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BritishJournalofOphthalmology, 1991,75,31-33 31 in unilateral ophthalmic disease Br J Ophthalmol: first published as 10.1136/bjo.75.1.31 on 1 January 1991. Downloaded from

Russell V Pearson, Geoffrey E Rose

Abstract assessed in a room with uniform illumination of Pupiliary diameters in the affected and moderate intensity (approximately 1000 lux). unaffected eyes of 327 patients with uniocular The patient was instructed to fixate a distant, were assessed during fixation of a non-accommodative target at 3 metres, and the distant target. The mean pupiliary diameters pupillary diameters were assessed by matching were similar in the unaffected eyes in each of with a comparative scale. The scale was held eight diagnostic groups, but were significantly alongside the , care being taken to avoid the different (F=3.84, p<0-001) in the diseased visual axis of the patient. The scale had 'half- eyes. With corneal abrasions (p<0-001), pupil' marks along one edge, with diameter marginal (p<005), and acute anterior incrementsof1 mm, therebypermittingdiameter (p<0-001) the mean pupillary diameter estimates to 0 5 mm gradations. for the affected eye was significantly smaller After recording the assessment ofpupil size, a than that of the unaffected eye. The observed problem orientated history and ophthalmic differences of pupillary diameter probably examination was performed. The colour was reflect the role of neuronal and autocoid also recorded. mechanisms in the unilateral control of pupillary size. Results Three hundred and twenty-seven patients (213 The ocular response to injury comprises a reduc- male, 114 female) were enrolled in the study. In tion in the blood-ocular barrier, an intraocular 317 patients the condition was one ofeight major pressure rise, and miosis.'4 It is probable that diagnostic categories (Table 1), and others (6 the changes in the blood-ocular barrier and male, 4 female) having various conditions, intraocular pressure are due to concentration of namely trauma (5 eyes), stromal keratitis (2 within the eye,24 this being a eyes), corneal abscess (1 eye), chemical injury (1 result of both increased production within45 and eye), and acute angle-closure (1 eye). decreased clearance from" the eye. The miosis, There was a predominance of males over however, is probably caused both by intra- femalesinalldiagnostic groupsexceptepiscleritis cameral accumulation and by (with a similar sex incidence). Dendritic keratitis

substance P acting on the smooth muscle of the and corneal foreign bodies occurred almost http://bjo.bmj.com/ sphincter pupillae, this neuropeptide being exclusively in men (Table 1). released from trigeminal sensory radicals within There was a significant difference between the the iris."' The stimulus for the release of mean ages at presentation (Table 1. One-way substance P is probably depolarisation ofafferent analysis of variance: F7;309=4-92, p<0-001). sensory trigeminal fibres in the and other Patients with subconjunctival haemorrhage were ocular structures, with the efferent path being significantly older than those in each ofthe other mediated through an axonal reflex.'2 Central or seven diagnostic groups - that is, marginal or on September 27, 2021 by guest. Protected copyright. peripheral trigeminal denervation reduces the dendritic keratitis (p<005), corneal foreign accumulation of substance P and the miosis in body, or iritis (p<0-01), and con- response to injury.10 Calcitonin gene-related junctivitis or corneal abrasion (p<0-001). peptide (CGRP) occurs within trigeminal nerve Similarly, those patients with marginal keratitis fibres-'-" and dilates ocular blood vessels. CGRP were significantly older than those with conjunc-. and substance P might act synergistically in tivitis (p<0-01) or corneal abrasion (p<005), mediation of the ocular response to injury.16 17 and those with iritis were significantly older than Miosis within an inflamed eye, as compared to those with (p<0 05). the unaffected fellow eye, is generally recognised In the group overall, the side of involvement among ophthalmologists as frequently being a was similar (162 right, 155 left), though there sign of significant ocular pathology. The actual was some variability between the subgroups. incidence in various diseases would not, how- Likewise, with the exception of episcleritis, the ever, appear to have been recorded. ratio of involvement of blue/grey eyes with In the present report the changes of pupillary respect to brown/green was similar in all the diameter are determined for various diseases groups (Table 1). causing uniocular red eye, and the changes are The average pupillary diameters in the considered in relation to the neuronal and auto- unaffected 'white' eyes in the eight categories Moorfields Eye Hospital, coid mechanisms affecting pupillary diameter in were not significantly different (Table 2, F7;309= London EC1V 2PD a single eye. 1-57). In contrast, for the 'red' eyes there were R V Pearson significant differences between the mean G E Rose various Correspondence to: diameters for the diagnoses F7;309=3-84, Mr G E Rose, Moorfields Eye Patients and methods p

Table 1 Characteristics and diagnosisfor 317 patients with unilateral ophthalmic disease frequency of anisocoria in blue/grey eyes as

Sex Inflamed Iris compared with brown/green eyes with the same Br J Ophthalmol: first published as 10.1136/bjo.75.1.31 on 1 January 1991. Downloaded from Number ratio Age (yr) eye colour diagnosis ranged from 1-0 for subconjunctival of (male/ mean (SD) (rightd (bluel haemorrhage or conjunctivitis to 5-0 for iritis Diagnosis patients female) (range) left) brown) (Table 3). This contrasts with an iris colour Subconjunctival 23 16/7 53-6 (17-9) 10/13 15/8 haemorrhage (2 29) (19-84) (1-88) frequency-ratio of 1 71 for blue/grey eyes with Conjunctivitis 131 75/56 36-3 (14-7) 70/61 83/48 respect to brown/green eyes. (1-34) (9-70) (1-73) Episcleritis 13 6/7 37-6 (13-7) 6/7 5/8 In the 80 eyes with anisocoria, 'red eye smaller' (0 86) (23-67) (0 62) anisocoria occurred in 70 eyes, and the propor- Corneal foreign 16 15/1 38-8 (10-3) 5/11 10/6 body (15-0) (23-59) (1.67) tion was similar in the two groups of iris Corneal 51 35/16 37 0(11-5) 25/26 34/17 colouration (for each ofthe diagnoses - Table 3). abrasion (2.19) (16-62) (2 00) Marginal 31 21/10 44-4 (14-5) 20/11 19/12 The incidence of 'red eye smaller' anisocoria, keratitis (2.10) (19-69) (1.58) without respect to iris colour, ranged from 0% Dendritic 8 8/0 36-8 (16-3) 1/7 5/3 keratitis (-) (20-60) (1.67) (with subconjunctival haemorrhage) to greater Acute Anterior 44 31/13 41-8 (16-8) 25/19 29/15 than 90% (marginal keratitis, iritis, corneal uveitis (2 38) (19-79) (1.94) abrasion, or dendritic ulceration). The prob- Totals 317 207/110 (39 4yr) 162/155 200/117 ability of drawing the incidences as observed, or (1-88) (9-84) (1-71) ones more extreme, is presented in Table 3. In each of the three conditions with significant Table 2 Estimates ofpupillary diameters in each ofeightdiagnostic categories ofpatients with anisocoria the symptoms were ofsimilar duration unilaterally inflamed ('red') eye in those eyes with and those without unequal . With marginal keratitis the mean Number Pupil diameter* of: Difference* (mm) of duration of symptoms in the anisocoric group Diagnosis patients 'white' eye 'red' eye ('white'-'red') was 4-6 days (SD 8-3 days, 10 eyes), whereas Subconjunctival 23 3-89 (0 64) 3-96 (0 67) -0-065 (0-23) those with equal pupils had 3-9 days' mean haemorrhage t= 1-36, p>O I duration (SD 3 1 days, 21 eyes), and, similarly, Conjunctivitis 131 4-31 (1 00) 4-27 (0 48) +0-042 (0 26) t= 1*84, p>005 with corneal abrasion (anisocorics: 2-6, SD 4-4 Episcleritis 13 3-77(1-11) 3-77(1-11) (-) days, 21 eyes; isocorics: 2-3, SD 3-2, days, 30 Corneal foreign 16 3-75 (0 97) 3-63 (0 92) +0-125 (0 34) body t= 1-47, p>0 1 eyes) and with iritis (anisocorics: 5-0, SD 7-2, Corneal 51 4-08(1-14) 3-74(1-05) +0 343(0-51) days, 24 eyes; isocorics: 9-8, SD 15-6, 20 eyes) abrasion t=4-80, p<0001 Marginal 31 4.10(1-29) 3-89(1-22) +0-210(0-51) keratitis t=2-29, p<005 Dendritic 8 3 75 (0-76) 3 25 (0 89) +0 500 (0 66) keratitis t=2-14, p>0.05 Discussion Acute anterior 44 4-10 (0-87) 3 65 (0 84) +0 455 (0 62) In the present investigation a relative miosis, uveitis t=4-87, p<0001 significant in both degree and incidence, was *Mean (standard deviation). present in eyes with corneal abrasion, marginal keratitis, and acute anterioruveitis. This possibly Table 3 The incidence ofanisocoria in each diagnosis and thefrequency ofanisocoria in which reflects the mechanisms involved in the ocular http://bjo.bmj.com/ the pupil is smaller on the affected ('red') side response to injury. Corneal is associated with marked Number(%) of abrasion patients with stimulation of afferent fibres of the' trigeminal anisocoria Number with red eye smaller antsocoria nerve, manifest clinically as extreme pain. In All Blue Brown Significance these eyes it is probable that the miosis is Diagnosis (bluelbrown) eyest eyes eyes (p)* mediated through a trigeminal axon reflex, with on September 27, 2021 by guest. Protected copyright. Subconjunctival 2 (9%) 0/2 0 0 0-48 release of substance P (and possibly CGRP) at haemorrhage (1/1) nerve fibres on the sphincter pupillae. Conjunctivitis 14(11%) 11/14 6 5 0-06 (7/7) With acute anterior uveitis the miosis is Episcleritis 0 (0%) 0 0 0 - probably due to an accumulation of prosta- Corneal foreign 5 (31%) 4/5 3 1 0 37 body (3/2) glandins and other autocoids within the inflamed Corneal 21 (41%) 20/21 13 7 <0-0001 eye.17-'9 The presence of pain with acute anterior abrasion (14/7) Marginal 10(32%) 9/10 6 3 <0 03 uveitis might, however, imply a partial mediation keratitis (7/3) through trigeminal axon reflexes. Similarly, the Dendritic 4(50%) 4/4 3 1 0-13 keratitis (3/1) miosis of marginal keratitis is probably induced Acute anterior 24(55%) 22/24 19 3 <0-0002 by both neuronal and antocoid mechanisms, uveitis (20/4) marginal keratitis being an immune process Two-tail probability ofdrawing observed overall incidence (t) of 'red eye smaller' anisocoria. occurring at a site rich in trigeminal sensory innervation. Subconjunctival haemorrhage, conjunctivitis, subconjunctival haemorrhage (3 96 mm, 23 eyes) and episcleritis did not cause a significant miosis and dendritic keratitis (3 25 mm, 8 eyes; in the present investigation, perhaps because p

smaller area than that with most corneal 5 Bhattacherjee P, Eakins KE. Inhibition of the prostaglandin synthetase systems in ocular tissues by indomethacin. BrJ

abrasions. Moreover, whereas an abrasion Ophihalmol 1974; 50: 227-30. Br J Ophthalmol: first published as 10.1136/bjo.75.1.31 on 1 January 1991. Downloaded from exposes nerve endings, those under a foreign 6 Bito LZ, Salvador EV. Intraocular fluid dynamics. III. The site and mechanism of prostaglandin transfer across the body are not exposed to the external environ- blood-intraocular fluid barriers. Exp Eye Res 1972; 14: ment. The relatively painless nature of corneal 233-41. 7 Bito LZ. The effects of experimental uveitis on anterior uveal foreign bodies, as compared with abrasions, is prostaglandin transport and aqueous humor composition. compatible with a reduced trigeminal afferent Invest Ophthalmol Vis Sci 1974; 13: 959-65. 8 Bito LZ, Wallenstein MC. Transport of prostaglandins across stimulation. The lack ofa significant miosis with the blood-brain and blood-aqueous barriers and the physio- herpetic dendritic keratitis is probably due to logical significance of these absorptive transport processes. Exp Eye Res 1977; 25 (suppl): 229-43. insufficient numbers in this group (eight cases). 9 Bill A, Stjernschantz J, Mandall A, Brodin E, Nilsson G. It is possible, however, that both the absence of Substance P: release on trigeminal nerve stimulation and effects on the eye. Acta PhysiolScand 1979; 106: 371-3. intraocular inflammation and a malfunctioning 10 Butler JM, Powell D, Unger WG. Substance P levels in normal of virus affected trigeminal neurons might and sensorily denervated rabbit eyes. Exp Eye Res 1980; 30: 311-3. reduce the incidence ofmiosis in such eyes. 11 Stjernschantz J, Sears M. Involvement of substance P in the To elucidate further the mechanisms causing antidromic vasodilation and barrier disruption of the rabbit eye. Invest Ophthalmol Vis Sci (ARVO suppl) 1982; 22: 180. miosis in ocular disease it would be of particular 12 Butler JM, Unger WG, Cole DF. Axon reflex in ocular injury: interest to ascertain whether blockage of the sensory mediation of the response of the rabbit eye to laser irradiation ofthe iris. QJ Exp Physiol 1980; 65: 261-72. trigeminal afferent response with topical 13 Terenghi G, Polak JM, Ghatei MA, et al. Distribution and anaesthesia reduces or prevents the miosis in, for origin of calcitonin gene-related peptide (CGRP) immuno- reactivity in the sensory innervation of the mammalian eye. example, patients with corneal abrasion. J CompNeurol 1985; 233: 506-15. Similarly, the use ofantagonists to prostaglandin 14 Stone RA, Kuwayama Y, Terenghi G, Polak JM, Calcitonin gene-related peptide: occurrence in corneal sensory nerves. synthesis might prevent the miosis associated Exp Eye Res 1986; 43: 279-90. with marginal keratitis or acute anterior uveitis, 15 Stone RA, McGlinn AM. Calcitonin gene-related peptide immunoreactive nerves in human and rhesus monkey eyes. this reflecting a role for autocoids in these Invest Ophthalmol VisSci 1988; 29: 305-10. diseases. 16 Wahlstedt C, Beding B, Ekman R, Oksala 0, Stjernschantz J, Hakanson R. Calcitonin gene-related peptide in the eye: release by sensory nerve stimulation and effects associated with neurogenic inflammation. RegulPept 1986; 16: 107-15. 1 Podos SM. Prostaglandins, non-steroidal anti-inflammatory 17 Unger WG, Terenghi G, Ghatei MA, et al. Calcitonin gene- agents and . Trans Am Ophthalmol Soc 1976; 74: related polypeptide as a mediator ofneurogenic ocular injury 637-60. response.J OculPharmacol 1985; 1:189-99. 2 Hal DWR,BontaIL. Prostaglandins and ocular inflammation. 18 Bhattacherjee P. Release of prostaglandin-like substances by Doc Ophthalmol 1977; 44: 435-44. shigella endotoxin and its inhibition by non-steroidal anti- 3 Bhattacherjee P. Prostaglandins and inflammatory reactions in inflammatory compounds. Br J Pharmacol 1975; 54: the eye. Methods Find Exp Clin Pharmacol 1980; 2: 17-31. 489-94. 4 Eakins KE. Prostaglandin and non-prostaglandin breakdown 19 Eakins KE, Whitelocke RAF, Bennett A, Martenet AC. ofthe blood-aqueous barrier. Exp Eye Res 1977; 25 (suppl): Prostagland-like activity in ocular inflammation. Br Med J 483-98. 1972; ii: 452-3. http://bjo.bmj.com/ on September 27, 2021 by guest. Protected copyright.