Review Article Equine Glaucomas F

EQUINE VETERINARY EDUCATION / AE / JUNE 2010 299

Review Article Equine glaucomas F. Ollivier* and S. Monclin† Animal Eye Doctor, Meylan, and Clinique Vétérinaire Advetia, Paris, France; and †Rutland House Referrals, St. Helens, UK.

Keywords: horse; glaucoma; intraocular pressure; laser; photocyclocoagulation; anti-glaucomatous medications

Summary also been previously reported in Thoroughbred, Arabian and Standardbred foals but is relatively uncommon with no The glaucomas are diseases that lead to the destruction of breed predisposition (Gelatt 1973; Wilcock et al. 1991; retinal ganglion cells and their axons via a number of Barnett 1998; Lassaline and Brooks 2005). Active or mechanisms such as direct pressure damage, hypoxic quiescent iridocyclitis, age (>15 years) and breed and toxic injuries. The aim of this article is to present a (Appaloosas) represent risk factors for development of review of this condition in horses in order to have a glaucoma in horses (Wilcock et al. 1991; Miller et al. 1997; proactive attitude and to enable an early diagnosis to be Wilkie et al. 2001; Brooks and Matthews 2007). made in order to determine the most adequate prophylactic (on predisposed individuals) and therapeutic treatment. Physiology of the aqueous humour

Introduction Aqueous humour fills the anterior and posterior chambers of the anterior segment of the eye and serves to carry The glaucomas are a group of diseases that lead to the nutrients to, and help remove waste from, the avascular destruction of retinal ganglion cells and their axons via a lens and cornea. As aqueous is formed by the ciliary body, number of mechanisms such as direct pressure damage, it accumulates in the posterior chamber and passed, hypoxic and toxic injuries (Wilcock et al. 1991; Wilkie and between the pupil and lens into the anterior chamber. In Gilger 2004; Lassaline and Brooks 2005). These diseases horses, as in many other animal species, its formation have been recognised in several domestic species, occurs via 3 separate processes: active secretion, including the horse and clinical presentations vary widely ultrafiltration and simple diffusion. Active secretion (primary between them. Equine glaucomas are usually slow to process) involves energy and carbonic anhydrase, an progress with discreet signs of pain and insidious loss of enzyme located in the nonpigmented ciliary body vision with an estimated incidence in the USA (Miller et al. epithelium that is constantly recycled. Only a small portion 1997; Wilkie et al. 2001; Brooks and Matthews 2007). of aqueous humour production arises from ultrafiltration of Following a review of the epidemiology and aetiology, this blood present in the ciliary body circulation. There are 2 article will present the physiology of the aqueous humour, main routes that aqueous may follow to exit the eye: the pathogenesis, clinical signs and various treatments for conventional and unconventional outflow pathways equine glaucomas. (Smith et al. 1986; Samuelson et al. 1989; De Geest et al. 1990; Glenwood et al. 2007). The conventional pathway Epidemiology and aetiology makes reference to aqueous outflow via the iridocorneal angle (ICA), which is delimited anteriorly by the peripheral Equine glaucoma usually represents a secondary ocular cornea and perilimbal sclera and posteriorly by the disease similarly to glaucoma in the cat. The initial insult peripheral iris and ciliary body (Fig 2). A stout pectinate that leads to its development is usually uveitis (Fig 1), ligament separates the anterior chamber from the ICA in although intraocular neoplasia, lens luxation and trauma the horse eye, and is visible at the limbus, medially and are also possible causes (Fig 1) (Gelatt 1973; Wilkie et al. laterally (Smith et al. 1986; Samuelson et al. 1989; De Geest 2001). Congenital glaucoma (i.e. goniodysgenesis) has et al. 1990; Barnett et al. 2004; Glenwood et al. 2007). Aqueous humour that exits the eye via the ICA reaches the corneoscleral and uveoscleral trabecular meshworks to *Corresponding author. Email: [email protected] ultimately access venous circulation via the vortex veins.

a) c)

b) d)

Fig 1: Main causes of secondary glaucoma in horses: (a, b) uveitis (fibrin clot and posterior synechiae can lead to secondary glaucoma) (c) intraocular neoplasm, in this case an iris melanoma (masses can interfere with the drainage of the aqueous and lead to glaucoma) (d) lens luxation.

a route of aqueous clearance as prominent as the conventional outflow, whereas the latter is most important in small animals (Smith et al. 1986; Samuelson et al. 1989; De Geest et al. 1990; Barnett et al. 2004; Glenwood et al. 2007). Aqueous formation is balanced by its drainage from the eye and this equilibrium results in an intraocular pressure (IOP). A range of 15–30 mmHg is reported as being physiologically normal in the horse and a measurement above this range leads to the diagnosis of intraocular hypertension (Miller et al. 1990; Dziezyc et al. 1992; van der Woerdt et al. 1995; Knollinger et al. 2005; Lassaline and Brooks 2005). Sustained elevated intraocular hypertension will lead to the death of retinal ganglion cells (RGC) and this is termed glaucoma. However, an eye that suffers from glaucoma may present with no detectable vision loss Fig 2: Iridocorneal angle in the horse: The conventional pathway is during a period of normal IOP. Equally interesting is the fact the aqueous drainage through the iridocorneal angle (ICA). In the horse, a thick pectinate ligament separate the ICA from the that IOP in horses may be as high as 50 mmHg for several anterior chamber and is easily visible medially and laterally at the days with no detectable vision loss, which is unthinkable in limbus. other domestic animals such as dogs and cats. The examiner should be aware that several external factors This pathway is influenced by intraocular pressure. The influence IOP. If tonometry is performed without an unconventional pathway refers to the outflow of aqueous auriculopalpebral nerve block, it may result in a slight humour via the uveoscleral route, through which aqueous is overestimation of the IOP; if it is performed while the horse’s absorbed by the iris, ciliary body and sclera. This route is not head is lower than its heart, it may result in a 32% increase affected by intraocular pressure but by the state of the compared to when it is measured with the head held ciliary body. When the ciliary body is relaxed, outflow is higher; and, inversely, if performed on a horse under the enhanced. Although both pathways are important for effects of a sedative (i.e. xylazine) it may result in a 23–27% aqueous removal, interspecies differences exist. In the decrease in IOP reading (van der Woerdt et al. 1995; Garg horse, the unconventional outflow pathway is thought to be et al. 2005).

Pathogenesis of glaucoma

Glaucoma is not an uncommon ocular disease in horses but unfortunately little is know about the pathogenesis and development of equine glaucoma in comparison with other animal species. When glaucoma is secondary to uveitis, adhesions of the peripheral iris (i.e. peripheral synechiae) (Fig 1b) may lead to the partial closure of the ICA and adhesions of the pupil to the anterior lens surface may impede the free flow of aqueous into the anterior chamber, causing a pupil block glaucoma (Wilcock et al. 1991; Barnett et al. 2004). In addition, preiridal fibrovascular membranes may form and span the iridocorneal angle altering its ability to allow the passage of aqueous humour out of the eye. Debris composed of neoplastic cells; inflammatory cells and/or proteinaceous material may also be deposited in the iridocorneal angle, further blocking the exit of aqueous Fig 3: Optic nerve head ‘cupping’. Enlargement of the optic cupule (Figs 1a,b). Lastly, blockage of the iridocorneal angle is commonly seen in cases of chronic glaucoma due to the reduction of the number of axons, compression of the lamina and may be seen, in association with space occupying lesions enlargement of the scleral canal. These changes at the level of the in the eye (Wilcock et al. 1991; Wilkie et al. 2001; Wilkie lamina and the axons lead to a phenomenon of excavation and Gilger 2004). The obstruction of the pupil or the (cupping) of the optic nerve head. ICA can also be a result of anterior lens luxation and vitreal prolapse, common conditions seen in Appaloosas the processes described above, also affect the equine and Rocky Mountain Horses (Figs 1c,d) (Barnett et al. retina and optic nerve during the development and 2004). These processes, which mostly affect the progression of glaucoma (Wilcock et al. 1991; Brooks et al. conventional outflow, appear to be very relevant in the 1995; Wilkie and Gilger 2004), but more research is needed pathogenesis of secondary glaucoma in equids. to elucidate the pathogenesis of this disease in horses and Interestingly, the presence of a large ICA in the horse and its relationship with equine recurrent uveitis (ERU). the importance of the unconventional outflow in this species may, in part, explain the relative low incidence of Clinical signs glaucoma in this species when compared to dogs and man (Wilcock et al. 1991). Clinical signs of glaucoma in horses can be very subtle as An increase in IOP causes a compressive often only slight pupil dilation and very limited discomfort conformational distortion within the scleral lamina cribrosa may be present. In addition, the IOP variations in this (i.e. site where the RGC leave the retina to enter the optic species can be relatively large. These 2 facts make the nerve) with a collapse of the laminar pores and laminar diagnosis of equine glaucoma difficult to establish and channels such that optic nerve axoplasmic flow is reduced frequently repeating IOP measurements may be necessary and eventually blocked to cause RGC death (Brooks et al. to detect the transient IOP spikes (Miller et al. 1997; 1995, 1999; Chen et al. 2008). Optic nerve head (ONH) cup Lassaline and Brooks 2005). It is also important to note that enlargement is associated with advanced glaucoma in even though this condition is not uncommon in horses, the horse and is termed ‘cupping’ (Fig 3). This is the result of limited information is still available. axonal loss, laminar plate compression, outward bowing of Clinical signs of early glaucoma vary according to the the lamina cribrosa, and a widening of the scleral canal cause of glaucoma and the IOP but can include: afferent (Brooks et al. 1999; Lassaline and Brooks 2005). These pupillary light reflex and visual deficits, mild buphthalmos concomitant laminar and axonal changes leading to the (Fig 4), blepharospasm, generalised mild corneal oedema, ONH cupping are unique to glaucoma and are not closed ICA, deep linear branching corneal ‘band encountered in other optic neuropathies. opacities’ (i.e. thinned areas of Descemet’s membrane), Studies in models of glaucoma have concluded that as pupil dilation and mild iridocyclitis (Fig 4). Some eyes may RGC die, neurotransmitter glutamate is released into the have a subluxated or a luxated lens. In ERU cases, meiosis, extracellular environment, which can cause other retinal posterior synechia and iris bombe might be present (Gelatt cells to die (Brooks et al. 1995, 1999; Chen et al. 2008). In 1973; Miller et al. 1997; Barnett 1998; Wilkie et al. 2001; addition, some cases of primary glaucoma fail to maintain Barnett et al. 2004; Wilkie and Gilger 2004; Lassaline and an adequate blood supply to the optic nerve head and, Brooks 2005; Brooks and Matthews 2007). possibly, other parts of the retina, influencing the Although the iridocyclitis associated with ERU usually progression of the disease even in periods of normotension leads to hypotony due to decreased production of (Brooks et al. 1999; Alyahya et al. 2007). Some, if not all of aqueous humour by the ciliary body, some of these cases

a) c) f)

g) b)

Fig 4: Clinical signs of glaucoma in the horse: Reduced or absent papillary reflexes and menace response, slight buphthalmia (a), blepharospasm, closure of the ICA, diffuse corneal oedema (b, c), presence of linear corneal opacities (c, d, e) (which are thinning of the Descemet’s membrane), mydriasis (b, c) and slight iridocyclitis are the clinical signs commonly observed. Advanced or chronic glaucoma show dense corneal oedema (a, f, g), corneal neovascularisation (g), ulcerative keratitis by exposure, severe buphthalmia, retinal degeneration, optic nerve head cupping, blindness and pain. may present secondary glaucoma if they enter a phase of Treatments for equine glaucoma ocular hypertension (elevated IOP). It is usually not possible to differentiate true glaucoma cases from uveitic ocular Therapy for equine glaucoma aims to preserve vision and hypertension in horses, unless the inflammatory signs are to minimise discomfort. Medical and surgical treatments for really pronounced (such as meiosis, flare, synechiae) but equine glaucoma directed at decreasing the IOP act by both conditions cause RGC death (Lassaline and Brooks reducing the production of aqueous or, more importantly, 2005; Brooks and Matthews 2007). by increasing outflow of aqueous humour. Combinations of Advanced and chronic cases of equine glaucoma drugs and surgery may be necessary to reduce the IOP may develop dense corneal oedema and vascularisation, to an ideal ‘target IOP’ that not only improves vision but ulcerative exposure keratitis leading to ulcerative disease, also is compatible with its preservation. This is achieved buphthalmos retinal degeneration, ONH cupping and by resolving corneal oedema and increasing vascular degeneration, blindness and ocular pain (Fig 4). Although perfusion. An IOP lower than 20 mmHg represents a initially, the equine eye appears to tolerate elevations in reasonable target IOP for this purpose (Lassaline and IOP that would quickly blind a dog, blindness is also the Brooks 2005; Brooks and Matthews 2007). end result in this species (Lassaline and Brooks 2005; Brooks The medical management of equine glaucoma in and Matthews 2007). horses follows very similar guidelines as those in other

a) b)

Fig 5: Medical treatment of glaucoma in the horse. Glaucomatous eye of a horse before (a) and after (b) 6 weeks of medical treatment. species (Fig 5). The objectives are to reduce IOP and, in appear to have any antihypertensive properties so its use is most equine cases, to suppress the iridocyclitis. The initial no longer considered warranted (Mughannam et al. 1999; response to medical therapy in early cases of equine Herring et al. 2000; Lassaline and Brooks 2005; Brooks and glaucoma is usually good but the long-term prognosis for Matthews 2007). vision with medical therapy alone is guarded. Glaucoma in When medical therapy is inadequate, surgery should be Appaloosas in particular is aggressive and difficult to utilised to control IOP and preserve vision. However, surgery control (Lassaline and Brooks 2005; Brooks and Matthews offers the best potential for preserving vision if glaucoma is 2007). detected early (Lassaline and Brooks 2005; Brooks and Aqueous production may be decreased with the Matthews 2007). Surgical therapy is directed toward topical application of a beta-adrenergic blocker such reducing the production of aqueous humour by selectively as 0.5% timolol maleate, which reduces IOP by 17% damaging the ciliary body (i.e. cycloablation) with laser (administered b.i.d. in clinically normal horses), and the energy (i.e. cyclophotocoagulation) and/or increasing topical use of a carbonic anhydrase inhibitors, such as 2% aqueous outflow with the implantation of a gonio-filtration dorzolamide or 1% brinzolamide, which reduces IOP by 10 device (i.e. goinioimplant). Nitrous oxide (i.e. and 21% when administered b.i.d. in clinically normal cyclocryotherapy) may also be used for cycloablation horses, respectively (van Der Woerdt et al. 1998; Willis et al. (Fig 6a) but it is not commonly performed because 2002; Germann et al. 2008). Topical cholinergics, such as of the severe post operative iridocyclitis and short-termed 2% pilocarpine, and prostaglandin analogues such as IOP lowering effects (Frauenfelder and Vestre 1981; 0.005% latanoprost, increase uveoscleral outflow in many Lassaline and Brooks 2005; Brooks and Matthews 2007). mammals by constricting the ciliary muscles and opening Transcleral cyclophotocoagulation (TSCPC) with the use of the trabecular meshworks. However, they seem to have Neodymium:yttrium-aluminium-garnet (Nd : YAG) or diode small effect on the IOP of horses and should be used with laser (Fig 6b) on the other hand, represents a viable surgical great caution as they exacerbate iridocyclitis (van Der alternative for long-term IOP control. However, uveitis and Woerdt et al. 1998; Willis et al. 2001). Systemic carbonic corneal oedema will increase initially following this anhydrase inhibitors such as acetazolamide (2–3 mg/kg procedure and superficial corneal ulcers may develop from bwt per os b.i.d. to q.i.d.), dichlorphenamide (1 mg/kg bwt corneal desensitisation and exposure during surgery b.i.d.), and methazolamide (0.25 mg/kg bwt) can be used (Whigham et al. 1999; Miller et al. 2001; Lassaline and Brooks for short-term IOP reduction in horses (Alberts et al. 2000; 2005; Brooks and Matthews 2007). Recently, a procedure Willis et al. 2001; Lassaline and Brooks 2005). using an endolaser was developed in dogs and has shown Anti-inflammatory therapy to control iridocyclitis interesting results in controlling the IOP in this species: this may include topically administered corticosteroids technique could be used in horses. Gonioimplantation such as prednisolone acetate, or topical nonsteroidal involves bypassing the obstructed ICA and directing the anti-inflammatory drugs (NSAIDs), such as diclofenamic outflow of aqueous humour to the subconjunctival space. acid, as well as systemically administered NSAIDs, The main complication of this surgery is fibrosis of the such as of phenylbutazone and flunixin meglumine, or drainage tube and/or filtration bleb formation, which corticosteroids, such as dexamethasone (Lassaline and reduce the life of the implant. Despite apparent success, Brooks 2005; Brooks and Matthews 2007). the use of this procedure in horses remains anecdotal Although topically applied atropine was once (Lassaline and Brooks 2005; Brooks and Matthews 2007). recommended to treat equine glaucoma, especially in Chronically painful and blind, buphthalmic globes cases with uveitis, it may cause IOP spikes and does not should undergo ciliary body ablation (CBA), be

a) b)

Fig 6: Surgical treatments of glaucoma in horses. Cryocycloablation is one of the ablation techniques but it is rarely utilised as it induces a severe uveitis post operatively and a short control of the intraocular pressure (a). Transcleral photocycloablation is another technique but has transitory side effects (b).

2005; Brooks and Matthews 2007). Enucleation surgery may be recommended for eyes with glaucoma secondary to infection or intraocular tumours and enucleation or evisceration with intrascleral silicone prosthesis (alternative to enucleation) may be recommended for eyes with painful lens luxation, chronic pain and blindness and severe buphthalmia. As with intrascleral silicone implants, intraorbital silicone implants may be offered for cases that undergo enucleation if cosmesis is important, as this minimises the pitting of the skin post surgically (Meek 1988; Lassaline and Brooks 2005; Brooks and Matthews 2007). Glaucomas in horses progress slowly and insidiously, which makes diagnosis difficult and often too late to allow

Fig 7: A salvage procedure in glaucomatous eye. The chemical optimal treatment. However, diagnostic techniques have ciliary body ablation. Chemical destruction of the ciliary body is improved greatly in recent years, as have the therapeutic recommended when the eye is blind but the pressure is still not techniques and the aim of this review article is to review controlled with the medical treatment. Picture of an eye 7 days the condition in horses in order to allow an early diagnosis post injection. to be made in order to determine the most adequate prophylactic (on predisposed individuals) and therapeutic enucleated or have an intrascleral prosthesis implanted treatment. (Lassaline and Brooks 2005; Brooks and Matthews 2007). Chemical ablation of the ciliary body (CBA) may References be recommended for a blind eye with medically uncontrolled IOP. This consists of an injection into the Alberts, M.K., Clarke, C.R., MacAllister, C.G. and Homer, L.M. (2000) Pharmacokinetics of acetazolimide after intravenous and oral vitreous of gentamycin for i.v. use (25–40 mg with 1 mg administration in horses. Am. J. vet. Res. 61, 965-968. dexamethasone), which induces a permanent decrease Alyahya, K., Chen, C.T. and Mangan, B.G. (2007) Microvessel loss, of aqueous humour production and results in varying vascular damage and glutamate redistribution in the retinas of dogs degrees of pain reduction (Fig 7). The surgeon should be with primary glaucoma. Vet. Ophthalmol. 1, 70-77. aware that chemical ablation of the ciliary body may also Barnett, K.C. (1998) Bupthalmos in a Thoroughbred foal. Equine vet. J. result in a marked reduction of aqueous humour followed 20, 132-135. by phthisis bulbi. A single injection is typically sufficient to Barnett, K.C., Crispin, S.M., Lavach, J.D. and Matthews, A.G. (2004) Anterior chamber, aqueous and glaucoma. In: Equine achieve the desired result although in some cases a Ophthalmology. An Atlas and Text, 2nd edn., W.B. Saunders, second injection may be necessary (Lassaline and Brooks London. pp 149-163.

Brooks, D.E. and Matthews, A.G. (2007) Equine ophthalmology. Miller, T.R., Brooks, D.E., Smith, P.J. and Sapienza, J.S. (1997) Equine Veterinary Ophthalmology, 4th edn., Ed: K.N. Gelatt, W.B. Saunders, glaucoma: clinical findings and response to treatment in 14 horses. Philadelphia. pp 1237-1243. Vet. Comp. Ophthalmol. 5, 170-182. Brooks, D.E., Blocker, T.L. and Samuelson, D.A. (1995) Histomorphometry Miller, P.E., Pickett, J.P. and Gilger, L.J. (1990) Evaluation of two of the optic nerves of normal horses and horses with glaucoma. Vet. applanation tonometers in horses. Am. J. vet. Res. 51, 935-937. Comp. Ophthalmol. 5, 193-210. Miller, T.L., Willis, A.M., Wilkie, D.A., Hoshaw-Woodard, S. and Stanley, J.R. Brooks, D.E., Komaromy, A.M. and Kallberg, M.E. (1999) Comparative (2001) Description of ciliary body anatomy and identification of optic nerve physiology: implications for glaucoma, neuroprotection sites for transscleral cyclophotocoagulation in the equine eye. Vet. and neuroregeneration. Vet. Ophthalmol. 2, 13-25. Ophthalmol. 4, 183-190. Chen, C.T., Alyahya, K. and Gionfrido, J.R. (2008) Loss of glutamine Mughannam, A.J., Buyukmihci, N.C. and Kass, P.H. (1999) Effect of synthetase immunoreactivity from the retina in canine primary topical atropine on intraocular pressure and pupil diameter in the glaucoma. Vet. Ophthalmol. 3, 150-157. normal horse eye. Vet. Ophthalmol. 2, 213-215. De Geest, J.P., Lauwers, H. and Simoens, P. (1990) The morphology of Samuelson, D.A., Smith, P.J. and Brooks, D.E. (1989) Morphologic the equine iridocorneal angle: a light and scanning electron features of the aqueous humor drainage pathway in horses. Am. J. microscopic study. Equine vet. J., Suppl. 3, 30-35. vet. Res. 50, 720-727. Dziezyc, J., Millichamp, N.J. and Smith, W.B. (1992) Comparison of Smith, P.J., Samuelson, D.A., Brooks, D.E. and Whitley, R.D. (1986) applanation tonometers in dogs and horses. J. Am. vet. med. Ass. Unconventional aqueous humor outflow of microspheres perfused 201, 430-433. into the equine eye. Am. J. vet. Res. 47, 2445-2453. Frauenfelder, H.C. and Vestre, W.A. (1981) Cryosurgical treatment van der Woerdt, A., Gilger, B.C., Wilkie, D.A. and Strauch, S.M. (1995) of glaucoma in a horse. Vet. Med. small anim. Clin. 76, 183- Effect of auriculo-palpebral nerve block and intravenous 186. administration of xylazine on intraocular pressure and corneal thickness in horses. Am. J. vet. Res. 56, 155-158. Garg, C.D., Ying, G.S., Liu, C. and Komoraromy, A.M. (2005) The effect van Der Woerdt, A., Gilger, B.C., Wilkie, D.A., Strauch, S.M. and Orczeck, of head position on intraocular pressure in horses. Abstract. In: American College of Veterinary Ophthalmologists Annual Meeting, S.M. (1998) Normal variation in, and effect of 2% pilocarpine on, intraocular pressure and pupil size in female horses. Am. J. vet. Res. Nashville. p 46. 59, 1459-1462. Gelatt, K.N. (1973) Glaucoma and lens luxation in a foal. Vet. Med. small Whigham, H.M., Brooks, D.E., Andrew, S.E., Gelatt, K.N., Strubbe, D.T. and anim. Clin. 3, 261. Biros, D.J. (1999) Treatment of equine glaucoma by transscleral Germann, S.E., Matheis, F.L., Rampazzo, A., Burger, D., Roos, M. and neodymium:yttrium aluminum garnet laser cyclophotocoagulation: Spiess, B.M. (2008) Effects of topical administration of 1% a retrospective study of 23 eyes of 16 horses. Vet. Ophthalmol. 2, brinzolamide on intraocular pressure in clinically normal horses. 243-250. Equine vet. J. 40, 662-665. Wilcock, B.P., Brooks, D.E. and Latimer, C.A. (1991) Glaucoma in horses. Glenwood, G.G., Gelatt, K.N. and Esson, D.W. (2007) Physiology of the Vet. Pathol. 28, 74-78. eye. In: Veterinary Ophthalmology, 4th edn., Ed: K.N. Gelatt, W.B. Wilkie, D.A. and Gilger, B.C. (2004) Equine glaucoma. Vet. Clin. N. Am.: Saunders, Philadelphia. pp 149-182. Equine Pract. 20, 381-391. Herring, I.P., Pickett, J.P., Champagne, E.S., Troy, G.C. and Marini, M. Wilkie, D.A., Peckham, E.S. and Paulic, S. (2001) Equine glaucoma and (2000) Effect of topical 1% atropine sulfate on intraocular pressure in diode laser transscleral cyclophotocoagulation: 27 cases. Vet. normal horses. Vet. Ophthalmol. 3, 139-143. Ophthalmol. 4, 294-299. Knollinger, A.M., La Croix, N.C., Barrett, P.M. and Miller, P.E. Willis, A.M., Robbin, T.E., Hoshaw-Woodard, S., Wilkie, D.A. and Schmall, (2005) Evaluation of a rebound tonometer for measuring M.L. (2002) Effect of topical administration of 2% dorzlamide intraocular pressure in dogs and horses. J. Am. vet. med. Ass. 227, hydrochloride or 2% dorzlamide hydrochloride-0.5% timolol maleate 244-248. on intraocular pressure in clinically normal horses. Am. J. vet. Res. 62, Lassaline, M.E. and Brooks, D.E. (2005) Equine glaucoma. Equine 709-713. Ophthalmology , 1st edn., Ed: B.C. Gilger, Elsevier, St Louis. pp Willis, A.M., Diehl, K.A., Hoshaw-Woodard, S., Kobayashi, I., Vitucci, M.P. 323-339. and Schmall, L.M. (2001) Effects of topical administration of 0.005% Meek, L.A. (1988) Intraocular silicone prosthesis in a horse. J. Am. vet. latanoprost solution on eyes of clinically normal horses. Am. J. vet. med. Ass. 193, 343-345. Res. 62, 1945-1951.

Advertisers’ Index

Bayer...... 274 Boehringer Ingleheim ...... 298a, 298b, Cover 3 IDEXX ...... Cover 2 Intervet ...... 266b Luitpold...... 266a Purina ...... 289