing malignant hyperthermia.Although it is true that lidocaine belongs to the category of "-caine" drugs purported to cause or exacerbate malignant hyperthermia, to our knowledge, there has never been a case reported to have been triggered by lidocaine. Moreover, in 1979, Wingard and Bobko2 were unable to induce malignant hyperthermia with intravenous (IV) lidocaine in swine that were genetically predisposed to malignant hyperthermia. We reviewed References 1. Sedwick LA, Romano PE: Malignant hyperthermia: Considerations for the ophthalmologist . Surv Ophthalmol 1981;25:378-382.Crossref 2. Wingard DW, Bobko S: Failure of lidocaine to trigger porcine malignant hyperthermia . Anesth Analg 1979;58:99-103.Crossref 3. Krakowiak FJ, Vatral JJ, Moore RC, et al: Malignant hyperthermia: Report of two cases . Oral Surg 1979;47:218-222.Crossref 4. Britt BA: Malignant hyperthermia: A pharmacogenetic disease of skeletal and cardiac muscle . N Engl J Med 1974;290:1140-1142.Crossref 5. Demeyere R: Malignant hyperthermia . Acta Anesthesiol Belg 1978;29:101-120.
Brandt, David E.;Fitzgibbons, Desiray C.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030845027
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 To the Editor. —We have read with interest the excellent Archives article by Dodd et al. After reading this review, one is tempted to believe that the triggering of malignant hyperthermia can be prevented by use of a "safe" anesthetic agent.We, however, have had the disconcerting experience of seeing a phenomenon, to our knowledge not previously reported—development of an episode of malignant hyperthermia after oral pretreatment with dantrolene sodium and administration of an anesthetic agent suggested by most to be nontriggering. Details of this ophthalmic case can be found in Anesthesiology (1981;54:1-2, 73-75). This first reported case of such an occurrence stresses the continued vigilance one must maintain despite following the usual and accepted protocol for patients suspected of having malignant hyperthermia.Other details associated with malignant hyperthermia that we would emphasize are as follows: There may not be any temperature rise in a specific person in whom
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030845028
Abstract To the Editor. —Dodd et al underscored several points that should be of intense interest to both ophthalmologists and anesthesiologists. I applaud the authors' emphasis on the importance of a thorough anesthetic and family history. Furthermore, as the authors stated, the increased incidence of malignant hyperthermia in patients with such muscular defects as strabismus and ptosis must be appreciated, as well as the fact that local anesthetics of the "-amide" variety (eg, lidocaine hydrochloride, mepivacaine hydrochloride, bupivacaine hydrochloride, and others) may be mild triggering agents. However, as an anesthesiologist, I believe that certain other areas of this article are deserving of comment. Of extreme concern is the fact that the patient received a second dose of IV succinylcholine, despite the fact that masseter spasm and tachycardia were noted "almost immediately" after the initial administration of succinylcholine. Isolated masseter muscle spasm after succinylcholine must be assumed to portend malignant hyperthermia References 1. Donlon JV, Newfield P, Streter F, et al: Implications of masseter spasm after succinylcholine . Anesthesiology 1978;49:298-301.Crossref 2. Ellis FR, Clarke IMC, Modgill M, et al: Evaluation of creatine phosphokinase in screening of patients for malignant hyperpyrexia . Br Med J 1975;3:511-513.Crossref 3. Owen G, Kerry RJ: Anesthesia during raised CPK activity . Br Med J 1974;4:75-76.Crossref 4. Zsigmond EK, Starkweather WH, Duboff GS, et al: Abnormal creatine phosphokinase isoenzyme pattern in families with malignant hyperpyrexia . Anesth Analg 1972;51:827-840. 5. Meltzer HY, Hassan SB, Russo P, et al: Isoenzymes of creatine phosphokinase in serum of families with malignant hyperpyrexia . Anesth Analg 1976;55:797-799.Crossref 6. Zsigmond EK, Penner J, Kothary SP: Normal erythrocyte fragility and abnormal platelet aggregation in MH families: A pilot study , in Aldrete JA, Britt BA (eds): Second International Symposium on Malignant Hyperthermia . New York, Grune & Stratton Inc, 1978, pp 213-219. 7. Solomons CC, Tan S, Aldrete JA: Platelet metabolism and malignant hyperthermia , in Aldrete JA, Britt BA (eds): Second International Symposium on Malignant Hyperthermia . New York, Grune & Stratton Inc, 1978, pp 221-225. 8. Ellis FR, Cain PA, Harriman DGF: Multifactorial inheritance of malignant hyperthermia susceptibilty , in Aldrete JA, Britt BA (eds): Second International Symposium on Malignant Hyperthermia . New York, Grune & Stratton Inc, 1978, pp 329-338.
Dodd, Michael J.;Phattiyakul, Pricha;Silpasuvan, Suwat
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030845029
Abstract In Reply. —Thank you for bringing the four letters to our attention. Drs Porter and McGoldrick mentioned that we erred in not discussing the second dose of succinylcholine given to the patient described in our article. We agree that we were remiss in not mentioning the important point that it is inappropriate to give a second dose of succinylcholine in a clinical setting of tachycardia and masseter muscle rigidity that follows the initial succinylcholine administration. Such a case should be considered malignant hyperthermia until proved otherwise, and the treatment should be discontinued, with careful monitoring of the patient's condition.1However, at the time our case occurred (Oct 3, 1978), this fact was not universally appreciated. We were concerned that the 10-mg dose of succinylcholine may have been inadequate and that the rigidity was an abnormal manifestation of generalized fasciculations without relaxation and that the tachycardia was caused by the References 1. Donlon JV, Newfield P, Streter F, et al: Implications of masseter spasm after succinylcholine . Anesthesiology 1978;49:298-301.Crossref 2. Barnes PK: Masseter spasm following intravenous suxamethonuium . Br J Anaesth 1973;45:759-760.Crossref 3. Wingard DW, Bobko S: Failure of lidocaine to trigger porcine malignant hyperthermia . Anesth Analg 1979;58:99-103.Crossref 4. Klimanek J, Majewski W, Walencik K: A case of malignant hyperthermia during epidural anesthesia . Anaesth Resuscitation Intensive Therap 1976;4:143-145. 5. Fitzgibbons DC: Malignant hyperthermia following preoperative oral administration of dantrolene . Anesthesiology 1981;54:73-75.Crossref
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030847030pmid: 7082214
Abstract To the Editor. —I read with great interest the article entitled "Central Ocular Motor Abnormalities in Duane's Retraction Syndrome" by Gourdeau et al in the Archives (1981;99:1809-1810). These authors suggest that Duane's retraction syndrome is produced by a primary brainstem abnormality involving premotor structures. This conclusion is based on eye movement studies on five patients with type 1 Duane's retraction syndrome.When only a limited number of patients are studied, it would seem that each case should be typical of the syndrome. One patient had a large amount of esotropia (30 PD), and one patient was exotropic (16 PD). Wong et al1 reported only 12% of all their esotropic patients with Duane's retraction syndrome had a deviation as large as 30 PD (6% of their entire series). The esotropia averaged 16 PD. Danis2 found only 15% of his patients with Duane's retraction syndrome were exotropic.In the article References 1. Wong GY, Jampolsky A, Scott AB: Primary position deviation in Duane's syndrome . Med Coll Va Q 1972;8:302-303. 2. Danis P: Sur les anomalies congénitales de la motilite oculaire d'origine musculaire et en particulier sur le syndrome de Stilling-Turk-Duane . Ann Ocul 1948;81:148-181. 3. Metz HS, Scott AB, Scott WE: Horizontal saccadic velocities in Duane's syndrome . Am J Ophthalmol 1975;80:901-906.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030848032pmid: 7082215
Abstract To the Editor. —Angell et al, in the December Archives (1981;99:2137-2139), described the refraction, visual acuity, and limited ocular biometry of seven patients with unilateral ruptures of Descemet's membrane. They found that the involved eye was more myopic than the normal fellow eye. They suggested there might be a human parallel to the recently reported development of axial myopia in monkeys with experimental corneal opacities.1Each of us views data from a different perspective, and working in a glaucoma clinic, it was easy to consider the possibility that some of these eyes (if not all) represent examples of arrested childhood glaucoma occurring unilaterally. As previously reported,2 the prevalence of spontaneously arrested glaucoma may be as high as 7% in children initially seen with findings compatible with glaucoma. Furthermore, trauma can cause both acute and chronic glaucoma. Robin et al2 describe eyes with histories of trauma severe enough References 1. Wiesel TN, Raviola E: Increase in axial length of the macaque monkey eye after corneal opacification . Invest Ophthalmol Vis Sci 1979;18:1232-1236. 2. Robin AL, Quigley HA, Pollack IP, et al: An analysis of visual acuity, visual fields, and disc cupping in childhood glaucoma . Am J Ophthalmol 1979;88:847-858.
Angell, Linda K.;Robb, Richard M.;Berson, Frank G.
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030848033
Abstract In Reply. —The comments of Dr Quigley are interesting and worthy of consideration. Congenital glaucoma may be excluded in our group of patients for various reasons. As mentioned in our article, the corneal breaks were vertical and not horizontal or concentric with the limbus in the periphery (inconsistent with glaucoma). Also described in our article were the myopic retinal changes in the histories of cases 1 through 4. Not included in our article were the specific findings that the disc changes were those of a myopic configuration, rather than a glaucomatous excavation, and the corneal diameters were normal in all our patients.The IOPs for five of our seven patients have been recorded between 14 and 19 mm Hg. In no case was the IOP greater in the involved eye than in the fellow eye. The IOPs were unavailable for two patients, and these patients are unavailable for follow-up.We References 1. Shaffer RN: New concepts in cogenital glaucoma . Can J Ophthalmol 1967;2:243-247.
Miller, Neil R.;Zee, David S.;Gourdeau, Alain;Morris, Jacqueline
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030847031
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 In Reply. —We appreciate the comments by Dr Metz regarding our article. While we agree that one of the patients had a large esotropia and another patient was exotropic, these patients, nevertheless, represent "typical" examples of type 1 Duane's retraction syndrome, in that they had severe limitation of abduction, slight limitation of adduction, and narrowing of the palpebral fissure with retraction of the globe on attempted adduction. In addition, our fifth patient, who had an exotropia of 15 diopters at distance and 30 D at near, has subsequently undergone an autopsy, with pathologic findings of Duane's retraction syndrome. An article concerning these findings is presently in press.With regard to peak saccadic velocities determined for 20° abducting saccades, velocities were determined to and from the primary position toward the field in which abduction was limited rather than in the field in which abduction was limited, as the footnote to Table
1982 Archives of Ophthalmology
doi: 10.1001/archopht.1982.01030030868034
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.