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Br J Ophthalmol: first published as 10.1136/bjo.71.11.844 on 1 November 1987. Downloaded from

British Journal of , 1987, 71, 844-849

Glaucoma in Fuchs' heterochromic cyclitis associated with congenital Horner's syndrome

LUCIAN S REGENBOGEN AND NAVA NAVEH-FLOMAN From the Maurice and Gabriela Goldschlager Eye Institute, Sheba Medical Center, Tel Hashomer, Sackler School ofMedicine, Tel Aviv University, Tel Aviv, Israel

SUMMARY We report a retrospective study of five patients with monocular Fuchs' heterochromic cyclitis associated with an ipsilateral Horner's syndrome. The minimum follow-up was 10 years. The presenting findings were cyclitis in three of the patients and heterochromia iridis associated with blepharoptosis in the other two. The major factors affecting all five patients were and glaucoma. The was uncontrolled even with maximal therapy, and anti- glaucomatous surgery was performed in all cases. A short period of good postoperative control was followed by an intractable ocular , causing loss of useful vision in all patients. The remarkable combination of Horner's syndrome with glaucoma and their interaction is discussed.

Fuchs' heterochromic cyclitis (FHC) is a commoner inflammations in the left eye during the preceding ocular disorder than has generally been recognised.f three years. Drooping of the and discoloration It is frequently overlooked when the heterochromia of the had been evident in the affected eye since is slight or when all its clinical features are not present early childhood. at the same time. His best corrected visual acuity was 6/7 (20/25) in One of the most serious complications of the the right eye (RE) and limited to light perception in disease is glaucoma, which has been observed in the left eye (LE). The intraocular pressure (IOP) in 18*6% of the studied cases.6 Although there is no the LE while the patient was on 4% and unanimity on the prognosis for the glaucoma in this 250 mg was 28 mmHg. The IOP in the http://bjo.bmj.com/ syndrome,357 recent communications"" suggest that RE was 14 mmHg, and when the patient was it usually becomes resistant to medical therapy, and submitted to a provocative topical surgery is only moderately successful. test the eye did not react with a significant rise in The purpose of this report is to describe the tension. manifestations of unilateral FHC associated with External examination of the LE revealed 2 mm Horner's syndrome and complicated by ipsilateral blepharoptosis. Slit-lamp biomicroscopy disclosed a

glaucoma in five patients. To the best of our know- normal RE and a few white keratic precipitates (KP) on October 2, 2021 by guest. Protected copyright. ledge, no similar cases have been previously with flare and cells in the anterior chamber in the LE. reported. We discuss the significance of the associa- The right iris was brown and rich in crypts in marked tion and the implications regarding the unfavourable to that of the left eye, which was light grey, course of the glaucoma in these patients. without crypts, and showed transillumination throughout an extensive depigmented area. Gonio- Case reports scopy showed a few engorged blood vessels in the LE and wide open angles in both eyes. Ophthalmoscopic CASE 1 examination showed a normal right fundus, whereas A 53-year-old male was first seen in May 1970 visualisation in the LE was impossible owing to an because of a progressive decrease in visual acuity, almost mature cataract. elevated intraocular pressure (IOP), and recurrent Two weeks after discontinuation of topical anti- glaucoma both reacted to light and , and of 1-5 mm was disclosed Correspondence to Professor L S Regenbogen, Maurice and Gabriela Goldschlager Eye Institute, Sheba Medical Center, Tel in the LE; 4% hydrochloride failed to dilate Hashomer 52621, Israel. the left but fully dilated the right. Marked left 844 Br J Ophthalmol: first published as 10.1136/bjo.71.11.844 on 1 November 1987. Downloaded from

Glaucoma in Fuchs' heterochromic cyclitis associated with congenital Horner's syndrome 845 pupillary dilatation was observed after further instil- remained uncontrolled (32 mmHg) despite maxi- lations of 1% epinephrine. mum medical therapy. The left became In January 1972 cyclodialysis was performed in the progressively damaged, and the showed a LE because of uncontrollable IOP despite supple- significant superior nasal . In July 1978 mentary medication. After an apparently good post- was performed, with subsequent operative period of three months the IOP increased bleeding into the anterior chamber. The hyphaema, progressively to 30 mmHg despite resumption of not absorbed after seven postoperative days, medical therapy. required surgical removal. No filtering bleb After an uneventful left intracapsular extraction developed, though the IOP decreased to 15 mmHg. carried out in April 1972, which restored the vision to The patient was seen incidentally in April 1983 6/10, a 0 40 glaucomatous cupping and involvement because of a traumatic in the RE. The of the inferior temporal rim were noticed. The left IOP was RE 14 mmHg and LE 30 mmHg despite visual field showed a small step. In March 1977 maximally tolerated medical therapy. In the LE trabeculectomy was performed because of further vision was reduced to 1/20, and the visual field deterioration in the left visual field. A 2 mm consisted of a central zone connected by a narrow hyphaema was noted after the operation. Transient bridge to a temporal island due to a totally cupped good postoperative control of the IOP was followed optic disc. by persistent elevation to 35 mmHg. The patient was not seen again until 1984, when the IOP in the LE was CASE 3 uncontrolled despite maximum medical therapy. The A 60-year-old female presented in March 1975 with a optic disc was totally cupped, and the visual field was 48-hour history of loss of vision in her painful RE. reduced to 'tubular', with an additional isolated The patient claimed to have had a 'smaller' right eye temporal island. The RE remained normal. and ipsilateral iris hypochromia since childhood. For many years she had received intermittent topical CASE 2 for chronic inflammation in the RE. A 51-year-old female was referred for consultation in Ocular examination revealed visual acuity limited January 1973 because of a history of recurrent to light perception in the RE and 6/6 (20/20) in inflammation and decreased vision in the LE. During the LE. The anterior segment of the RE showed the previous 10 months the affected eye had blepharoptosis of 2-5 mm, with the lower lid slightly developed , and 4% pilocarpine higher than that of the left side. Biomicroscopy of the and were administered. RE disclosed perikeratic congestion, hazy , a On examination her corrected visual acuity was few hyaline posterior deposits, turbid aqueous, a

RE 6/6 (20/20) and LE counting fingers. The IOP was hypochromic iris, and a hypermature cataract. The http://bjo.bmj.com/ 25 mmHg in the LE (under topical medication) and LE was normal. Applanation tonometry values were 15 mmHg in the RE. The RE was normal, and its IOP RE 50 mmHg and LE 18 mmHg. On the did not react to topical steroid testing. angles were open. Right phakolytic glaucoma was The left upper eyelid had 2 mm of blepharoptosis diagnosed, and uneventful intracapsular cataract with good elevator function; a picture taken when the extraction was performed. After the operation the patient was 10 years old confirmed the presence of best corrected visual acuity in the RE improved to 6/9 this abnormality since childhood. The right eyelid (20/30), and the IOP dropped to 22 mmHg. The right on October 2, 2021 by guest. Protected copyright. was normal. optic disc had a deep cup with involvement of the Biomicroscopy disclosed typical FHC findings with inferotemporal rim and a corresponding visual field a mature cataract in the LE. Gonioscopic examina- defect. The iridocorneal angle remained open all tion revealed open angles with around without synechiae. A few months later the visible. A few large vessels were seen in the angle of IOP progressively increased to 30 mmHg and the LE. remained at this level despite maximal medical The left pupil was miotic and unresponsive to 4% therapy. cocaine (administered while the patient was off Cyclodialysis was performed in February 1976, but pilocarpine treatment for 10 days), but dilatation was its hypotensive effect was only transitory. Six months observed after repeated instillations of 1% epine- later the IOP increased again to 32 mmHg despite phrine. The right pupil reacted normally. maximal topical and systemic medication. In the 10 Uneventful left intracapsular cataract extraction years' follow-up the IOP remained uncontrolled and was performed in January 1974 with subsequent the optic disc was progressively damaged. In the improvement in visual acuity to 6/12 (20/40). At this unaffected eye the IOP remained normal, and a stage both optic discs were normal. dexamethasone test was negative. During the following years the IOP in the LE The patient refused additional surgical treatment. Br J Ophthalmol: first published as 10.1136/bjo.71.11.844 on 1 November 1987. Downloaded from

846 Lucian S Regenbogen and Nava Naveh-Floman

CASE 4 On ocular examination his best refracted visual A 52-year-old woman was first seen in December acuity was RE 6/6 (20/20) and LE 6/24 (20/80). 1971 because of a 14-year history of heterochromic External examination of the LE revealed a blep- cyclitis, cataract, and ocular hypertension in her RE. haroptosis of 2-5 mm; slit-lamp biomicroscopy dis- The ocular inflammation and the IOP responded closed in the LE a few KP with filaments and a favourably to topical therapy. The patient reported hypochromic iris. The normal crisp appearance ofthe that the affected eye had been 'smaller' than the left iris was absent, and the iris surface was blurred. A eye ever since she could remember. transillumination defect of the iris and gaps in the Slight and blepharoptosis of 2 mm pigment ruff were noted. Gonioscopy revealed an with dropping of the lower lids was noted in the open angle with few dilated blood vessels. The affected eye. showed an incipient subcapsular posterior cataract. Best corrected visual acuity was RE 6/60 (20/200) A deep cup was noted. The IOP was 30 mmHg, and a and LE 6/7M5 (20/25). The IOP in the RE was small nasal defect was disclosed in the visual field. controlled with 4% pilocarpine and acetazolamide The RE was completely normal. Its IOP was 12 250 mg. The IOP in the LE was normal and did not mmHg, and the eye did not react to a provocative react to topical testing. topical dexamethasone test. Biomicroscopy ofthe RE disclosed a few dispersed Both pupils reacted normally to light and accom- KP and minimal flare in the anterior chamber. The modation. Miosis of 1*5 mm was present in the LE. iris was hypochromic, with a dull surface, and show- After instillation of 4% cocaine the left pupil ing patchy areas of transillumination. Gonioscopic- remained unchanged, while the right pupil reacted ally the angle was partially closed in the upper half with 5 mm dilatation. but otherwise open to the . A posterior Over a one-year period the IOP in the LE subcapsular immature cataract was present. The optic remained uncontrolled despite strong topical and disc seemed normal. The LE was absolutely normal. systemic medication, and a significant progression in The miotic right pupil, two weeks after discon- loss ofvisual field was disclosed. Trabeculectomy was tinuation of topical medication, reacted normally to performed in January 1976. Hyphaema occurred light and accommodation but failed to respond to a during surgery. No distinct conjunctival bleb 4% cocaine test, whereas the normal opposite pupil developed postoperatively. The IOP remained con- dilated widely. trolled for nine months without medication. In May In June 1973 an uneventful extracapsular extrac- 1977 extensive rubeosis was noted, and the IOP tion in the RE followed by discission of a secondary increased to 36 mmHg despite the reinstitution of cataract restored vision to 6/18 (20/60). After surgery antiglaucoma medical therapy. The patient was lost slight atrophy of the optic disc was disclosed, and a to follow-up, but when he was last seen, in May

1984, http://bjo.bmj.com/ nasal field defect was detected. The IOP was normal the IOP in the LE exceeded 40 mmHg, and vision was but after 10 months measured 30 mmHg despite. reduced to temporal light perception only. The left maximally tolerated medical therapy. Cyclodialysis optic disc was totally cupped. The RE remained performed in April 1974 controlled the IOP for a normal. period of eight months, but was followed by refrac- tory ocular hypertension during the subsequent Discussion years. A Scheie filtering procedure performed in March 1977 was followed by hyphaema and had a The distinctive features of FHC are slowly pro- on October 2, 2021 by guest. Protected copyright. hypotensive effect that lasted only a year after gressive with non-pigmented KP, minimal surgery. cells and flares in the anterior chamber, atrophy of In December 1984 a follow-up examination the iris with hypochromia, and absence of posterior showed that the right optic disc was totally damaged, synechiae. The disorder is often associated with and the visual field was reduced to two temporal cataract and sometimes with glaucoma. islands. The LE remained normal. The aetiology of FHC is still subject to con- troversy. Some investigators consider that we are CASE 5 dealing with an immunological disease related to a A 56-year-old male was referred to us in May 1974 defect in supressor T-cell activity.'0 Earlier theories because of a gradual decrease in visual acuity in the pointed to the possible role of an initial infectious LE during the preceding three years. The patient had process.' More recent studies -have demonstrated a long history of repeated episodes of inflammation, chorioretinal lesions, particularly suggestive of toxo- as well as a lighter coloured iris in that eye. He also plasmosis."I 12 The neurogenic theory of Passow'3 reported that the left upper lid had drooped since his proposed that damage to the sympathetic nervous youth. system can mediate the changes in FHC; the pre- Br J Ophthalmol: first published as 10.1136/bjo.71.11.844 on 1 November 1987. Downloaded from

Glaucoma in Fuchs' heterochromic cyclitis associated with congenital Horner's syndrome 847 sumption originates from the fact that sympathetic Franceschetti2 and Smith and O'Connor'" but differs lesions due to neonatal injury may be followed by from the experience of Ward and Hart,'6 Norn,'7 ipsilateral iris hypochromia. The hereditary theory6 and Liesegang,8 who found a high prevalence of originates from the fact that the more important hyphaema, extensive peripheral synechiae, corneal types of iris heterochromia are hereditary in origin. oedema, and persistent pupillary membranes. Our Horner's syndrome is an uncommon condition results also differ from the findings of Hart and deriving from an interruption of the sympathetic Ward,'8 which indicated that lens extraction has a pathway at any point along its course between the deleterious effect on the dynamics of the TOP in eyes hypothalamus and the . The syndrome accom- with FHC. Because previous patients with FHC who panied by iris heterochromia usually indicates a long- underwent extracapsular cataract extraction with standing cervical sympathetic denervation. posterior chamber lens implantation did not show a We report here a follow-up for 10 to 14 years offive tendency to ocular hypertension,"' the use of this patients with monocular FHC associated with procedure seems advisable, especially in monocular ipsilateral Horner's syndrome and complicated by cases. glaucoma. The diagnosis of FHC was based on the The most serious in FHC remains the presence of the above mentioned features of the development of glaucoma. There has been a statistic- condition. The diagnosis of Horner's syndrome was ally significant increase in the incidence of this based on the presence of blepharoptosis and miosis complication over the last 30 years. Whether the and the failure of the affected pupil to respond to 4% increase is merely an expression of improved diag- cocaine, whereas the opposite pupil dilated briskly. nostic methods and better attention or is due to In every case Horner's syndrome was considered to indiscriminate employment of topical steroids be of congenital origin, as a 'smaller' eye had been remains uncertain. noted since early childhood. The cause of glaucoma in FHC is poorly under- Cyclitis was the presenting sign of FHC in three stood. Huber3 considered the main cause of ocular patients (cases 2, 4, and 5) followed by iris hypo- hypertension to be an increase of the outflow resist- chromia. In the two other patients (cases 1 and 3) ance located in the trabeculum. Chandler and Grant'9 heterochromia associated with blepharoptosis was stated that rubeosis of the iris in the anterior chamber the first apparent finding of the syndrome, occurring angle induces the development of chronic secondary during youth and preceding other signs of uveitis by glaucoma. 20 to 30 years. In this regard O'Connor'" confirmed In the current series all five patients with unilateral that a significant number of patients with FHC have FHC had ipsilateral ocular hypertension resembling iris heterochromia since birth or early childhood. chronic open angle glaucoma in its course and

We believe that the detection of a previous symptomatology. One patient (case 3) presented http://bjo.bmj.com/ ipsilateral Horner's syndrome, as in cases 1 and 3, with phakolytic glaucoma at the time of initial diag- suggests the possibility that sympathetic damage nosis, but after the cataract extraction extensive exerts a trophic influence on the development of iris damage to the optic disc indicated also long-standing hypochromia and perhaps mediates other changes in open angle glaucoma. The onset and duration of FHC. In cases 2, 4, and 5 both immunological and/or glaucoma varied: in one of the patients (case 4) sympathetic mechanisms may be taken into con- glaucoma became evident concurrently with the

sideration. In this connection Calmettes and associ- appearance of cyclitis, while it was only a subsequent on October 2, 2021 by guest. Protected copyright. ates'4 reported a remarkable case in which Horner's development in the remaining four patients. All syndrome following stellate ganglionectomy and patients developed glaucoma before cataract extrac- FHC developed consecutively in the same eye. tion. Cataract was a major problem affecting all five There is no general agreement on the prognosis of patients in the current series: four patients developed glaucoma in FHC, and most authors report their posterior subcapsular cataract within four to 20 years conclusions on cases with a short control period. after the first manifestation of FHC; in one patient Some workers72" claimed a favourable outlook when (case 5) cataract was detected very early in the course the glaucoma was treated early. Other studies4"' of the disease. Four patients underwent uneventful suggest that glaucoma usually becomes refractory cataract extraction (three intracapsular and one to medical treatment. In the series reported by extracapsular) with prompt improvement in vision. Liesegang,8 the prognosis was poorer than previously In our experience the prognosis for cataract extrac- reported, although the author demonstrated success tion in FHC is fair and the operation is no more likely in controlling IOP by combined medical and surgical to be complicated than an~' routine . therapy in 21 of 32 patients. The cyclitis was not worse after than before the In the current series maximum medical therapy operation. This confirms the good prognosis noted by (two topical agents with or without a carbonic Br J Ophthalmol: first published as 10.1136/bjo.71.11.844 on 1 November 1987. Downloaded from

848 Lucian S Regenbogen and Nava Naveh-Floman

anhydrase inhibitor) and cataract extraction were significant reduction of IOP in 21 patients with third unsuccessful in controlling the IOP. Therefore anti- nerve Horner's syndrome. glaucomatous surgery was performed in all cases: Because of the rarity of the clinical reports associ- three patients (cases 1, 2, and 5) underwent trabecu- ating Horner's syndrome and glaucoma in the same lectomy, one patient (case 3) cyclodialysis, and one eye, it is difficult to speculate on their relation. patient (case 4) cyclodialysis followed by a Scheie However, Julien and Vincendeaul reported a case of filtering operation. None of these procedures, FHC complicated by glaucoma that showed homo- though performed correctly, presented a well formed lateral sympathetic injury after high dosage of functioning conjunctival bleb. Hyphaema was fre- ingestion. Weinstein and Laugham27 quent, and immediate postoperative complications described a patient with congenital Horner's syn- and extensive rubeosis developed in one patient (case drome in whom bilateral open glaucoma was 5) a few months after . In all cases detected at the age of 57 years. Brazier28 reported a surgical procedures resulted in a short-term hypoten- case of bilateral cervical sympathectomy associated sive effect followed by intractable ocular hyperten- with unilateral Horner's syndrome in which the IOP sion. In some of these patients the vascular accidents was normal in the eye with Horner's syndrome, but appear to have compromised the surgical result. ocular hypertension (in the presence of normal visual The cases in our study were selected out of a large field and optic disc) was disclosed in the contralateral group of 56 patients with FHC who were under eye. The author suggested that the normal IOP in the long-term observation at the same period. Eight eye with Horner's syndrome, and the normal visual additional cases were also complicated by glaucoma field and optic disc in the fellow eye, might be due to but were not associated with Horner's syndrome. Of some antiglaucomatous 'protective' mechanism pro- these cases (two of them in the aphakic eye), the IOP duced by the sympathetic denervation. In view of the could be kept under control with medical treatment hypotensive effects of sympathetic lesions on ocular in only one patient. Though the number of cases is dynamics23 I one is surprised that, in cases with FHC, small and statistically insignificant, it appears that in the associated Horner's syndrome in the ipsilateral more than 90% of patients the glaucoma, if the eye had no prophylactic, or at least, alleviating follow-up period is prolonged, becomes completely influence on the complicating glaucoma. refractory to any form of therapy and is eventually In the cases described here the mechanism of the cause of loss of useful vision. In this matter our the interaction between Horner's syndrome and experience is different from all statistics showing a glaucoma may have several possible causes. First, the better prognosis. occurrence of these two conditions was entirely No IOP abnormalities were detected in the unin- independent and simply coincidental. A second volved eye of patients in the present series. A possibility might be that Horner's syndrome is, if not provocative topical dexamethasone test was carried responsible for the glaucoma, then at least an aggra- http://bjo.bmj.com/ out in these eyes; only one fellow eye reacted with a vating factor. This is unlikely, because there is no significant rise in IOP and was classified as an clinical or experimental evidence that the IOP can intermediate steroid responder. rise as a result of ocular sympathetic denervation in The remarkable combination of Horner's syn- humans. A third possibility is that Horner's syn- drome with glaucoma and their interaction seems drome preceded the development of the cyclitis and inconsistent with what had been expected in such glaucoma by many years and might have been

cases. The relationship between Horner's syndrome associated with normal or hypotensive IOP before on October 2, 2021 by guest. Protected copyright. and IOP has been studied both in animal experiments and in the first stages of the FHC; later, with the and by clinical observations in patients who have aggravation of cyclitis, the augmented protein levels suffered sympathetic denervation. Experimental in the anterior chamber produced inflammatory studies, mainly in rabbits2' and cats,22 produced a damage to the trabeculum, overcoming the eventual short-term reduction of IOP following sympathec- ocular hypotensive effect of Horner's syndrome. This tomy; long-term effects appear to have been variable possibility seems to be the most satisfactory explana- or absent. tion. Cervical sympathectomy, by excision of the A long follow-up of patients with FHC and superior cervical ganglion, was used for the treat- Horner's syndrome illustrates the therapeutic diffi- ment of chronic simple glaucoma at the turn of the culties encountered when this peculiar combination century.2324 Swegmark25 studied aqueous dynamics in is complicated by glaucoma. The reason for the patients with unilateral Homer's syndrome and con- complete resistance of ocular hypertension to cluded that sympathetic denervation reduced medical and surgical therapy in such cases is not aqueous production and thus IOP in the ipsilateral clear. eye. Wentworth and Brubanker26 found a statistically Additional studies are necessary to evaluate the Br J Ophthalmol: first published as 10.1136/bjo.71.11.844 on 1 November 1987. Downloaded from

Glaucoma in Fuchs' heterochromic cyclitis associated with congenital Horner's syndrome 849 incidence of sympathetic nervous damage in patients d'heterochromie de Fuchs et de syndrome de Claude Bernard- Horner. Rev Oto-Neuro-Ophthalmnol 1953; 25: with FHC and to perceive its effect on the outcome of 399-40(X. 15 Smith RE, O'Connor GR. Cataract extraction in Fuchs' syn- the glaucoma. drome. Arch Ophthalmol 1974; 91: 39-41. 16 Ward DM, Hart CT. Complicated cataract extraction in Fuchs' References hetcrochromic uveitis. BrJ Ophthalmol 1967; 51: 530-8. 17 Norn MS. Cataract extraction in Fuchs' heterochromia. Acta I Fuchs E. Ueber Komplikationen der Hcterochromie. Z Ophthalmol (Kbh) 1968; 46: 685-99. Augenheilkd 1906; 15: 191-212. 18 Hart CT, Ward DM. Intraocular pressure in Fuchs' hetero- 2 Franceschetti A. Heterochromic cyclitis (Fuchs' syndrome). Am chromic uveitis. BrJ Ophthalmol 1967; 51: 739-43. J Ophthalmol 1955; 39: 50-8. 19 Chandler PA, Grant WM. Lectures on glaucoma. Philadelphia: 3 Huber A. Das Glaucom bei komplizierten Hetcrochromie Lea and Febiger, 1965. Fuchs. Ophthalmologica 1961; 142: 66-115. 20 Velicky J. Vyskyt a diagnostika glaucomu pri komplikovane 4 Kimura SJ, Hogan MJ, Thygcson P. Fuchs' syndrome of heterocrommi. Cesk Oftalmol 1964; 20: 298-301. heterochromic cyclitis. Arch Ophthalmol 1955; 54: 179-86. 21 Sears ML, Barany EH. Outflow resistance and adrenergic 5 Julien RG, Vincendeau J. Heterochromie de Fuchs, glaucome et mechanism. Arch Ophthalmol 1960; 64: 839-48. sympathectomimetiques. Bull Soc Ophthalmol Fr 1956: 187-8. 22 Laugham ME, Taylor CB. The influence of pre- and post- 6 Dernouchamps JP. Fuchs' Heterochromic cyclitis. Acta ganglionic section of the cervical sympathetic on the intraocular Ophthalmol (Kbh) 1984; 163 (suppl): 49. pressure of rabbits and cats. J Physiol (Lond) 1960; 152: 437-46. 7 Lemke L. Das Glaucoma bei Heterochromiecyclitis. Ophthal- 23 Abadie C. Nature et traitement du glaucome. Arch Ophtalmol mologica 1966; 151: 457-64. (Paris) 1899; 19: 94-101. 8 Liesegang TJ. Clinical features and prognosis in Fuchs' uveitis 24 lonesco T. Die Resection des Halssympaticus in der Behandlung syndrome. Arch Ophthalmol 1982; 100: 1622-6. des Glaukoma. Wien Klin Wochenschr 1899; 12: 483-6. 9 O'Connor GR. Heterochromic iridocyclitis. Trans Ophthalmnol 25 Swegmark G. dynamics in Horner's syn- Soc UK 1968; 104: 219-30. drome. Trans Ophthalmol Soc UK 1963; 83: 255-61. 10 O'Connor GR. Heterocromic iridocyclitis. Doyne lecture. Trans 26 Wentworth WO, Brubanker RF. Aqueous humor dynamics in a Ophthalmol Soc UK 1985; 104: 219-31. series of patients with third neuron Horner's syndrome. Am J 11 de Abreu MT, Belfort R, Hirata P. Fuchs' heterochromic cyclitis Ophthalmol 1981; 92: 407-15. and ocular toxoplasmosis. Am J Ophthalmol 1982; 93: 739-44. 27 Weinstein GM, Laugham ME. Horner's syndrome and 12 Arffa RC, Schlaegel Jr TF. Chorioretinal scars in Fuchs' hetero- glaucoma. Arch Ophthalmol 1969; 82: 483-6. chromic iridocyclitis. Arch Ophthalmol 1984; 102: 1153-5. 28 Brazier DJ. Ocular sympathetic denervation associated with 13 Passow A. Hornersyndrom, Heterochromie, und Status dystro- ocular hypertension: a case report. Br J Ophthalmol 1983; 67: phicus, ein Symptomkomplex. Arch Augenheilkd 1933; 197: 297-301. 1-51. 14 Calmettes ML, Deodati R, Amalric P. Un cas d'association Acceptedforpublication 31 October 1986. http://bjo.bmj.com/ on October 2, 2021 by guest. Protected copyright.