Choroidal neovascularization (CNV) consists of new vessels of choroidal origin extending through Bruch's membrane into the sub-retinal-pigment-epithelial (subRPE ) or sub-neurosensory retinal space. The significance of these vessels was first recognized by Gass in 1967, when he suggested that they play a role in the pathogenesis of disciform macular detachment associated with senile macular degeneration1 and possibly with angioid streaks.2 In 1973, Gass demonstrated that CNV occurs in a variety of clinical syndromes and predisposes the eyes to serous and hemorrhagic macular detachment.3 A 4-year-old boy with CNV and optic nerve head drusen was reported as one of the case examples. Seven of the eight clinical syndromes reported by Gass to be associated with choroidal neovascular membranes can be seen in the pediatric population.3 The report also emphasized that good quality, rapidsequence fluorescein angiography (FA) is required for detecting CNV and determining candidates for photocoagulation treatment.
We wish to reacquaint the pediatric ophthalmologist with CNV, a sight-threatening but potentially treatable condition. A review of the literature, with reference to the pediatric age group, and five illustrative cases are presented. Guidelines to recognition, parent and patient instruction, and the selective use of FA are then emphasized. The Table represents the most complete and updated available list of conditions associated with CNV in children and adolescents.
CASE 1: A 10-year-old boy had a 2-week history of metamorphopsia and slight blurring of vision of the right eye. Visual acuity was 20/40 OD and 20/20 OS. A small scotoma with surrounding metamorphopsia just inferior to fixation in the right eye appeared on Amsler grid viewing. Ophthalmoscopy revealed a small ring-shaped pigmented lesion just above the fovea of the right eye with a disc diameter of elevated RPE and a hint of subretinal blood (Figure 1). The left eye was normal. Neither eye demonstrated features of presumed ocular histoplasmosis syndrome (POHS) or any other known predisposing condition for CNV. Fluorescein angiography (FA) showed an active choroidal neovascular membrane near the fovea of the right eye (Figure 2). Krypton laser photocoagulation under topical anesthesia guided by projected FA was performed. Several subsequent FAs demonstrated successful obliteration of the CNV. Visual acuity remains 20/30 in the right eye without metamorphopsia 18 months after treatment. Daily Amsler grid viewing continues to be stressed for each eye.
FIGURE 1: Case 1. Idiopathic CNV in a 10-year-old boy.
FIGURE 2: Case 1. Fluorescein angiogram demonstrating CNV superior to the fovea.
FIGURE 3: Case 2. CNV with adjacent subretinal hemorrhage in a 14-year-old girl.
FIGURE 4: Case 2. Fluorescein angiogram demonstrating peripapillary CNV. Subretinal blood has diminished.
CASE 2. A 14-year-old girl had a history of approximately 2 months of blurred vision and metamorphopsia of the right eye. Visual acuity was 20/200 OD and 20/15 OS. Ophthalmoscopy revealed a pale discoloration extending from the inferior temporal border of the right optic disc, which bordered a large subretinal hemorrhage involving the foveal area (Figure 3). FA verified a choroidal neovascular membrane with associated subretinal blood (Figure 4). After resorption of subretinal blood and photocoagulation of the CNV, vision improved to 20/100. Peripapillary atrophy in both eyes suggested POHS. No peripheral punched-out lesions were present, however, in either fundus.
CASE 3: A 15-year-old girl came to us 19 months after a rock had struck her right eye, resulting in a posterior choroidal rupture without initial acuity loss. She complained of "fuzzy" vision. Visual acuity was 20/30 - 1 OD and 20/15 OS. On ophthalmoscopy, at the superior edge of a curvilinear choroidal rupture, a subtle dirty-grey lesion two thirds of a disc diameter was seen surrounded by a fine lacy border of subretinal blood (Figure 5). FA verified a choroidal neovascular membrane bordered by the blocked fluorescence pattern of the subretinal blood (Figure 6). Over the next several months vision decreased to counting fingers despite attempts to arrest progression of the CNV and its attendant scarring with argon laser photocoagulation. Follow-up examinations have revealed no change in acuity.
CASE 4. A 12-year-old girl had a central visual loss for approximately 3 months OS. She was reported to have had a normal eye examination 5 years prior. A recent examination by the referring ophthalmologist revealed blurred disc margins in both eyes and a pigmented chorioretinal lesion of the left fundus. Neurologic examination was normal. Visual acuity was 20/20 OD and 20/400 OS. Ophthalmoscopy revealed blurred, scalloped margins to both discs. A yellow spot in the center of the left disc was felt to be a visible druse. Marked atrophy of the RPE was present in the papillomacular bundle of the left eye, including the fovea. A raised pigmented chorioretinal scar with a small amount of neurosensory elevation was present just adjacent to the temporal border of the left disc, suggesting late effects of CNV (Figure 7). FA also suggested CNV. Treatment was not felt to be potentially beneficial. Amsler grid viewing was strongly advised for the unaffected right eye. Two and one half years later Amsler grid distortion and episodic blurring were noticed in the right eye. Ophthalmoscopy revealed CNV at the border of the right disc at the 9 o'clock position. A modest amount of RPE atrophy and a characteristic pigmented ring were present (Figure 8). FA verified CNV. Vision remained 20/20 OD. Close follow-up was chosen over photocoagulation, because the symptoms had been fleeting and the acuity remained excellent. The lesion gradually involuted, becoming a fiat pigmented chorioretinal scar. Amsler grid viewing continues daily.
FIGURE 5: Case 3. CNV extending from the edge of a traumatic choroidal rupture in a 15-year-old girl.
FIGURE 6: Case 3. Fluorescein angiogram demonstrating CNV and choroidal rupture.
FIGURE 7: Case 4. Chorioretinal scarring from CNV associated with disc drusen in the left eye of a 12-year-old girl.
FIGURE 8: Case 4. Active peripapillary CNV in the right eye 2½ years after CNV developed in the left eye.
FIGURE 9: Case 5. Subfoveal CNV in a 18-year-old with rubella retinopathy.
FIGURE 10: Case 5. Disciform scar 11 months after initial visual symptoms of CNV.
Reported Associations With Choroidal Neovascularization in Children and Adolescents
CASE 5: An 18-year-old man was examined for poor vision in his left eye. Acuity, documented to be normal in the past, was 20/20 OD and 20/200 OS. His mother had a documented rubella infection during pregnancy. He was systemically well and possessed normal hearing. Sub-foveal blood and pigmentary clumping was present in the left eye on ophthalmoscopy (Figure 9). Widespread retinal pigment epithelial mottling was seen in both eyes in a pattern typical for rubella retinopathy. An electroretinogram (ERG) was normal. FA confirmed the presence of sub-foveal CNV. Treatment was not felt to be indicated based on the subfoveal location of the CNV and the uncertain natural history of such membranes. Eleven months after initial examination, a disciform scar evolved in the macula of the left eye (Figure 10). Visual acuity is 20/20 OD and 20/400 OS. Amsler grid viewing is continuing daily in the right eye, which has better visual acuity.
Choroidal neovascularization most commonly occurs in either a macular or peripapillary location. New vessels extend through Bruch's membrane or around its peripapillary end. Conditions such as traumatic choroidal rupture, angioid streaks, and myopic lacquer cracks predispose to CNV secondary to breaks in Bruchs membrane. Optic nerve head drusen and congenital optic pits could disturb the peripapillary end of Bruch's. In addition, it is now known that new choroidal vessels can digest an intact Bruch's membrane.4 CNV thus has been reported in association with many diverse disturbances of the retina, choroid, and RPE,5 and represents an important cause of late visual loss in many of these conditions. The Table lists only conditions that have been associated with CNV in children and adolescents.
When CNV occurs in the absence of any demonstrable associated condition, it is classified as idiopathic. A recent series of idiopathic CNV represented a wide range of ages.6 We report a 10-year-old boy (Case 1) with an idiopathic CNV successfully treated with photocoagulation near the fovea, preserving good central acuity.
The presumed ocular histoplasmosis syndrome (POHS) is most commonly associated with CNV in young adults, and has also been reported to occur in the pediatric population. In 1977, Klein et al reported on 208 FAs of CNV in POHS with an age range of 15 to 59 years (average age 39 years).7 Age was found to be unrelated to visual prognosis. Gutman later reported a series of 108 eyes in 83 patients with CNV in POHS.8 Forty-nine percent of patients were less than 40 years old. Four cases (4%) were between 10 and 19 years old, each with the neovascular process extending beneath the fovea.8 An additional 82 patients with subfoveal or juxtafoveal CNV in POHS were reported by Olk et al, including three patients less than 20 years old.9 Again, a full 50% of patients in this series were less than 40 years old. An early report of 19 eyes with CNV in POHS10 helped establish that with rapid sequence FA, new vessels could be demonstrated even before subretinal hemorrhage occurred. Although Case 2 does not present the full spectrum of POHS, the pattern of CNV extending toward the fovea with evidence of additional neovascular growth at several peripapillary locations (Figure 4) is a pattern not uncommon in more obvious POHS-associated CNV.
Choroidal rupture is a common consequence of blunt trauma to the eye. In 1974, Smith et al recognized that the most common reason for late vision loss after choroidal rupture in young people is CNV11 In 1975, Hilton reported four patients with CNV 6 to 14 months following traumatic choroidal rupture.12 All were under 30 years old; the youngest was 16. The author stated that the long-term prognosis for macular function should be guarded in any patient with traumatic choroidal rupture near the macula due to a predisposition for CNV. Case 3 is an example of CNV recognized 19 months following choroidal rupture. In this case, progression to serious visual loss occurred despite attempted laser obliteration.
Optic disc drusen are known to simulate papilledema in children and adolescents. Associated hemorrhages have been recognized since 1895.13 More recently, however, it has become apparent that although superficial intraretinal hemorrhages are relatively innocuous, hemorrhages beneath the pigment epithelium are much more serious.14 These subretinal hemorrhages are the direct result of CNV and can threaten central vision, especially when occurring on the temporal aspect of the disc. As stated earlier, Gass reported CNV associated with disc drusen in a 4-year-old child in his classic 1973 paper.3 Twenty-three patients, aged 6 to 70 years with optic disc drusen and subretinal hemorrhage, were reported in 1974. 14 The authors stressed that progression of CNV to involve the macula may be rapid, and treatment with photocoagulation should be instituted promptly14 In contradistinction, Harris et al15 stated that many of these neovascular nets will involute spontaneously and thus require no treatment. Seven eyes of four patients, ages 8, 12, 12, and 24 years, were reported. Case 4 illustrates that disc drusen, as well as some other predisposing conditions, may put the patient at risk for bilateral CNV. An extensive chorioretinal scar was present in the left eye on initial examination. Daily Amsler grid viewing with the right eye was rewarded by early detection of a neovascular process that fortunately involuted without treatment.
Rubella retinopathy is considered a benign manifestation of the congenital rubella syndrome that presents no threat to vision.16,17 In 1978, however, two reports described five patients, ages 7, 10, 11, 14, and 17 years, with rubella retinopathy and CNV.18,19 Vision was reduced from normal or near normal to the 20/200 range in all affected eyes. In 1982, a 28-year-old patient was reported to have spontaneous resolution of a rubella retinopathy-associated CNV, with recovery of 20/20 vision.20 The diagnosis of rubella retinopathy in Case 5 was made presumptively based on typical ophthalmoscopic findings, a normal ERG, and a history of rubella infection in the mother during pregnancy.
Chronic uveitis has been shown to lead to CNV rarely When it occurs, however, it is usually in the pediatric population. A 17-year-old girl with bilateral peripapillary CNV in chronic uveitis was described in 1978.21 Two patients, ages 9 and 12 years, with chronic uveitis of unknown etiology, were reported to develop CNV in 1980.22 One developed unilateral peripapillary CNV, the other developed bilateral macular CNV. The chronic inflammation, the authors theorized, damaged the choriocapillaris/ Bruch's membrane/retinal-pigment-epithelial interface, providing a route for vascular ingrowth into the subpigment-epithelial and sub-neurosensory retinal spaces.22 Two patients (ages 9 and 17 years) with presumed sarcoid uveitis and CNV also have been reported.23
Angioid streaks are seen in the pediatric population, usually with pseudoxanthoma elasticum. CNV is commonly reported in adults24 and less commonly reported in pediatric patients with angioid streaks.25 This frequency also applies to degenerative myopia. Although CNV is much more commonly associated with degenerative myopia in adulthood, an occasional pediatric patient is also affected.25 A recent retrospective analysis of 354 eyes of 188 patients with degenerative myopia (ages 14 to 80 years) revealed 149 eyes with evidence of CNV.26 CNV occurred in this series from the teens to the 80s.
In 1970, Gass reported evidence of new vessels of choroidal origin, subretinal hemorrhage, and subsequent chorio-retinal anastomosis in macular scarring secondary to Toxocara canis (ages 10, 12, and 14).27 This finding was subsequently verified histopathologically.28
In 1976, a 9-year-old boy with Bests vitelliform macular dystrophy and a 2-week history of metamorphopsia was reported to have CNV in the macula of his left eye.29 Many authors have noted subretinal hemorrhage in some cases during the disruptive phase of vitelliform lesion,30 but this report presented the first convincing evidence that CNV can be an integral part of Best's disease.29
Ocular toxoplasmosis was added to the growing list of disease processes documented to lead to CNV in the pediatric age group with a 1981 report from Fine et al31 of two patients (ages 13 and 18) with subfoveal neovascularization. The following year, reports of patients ages 7 and 8 with optic nerve pits associated with CNV, 32 ana a 15-yearold boy with bilateral choroidal osteoma and CNV,33 appeared. Isolated reports of young patients with CNV associated with fundus flavimaculatus (age 14),34 and choroideremia (age 14),35 also have been documented.
Photocoagulation, the only established treatment for CNV, also is well known to damage Bruch's membrane at times and actually stimulate choroidal new vessel growth.36,37 Photocoagulation has even been used to create CNV in monkeys.38 CNV after photocoagulation for sickle cell retinopathy was reported in a 5-year follow-up study in 1980.39 Six patients with CNV in this study were 14 to 19 years old. The following year, Condon et al40 presented evidence that the younger, treated sickle cell patient actually developed the complication of CNV more commonly than the older patients. Neovascular growth of choroidal origin also was reported to occur in sickle cell retinopathy without prior photocoagulation.41
The list of CNV-assoeiated conditions is growing as recognition improves. Also, it is not uncommon in our experience to see young patients with a history of poor vision in an eye secondary to a disciform scar. One of the conditions in the Table is often present. Often, no specific onset for the vision loss can be illicted. Verhoeff coined the phrase "juvenile disciform degeneration" to describe this process, which he stated was often hemorrhagic during its evolution.42 CNV is undoubtedly the precipitating event leading to scarring in many of these patients. The disciform process has been reported to occur rapidly at times in young patients.43
DIAGNOSIS AND TREATMENT
Presentation: Patients usually have metamorphopsia, blurring, or vision loss of uncertain onset. Occasionally, a suspicious clinical appearance is seen on routine fundus examination. Cases 1, 2, and 4 demonstrate the importance of metamorphopsia, the most common presenting symptom of CNV in any age group. Subtle distortions or scotoma can be accentuated by having the patient view an Amsler grid at 14 inches uniocularly.
Clinical Fundus Exam and Fluorescein Angiography: Gass described the fundus findings of CNV as a dirty, yellow, or greyish, usually circular or oval patch; a pigmented ring; or a pigmented mound beneath the retina in the macula or peripapillary areas. He also noted that one or more splotchy areas or a ring of subretinal blood may be present along the outer edge of the neovascular membrane.3 Henkind described a dirty grey or greenish subretinal blemish that is often visible, but noted that neovascular vessels may remain invisible clinically until bleeding occurs beneath the RPE or neurosensory retina.44 We therefore recommend FA for patients with unexplained metamorphopsia or vision loss, especially when accompanied by one of the predisposing conditions listed in the Table. When subretinal fluid, blood, or exudate is present, or a dirty grey hue is seen, FA also should be performed. The major fluorescein angiographic features of CNV are lacy, nodular, or irregular hyperfluorescence in the early phase, with pooling of dye in the sub-neurosensory retinal space during the late phase of the angiogram. Gass has written that often a bicycle-wheel pattern is formed by the radiating capillaries, which are then obscured during recirculation of dye by leakage into the connective tissue and exudate surrounding the new vessels.3
Patient and Parent Instructions; Any patient with a history of previous CNV, or a predisposing fundus condition, is instructed to occlude each eye alternately and view the environment briefly on a daily basis. In addition, an Amsler grid is viewed at reading distance with each eye daily, in older adolescents, we advise taping the grid to the bathroom mirror for quick, convenient daily viewing. The importance of monocular viewing, especially of the Amsler grid, cannot be overemphasized. Metamorphopsia and blurring can go undetected without this simple technique. Patients with angioid streaks, POHS scars, and traumatic choroidal ruptures near the macula should be encouraged to use the Amsler grid viewing technique. These patients are at high risk of vision loss should CNV extend from these perifoveal disturbances. We urge patients to report visual changes promptly, and we stress the need for long-term follow-up. If visual changes occur, we have the patient draw the distortion on the grid or circle the lines that appear distorted or missing. This is then filed for future comparisons.
Treatment: The Macular Photocoagulation Study Group (MPSG) has shown that laser photocoagulation can be effective in treating select patients with idiopathic CNV45 and CNV associated with age-related macular degeneration46 or POHS47 when located 200 to 2500 µm from the center of the foveal avascular zone. The precise role of treatment for CNV in other conditions or locations is less clear and beyond the scope of this article. Although improvement is sometimes seen, preventing further visual deterioration is the goal of treatment. Even this goal is not always attained, as seen in Case 3. Also, recurrence of CNV at the margins of treatment is disturbingly high.48 Indefinite follow-up is thus recommended.
Case 1 is now more than 18 months post-treatment without recurrence. This patient is, to the best of our knowledge, the youngest reported successfully treated with krypton laser photocoagulation near the fovea. With better recognition and earlier diagnosis, successful treatment in younger patients should become more common.
1. Gass JDM: Pathogenesis of disciform detachment of the neuroepithelium: III. Senile disciform macular degeneration. Am J Ophthalmol 1967; 63:617-644.
2. Gass JDM: Pathogenesis of disciform detachment of the neuroepithelium: V. Disciform macular degeneration secondary to focal choroiditis. Am J Ophthalmol 1967; 63:661-687.
3. Gass JDM: Choroidal neovascular membranes: Their visualization and treatment. Trans Am Acad Ophthalmol Otolaryngol 1973; 77:310-320.
4. Heriot WJ, Henkind P, Bellhorn RW, et al: Choroidal neovascularization can digest Bruch's membrane: A prior break is not essential. Ophthalmology 1984; 91:1603-1608.
5. Green WR, Wilson DJ: Choroidal neovascularization. Ophthalmology 1986; 93:1169-1176.
6. Cleasby GW: Idiopathic focal subretinal neovascularization. Am J Ophthalmol 1976; 81:590-596.
7. Klein ML, Fine SL, Knox DL, et al: Follow-up study in eyes with choroidal neovascularization caused by presumed ocular histoplasmosis. Am J Ophthalmol 1977; 83:830-835.
8. Gutman FA: The natural course of active choroidal lesions in the presumed ocular histoplasmosis syndrome. Trans Am Ophthalmol Soc 1979; 77:515-541.
9. Olk RJ, Burgess DB, McCormick PA: Subfoveal and juxtafoveal subretinal neovascularization in the presumed ocular histoplasmosis syndrome: Visual prognosis. Ophthalmology 1984; 91:1592-1602.
10. Krill AE, Archer D: Choroidal neovascularization in multifocal (presumed histoplasmin) choroiditis. Arch Ophthalmol 1970; 84:595-604.
11. Smith RE, Kelley JS, Harbin TS: Late macular complications of choroidal ruptures. Am J Ophthalmol 1974; 77:650-658.
12. Hilton GF: Late serosanguineous detachment of the macula after traumatic choroidal rupture. Am J Ophthalmol 1975; 79:997-1000.
13. Gifford H: An unusual case of hyaline bodies in the optic nerve. Arch Ophthalmol 1895; 24:395-401.
14. Wise GN, Henkind P, Alterman M: Optic disc drusen and subretinal hemorrhage. Trans Am Acad Ophthalmol Otolaryngol 1974; 78:212-219.
15. Harris MJ, Fine SL, Owens SL: Hemorrhagic complications of optic nerve drusen. Am J Ophthalmol 1981; 92:70-76.
16. Hertzberg R: Twenty-five-year follow-up of ocular surgery defects in congenital rubella. Am J Ophthalmol 1968; 66:269-271.
17. Krill AE: Retinopathy secondary to rubella. Int Ophthalmol Clin 1972; 12:89-103.
18. Frank KE, Purnell EW: Subretinal neovascularization following rubella retinopathy. Am J Ophthalmol 1978; 86:462-466.
19. Deutman AF, Grizzard WS: Rubella retinopathy and sub-retinal neovascularization. Am J Ophthalmol 1978; 85:82-87.
20. Bonomo PP: Involution without disciform scarring of subretinal neovascularization in presumed rubella retinopathy. A case report. Acta Ophthalmol 1982; 60:141-146.
21. Schwartz PL, Gradoudas ES, Lapus JV: Peripapillary subretinal neovascularization in chronic uveitis. Arch Ophthalmol 1978; 96:836-838.
22. Augsburger JJ, Benson WE: Subretinal neovascularization in chronic uveitis. Graefes Arch Clin Exp Ophthalmol 1980; 215:43-51.
23. Gragoudas ES, Regan CDJ: Peripapillary subretinal neovascularization in presumed sarcoidosis. Arch Ophthalmol 1981; 99:1194-1197.
24. Watzke RC: Acquired macular disease, in Duane TD (ed): Clinical Ophthalmology, Philadelphia, Harper and Row, 1986, vol 3, chap 23.
25. Augsburger JJ, Goldberg RE, Magargal LE: Retinal and choroidal vascular abnormalities and fluorescein angiography, in Harley RD (ed): Pediatric Ophthalmology, Philadelphia, WB Saunders, 1983, vol 1, chap 21.
26. Avila MP, Weiter JJ, Jalkh AE, et al: Natural history of choroidal neovascularization in degenerative myopia. Ophthalmology 1984; 91:1573-1581.
27. Gass JDM: Stereoscopic Atlas of Macular Diseases, St Louis, CV Mosby, 1970, pp 62-65.
28. Green WR, Gass JDM: Senile disciform degeneration of the macula: Retinal arterialization of the fibrous plaque demonstrated clinically and histopathologically. Arch Ophthalmol 1971; 86:487-494.
29. Miller SA, Bresnick GH, Chandra SR: Choroidal neovascular membrane in Best's vitelliform macular dystrophy. Am J Ophthalmol 1976; 82:252-255.
30. Benson WE, Kolker AE, Enoch JM, et al: Best's vitelliform macular dystrophy. Am J Ophthalmol 1975; 79:59-66.
31 . Fine SL, Owens SL, Haller JA, et al: Choroidal neovascularization as a late complication of ocular toxoplasmosis. Am J Ophthalmol 1981; 91:318-322.
32. Borodic GE, Gragoudas ES, Edward WO, et al: Subretinal neovascularization and serous macular detachment: Association with congenital optic pits. Arch Ophthalmol 1984; 102:229-231.
33. Avila MP, El-Markabi H, Azzolini C, et al: Bilateral choroidal osteoma with subretinal neovascularization. Ann Ophthalmol 1984; 16:381-385.
34. Klein R, Lewis RA, Meyers SM, et al: Subretinal neovascularization associated with fundus flavimaculatus. Arch Ophthalmol 1978; 96:2054-2057.
35. Robinson D, Tiedeman JS: Choroideremia associated with subretinal neovascular membrane formation (poster abstract). Ophthalmology 1986; 93(August suppl):125.
36. Francois J, Delaey JJ, Cambie E, et al: Neovascularization after argon laser photocoagulation of macular lesions. Am J Ophthalmol 1975; 79:206-210.
37. Fine SL, Patz A, Orth DH, et al: Subretinal neovascularization developing after prophylactic argon laser photocoagulation of atrophic macular scars. Am J Ophthalmol 1976; 82:352-357.
38. Ryan SJ: Subretinal neovascularization: Natural history of an experimental model. Arch Ophthalmol 1982; 100:1804-1809.
39. Condon PI, Serjeant GR: Photocoagulation in proliferative sickle retinopathy: Results of a 5-year study. Br J Ophthalmol 1980; 64:832-840.
40. Condon PI, Jampol JM, Ford SM, et al: Choroidal neovascularization induced by photocoagulation in sickle cell disease. Br J Ophthalmol 1981; 65:192-197.
41. Liang JC, Jampot LM: Spontaneous peripheral chorioretinal neovascularization in association with sickle cell anaemia. Br J Ophthalmol 1983; 67:107-110.
42. Verhoeff FH, Grossman HP: Pathogenesis of disciform degeneration of the macula. Arch Ophthalmol 1937; 18:561-585.
43. Doran RML, Hamilton AM: Disciform macular degeneration in young adults. Trans Ophthalmol Soc UK 1982; 102:471-480.
44. Henkind P: Ocular neovascularization: The Krill memorial lecture. Am J Ophthalmol 1978; 85:287-301.
45. Macular Photocoagulation Study Group: Argon laser photocoagulation for idiopathic neovascularization: Results of a randomized clinical trial. Arch Ophthalmol 1983; 101:1358-1361.
46. Macular Photocoagulation Study Group: Argon laser photocoagulation for senile macular degeneration: Results of a randomized clinical trial. Arch Ophthalmol 1982; 100:912-918.
47. Macular Photocoagulation Study Group: Argon laser photocoagulation for ocular histoplasmosis: Results of a randomized clinical trial. Arch Ophthalmol 1983; 101:1347-1357.
48. Sorenson JA, Yannuzzi LA, Shakin JL: Recurrent subretinal neovascularization. Ophthalmology 1985; 92:1059-1074.
Reported Associations With Choroidal Neovascularization in Children and Adolescents