Ординатура / Офтальмология / Английские материалы / Veterinary Ocular Pathology A Comparative Review_Dubielzig, Ketring, McLellan_2010

*

Figure 12.15  Extension of meningioma from the calvarium into the optic nerve. Gross photograph showing the brain from a dog with a ventral meningioma (*) extending down the optic nerve meninges on both sides (arrows).

Morphologic features of optic nerve head medulloepithelioma in horses include:

•Medulloepithelioma is characterized by the presence of thick tubular rosettes, with a complex cellular lining that is several cells thick and a distinct lumen

•More simple Flexner–Wintersteiner or Homer–Wright rosettes may also be identified in medulloepithelioma but they are not the defining feature

•The neoplasm may also arise from the neuroepithelium of the anterior uvea or, theoretically, the neural retina (see Chapters 9 and 11 for more detailed discussion of the morphologic and immunohistochemical features of medulloepithelioma).

Proliferative optic neuropathy in horses

•These unilateral, benign lesions of the optic nerve head are not uncommon in older horses and do not appear to have a significant impact on vision

■Due to their benign nature, and appearance in older animals, enucleation and submission to a pathology service is seldom considered and there are no examples in the COPLOW collection

•The clinical appearance is of a well-defined, pedunculated white mass protruding from the optic nerve head into the vitreous cavity, that appears static or very slowly progressive

•Published reports have presented similar morphological features, but alternate diagnoses for proliferative optic neuropathy

■Large, thin-walled cells with foamy cytoplasm have been described, that were thought to contain lipid

•The lesion should be distinguished from traumatic, exudative optic neuropathy which is associated with loss of vision, and from glioma/astrocytoma (see above).

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Figure 12.16  Optic nerve glioma, fundus. Saint Bernard, 5 years old: the white elevation on the disc margin was diagnosed as a glioma. It involved the optic nerve and optic chiasm in this blind dog.

Comparative Comments

•The two major tumors of the human optic nerve are glioma and meningioma, both of which most commonly affect the retrobulbar portion of the optic nerve

•The most common type of astrocytoma is the juvenile pilocytic astrocytoma

–These are usually low-grade tumors that occur in the first decade of life

•More than 10% of human patients with optic nerve astrocytomas have neurofibromatosis (NF1)

•Meningiomas of the optic nerve may occur at any age but predominate in middle age and in females

–They may be unilateral or bilateral and are frequently associated with independent meningiomas within the cranium

–Tumor growth is slow, and the tumor may invade the optic nerve itself and the eye

–Microscopically, optic nerve meningiomas are usually of the meningotheliomatous type, with compact masses of protoplasm-rich cells arranged in whorls. Laminated and calcareous concretions (psammoma bodies) are common

•Other less common tumors that principally affect the optic nerve head are melanocytoma, peripapillary choroidal melanoma, pigment epithelial neoplasms, and hemangioma. Leukemic or lymphomatous infiltration of the optic nerve is occasionally seen. Local extension into the optic nerve from retinoblastoma is common, and carcinomatous metastases to the optic nerve have also been reported.

Introduction and normal anatomy

Brooks, D.E., Blocker, T.L., Samuelson, D.A.,

et al., 1995. Histomorphometry of the optic nerves of normal horses and horses with glaucoma. Vet. Comp. Ophthalmol. 5, 193–210.

Brooks, D.E., Strubbe, D.T., Kubilis, P.S., et al., 1995. Histomorphometry of the optic nerves of normal dogs and dogs with hereditary glaucoma. Exp. Eye. Res. 60, 71–89.

Brooks, D.E., Komaromy, A.M., Kallberg, M.E., 1999. Comparative retinal ganglion cell and optic nerve morphology. Vet. Ophthalmol.

2, 3–11.

Miyake, E., Imagawa, T., Uehara, M., 2004. Fine structure of the retino-optic nerve junction in dogs. J. Vet. Med. Sci. 66, 1549–1554.

Radius, R.L., Bade, B., 1982. The anatomy at the lamina cribrosa in the normal cat eye. Arch. Ophthalmol. 100, 1658–1660.

Ng, A.Y., Stone, J., 1982. The optic nerve of the cat: Appearance and loss of axons during normal development. Brain Res. 281, 263–271.

Brooks, D.E., 2007. Diseases of the canine optic nerve. In: Gelatt, K.N. (Ed.), Veterinary ophthalmology, 4th edn. Blackwell, Oxford, pp. 1059–1092.

Optic nerve hypoplasia and achiasma

Ernest, J.T., 1976. Bilateral optic nerve hypoplasia in a pup. J. Am. Vet. Med. Assoc. 168, 125–128.

Kern, T.J., Riis, R.C., 1981. Optic nerve hypoplasia in three Miniature poodles. J. Am. Vet. Med. Assoc. 178, 49–54.

da Silva, E.G., Dubielzig, R., Zarfoss, M.K., et al., 2008. Distinctive histopathologic features of canine optic nerve hypoplasia and aplasia: A retrospective review of 13 cases. Vet.

Ophthalmol. 11, 23–29.

Negishi, H., Hoshiya, T., Tsuda, Y., et al., 2008. Unilateral optical nerve hypoplasia in a Beagle dog. Lab. Anim. 42, 383–388.

Hogan, D., Williams, R.W., 1995. Analysis of the retinas and optic nerves of a chiasmatic Belgian sheepdogs. J. Comp. Neurol. 352, 367–380.

Optic disc coloboma

Barnett, K.C., Knight, G.C., 1969. Persistent pupillary membrane and associated defects in the Basenji. Vet. Rec. 85, 242– 248.

Gelatt, K.N., Huston, K., Leipold, H.W., 1969. Ocular anomalies of incomplete albino cattle: Ophthalmoscopic examination. Am. J. Vet. Res. 30, 1313–1316.

Barnett, K.C., Ogien, A.L., 1972. Ocular colobomata in Charolais cattle. Vet. Rec. 91, 592.

Papilledema

Hayreh, S.S., 1977. Optic disc edema in raised intracranial pressure. VI. Associated visual disturbances and their pathogenesis. Arch. Ophthalmol. 95, 1566–1579.

Tso, M.O., Hayreh, S.S., 1977. Optic disc edema in raised intracranial pressure. III. A pathologic study of experimental papilledema. Arch. Ophthalmol. 95, 1448–1457.

Tso, M.O., Hayreh, S.S., 1977. Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema. Arch. Ophthalmol. 95, 1458–1462.

Wirtschafter, J.D., 1983. Optic nerve axons and acquired alterations in the appearance of the optic disc. Trans. Am. Ophthalmol. Soc. 81, 1034–1091.

Palmer, A.C., Malinowski, W., Barnett, K.C., 1974. Clinical signs including papilloedema

associated with brain tumours in twenty-one dogs. J. Small Anim. Pract. 15, 359–386.

Morgan, W.H., Chauhan, B.C., Yu, D.-Y., et al., 2002. Optic disc movement with variations in intraocular and cerebrospinal fluid pressure. Invest. Ophthalmol. Vis. Sci. 43, 3236–3242.

Vitamin A deficiency

Hayes, K.C., Nielsen, S.W., Eaton, H.D., 1968. Pathogenesis of the optic nerve lesion in vitamin a-deficient calves. Arch. Ophthalmol. 80, 777–787.

Barnett, K.C., Palmer, A.C., Abrams, J.T., et al., 1970. Ocular changes associated with hypovitaminosis a in cattle. Br. Vet. J. 126, 561–573.

Booth, A., Reid, M., Clark, T., 1987. Hypovitaminosis a in feedlot cattle. J. Am. Vet. Med. Assoc. 190, 1305–1308.

Optic nerve trauma

Martin, L., Kaswan, R., Chapman, W., 1986. Four cases of traumatic optic nerve blindness in the horse. Equine. Vet. J. 18, 133–137.

Rebhun, W.C., 1992. Retinal and optic nerve diseases. Vet. Clin. North Am.: Equine Pract. 8, 587–608.

Gelatt, K.N., 1979. Neuroretinopathy in horses. J. Equine. Med. Surg. 3, 91–96.

Hardy, J., Robertson, J.T., Wilkie, D.A., 1990. Ischemic optic neuropathy and blindness after arterial occlusion for treatment of guttural pouch mycosis in two horses. J. Am. Vet. Med. Assoc. 196, 1631–1634.

Gilger, B.C., Hamilton, H.L., Wilkie, D.A., et al., 1995. Traumatic ocular proptoses in dogs and cats: 84 cases (1980–1993). J. Am. Vet. Med. Assoc. 206, 1186–1190.

Stiles, J., Buyukmihci, N.C., Hacker, D.V., et al., 1993. Blindness from damage to optic chiasm. J. Am. Vet. Med. Assoc. 202, 1192.

Optic neuritis

Fischer, C.A., Jones, G.T., 1972. Optic neuritis in dogs. J. Am. Vet. Med. Assoc. 160, 68–79.

Nafe, L.A., Carter, J.D., 1981. Canine optic neuritis. Comp. Contin. Edu. Pract. Vet. 3, 978–981.

Nell, B., 2008. Optic neuritis in dogs and cats. Vet. Clin. North Am. Small Anim. Pract. 38, 403–415, viii.

Fischer, C.A., Liu, S.-K., 1971. Neuroophthalmologic manifestations of primary reticulosis of the central nervous system in a dog. J. Am. Vet. Med. Assoc. 158, 1240– 1248.

Smith, J.S., de Lahunta, A., Riis, R.C., 1977. Reticulosis of the visual system in a dog. J. Small Anim. Pract. 18, 643–652.

Cordy, D.R., 1979. Canine granulomatous meningoencephalomyelitis. Vet. Pathol. 16, 325–333.

Thomas, J.B., Eger, C., 1989. Granulomatous meningoencephalomyelitis in 21 dogs. J. Small Anim. Pract. 30, 287–293.

Munana, K.R., Luttgen, P.J., 1998. Prognostic factors for dogs with granulomatous meningoencephalomyelitis: 42 cases (1982–1996). J. Am. Vet. Med. Assoc. 212, 1902–1906.

Cherubini, G.B., Platt, S.R., Anderson, T.J., et al., 2006. Characteristics of magnetic resonance images of granulomatous meningoencephalomyelitis in 11 dogs. Vet. Rec. 159, 110–115.

Adamo, P.F., Adams, W.M., Steinberg, H., 2007. Granulomatous meningoencephalomyelitis in dogs. Compend Contin. Edu. Vet. 29, 678–690.

Jubb, K.V., Saunders, L.Z., Coates, H.V., 1957. The intraocular lesions of canine distemper. J. Comp. Pathol. 67, 21–29.

Vandevelde, M., Higgins, R.J., Kristensen, B.,

et al., 1982. Demyelination in experimental canine distemper virus infection: Immunological, pathologic, and immunohistological studies. Acta. Neuropathol. 56, 285–293.

Vandevelde, M., Zurbriggen, A., 1995. The neurobiology of canine distemper virus infection. Vet. Microbiol. 44, 271–280.

Vandevelde, M., Zurbriggen, A., 2005. Demyelination in canine distemper virus infection: A review. Acta. Neuropathol. 109, 56–68.

Optic nerve neoplasia

Buyukmihci, N.C., Chancellor, K.E., Bouldin, T.W., 2002. Optic nerve neoplasia. In: Peiffer, R.L., Jr., Simons, K.B. (Eds), Ocular tumors in animals and humans. Iowa State Press, Ames, Iowa, pp. 289–304.

Barnett, K.C., Singleton, W.B., 1967. Retrobulbar and chiasmal meningioma in a dog. J. Small Anim. Pract. 8, 391–394.

Langham, R.F., Bennett, R.R., Zydeck, F.A., 1971. Primary retrobulbar meningioma of the optic nerve of a dog. J. Am. Vet. Med. Assoc. 159, 175–176.

Buyukmihci, N., 1977. Orbital meningioma with intraocular invasion in a dog. Histology and ultrastructure. Vet. Pathol. 14, 521–523.

Dugan, S.J., Schwarz, P.D., Roberts, S.M., et al., 1993. Primary optic nerve meningioma and pulmonary metastasis in a dog. J. Am. Anim. Hosp. Assoc. 29, 11–16.

Mauldin, E.A., Deehr, A.J., Hertzke, D., et al., 2000. Canine orbital meningiomas:

A review of 22 cases. Vet. Ophthalmol. 3, 11–16.

Perez, V., Vidal, E., Gonzalez, N., et al., 2005. Orbital meningioma with a granular cell component in a dog, with extracranial metastasis. J. Comp. Pathol. 133, 212–217.

Barnhart, K.F., Wojcieszyn, J., Storts, R.W., 2002. Immunohistochemical staining patterns of canine meningiomas and correlation with published immunophenotypes. Vet. Pathol. 39, 311–321.

Montoliu, P., Anor, S., Vidal, E., et al., 2006. Histological and immunohistochemical study of 30 cases of canine meningioma. J. Comp. Pathol. 135, 200–207.

Reis, J.L., Kanamura, C.T., Machado, G.M., et al., 2007. Orbital (retrobulbar) meningioma in a Simmental cow. Vet. Pathol. 44, 504–507.

Yoshitomi, K., Everitt, J.I., Boorman, G.A., 1991. Primary optic nerve meningiomas in F344 rats. Vet. Pathol. 28, 79–81.

Spiess, B.M., Wilcock, B.P., 1987. Glioma of the optic nerve with intraocular and intracranial involvement in a dog. J. Comp. Pathol. 97, 79–84.

Caswell, J., Curtis, C., Gibbs, B., 1999. Astrocytoma arising at the optic disc in a dog. Can. Vet. J. 40, 427–428.

Siso, S., Lorenzo, V., Ferrer, I., et al., 2003. An anaplastic astrocytoma (optic chiasmatichypothalamic glioma) in a dog. Vet. Pathol. 40, 567–569.

Lipsitz, D., Higgins, R.J., Kortz, G.D., et al., 2003. Glioblastoma multiforme: Clinical findings, magnetic resonance imaging, and pathology in five dogs. Vet. Pathol. 40, 659–669.

Naranjo, C., Schobert, C., Dubielzig, R., 2008. Canine ocular gliomas: A retrospective study. Vet. Ophthalmol. 11, 356–362.

Eagle, R.C., Jr., Font, R.L., Swerczek, T.W., 1978. Malignant medulloepithelioma of the optic nerve in a horse. Vet. Pathol. 15, 488–494.

Bistner, S.I., 1974. Medullo-epithelioma of the iris and ciliary body in a horse. Cornell Vet. 64, 588–595.

Knottenbelt, D.C., Hetzel, U., Roberts, V., 2007. Primary intraocular primitive neuroectodermal tumor (retinoblastoma) causing unilateral blindness in a gelding. Vet. Ophthalmol. 10, 348–356.

Riis, R.C., Scherlie, P.H., Rebhun, W.C., 1990. Intraocular medulloepithelioma in a horse. Equine Vet. J. (Suppl 10), 66–68.

Gelatt, K.N., Leipold, H.W., Finocchio, E.J., et al., 1971. Optic disc astrocytoma in a horse. Can. Vet. J. 12, 53–55.

Saunders, L.Z., Bistner, S.I., Rubin, L.F., 1972. Proliferative optic neuropathy in horses. Vet. Pathol. 9, 368–378.

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CHAPTER CONTENTS

General considerations

Structure and function of the normal aqueous outflow pathways

The glaucomas: significance and general principles

Definition

Significance to a mail-in ocular pathology service

Non-specific changes in ocular tissues associated with elevated intraocular pressure

Underlying pathogenesis

Critical events in the pathogenesis of the glaucomas

The canine glaucomas

Goniodysgenesis associated glaucoma (primary glaucoma, acute primary angle-closure glaucoma, primary open-angle closed-cleft glaucoma)

Sequential changes in the drainage angle following acute IOP elevation in goniodysgenesis-related glaucoma

Chronic changes

Sequential changes in the retina following acute IOP elevation in goniodysgenesis-related glaucoma

Chronic changes

Sequential changes in the optic nerve following acute IOP elevation in goniodysgenesis-related glaucoma

Chronic changes

Canine primary open-angle glaucoma (POAG) Lens luxation glaucoma

Neovascular glaucoma

Glaucoma in canine ocular melanosis

Multiple thin-walled iridociliary cysts, pigmentary uveitis in Golden Retrievers

Glaucoma associated with neoplasia in dogs

The feline glaucomas

Some general features of feline glaucoma compared to canine glaucoma

The majority of cases of feline glaucoma are secondary to other ocular disease

Lymphoplasmacytic uveitis

Glaucoma associated with feline diffuse iris melanoma

GENERAL CONSIDERATIONS

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Structure and function of the normal

space and vortex veins. Uveoscleral outflow has been estimated to account for about 3% of aqueous outflow in normal cats, and about 15% of aqueous outflow in normal dogs.

The glaucomas: significance and general principles

Definition

The glaucomas represent a large, diverse group of pressure dependant neurodegenerative disorders, that all result in loss of normal function and integrity of the retinal ganglion cells and their axons in the optic nerve and ultimately lead to loss of vision.

•In veterinary patients, the single most consistently recognized feature of all glaucomas characterized to date is elevation in intraocular pressure (IOP).

Significance to a mail-in ocular pathology service

•Glaucoma leads to loss of vision, with varying degrees of ocular pain or discomfort. Despite advances in medical and surgical therapy, the prognosis for restoration and maintenance of vision remains quite poor. Given this relatively poor prognosis for vision, and that therapy can be costly for control of a disease that is often a source of significant discomfort, glaucoma is a common reason for enucleation and subsequent submission of the globe to a pathology service

•41% of canine submissions to COPLOW have glaucoma as a part of the syndrome

•29% of feline submissions to COPLOW have glaucoma as a part of the syndrome

•Glaucoma is probably under-represented in equine submissions. The condition often goes clinically undiagnosed in horses as tonometry is less frequently performed in this species and the pain of glaucoma is not manifest as acutely as it is in dogs.

Non-specific changes in ocular tissues associated with elevated intraocular pressure (Fig. 13.2)

Many of the changes listed below can represent either a cause or an effect of glaucoma. It is often difficult to determine which, with confidence.

•Cornea and sclera

■Corneal edema

■Descemet’s streaks (Haab’s striae) associated with tears or splits in Descemet’s membrane

■Corneal vascularization

■Scleral atrophy at the limbus

■Thinning, stretching and enlargement of the globe (buphthalmos)

–This is more commonly seen in animals than in humans with glaucoma

–Globe enlargement is more dramatic in young animals and children than in adults

■Equatorial and limbal staphyloma

•Uvea

■Collapse of the ciliary cleft

■Atrophy of the corneoscleral trabecular meshwork

■Iris atrophy

■Ciliary body atrophy

■Decreased choroidal perfusion

•Lens

■Cataract

■Lens subluxation or luxation

•Neurosensory retina

■Loss of retinal ganglion cells (all species)

■Full thickness retinal atrophy and gliosis, dogs only

■Less atrophy of the superior (tapetal retina relative to the inferior (non-tapetal) retina, dogs only

•Optic nerve

■Necrosis is an early feature, followed by malacia, gliosis and the formation of a deep cup. In species other than the dog the development of gliosis and cupping follows a less precipitous course

■In glaucomatous optic neuropathy, there is a loss of large diameter optic nerve axons.

Underlying pathogenesis

It can be challenging for the pathologist to differentiate primary and secondary changes and suggest the underlying pathogenesis, in the absence of an informative clinical history. For example, lens subluxation may lead to, or result from, glaucoma. Consideration of breed predispositions may increase the index of suspicion for either primary or secondary causes of glaucoma.

Critical events in the pathogenesis of the glaucomas

Many of the critical events in the pathogenesis of the glaucomas remain poorly understood including the following:

•The precise mechanism responsible for the control and regulation of intraocular pressure, particularly at the level of aqueous outflow, is incompletely understood in both normal and glaucomatous animals.

Mechanisms for IOP elevation

•To date, no instances of glaucoma related to increased aqueous humor formation have been documented in veterinary glaucoma patients

•The key mechanisms for IOP elevation are therefore:

■Reduction in capacity for aqueous outflow, and/or

■Increase in episcleral venous pressure (i.e. ‘back pressure’)

•Reduction in the capacity for aqueous outflow may be:

■Primary (goniodysgenesis):

–Due to an inherent abnormality in the aqueous outflow pathways

It is worth emphasizing that the cause of increased resistance in the aqueous outflow pathway in goniodysgenesis is not yet known. The possibility that aqueous outflow obstruction might actually prove to be secondary and not primary cannot be discounted

–Primary glaucoma is fairly common in certain breeds of dog

–Primary glaucoma is seldom encountered in other domestic species

■Secondary to other ocular or systemic disease processes, as a relatively frequent complication of:

–Uveitis

–Synechiae

–Pre-iridal fibrovascular membrane

–Cataract

–Lens luxation

–Intraocular neoplasia

–Intraocular hemorrhage

–Retinal detachment

•Increase in episcleral venous pressure may occur:

■In animals with orbital space occupying lesions

■Transiently, as a result of inappropriate restraint restricting jugular blood flow, including tight collars

•Mechanisms for aqueous outflow obstruction:

■Pupil block

–Anterior lens luxation, anterior vitreous prolapse, intumescent cataract and extensive posterior synechiae are all relatively common causes of pupil block glaucoma

–Flow of aqueous humour from the posterior chamber to the anterior chamber is obstructed at the level of pupil and aqueous is therefore unable to exit through the conventional outflow pathways via the irido-corneal angle and ciliary cleft

–Elevation in pressure within the posterior chamber leads to forward displacement of the iris, collapse of the ciliary cleft, narrowing of the irido-corneal angle and a shallow anterior chamber. The anterior chamber may be diffusely shallow, or may vary in depth as in iris bombé.

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■Angle closure

–Secondary angle closure glaucoma may occur as a sequela of pupil block, as the iris is ‘pushed forward’, occluding the opening of the irido-corneal angle. Multiple iridociliary cysts, as sporadically encountered in the Golden Retriever and Great Dane breeds, may also lead to anterior displacement of the ciliary zone of the iris contributing to secondary angle closure

Theoretically, in such cases, it should be possible to ‘open’ the angle during indentation gonioscopy, but as the ciliary cleft collapses, angle closure can become permanent

–Alternatively, the iris may be ‘pulled forward’, as occurs in association with contracture of pre-iridal fibrovascular membranes (PIFVM), in a mechanism that can ultimately lead to extensive peripheral anterior synechiae

–Obstruction of the trabecular meshwork and/or obliteration of the ciliary cleft by cellular infiltrates or debris may lead to the development of glaucoma secondary to neoplasia, uveitis and intraocular hemorrhage

•Clinical and pathological nomenclature: open-angle versus closed-angle

■Traditionally, veterinary ophthalmologists have tended to classify glaucomas clinically, on the basis of gonioscopic findings, as either ‘open-angle’ or ‘closed-angle’. In reality, what we are really referring to is not simply the irido-corneal angle (ICA), but the opening to the ciliary cleft

■In contrast, veterinary pathologists have tended to classify many of the primary glaucomas as ‘open-angle, closed-cleft’. This has led to confusing discrepancies in the clinical and histopathological classification of the canine and feline glaucomas

■Until relatively recently our ability to visualize and clinically characterize the ciliary cleft in vivo was extremely limited. Refined imaging techniques, such as ultrasound biomicroscopy (UBM), with probe frequencies around

50 MHz, and high resolution ultrasonography (HRUS), with probe frequencies around 20 MHz, offer us a greater appreciation for the dynamic changes that take place within the aqueous outflow pathways in our glaucomatous patients. These new technologies should facilitate the harmonization of clinical and pathological classification schemes as well as improve our insight into the pathogenic mechanisms involved in each individual patient

Because of the confusion, in this chapter we will avoid the use of this terminology altogether.

Mechanisms of optic nerve and retinal damage

The mechanisms of optic nerve and retinal damage in the glaucomas remain subject to debate. Proposed mechanisms include the following:

•Elevated intraocular pressure leads to deformation of the optic nerve axons at the lamina cribrosa and the blockage of anterograde and retrograde axonal transport which, in turn, leads to the death of retinal ganglion cells. Cell death is due, at least in part, to an interruption in the supply of neurotrophic factors from the CNS

•Elevated intraocular pressure leads to deformation of the lamina cribrosa, leading to a decrease in vascular perfusion of the optic nerve head microcirculation, that results in a

loss of axonal integrity and subsequent death of retinal ganglion cells

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•Elevated intraocular pressure leads to tissue infarction and subsequent gliosis

•Retinal ganglion cell loss may also be due to the pathologic release of glutamate from within the damaged retina, which initiates the process of apoptosis by a mechanism termed ‘excitotoxicity’

•Decreased choroidal perfusion causes a segmental retinal degeneration affecting both inner and outer retina

•Recent evidence suggests that different mechanisms may be involved in the death of the retinal ganglion cell bodies, axons and dendritic trees.

Mechanisms of retinal and optic nerve degeneration

The relevance of the various proposed mechanisms of retinal and optic nerve degeneration to the spontaneous glaucomas of dogs and cats:

•Any or all of these proposed mechanisms might be in play, depending on the species and also the underlying pathophysiology of the different glaucoma syndromes in dogs and cats

•The pathogenic mechanisms in play, and their relative importance, appear to differ considerably between glaucomatous dogs, cats and humans

■In the dog, the changes in the retina and the optic nerve head suggest that abnormal vascular perfusion and ischemia are major factors in the pathogenesis of optic nerve and retinal damage encountered in glaucoma syndromes.

Severe damage to the inner and outer retina and optic nerve can be observed in dogs at a very acute stage of

disease. In acute congestive canine glaucoma, where IOP is frequently >50 mmHg, there is evidence to support an important role for ischemia in cell death within both the inner and outer retina. Breakdown in the blood-ocular barrier and inflammation may also contribute to retinal degeneration

■In the cat, the retinal disease is more restricted to the ganglion cell layer, and optic nerve necrosis and malacia is less common.

Comparative Comments

As is the case in other animal species, ‘glaucoma’ in human ophthalmology is generally considered a generic term for a common group of ocular diseases that, if untreated, can cause an irreversible loss of visual function. The common underlying factor in all forms of glaucoma is an inappropriate intraocular pressure, which is associated with damage to the retina and optic nerve head.

Glaucoma in humans is usually divided into five main categories:

1.Congenital glaucoma

2.Primary open-angle glaucoma

3.Primary angle-closure glaucoma

4.Secondary open-angle glaucoma

5.Secondary closed-angle glaucoma.

Unlike the situation described with canine and feline glaucoma, in developed countries enucleation is practically never carried out for uncomplicated primary open-angle glaucoma. It is, however, sometimes performed for the secondary types of glaucoma, particularly in cases of tumors, vascular disease, uveitis, and trauma.