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Do we need a retinal pigment epithelium (or choroid) for the maintenance of retinal apposition?
344
Surv Ophthalmol
30(5) March-April
1986
CURRENT
OPHTHALMOLOGY
develop in them. In the absence of localized scleral ectasias it is most unlikely that the typical circumscribed areas of myopic chorioretinal degeneration will emerge. Visual-input myopia will make an excellent animal model for intermediate myopia, however. In this type of myopia there is excessive elongation of the eye with crescent formation and thinning of the retinal pigment epithclium (RPE) but posterior staphyloma is absent (Curtin BJ: The &~o@c: Bnsir Science and CXnica( Management. Philadelphia, Harper and Row, 1985, p lG9j. Like most well-constructed research, these experiments raise more questions than they answer. Surely, there should be added studies to determine the tissue changes that are associated with this unusual response to vrisual input. Histologic and biochemical studies of the vitreous and sclera should he included inasmuch as Coulombre and his coworkers have demonstrated that these components represent the expansion and resistance force, respectively, ofthe developing eye. Coulombre demonstrated that cannularization and resultant decompression of the vitreous cavity produced a marked arrest in the expansion of the developing chick eye. Removal of the cannula permitted the intraocular pressure to rise and the expansion to resume. This expansion was restricted, however, by the sclera which had continued its own growth and had become less distensible (Coulombre AJ: J E.xj~ 2001 233:21 1, 1956) (Coulombre ‘45: 7’he Eve in Organogenesis. New York, Holt, Rinehart and Winston, 1965, p 240). Flat RPE specimens also should be studied to determine the areas of the ocular wall that are predominantly involved in the expansion process. Two studies, those of Tso and Friedman (Tso MOM, Friedman E: Arch Ophthalmol80;214, 1971) and Strectan (Streetan BI1’: Arch Ophthalmol81:383, 1971), indicate that normal postnatal expansion affects the ora-equatorial zone with gradually less flattening and increases in diameter of the RPE cells seen as the posterior pole is approached. The orientation of the neuroepithelial elements of the retina is also of interest. /Ye have always held the erroneous concept of the retina having a passivre, receptor function. The studies of Enoch et al (Enoch JM, VanLooJA, Okun E: Imest Ophthalmol 12:849, 1973) (F,noch JM, Birch IX: Ophthnlmologv 87:82 1, 1980) indicate that the retina is actually an active image-seeking tissue. \vhen needed, it is capable ofthe reorientation ofits sentient elements for optimum image formation. When we consider the retina as a source of vitreous formation, the possihlr effect of disorientation of these elements upon ocular growth appears possible. Certainly we must be grateful to I)rs. \t’iesel and Raviola for giving us a greater appreciation of‘ the importance of early visual experience upon the development of the rye. As the authors validly state, ocular refraction is largely programmed on a genetic basis. Their studies and the added clinical reports of‘myopia occurring in children as a consequence of opacification of the media. clearly indicate that some forms of myopia are, indeed, products of environmental impact. As such, these forms of myopia are treatable and the attempts to develop effective therapeutic regimes should he actively encouraged hencrlbrth. BKI.ZN J. ~I.KTIN, hl.])., P.c:. NlC\V YOKK, xi,:\\ YOliK
Do We Need A Retinal Pigment Epithelium (or Choroid) for the Maintenance Apposition?, by W.S. Foulds. BrJ Op~~~uZrno~ 69:237-239, 1985
of Retinal
Many structural and dynamic factors have been suggested as being important in the maintenance ofretinal apposition within its bed. These include interdigitation of retinal receptor cell outer segments with the apical processes of the retinal pigment epithelium, the presence of the inner photoreceptor matrix between the outer retina and the retinal pigment epithelium, and active transport of molecules from the potential subretinal space to the choroid by the cells ofthe retinal pigment epithelium. All these suggested mechanisms presuppose either a structural or functional role for the retinal pigment epithelium in maintenance of retinal pigment however, has indicated that surgical apposition. Experience of local resection of choroidal melanomas, removal of extensive areas of the choroid and retinal pigment epithelium does not commonly lead to retinal detachment. The relative rarity of retinal detachment following this extensive surgical resection of choroid and retinal pigment epithelium suggests that neither of these tissues are necessary for retinal attachment. (Author’s address: Prof. W.S. Foulds, Tennent, Institute of Ophthalmology, Western Infirmary, Glasgow, G11 6NT, Scotland.)
CURRENT
315
OPHTHALMOLOGY
Comment Foul&’ remarkable results with local resection of choroidal melanomas show clearly that retina stays This observation attached t’ven when there is no retinal pigment epithelium (RPE) or choroid underneath. may seem puzzling, inasmuch as a number of authors (myselfincludcd) ha\.c emphasized thr importance of the RPE in maintaining retinal adhesion. Is the RPE really necessary. as Foulds queries’? The answer lies in the fact that both active and passi\~e systems colltrihute to retinal adhesion, and the RPE has both acti1.e and passive functions within the eye. Under normal conditions, retinal adhesion is maintainccl in part hy metabolic activity of the RPE (which pumps fluid out of the suhretinal space, synthesizes a \kous matrix and controls the movement of microvilli which wrap around the ends of the photoreceptors). and passiise physical factors which include intraocular pressure and the osmotic pressure of the choroid (hot11 of which draw fluid from \ritreous to choroid, serving to push the retina outward and dch>,drate the subrcbtinal space). The metabolic systems predominate in an intact eye, hecauxe the RPE (as a part of the blood/retinal barrier) is such an impediment to fluid movement that the pashi\-c s!-stems are rendered relati\.ely inefrective. Hu\vevckr, if the RPE barrier is destroyed, retina will flatten o\.cr ttle damaged arra because of passi1.e fluid movc’mtml. Thus, the KPE is not strictly necessary for retinal adhesion. But it is absoluteI>- ncccssar~ l&r retinal ht%aith and func~tion. and the price we must pay for having RPE undcar the rrtina is that the pass’\“’ mcchanistns of adhesion (,\vhich account for Foulds’ observation) no longer \vork \‘er); well. \\‘h~n the RPE; is intact, the RPE ic \‘ery much ne4f.d for adhesion; when the RPE is absent. the rc,tlna I$ ill adhere but it \vill not \vork. III(:~l.\l:l. 3L.\K\IOII, hl.1). S-r\sl OKI). ~:.\1.11~01111.\
Pupillary Constriction to Darkness, by M.J. Br j 0phthaLmol 69~204-2 11, 1985
Price, .J.S. Thompson,
G.F. Judisch,
and .J.
Corbett.
(:hildrcn with congenital stationary night blindness and congenital achromatopsia have bcrn fi)und to havf unusual pupillary reactions. When the lights are turned out their pupils briefly constrict hefore they dilatr in the customary way. The authors have examined 50 normal subjects and 108 patients lvith retinal and optic ncr\‘c dysl‘unction to set ifany had initial pulmonary constriction to darkness. They used a new infrared trlcxfision apparatus. Four patitlnts with congenital stationary night blindness, four with achrtrmatopsia, tbvo with bilateral optic nruritis, and ant‘ bvith dotninant optic atrophy showed the phetlomrna. In the patients ivho sho\~cd this unusual it was the first observable cvc‘nt c’\‘cry time the lights wcr(’ rurncti oft’. 7‘11~ pupillary response to darkness, constriction could usually hr seen with a hand light, and it \\as similar in latcnc): 10 tht, normal pupillar) dilatation to darkness. Pupillary constriction to darkness is a clinic~;tll\~ valuable sign that can tw l~scd in the detection of congenital retinal disease in children with poor vision. ~.\uthor‘s atidrrss: hlichatl ,J. Pric,c,. (1,s.. O’Brien I,ihr;try, Department of’ Ophthalmology, Vniversit); of Io\v;t Hospitals. Io\va City, Io\~a ,?L’2&2.I
Comment The authors, in this article, share their experience searching ii)r al)normal pupillary constriction to darkness in 50 normal subjects and 108 patients with retina and optic ncrv~~ dyst’unctions. The), hacts cic\~clop~d bvith &the-shelf technology, a simple but effective infrared telrvision apparatus which the), also drscrihc. Frame h). framr analysis of the video picture was used to construct cur\Tcs of pupillary response to darkness. r\mong the 108 patients. the paradoxical pupillary response to darkness was seen most fi-equentl>- in congc~nital thr autosomal rccessivc or S-linked varict): achromats (67%) and congenital stationary night blintlncss, (33%). It is also seen in dominant optic atrophy (12%) and hilatcral optic neuritis (8.7% ). so norma! t(J darkness in the a&cted subjects displayed the phenomenon. The latency of ttw pupillan corlstriction subjects was similar t(J the latency ofthe normal suttjrcts dilatation to darkness. Thr authors do not commfbnt
Surv Ophthalmol
30(5) March-April
1986
CURRENT
OPHTHALMOLOGY
develop in them. In the absence of localized scleral ectasias it is most unlikely that the typical circumscribed areas of myopic chorioretinal degeneration will emerge. Visual-input myopia will make an excellent animal model for intermediate myopia, however. In this type of myopia there is excessive elongation of the eye with crescent formation and thinning of the retinal pigment epithclium (RPE) but posterior staphyloma is absent (Curtin BJ: The &~o@c: Bnsir Science and CXnica( Management. Philadelphia, Harper and Row, 1985, p lG9j. Like most well-constructed research, these experiments raise more questions than they answer. Surely, there should be added studies to determine the tissue changes that are associated with this unusual response to vrisual input. Histologic and biochemical studies of the vitreous and sclera should he included inasmuch as Coulombre and his coworkers have demonstrated that these components represent the expansion and resistance force, respectively, ofthe developing eye. Coulombre demonstrated that cannularization and resultant decompression of the vitreous cavity produced a marked arrest in the expansion of the developing chick eye. Removal of the cannula permitted the intraocular pressure to rise and the expansion to resume. This expansion was restricted, however, by the sclera which had continued its own growth and had become less distensible (Coulombre AJ: J E.xj~ 2001 233:21 1, 1956) (Coulombre ‘45: 7’he Eve in Organogenesis. New York, Holt, Rinehart and Winston, 1965, p 240). Flat RPE specimens also should be studied to determine the areas of the ocular wall that are predominantly involved in the expansion process. Two studies, those of Tso and Friedman (Tso MOM, Friedman E: Arch Ophthalmol80;214, 1971) and Strectan (Streetan BI1’: Arch Ophthalmol81:383, 1971), indicate that normal postnatal expansion affects the ora-equatorial zone with gradually less flattening and increases in diameter of the RPE cells seen as the posterior pole is approached. The orientation of the neuroepithelial elements of the retina is also of interest. /Ye have always held the erroneous concept of the retina having a passivre, receptor function. The studies of Enoch et al (Enoch JM, VanLooJA, Okun E: Imest Ophthalmol 12:849, 1973) (F,noch JM, Birch IX: Ophthnlmologv 87:82 1, 1980) indicate that the retina is actually an active image-seeking tissue. \vhen needed, it is capable ofthe reorientation ofits sentient elements for optimum image formation. When we consider the retina as a source of vitreous formation, the possihlr effect of disorientation of these elements upon ocular growth appears possible. Certainly we must be grateful to I)rs. \t’iesel and Raviola for giving us a greater appreciation of‘ the importance of early visual experience upon the development of the rye. As the authors validly state, ocular refraction is largely programmed on a genetic basis. Their studies and the added clinical reports of‘myopia occurring in children as a consequence of opacification of the media. clearly indicate that some forms of myopia are, indeed, products of environmental impact. As such, these forms of myopia are treatable and the attempts to develop effective therapeutic regimes should he actively encouraged hencrlbrth. BKI.ZN J. ~I.KTIN, hl.])., P.c:. NlC\V YOKK, xi,:\\ YOliK
Do We Need A Retinal Pigment Epithelium (or Choroid) for the Maintenance Apposition?, by W.S. Foulds. BrJ Op~~~uZrno~ 69:237-239, 1985
of Retinal
Many structural and dynamic factors have been suggested as being important in the maintenance ofretinal apposition within its bed. These include interdigitation of retinal receptor cell outer segments with the apical processes of the retinal pigment epithelium, the presence of the inner photoreceptor matrix between the outer retina and the retinal pigment epithelium, and active transport of molecules from the potential subretinal space to the choroid by the cells ofthe retinal pigment epithelium. All these suggested mechanisms presuppose either a structural or functional role for the retinal pigment epithelium in maintenance of retinal pigment however, has indicated that surgical apposition. Experience of local resection of choroidal melanomas, removal of extensive areas of the choroid and retinal pigment epithelium does not commonly lead to retinal detachment. The relative rarity of retinal detachment following this extensive surgical resection of choroid and retinal pigment epithelium suggests that neither of these tissues are necessary for retinal attachment. (Author’s address: Prof. W.S. Foulds, Tennent, Institute of Ophthalmology, Western Infirmary, Glasgow, G11 6NT, Scotland.)
CURRENT
315
OPHTHALMOLOGY
Comment Foul&’ remarkable results with local resection of choroidal melanomas show clearly that retina stays This observation attached t’ven when there is no retinal pigment epithelium (RPE) or choroid underneath. may seem puzzling, inasmuch as a number of authors (myselfincludcd) ha\.c emphasized thr importance of the RPE in maintaining retinal adhesion. Is the RPE really necessary. as Foulds queries’? The answer lies in the fact that both active and passi\~e systems colltrihute to retinal adhesion, and the RPE has both acti1.e and passive functions within the eye. Under normal conditions, retinal adhesion is maintainccl in part hy metabolic activity of the RPE (which pumps fluid out of the suhretinal space, synthesizes a \kous matrix and controls the movement of microvilli which wrap around the ends of the photoreceptors). and passiise physical factors which include intraocular pressure and the osmotic pressure of the choroid (hot11 of which draw fluid from \ritreous to choroid, serving to push the retina outward and dch>,drate the subrcbtinal space). The metabolic systems predominate in an intact eye, hecauxe the RPE (as a part of the blood/retinal barrier) is such an impediment to fluid movement that the pashi\-c s!-stems are rendered relati\.ely inefrective. Hu\vevckr, if the RPE barrier is destroyed, retina will flatten o\.cr ttle damaged arra because of passi1.e fluid movc’mtml. Thus, the KPE is not strictly necessary for retinal adhesion. But it is absoluteI>- ncccssar~ l&r retinal ht%aith and func~tion. and the price we must pay for having RPE undcar the rrtina is that the pass’\“’ mcchanistns of adhesion (,\vhich account for Foulds’ observation) no longer \vork \‘er); well. \\‘h~n the RPE; is intact, the RPE ic \‘ery much ne4f.d for adhesion; when the RPE is absent. the rc,tlna I$ ill adhere but it \vill not \vork. III(:~l.\l:l. 3L.\K\IOII, hl.1). S-r\sl OKI). ~:.\1.11~01111.\
Pupillary Constriction to Darkness, by M.J. Br j 0phthaLmol 69~204-2 11, 1985
Price, .J.S. Thompson,
G.F. Judisch,
and .J.
Corbett.
(:hildrcn with congenital stationary night blindness and congenital achromatopsia have bcrn fi)und to havf unusual pupillary reactions. When the lights are turned out their pupils briefly constrict hefore they dilatr in the customary way. The authors have examined 50 normal subjects and 108 patients lvith retinal and optic ncr\‘c dysl‘unction to set ifany had initial pulmonary constriction to darkness. They used a new infrared trlcxfision apparatus. Four patitlnts with congenital stationary night blindness, four with achrtrmatopsia, tbvo with bilateral optic nruritis, and ant‘ bvith dotninant optic atrophy showed the phetlomrna. In the patients ivho sho\~cd this unusual it was the first observable cvc‘nt c’\‘cry time the lights wcr(’ rurncti oft’. 7‘11~ pupillary response to darkness, constriction could usually hr seen with a hand light, and it \\as similar in latcnc): 10 tht, normal pupillar) dilatation to darkness. Pupillary constriction to darkness is a clinic~;tll\~ valuable sign that can tw l~scd in the detection of congenital retinal disease in children with poor vision. ~.\uthor‘s atidrrss: hlichatl ,J. Pric,c,. (1,s.. O’Brien I,ihr;try, Department of’ Ophthalmology, Vniversit); of Io\v;t Hospitals. Io\va City, Io\~a ,?L’2&2.I
Comment The authors, in this article, share their experience searching ii)r al)normal pupillary constriction to darkness in 50 normal subjects and 108 patients with retina and optic ncrv~~ dyst’unctions. The), hacts cic\~clop~d bvith &the-shelf technology, a simple but effective infrared telrvision apparatus which the), also drscrihc. Frame h). framr analysis of the video picture was used to construct cur\Tcs of pupillary response to darkness. r\mong the 108 patients. the paradoxical pupillary response to darkness was seen most fi-equentl>- in congc~nital thr autosomal rccessivc or S-linked varict): achromats (67%) and congenital stationary night blintlncss, (33%). It is also seen in dominant optic atrophy (12%) and hilatcral optic neuritis (8.7% ). so norma! t(J darkness in the a&cted subjects displayed the phenomenon. The latency of ttw pupillan corlstriction subjects was similar t(J the latency ofthe normal suttjrcts dilatation to darkness. Thr authors do not commfbnt